THE

RESPIRATORY
SYSTEM
 Function
Upper RT/ Conducting Airways Lower RT/Respiratory Zone
▪ Epiglottis – a valve flap; covers
the opening to the larynx during
swallowing
■ Larynx – 9 cartilages
■ Trachea – 16 – 20 cartilages; C-
shape
■ Carina – area where the trachea
divides into two main bronchi
LUNGS LUNG MEMBRANE
soft, spongy, cone-shaped organs;
main organ of respiration
Broncho pulmonary segment
is supplied by tertiary bronchioles
Alveoli/Air sac
300 million in the lungs, arranged in
clusters of 15 to 20.
Type I alveolar cells Visceral pleura – covers the lungs
Type II AC – metabolically active; Parietal pleura – lines the thorax
secretes surfactant Pleural fluid - 5-15 ml.
Type III AC – macrophages which - lubricate the lungs and
ingest foreign matter. thorax
- Helps the visceral and
parietal membrane stick
together
Muscles of Respiration
 Muscles of Respiration

Diaphragm
➢ principal muscle of inspiration
➢ innervated by the phrenic nerve roots, which
arise mainly from C4 but also from C3 and C5.
External intercostal muscles
➢ also aid in inspiration
Scalene muscles and the sternocleidomastoid
muscles
➢ Accessory muscles of inspiration
➢ deep forceful inspiration
Internal intercostal muscles and abdominal muscles
➢ used to increase expiratory effort
Neural Regulation
Respiratory Centers
a. Medulla Oblongata
inspiration center
expiratory center
➢ responsible for the
cyclic pattern of breathing
b. Pons of the brainstem
➢ modifies the output of the medullary
centers.
apnuestic center - prevent medullary
inspiratory neurons from switching off, creating a
prolonged, gasping inspiration.
pneumotaxic center - shorten inspiratory
time and increasing respiratory rate.
Chemoreceptors
➢ Monitor blood levels of
carbon dioxide, oxygen and
pH

Central chemoreceptor(medulla)
- increase in CO2 and H+
Peripheral (carotid and aortic bodies)
- decrease in PaO2
(decreases to about 60 mm Hg)

The primary stimulus for breathing in healthy

individuals is arterial CO2

The secondary stimulus for breathing in healthy

individuals is arterial hypoxemia, which is not clinically
significant until PaO2 is less than 60 mm Hg.
 Lung Receptors

Three Types
1. Stretch receptors
Hering –Breurer reflexes – baroreceptors in lung
tissue detect stretching and send impulses to the
medulla to depress the inspiratory center
2. Irritant receptors
- stimulated by noxious gases, cigarette smoke,
inhaled dust, and cold air
- Initiate periodic sighing and yawning

3. Juxtacapillary or J receptors
- are located in the alveolar wall, close to the
pulmonary capillaries: thought to sense lung congestion
Peripheral Proprioceptors

■ Proprioceptors in muscles, tendons, and joints

and pain receptors in muscles and skin send
stimulatory signals to the medullary
respiratory center
■ Proprioceptors in joints and tendons may be
important in initiating and maintaining
increased ventilation at the beginning of
exercise
HYPOTHALAMUS
-Modifies the output from the medulla
Emotions:
-Anger = increase RR
-Fright = gasp

CEREBRAL CORTEX
-Enables us to voluntarily change breathing
rate or rhythm
-Talking, singing
 NCM 103:
OXYGENATION
Assessment of
Respiratory Status
Assessment of Clients w/ Respiratory Disorders
 History
A. Present Hx
1. Biographic data
2. Chief complaint/presenting problem
 Dyspnea
 Cough
 Sputum production
 Hemoptysis
 Wheezing
 Stridor
 Chest pain
3. Lifestyle
4. Nutrition/diet
Assessment of Clients with Respiratory
Disorders
B. Past medical history
 Childhood / Infectious diseases
 Respiratory immunization
 Major illnesses / hospitalizations
 Medications
 Allergies
C. Family history
D. Psychosocial history and lifestyle
 Occupational or environmental exposure
 Geographic location
 Personal habits

 Years of smoking x packs/day =

pack years

 15 years of smoking x 2 packs/day

= 30 packs years
 WHAT’S UP?
WHAT’S UP?
■ [Where is it? (not applicable)]
■ How does it feel? Does breathing feel tight, gasping, suffocating?
■ Aggravating and alleviating factors? How much activity causes
the SOB? Does anything else aggravate it? What do you do to
lessen your SOB?
■ Timing? When did you first experience SOB? Does it happen
more at any particular time of day or year?
■ Severity? Rate your SOB on a scale of 0 to 10, with 0 being easy
breathing and 10 being the worst shortness of breath you can
imagine.
■ Useful other data? Do you have any other symptoms that occur
along with the shortness of breath?
■ Patient’s perception? What do you think is causing your
shortness of breath?
Physical Examination
Inspection
S/S of respiratory distress
I:E (Inhalation: Expiration) ratio (1:2)
Speech pattern
Chest wall configuration
Chest movement
Fingers and toes
 Normal Findings
Tracheal position

 Midline& straight; directly above

the suprasternal notch.
 The Allen test is a simple
method for assessing
collateral circulation in the
hand. Ensures circulation if
radial artery thrombosis
occurs.

Procedure:
1. Obliterate the radial and ulnar pulses
simultaneously by pressing on both
blood vessels at the wrist.
2. Ask the patient to clench and
unclench his fist until blanching of the
skin occurs
3. Release pressure on ulnar artery
(while still compressing radial artery).
Watch for return of skin color within 15
seconds.
Physical Examination
Palpation

Trachea
Chest wall
Thoracic excursion
Tactile fremitus
Sensation of sound vibrations produced
when the pt speaks.
 Normal Findings

 Vocal / Tactile Fremitus

 Sensation of sound vibrations
produced when the pt speaks.
 Examiner instructs the pt to say
“1,2,3” or “how-now-brown-cow.”
 As these words are spoken, the
examiner feels for the vibrations.
 Abnormal Responses
Increased fremitus
An ↑in vibratory sensation
 = consolidation of the lung caused
by fluid – filled or solid structures,
w/c would transmit the vibrations
better than air filled lungs.
Occurs w/ pneumonia or a tumor of
the lung.
 Abnormal Responses

Decreased fremitus
A ↓ in the vibratory sensation
 = more air than normal is blocked or
trapped in the lungs or pleural
space; vibrations of the spoken
voice are ↓ed.
Occurs w/ emphysema or a
pneumothorax.
Physical Examination
Percussion

Resonance
Hyperresonance
Dullness
Abnormal Responses - Percussion Tones

 Hyperresonance is abnormal sound heard during

percussion in adults.
- It represents air trapping as in obstructive lung
diseases.
 Resonance – over lungs
 Flat – over heavy muscles and bones
 Dullness – heart, liver
 Tympany - stomach
Physical Examination
 Auscultation : Normal breath sounds
 Bronchial (tracheal) – heard over the
manubrium in the large tracheal airways.
High-pitched & loud.
 Bronchovesicular – heard over the
bronchi. Moderate-pitched, w/ moderate-
amplitude.
 Vesicular – heard all over the chest &
heard best in the bases of the lungs. Low-
pitched and soft.
https://www.youtube.com/watch?v=O8OC7EiqBKQ
https://www.youtube.com/watch?v=TlgP8MzlMaw

SEQUENCE
OF CHEST
AUSCULTATION
Abnormal (Adventitious) Cause of Sound Description Associated Disorders
Sound
Moist bubbling sound, Pulmonary edema,
Coarse crackles Fluid in airways
heard bronchitis,
(rales) on inspiration or pneumonia
expiration
Velcro being torn apart, Heart failure, atelectasis
Fine crackles Alveoli popping
heard
(rales) open on
at end of inspiration
inspiration
Narrowed airways Fine high-pitched violins Asthma
Wheezes
mostly on expiration
Airway obstruction Loud crowing noise heard Obstruction from tumor
Stridor
without stethoscope or
foreign body
Sound of leather rubbing Pleurisy, lung cancer,
Pleural friction Pleura rubbing
together, grating pneumonia,
rub together
pleural irritation
Decreased air Faint lung sounds Emphysema,
Diminished
hypoventilation,
movement
obesity, muscular chest
wall
No air movement No sounds heard Pneumothorax,
Absent
pneumonectomy
Adventitious Breath Sounds
Crackles / rales-
 soft, appears during inspiration
- Fine - High-pitched, soft, crackling /
popping sound. (rolling strand of hair
bet. fingers)
- Coarse - Loud / low – pitched,
bubbling, gurgling (sounds like opening Velcro
fastener).

https://www.youtube.com/watch?v=TlgP8MzlMaw
Adventitious Breath Sounds
Wheezes
as a result of narrowed airways,
appears during expiration
- Sibilant rhonchi, High-pitched,
squeaking sound
- Sonorous rhonchi, Low – pitched,
musical snoring, moaning sound
 Voice Sounds
 Egophony
 Say prolonged “e”
 Auscultated as “a” indicating consolidation

 Whispered Pectorilogy
 Whisper “1,2,3”
 Auscultated as muffled 1,2,3
 If the words are distinct, this indicates consolidation

 Bronchophony
 say “ninety-nine”
 consolidation results in increased resonance and
the words are heard clearly.
 Adventitious Breath Sounds

Pleural friction rub – harsh, crackling,

coarse, low-pitches; grating sound.
 Normal Findings
 General appearance
 Appear relaxed; breathing is quiet & easy
w/o apparent effort; facial expressions & limb
movements are relaxed.
 Breathing pattern
 Smooth & regular, may have occasional
sighing respirations; breathing is quiet &
passive w/ symmetric chest expansion;
abdomen bulges slightly w/ inhalation.
 Respiratory rate
 12 – 20b/min.
 Normal Findings
 Skin
 Oral mucous membranes are pink; no
cyanosis or pallor present.
 Palpation of skin & chest wall reveals smooth
skin & a stable chest wall; no crepitations,
masses or painful areas.
 Nails
 Angulation bet. base of nail & finger; no
thickening of distal finger width; no clubbing.
Modality of
Care
Airway Management
Endotracheal
Intubation

 passing an endotracheal tube

through the nose or mouth into
the trachea as means of
providing an airway (method of
choice in emergency care)
 Comatose, upper airway
obstruction
 Patient needing mechanical
ventilation
Endotracheal Intubation

➢ tube is positioned about 2 cm

above the carina
➢ a cuff at the distal end of the
endotracheal tube is inflated
➢ secure the tube
➢ position of the endotracheal tube
is verified by checking end-tidal
carbon dioxide levels and
confirmed with chest x-ray.

Cuff pressures should be maintained between

20 and 25 mmHg (24 to 30 cm H2O)
➢ high cuff pressure can cause tracheal
bleeding, ischemia, and pressure necrosis
➢ low cuff pressure can increase the risk of
aspiration pneumonia.
 TRACHEOSTOMY
Artificial opening created into the trachea (at the level of
the second or third tracheal ring) to establish an airway
tracheotomy is a surgical incision into
the trachea for the purpose of
establishing an airway.
tracheostomy is the stoma or opening
that results from the tracheotomy

Purposes
1. provide or maintain open airway
2. permit the long-term use of mechanical
ventilation
3. allow removal of tracheobronchial secretions
4. prevent aspiration of oral or gastric secretions
in the unconscious or paralyzed patient
Types of tracheostomy tube

A. Fenestrated tube, which B. Double-cuffed tube. Inflating

allows patient to talk. the two cuffs
Nursing Intervention

a. Assess signs of respiratory distress

b. Encourage coughing and deep breathing.
c. Maintain a semi-Fowler's to high Fowler's
position.
d. Suction secretions as needed
e. Assess the stoma and secretions for blood
or
purulent drainage.
f. Clean the tracheostomy site and inner
cannula; usually, half-strength hydrogen
peroxide is used.
 SUCTIONING
A sterile procedure involving the removal of
respiratory secretions that accumulate in the
tracheobronchial airway when the client is unable
to expectorate secretions; performed to maintain a
patent airway.
purpose:
• remove excess saliva, secretions,
• relieve respiratory distress,
• clear the airways,
• promote adequate gas exchange,
• obtain sputum culture

oxygenation
SUCTIONING
Points to remember
All equipment that comes into direct contact with the patient’s lower
airway must be sterile to prevent sepsis.
suction is not applied when catheter is inserted
apply suction when pulling the catheter
circular or rotating motion
maximum time 10-15 seconds
oxygenate after suctioning

oxygenation
 MECHANICAL VENTILATION
process of delivering
gases into the lungs by
a mechanical device

two main indication

Inadequate ventilation
Hypoxemia
Indications
➢ respiratory failure
➢ compromised airway (endotracheal
intubation and mechanical ventilation)
➢ clinical evidence
➢ decrease inoxygenation (PaO2
➢ an increase in arterial carbon dioxide levels
(PaCO2)
➢ a persistent acidosis (decreased pH);
however, if the patient’s status
➢ thoracic or abdominal surgery
➢ drug overdose,
➢ neuromuscular disorders
➢ inhalation injury
➢ COPD, multiple trauma
➢ shock, multisystem failure, and coma may
lead to respiratory failure
Mechanical ventilator
The two general categories of
mechanical ventilators
1. negative-pressure
2. positive-pressure

Types of negative-pressure ventilators:

1. iron lung,
2. body wrap
3. chest cuirass
 Types Positive Pressure Of Mechanical Ventilation
1. Pressure-cycled ventilator
The ventilator pushes air into the
lungs until a specific airway pressure
is reached.
2.Volume-cycled ventilator
The ventilator pushes air into the
lungs until a preset volume is
delivered has elapsed.
A. The AVEA can be used to both
3. Time-cycled ventilator ventilate and monitor neonatal,
The ventilator pushes air into pediatric, and adult patients
the lungs until a preset time has B. The Puritan-Bennett 840
elapsed. Ventilator System has volume,
pressure, and mixed modes
designed for adult, pediatric, and
infant ventilation.
Types Positive Pressure Of Mechanical
Ventilation
4. High-Frequency Oscillatory Support Ventilators
➢ These types of ventilators deliver very high respiratory rates
(i.e., 180 to 900 breaths/min) that are accompanied by
very low tidal volumes and high airway pressures
➢ is used to open the alveoli in situations characterized by
closed small airways, such as atelectasis and ARDS and it
is also thought to protect the lung from pressure injury
Types Positive Pressure Of Mechanical
Ventilation

Noninvasive Positive-Pressure Ventilation (NIPPV)

➢ is a method of positive-pressure ventilation that
can be given via facemasks that cover the
nose and mouth
➢ nasal pillow (a small nasal cannula that
seals around the nares to maintain the
prescribed pressure)
➢ Eliminates the need for endotracheal
intubation or tracheostomy and decreases
the risk of nosocomial infections such as
pneumonia.
 MODES OF VENTILATION

1. Controlled
2. Assist-control (continuous mandatory ventilation)
3. Intermittent mandatory ventilation (IMV),
4. Synchronized intermittent mandatory ventilation (SIMV)
5. PSV – pressure support ventilation
6. Airway pressure release ventilation (APRV
 Modes of ventilation

1. Controlled
 used for clients who cannot initiate respiratory effort .
 if the client attempts to initiate a breath, the ventilator
blocks the effort.
2. Assist- Controlled (A/C ventilation)
 more commonly called continuous mandatory (volume or
pressure)ventilation (CMV)
 the ventilator delivers a preset tidal volume or pressure at
a preset rate of respirations
 allows the patient initiates a breath between the machine’s breaths,(
the ventilator delivers at the preset volume or pressure (assisted
breath)
Modes of ventilation
3. Intermittent Mandatory Ventilation
 provides a combination of mechanically assisted breaths and spontaneous breaths.
 Mechanical breaths are delivered at preset intervals and a preselected tidal volume,
regardless of the patient’s efforts.
 the patient can increase the respiratory rate by initiating inspiration ( these spontaneous
breaths are limited to the tidal volume generated by the patient
 allows patients to use their own muscles for ventilation to help prevent muscle atrophy
 It lowers mean airway pressure, which can assist in preventing barotrauma.
 “fighting the ventilator” or “bucking the ventilator” (i.e., trying to exhale when the
ventilator is delivering a breath) may increase
4. Synchronized Intermittent Mandatory Ventilation (SIMV)
 the ventilator senses patient breathing efforts and does not initiate a breath in opposition to the
patient’s efforts
 used as a weaning mode, (RR is decreased gradually, and the client gradually resumes
spontaneous breathing
5. PSV (Pressure Support Ventilation)
applies a pressure plateau to the airway throughout the patient triggered
inspiration to decrease resistance within the tracheal tube and ventilator
tubing.
6. Airway Pressure Release Ventilation (APRV)
 a time-triggered, pressure-limited, time-cycled mode of mechanical
ventilation
 allows unrestricted, spontaneous breathing throughout the ventilatory
cycle.
 The inflation period is long, and breaths may be initiated spontaneously as
well as by the ventilator.
 APRV allows alveolar gas to be expelled through the lungs’ natural recoil.
 Advantages : less ventilator-induced lung injury and fewer adverse effects
on cardiocirculatory function and being associated with lower need for
sedation and neuromuscular blockade
 Ventilator Controls and Setting

 Tidal volume
 Rate
 Fraction of inspired oxygen (Fio2)
 Sighs - The volumes of air that are 1.5 to 2
times the set tidal volume
 Peak inspiratory pressure
 I:E ratio
 Continuous positive airway pressure
 Positive end-expiratory pressure (PEEP)
 Pressure support ventilation
Normal is 15 to 20 cm H2O
Continuous positive airway pressure

application of positive airway pressure

throughout the entire respiratory cycle
for spontaneously breathing clients.
 to keeps the alveoli open during
inspiration and prevents alveolar
collapse.
 used primarily as a weaning
modality.
Positive end-expiratory pressure (PEEP)

Positive pressure is exerted during the

expiratory phase of ventilation.
- improves oxygenation by
enhancing gas exchange and
preventing atelectasis.
- Higher amounts of PEEP (more than
15) increase the chance of
complications such as barotraumas -
tension pneumothorax.
 Nursing Interventions
 Assess the client first and then assess ventilator.
 Assess vital signs, lung sounds, respiratory status,
and breathing patterns.
 Monitor skin color, particularly in the lips and
nailbeds.
 Monitor chest for bilateral expansion.
 Obtain pulse oximetry reading
 Monitor ABG results.
 Nursing interventions

 Assess the need for suctioning and observe

the type, color, and amount of secretions.
 Assess level of water in humidifier and
temperature of the humidification system
 Ensure that the alarms are set.
 Nursing interventions

 If a cause for an alarm cannot be determined,

ventilate the client manually with a resuscitation
bag until the problem is corrected.
 Empty the ventilator tubing when moisture collects.
 Turn the client at least q 2hours or get the client out
of bed, as prescribed, to prevent complications of
immobility.
 Have resuscitation equipment available at the
bedside.
 Causes of alarms :

High Pressure Alarms

Increased secretions in the airways
Wheezing or bronchospasm
The ET is displaced
The ET is obstructed (H2O or a kink in
the tubing)
Client coughs, gags, or bites on the
oral endotracheal tube
Client is anxious or fights the ventilator
 Causes of alarms : Ventilator

Low Pressure Alarms

Disconnection or leak in the
ventilator or in the client’s airway
cuff occurs
The client stops spontaneous
breathing
 Hypotension
Infections
Malnutrition
Pneumothorax
Complications
Ventilator
subcutaneous dependence
emphysema Muscular
deconditioning
stress ulcers
 PRIMARY INDICATORS
OF
RESPIRATORY DISORDERS
1. DYSPNEA
difficult or labored breathing
shortness of breath
TYPES
a. Exertional
b. Orthopnea
c. Paroxysmal nocturnal dypsnea
2. COUGH
results from irritation of the mucous
membranes anywhere in the
respiratory tract
Evaluate character of cough
Dry - URTI,
Severe changing - carcinoma

Time of cough
Am – bronchitis
Pm - asthma
3. SPUTUM PRODUCTION
is the reaction of the lungs to any
constantly recurring irritant.
Thick yellow - bacterial infection
Rust-colored sputum – pneumonia
Thin, mucoid sputum - viral bronchitis.
A gradual increase of sputum – chronic bronchitis
Pink-tinged mucoid sputum - lung tumor.
Profuse, frothy, pink material - pulmonary edema.
Foul-smelling sputum - lung abscess
4. CHEST PAIN
Chest pain associated with pulmonary
conditions may be sharp, stabbing, and
intermittent, or it may be
dull, aching, and persistent.

Chest pain may occur with

pneumonia,pulmonary embolism with
lung infarction, and pleurisy
5. WHEEZING
is often the major finding in a patient with
Bronchoconstriction or airway narrowing.
6. CLUBBING OF THE FINGERS
a sign of lung disease found in
patients with chronic hypoxic
conditions
7. HEMOPTYSIS
expectoration of blood from
the respiratory tract
The most common causes are:
• Pulmonary infection
• Carcinoma of the lung

Blood from the lung is usually

bright red, frothy, and mixed
with sputum
8. CYANOSIS
a bluish coloring of the skin, is a
very late indicator of hypoxia

Cyanosis appears when there

is 5 g/dL of unoxygenated hemoglobin

central cyanosis –tongue and lips

decrease in oxygen tension in the blood.
Peripheral cyanosis – due to decreased blood
flow to a certain area of the body
-vasoconstriction from exposure to cold
-nail bed, earlobe
 RESPIRATORY TRACT INFECTION

UPPER RESPIRATORY TRACT INFECTION

Disorders of the upper respiratory tract include problems occurring in the nose, sinuses, pharynx, larynx,
and trachea

VIRAL RHINITIS (COMMON COLD)

The term “common cold” often is used when
referring to an upper respiratory tract infection
that is self-limited and caused by a virus (viral
rhinitis).
The release of histamine and other substances
causes vasodilation and edema, which result in
symptoms.

S/Sx: Nasal congestion, rhinorrhea, sneezing, sore

throat, and general malaise

MEDICAL MANAGEMENT
No specific treatment, symptomatic treatment
Adequate rest, Increase oral fluid intake
Increase Vitamin C intake
Expectorants as needed
Warm salt-water gargle for sore throat
Antihistamines - to relieve sneezing, rhinorrhea,
and nasal congestion
Topical (nasal) decongestant agents
Zinc lozenges may reduce the duration of cold
symptoms if taken within the first 24 hours of
onset (Prasad, Fitzgerald, & Bao, 2000)

NURSING MANAGEMENT
Teach patient how to break chain of infection
Proper Hand Hygiene
Cough etiquette

PHARYNGITIS LARYNGITIS
is a sore throat, which could be due to a viral is an inflammation of the vocal cords in which the
infection or a bacterial infection. person partially or totally loses his/her voice.

LOWER RESPIRATORY TRACT INFECTION

Disorders of the lower respiratory tract include problems of the lower portion of the trachea, bronchi, bronchioles,
and alveoli.

PNEUMONIA
An acute inflammatory process involving the lung parenchyma
it is described as lung inflammation and alveolar filling with fluid

CAUSATIVE AGENTS
TYPES OF PNEUMONIA INCLUDING COMMON ETIOLOGIC AGENTS
a. COMMUNITY ACQUIRED PNEUMONIA (CAP)
- Occurs either in the community setting or within the first 48 hours of hospitalization.
- The agents that most frequently cause CAP requiring hospitalization are Streptococcus pneumoniae,
H. influenzae, Legionella, Pseudomonas aeruginosa, and other gram negative rods

b. HOSPITAL ACQUIRED PNEUMONIA (HAP)

- also known as nosocomial pneumonia, is defined as the onset of pneumonia symptoms more than 48
hours after admission to the hospital.
The common organisms responsible for HAP include Pseudomonas. aeruginosa Enterobacter species,
Escherichia coli, Klebsiella species, Proteus, and methicillin-sensitive or methicillin-resistant Staphylococcus aureus.

c. OPPORTUNISITIC PNEUMONIA
- Seen in clients with very poor immune systems: malnutrition, HIV/AIDS, transplant clients receiving
steroids, cancer clients.
- Opportunistic pneumonias are caused by Pneumocystis carinii, cytomegalovirus, and fungi.
D. ASPIRATION PNEUMONIA
- refers to the pulmonary consequences resulting from the entry of endogenous or exogenous
substances into the lower airway.
- This most often occurs in patients with decreased levels of consciousness or an impaired cough or
gag reflex. These conditions can occur with alcohol ingestion, stroke, general anesthesia, seizures, or
other serious illness.
E. HYPOSTATIC PNEUMONIA.
- Patients who hypoventilate because of bedrest, immobility, or shallow respirations are at risk for
hypostatic pneumonia.
- Secretions pool in dependent areas of the lungs and can lead to inflammation and infection.

4 STAGES OF PNEUMONIA

1. CONGESTION

2. RED HEPATIZATION

3. GRAY HEPATIZATION

4. RESOLUTION

Signs and symptoms:

fever, pleuritic chest pain, chills, increased RR, lethargy,

productive cough, shortness of breath, inspiratory
crackles, decreased breath sounds, dullness noted on
percussion over the lungs, egophony , increased tactile
fremitus

Diagnostic Exams SPUTUM RAINBOW: The colors of sputum

and their corresponding bacteria follow:
CBC
Blood Cultures RUST = Streptococcus pneumonia
Pulse Oximetry PINK = Staphylococcus aureus
ABG GREEN with odor = Pseudomonas aeruginoa
CXR and CT Scan
Sputum GSCS
Bronchoscopy Management:
Antibiotic therapy accdg. to causative agent
Respiratory precautions
Inhalation therapy
Postural drainage
Prevention: Bronchodilators
Hand washing Deep breathing exercises
Immunization Antipyretics
Respiratory precaution (masks and gloves Frequent rest periods
when handling secretions) Increase Oral Fluid Intake
Semi Fowlers position
 PATHOPHYSIOLOGY

TUBERCULOSIS_______________________

Is an infectious disease caused by bacteria

(Mycobacterium tuberculosis) that are usually
spread from person to person through the air.

MODE OF TRANSMISSION: airborne droplet;

coughing, sneezing, talking

TYPES:
PRIMARY TB – develops in previously unexposed and
unsensitized persons
- Clinically and radiologically silent
SECONDARY TB –reinfection from inhaled droplet
nuclei or reactivation of a previously healed primary
lesion

Classification
RISK FACTORS:
 PATHOPHYSIOLOGY

Diagnostic tests:
Mantoux test, PPD (Tuberculin Skin test)
Chest Xray
Sputam Exam

PREVENTIVE MEASURES
A. BCG IMMUNIZATION
B. IMPROVED SOCIAL CONDITIONS

Management:
1. Simultaneous administration of 3 or more drugs increases
the therapeutic effects of medication and decreases the
development of resistant bacteria
2. Course of treatment: average 6 – 12 mos.
3. DOTS (DIRECT OBSERVED TREATMENT SHORT COURSE)
- Is the name for a comprehensive strategy which
primary health care services around the world are
using to detect and cure TB.

TREATMENT REGIMEN IN THE NATIONAL TUBERCULOSIS PROGRAM (NTP)

REGIMEN TYPE OF TB PATIENT DRUG/DURATION

CATEGORY I -NEW PULMONARY SMEAR (+) CASES RIPE 2 MOS (INTENSIVE PHASE)
-NEW SERIOUSLY ILL PULMO. SMEAR (-) RI 4 MOS. (MAINTENANCE PHASE)
CASES WITH EXTENSIVE LUNG LESIONS
-NEW EXTRA-PULMO TB
-CONCOMITTANT HIV INFECTION

CATEGORY II FAILURE CASES RIPES 2 MONTHS

RELAPSE CASES RIPE 1 MONTH
RETURN AFTER DEFAULT (SMEAR +) RIE 5 MOS. MAINTENANCE
OTHER SMEAR (+) OR (–)

CATEGORY III NEW SMEAR (-) BUT WITH MINIMAL PTB RIPE 2 MONTHS
ON XRAY AS ASSESSSED BY TB RI 4 MONTHS
DIAGNOSTIC COMMITTEE
 ANTI- TUBERCULOSIS MEDICATIONS

DRUG SIDE EFFECTS

ISONIAZID (INH) Bactericidal Inhibits PERIPHERAL NEURITIS , HEPATITIS
mycobacterial cell
wall synthesis Implications: take meds on empty
stomach, no alcohol while on
treatment.
RIFAMPIN Bactericidal inhibits RNA Body secretions may turn to orange
synthesis (urine, tears, perspiration,)

Implications: expect orange-red

urine
ETHAMBUTOL Bacteriostatic given in resistant OPTIC NEURITIS (decreased red-
cases. Inhibit green color discrimination,
cellular metabolism decreased visual acuity)

Implications: check for visual acuity,

5. Streptomycin –. color perception.
S/E:
damage to CN VIII

PYRAZINAMIDE Both Bactericidal and Bacteriostatic Hyperuricemia, Hepatotoxicity

Implications: obtain baseline uric
acid levels
STREPTOMYCIN Bactericidal for resistant, severe OTOTOXICTY, NEPHROTOXICITY
TB
Implication: report for ringing,
fullness of ears, dizziness, vertigo.
NURSING CARE:
INSTRUCT PATIENT TO TAKE DRUGS IN CORRECT AMOUNTS AND ON SCHEDULE
BALANCED DIET, AVOID EXCESSIVE FATIGUE
USE HEPA RESIPARTOR MASK FOR ALL PEOPLE IN CLOSE CONTACT WITH PATIENT, IF SPUTUM IS POSITIVE
COUGH ETIQUETTE
HANDWASHING, DISCARD ALL SECRETIONS IN PLASTIC BAG

INFLUENZA__________________________________________________________________

Influenza, commonly referred to as the flu, is a viral infection of the respiratory tract.

MODE OF TRANSMISSION: via droplets from coughs and sneezes of infected individuals, direct contact
INCUBATION PERIOD: from time of exposure to onset of symptoms is 1 to 3 days.

Symptoms have an abrupt onset

• Nonproductive cough
• Fever over 101F, Chills and sweats • Muscle aches (myalgia)
• Fatigue and malaise • Watery, nasal discharge
• Headache • Sore throat

PREVENTION
: Yearly immunization

Treatment
Treatment is primarily symptomatic.
Acetaminophen is given for fever, headache, and
myalgia. Aspirin is avoided in children because it
increases the risk for Reye’s syndrome.
Rest and fluids.
Antibiotics are used only if a secondary bacterial
infection is present.
Antiviral drugs such as Amantadine (Symmetrel),
Zanamivir (Relenza) and Oseltamivir (Tamiflu) may
be helpful for high-risk patients if given within 48
hours of exposure.
Nursing management:
Administer medications as ordered.
Administer fluids and electrolytes as ordered.
Monitor respiratory status for rate, effort, use of
accessory muscles, skin color, and breath sounds.

REYE’S SYNDROME – acute encephalopathy with fatty liver degeneration

 SEVERE ACUTE RESPIRATORY SYNDROME (SARS)__________________________________________

- Is a serious, potentially life-threatening viral infection caused by a previously unrecognized virus from the
Coronaviridae family.
- The virus has been named the SARS-associated coronavirus (SARS-CoV).
- The epidemic of SARS appears to have started in Guangdong Province, China in November 2002.

Incubation period: 2-7 days after exposure to a SARS case, with a maximum of 10 days

Mode of transmission: droplet transmission, contact with contaminated objects

People at Risk: Direct contact with infected people

Health care workers
Travelers to regions where SARS is prevalent

Initial symptoms are flu-like and may include: fever,

myalgia, lethargy, gastrointestinal symptoms,
cough, sore throat and other non-specific
symptoms. The only symptom that is common to all
patients appears to be a fever above 38 °C (100.4
°F). Shortness of breath may occur later.

SARS may be suspected in a patient who has:

1. Any of the symptoms, including a fever of 38 °C (100.4 °F) or higher, and

2. Either a history of:
1. Contact (sexual or casual) with someone with a diagnosis of SARS within the last 10 days OR
2. Travel to any of the regions identified by the WHO as areas with recent local transmission of
SARS (affected regions as of 10 May 2003 were parts of China, Hong Kong, Singapore and the
province of Ontario, Canada).

Management: Quarantine and Isolation

Anti-viral medications
Steroid
Hydration and Oxygenation
Wearing Personal Protective Equipment

AVIAN FLU/BIRD FLU/ A(H5N1)________________________ HA codes for hemagglutinin, an antigenic

Is an infection caused by avian influenza viruses.
These influenza viruses occur naturally among birds. Wild birds
worldwide carry these viruses in their intestine, but usually
don’t get sick with them. However, it is very contagious among
birds and can make domesticated birds, including chicken,
ducks, and turkeys, very sick and kill them.
glycoprotein found on the surface of the influenza
viruses and is responsible for binding the virus to
the cell that is being infected. NA codes for
neuraminidase, an antigenic glycosylated enzyme
found on the surface of the influenza viruses. It
facilitates the release of progeny viruses from
infected cells.

Etiology: Type A strain of the Influenza virus, H5N1 virus
Incubation period: ranging from two to eight days and possibly
as long as 17 days.
Bird Flu Transmission:
Virus is transmitted to humans from infected birds
Birds shed the virus in saliva, nasal mucus and stool
The virus has not been transmitted from person to person
The hemagglutinin (HA) and neuraminidase (NA)
RNA strands specify the structure of proteins that
are most medically relevant as targets for antiviral
drugs and antibodies. HA and NA are also used as
the basis for the naming of the different subtypes
of influenza A viruses. This is where the H and N
come from in H5N1.

Signs and symptoms:  H5 stands for the fifth of several known

Most often resemble those of conventional influenza; including types of the protein hemagglutinin. N1
Fever, sore throat, cough, myalgia stands for the first of several known
types of the protein neuraminidase.
 Management: Precautions:
Acetaminophen for pain and fever Hand hygiene especially those who have been in
Cough and Decongestant medications close contact with infected animals
Antiviral medications Personal Protective Equipment
Oxygen therapy and Hydration

___________________________________________________SWINE FLU/ A (H1N1)

Influenza A (H1N1) is caused by a novel virus that resulted from the reassortment of 4 viruses from pigs, humans
and birds.
Novel influenza A (H1N1) is a new flu virus of swine origin that first caused illness in Mexico and the United States
in March and April, 2009.

MODE OF TRANSMUSSION: Exposure to droplets from the cough and sneeze of infected person
: direct contact with secretions
How long can an infected person spread influenza
- As long as they are symptomatic and possibly up to 7 days following disease onset

Signs and Symptoms: Management:

Similar to the regular flu Isolation or Quarantine
Fever, headache, muscle pains, sore throat, cough, Antiviral medications
runny nose, nausea or vomiting, diarrhea Rest
Hydration
Hand Hygiene
Cough Etiquette
Personal Protective Equipment

CHRONIC OBSTRUCTIVE PULMONARY DISEASE________________________

is a disease state characterized by airflow limitation that is not fully reversible
any process that limits airflow on expiration
group of chronic lung diseases associated with persistent or recurrent obstruction of airflow

EMPHYSEMA CHRONIC BRONCHITIS

PROBLEM WITH THE ALVEOLI THAT IS CHARACTERIZED BY A LOSS OF
ALVEOLAR ELASTICITY, OVERDISTENTION AND DESTRUCTION WHICH
REDUCES THE SURFACE AREA FOR GAS EXCHANGE
WITH SEVERE GAS EXCHANGE IMPAIRMENT
Types:
Panacinar
Involves the peripheral alveoli and extends to the central bronchioles
PROBLEM WITH THE AIRWAY CHARACTERIZED BY
EXCESSIVE MUSUS PRODUCTION, IMPAIRED CILIARY
FUNCTION WHICH DECREASES MUCUS CLEARANCE
Repeated lung inflammation damages the lungs
Causes scarring of the airway
Sometimes called “smoker’s cough”

Centriacinar
Affects the bronchioles in the central part of the respiratory lobules
Risk Factors:
Smoking Most Common Smoking
Heredity
Aging Process
Inherited deficiency of alpha 1 antitrypsin
MANIFESTATION:
1. thin in appearance 1. generally normal or overweight
2. cough is not common progressive dyspnea 2. increased chronic sputum production
3. sensation of air hunger 3. low pao2, cyanosis
4. use of accessory respiratory 4. productive cough
5. muscles 5. exercise intolerance
6. ABG is normal until late in the disease 6. SOB
7. generally without cardiac involvement 7. with cardiac involvement
8. cor pulmonale, late in the disease 8. persistent cough for 3 months in 2
9. anorexia consecutive years
10. weight loss 9. x-rays will reveal flattened diaphragm
11. respiratory acidosis 10. respiratory acidosis
12. decreased breath sounds with prolonged expiration 11. cyanosis
13. barrel chest 12. bloated appearance
14. pursed –lip breathing
15. hyper-resonant chest
 TYPES
OF
EMPHYS
EMA

Diagnostic Tests
(emphysema) (bronchitis)
• Pulmonary function test • pulse oximetry
– decreases in forced expiratory volume & total • ABG
lung capacity • chest x-ray
– decrease residual volume (dead space)
– impaired oxygenation
– poor ventilation
– acidosis.
• Radiologic Exam
• ABG
Management • Bronchodilators
• Bronchodilators • postural drainage
• Nebulization • chest percussion
• O2 therapy • proper hydration
• antimicrobials • High calorie;
• Breathing exercise • High CHON ; Low CHO
• Quit smoking (small, frequent, easily swallowed feeding)
• Prevent complications
• Resection of Bleb
 PATHOPHYSIOLOGY
Emphysema

PATHOPHYSIOLOGY
Bronchitis
 DISTINGUISHING MARKS
BRONCHITIS VS EMPHYSEMA

FEATURES BRONCHITIS EMPHYSEMA

Productive cough classic Late in course w/ infection

Dyspnea Late in course Common

Barrel chest Occasionally Classic
Prolonged expiration Always present Always present

Cyanosis Common Uncommon

Chronic hypoventilation Common Late in course

Polycythemia Common Late in course

Cor Pulmonale Commmon Late in course
Blood gases Hypercapnia & hypoxemia Normal until late
Appearance Blue bloaters Pink puffers
CHRONIC OBSTRUCTIVE
PULMONARY DISEASE

a disease characterized by
airflow limitation that is not fully
reversible.
( Global Initiative for Chronic Obstructive
Lung Disease, GOLD)

Most common form

Emphysema
Chronic bronchitis
 CAUSATIVE FACTORS

• SMOKING (most common)

•Air pollution
• HEREDITY
• AGING PROCES
• Inherited deficiency of alpha1-
antitrypsin
Pulmonary Emphysema (pink puffers)
Is a condition of the
lungs characterized by
abnormal permanent
enlargement of gas
exchange airways and
accompanied by
destruction of alveolar
wall

The major mechanism of

air flow limitation
Is loss of elastic recoil
BULLAE – hyperinflation of alveoli at lung
parenchyma
BLEB – near pleural membrane
Cigarette Stimulate INFLAMMATORY CELLS
release of ELASTASE & PROTEASES

smoking NORMALLY, protected by

ANTI-PROTEASE ENZYMES –
Alpha1-Antitrypsin

Digest ELASTIN

DESTRUCTION of ELASTIC RECOIL

DYSPNEA
Overdistention of ALVEOLI BARREL
-CHEST
Destruction of alveolar walls & Trapping of AIR ==
capillary beds (ACM) retention of CO2

Altered Blood Gas Exchange PURSED- LIP

breathing
HYPOXEMIA RESPIRATORY ACIDOSIS

WEAKNESS, ANOREXIA
 Types of Emphysema
1. PANACINAR
Dilatation and destruction involve entire acini

2. CENTIRACINAR
the central part of the acinus
Signs & Symptoms
 progressive dyspnea
 progressive cough and
increase in sputum
production
 Anorexia
 weight loss
 respiratory acidosis Tripod sitting
 use of accessory muscles
when breathing
 barrel chest
 pursed –lip breathing
 hyperresonant chest
 Decrease tactile fremitus
 Diagnostic Tests
Pulmonary function
test – TLC, FEV
Radiologic Exam
ABG
Ventilation-perfusion
lung scan
Serum alpha-
antitrypsin level
 Management
 Smoking cessation
 Bronchodilators
anticholinergic
 O2 therapy
 antimicrobials
 Breathing exercise
 Ressection of Bleb/
Bullectomy
Chronic Bronchitis

Chronic inflammation in the lungs

causes scarring of the airways
and excessive production of
mucus that results in a chronic
cough.
 Productive cough that last 3
months a for 2 consecutive
years
CHRONIC BRONCHITIS “BLUE BLOATER”
Cigarette smoking, RTI, pollutants

Inflammation of major and small airways- bronchioles/bronchi

HYPERTROPHY of submucosal glands in the Release of chemical/inflammatory

trachea & bronchi and HYPERSECRETION mediators
of Goblet cells
BRADYKININ, HISTAMINE,
Increased sputum production, PROSTAGLANDIN
bronchial congestion, decreased
mucociliary clearance
Increase CAPILLARY permeability
WHITE, thick secretions,
persistent COUGH, Fluid/cellular exudation
increased mucus
production
NARROWING of
BRONCHIOLES

dyspnea
BLOOD GASES IMBALANCE

HYPOXEMIA & HYPERCAPNIA

 BLOOD GASES IMBALANCE

HYPOXEMIA & HYPERCAPNIA

REFLEX VASOCONSTRICTION

Pulmonary Vessels Constrict

Pulmonary HYPERTENSION

RIGHT-SIDED HEART FAILURE

ASCITES,
COR PULMONALE Peripheral edema HEPATOMEGALY,
DISTENDED NECK VEINS
 Signs & Symptoms
 persistent cough that
last 3 months a year in
2 consecutive years
 sputum production
Primarily mucoid
Copius amount,
thick tenacious
 Cyanosis
 bloated appearance
 Diagnostic Tests Management

 ABG  Bronchodilators
 pulse oximetry  postural drainage
 chest x-ray  chest percussion
 proper hydration
 High calorie;
 High CHON ; Low CHO
(small, frequent, easily
swallowed feeding)
 Bronchiectasis

 Is a disorder that is
characterized by
permanent
dilatation and destruction
of cartilage containing
airways
CAUSES:

Smoking/ exposure to toxic gases

Cystic fibrosis
Repeated Lung infection
 3 Different types of
bronchiectasis.
Cylindrical or tubular
bronchiectasis involves dilated
airways alone.
Varicose bronchiectasis is
characterized by focal
constrictive areas between the
dilated airways.
Saccular or cystic
bronchiectasis is
characterized by progressive
dilatation of the airways, which
form grape-like clusters.
 Repeated infection & obstruction

Increase mucus production, damage to mucociliary

mechanism
Prevents bacterial clearance enhancing inflammatory
changes and intensifies productions of mucus

Stretching and enlargement of respiratory passages

Permanent dilatation, damage, scarring and deformity

of airway cartilage
Involvement of the bronchioles and
collapse of the alveoli
 Signs & Symptoms
o chronic cough,
o production of purulent sputum,
Layering out-frothy, clear layer,
dense particulate
o Hemoptysis
o clubbing of fingers
Diagnostic Test
Management
CT scan
bronchoscopy o Postural drainage
ABG o Bronchoscopy
o chest percussion
o smoking cessation
o antimicrobial therapy
o bronchodilators,
 ASTHMA
The condition with
widespread narrowing of
the bronchial airways.
May be precipitated by
exposure to one or more of
a wide range of stimuli
including:
Allergens, Exertion,
Emotion, Air pollution
 TYPES OF ASTHMA

1. Extrinsic asthma/IgE
mediated
 Allergic form; seen mostly
in children
 due to external agents of
specific allergens

2. Intrinsic/ non-allergic
 due to
o URTI
o emotional stress
o non-specific factors
 Inhaled Antigen or Irritant =Allergen (Extrinsic)
Inflammation (Intrinsic)

Antigen binds to sensitized mast cells on

mucosal surface of airways

RELEASE of CHEMICAL MEDIATORS

from IgE coated mast cells
HISTAMINE, BRADYKININ, PROSTAGLANDIN,
SEROTONIN, LEUKOTRIENES, ECF-A, SRS-A
BRONCHOSPASM BRONCHOCONSTRICTION
EDEMA of MUCOUS HYPERSECRETION of
MEMBRANE MUCUS

Narrowing of AIRWAYS Diaphoresis,cold

Tends to sit up; clammy skin;
restless; INCREASED work of breathing
wheezing,
tachypnea/dyspnea; retractions; pallor-
flaring of nostrils EXHAUSTION cyanosis

Slow reacting substance

SLOW, SHALLOW RESPIRATION of anaphylaxis
Eosinophils chemotaxic
Retention of CO2 (airtrapping)

HYPOXIA RESPIRATORY ACIDOSIS

Classical Signs
 cough with or without
sputum (phlegm)
production
 dyspnea
 Wheezing
STATUS ASTHMATICUS

 Severe asthma that is unresponsive

to usual emergency method of
treatment and ventilatory failure is
PRECIPATATED BY:
immenent Infection
Danger signs: Anxiety
Nebulizer abuse
 Unable to talk Dehydration
Aspirin hypersensitivity
 Absence of breath sound
 Cough becomes ineffective
despite being repetitive & hacking
 Diagnostic Tests
 pulmonary function
tests
 peak flow
measurements
 chest X-ray
 allergy testing by skin
testing or serum tests
 arterial blood gas
PEAK FLOW METERS

measure the highest airflow during a forced

expiration
- recommended to patient with moderate or
severe asthma
- helps measure asthma severity and indicates
the current degree of asthma control
3 ZONES OF MEASUREMENT ACCORDING TO
THE AMERICAN LUNG ASSOCIATION
 Management

Prevent recurrent exacerbation of

asthma
Maintain near-normal pulmonary function
Maintain normal activity level
Provide optimal pharmacotherapy with
minimal or no adverse effects
 Long-acting medications
 used on a regular basis to  used to relieve symptoms
prevent attacks, not for
treatment during an attack.
 Corticosteroids MDI
(Azmacort, AeroBid)
 Leukotriene inhibitors
(Singulair, Accolate)
 Long-acting
Bronchodilators
(famoterol, Serevent)
 Xanthine derivatives
(Aminophylline)
 Mast cell stabilizer
Cromolyn Na
Quick relief medications
during asthmab attack.
 Short-acting
bronchodilators
(e.g.Proventil, Ventolin,)
 oral or intravenous
corticosteroids
(e.g., prednisone,
methylprednisolone)
- Anticholinergic
ipratropium
 NURSING CARE

 during acute attacks, stay calm & stay with the patient
 position patient on MHBR or patient’s preference
 encourage relaxation techniques, pursed lip breathing, deep
breathing exercises
 observe clue for respiratory arrest
 patient cannot talk, decrease or absent breath sounds
Any disorder that LIMITS lung expansion and
RESTRICTS chest wall movement resulting in:

Decreased Lung Volume

Increased Work of Breathing
 Chest Trauma
 Injury to chest wall/lungs which interferes with
respiration

Often-life threatening
and results in
Hypoxemia
Hypovolemia
Cardiac failure
Classification of Chest Trauma

Blunt/ non penetrating

Damages of structures within the

chest cavity without disrupting
chest wall integrity.

Penetrating injury

Disrupts chest wall integrity and

within chest cavity; mostly
occurs as a result of gunshot,
stabbing
A. FRACTURED RIBS

Injury to bone on the ribs

: RIBS 4-8 ARE MOST COMMONLY
FRACTURED
ASSESSMENT FINDINGS:
 pain (inspiration)
 tenderness and bruising at injury site,
splinting with shallow rapid respirations
 diagnostic test: CXR reveals area and
degree of fracture
Medical management: narcotics
chest binder, surgical fixation
Nursing Interventions:
 Semi or High Fowler’s position
 Monitor client for complications
: bloody sputum indicative of lung
penetration
: observe for signs of hemothorax-
and pneumothorax
Chest Binder
Titanium plates
stabilize broken ribs
FRACTURE OF SEVERAL RIBS AND
INSTABILITY OF THE CHEST WALL
CHEST WALL UNABLE TO PROVIDE
BONY STRUCTURE NECESSARY FOR
ADEQUATE VENTILATION
: UNDERLYING TISSUE MOVE
PARADOXICALLY
 Paradoxical
chest movement

On expiration, the
On inspiration
flail segment bulges
the flail rib segment is
outward and the
sucked inward and the
mediastinal
mediastinal structures
structures shift back
shift to the unaffected
to the affected side.
side.
ASSESSMENT FINDINGS:
 paradoxical respirations
 Severe pain
 Tachypnea, shallow breathing
 cyanosis; tachycardia,
hypotension
MEDICAL MANAGEMENT
Supportive.Management includes
ventilatory support
clearing secretions from the lungs
controlling pain
The specific management depends on the degree of
respiratory dysfunction
Small segment of the chest
to clear the airway through positioning - coughing, deep
breathing
to aid in the expansion of the lung - suctioning
to relieve pain - intercostal nerve blocks, high thoracic
epidural blocks, IV opioids.
MEDICAL MANAGEMENT

Mild to moderate flail chest injuries

➢ Appropriate fluid replacement
➢ Closely monitored for further
respiratory compromise.
Severe flail chest injury
➢ Endotracheal intubation and
mechanical ventilation
➢ Surgery- internal or external
fixture
Surgical stabilazation of flail chest
Nursing Interventions:
Maintain open airway, suction
secretions
Monitor mechanical ventilation
Encourage turning, deep breathing
and coughing exercises
Monitor for signs of shock
Pneumothorax
Is the presence of air in the pleural
space cause by a rupture in the
visceral pleura or parietal pleura and
chest wall

SPONTANEOUS
Types: PRIMARY
SECONDARY
Spontaneous
TRAUMATIC
- Traumatic OPEN
Tension CLOSED
IATROGENIC
TENSION
 TYPES OF PNEUMOTHORAX

SPONTANEOUS PNEUMOTHORAX
Air enters the pleural space
through a breach of either the parietal or
visceral pleura

CAUSES
The rupture of bleb
PTB
Bronchogenic cancer
Emphysema
 TYPES OF PNEUMOTHORAX

TRAUMATIC PNEUMOTHORAX
Air enters the pleural space
through an opening in the chest wall; or
from a laceration in the lung itself

CAUSES
Fractured or dislocated ribs
Stab wound
Transthoracic needle aspiration
Intubation/mechanical ventilation
Complication of CPR
 TYPES OF
PNEUMOTHORAX
TENSION PNEUMOTHORAX
occurs when air is drawn into the pleural
space a small hole in the chest wall the air that
enters the chest cavity with each inspiration is
trapped; it cannot be expelled during expiration

a one-way valve
mechanism occurs
 One way valve mechanism

Inhalation: Air enters pleural space Exhalation: Air trapped

Compression atelectasis Compress mediastinum

s/sx:
Tracheal deviation;
distended neck veins;
Subcutaneous emphysema;
shock
Open/ Tension Pneumothorax
 Atmospheric air flows directly
PATHOPHYSIOLOGY
into Pleural cavity

Increases Pressure in the pleural

cavity

Prevents lung expansion during

respiration
•Sudden sharp
pleuritic pain
•Decrease vocal
ATELECTASIS fremitus
•Absent breath
Decrease total lung capacity, sounds on
vital capacity, lung compliance affected lung

V/Q IMBALANCES

•SOB
increase RR
HYPOXIA •Increase CR
blood in the pleural
cavity compresses the
lungs and can produce
blood loss resulting in
shock
 Management of
Pneumothorax

Chest tube placement

Tension P. initial treatment of choice is to insert
a large-bore needle into the second intercostal
space midclavicular line to relieve pressure
Oxygen therapy.
Pain management
(epidural catheter)

Bed rest
Pain medications:
monitor respirations
 Nursing Management
Nursing Diagnoses
Impaired Gas Exchange
Ineffective Airway Clearance

1. Assess respiratory status and breath sounds

2. Provide measures promote chest expansion and secretion
clearance (incentive spirometer, nebulization, head of bed
elevated 30 degrees, turn frequently,)
3. Perform chest physiotherapy to remove mucus. Teach
slow, pursed-lip breathing
4. Administer I.V. fluids and mucolytics to reduce sputum
viscosity.
5. Suction patient as needed
6. Care of client with chest tube
Collapse of lung tissue at
any structural level

 TYPES:
 PRIMARY – due to
decreased surfactant
factor
 SECONDARY – due to
airway obstruction and
lung compression
CLASSIFICATION OF ATELECTASIS

1.) NON-OBSTRUCTIVE/ COMPRESSION Atelectasis –

caused by external pressure

CAUSES
Pneumothorax
Pleural effusion
Large mass
2. OBSTRUCTIVE/Absorption Atelectasis –

If flow of air into an alveolus

is bloked,the air currently
inside would eventually
diffusses out and the
alveolus collapse
CAUSES
 Mucous plugging
 Foreign objects
 anesthesia, pain,
narcotics,
immobility)
 Assignmen: define on the
following types of atelectasis

1. Relaxation or passive atelectasis

2. Compression atelectasis
3. Adhesive atelectasis
4. Cicatrization atelectasis
5. Replacement atelectasis
Postoperative Atelectasis

 General anesthesia and surgical

manipulation lead to atelectasis by
causing diaphragmatic dysfunction and
diminished surfactant activity.
Pathophysiology Atelectasis

Clinical manifestation
ATELECTASIS Dyspnea
Tachypnea; tachycardia
Decrease total lung
Cyanosis
capacity, vital Diminished chest
capacity, lung expansion
compliance
Absence of breath
sounds
HYPOXIA Intercostal retractions
Diagnostic test:

Chest X-ray
CT scan
Bronchoscopy
Management
To improve ventilation
To remove secretions
Treating the underlying cause:
administration of surfactant, antimicrobial,
bronchodilators
Oxygen administration
Chest tube insertion
Removal of tumor, foreign body
PREVENTION: Ambulation and body
positioning that favor lung expansion
Deep breathing, coughing, incentive
spirometry, CPT
PULMONARY VASCULAR DISEASE
PULMONARY
An embolus blocking
the pulmonary artery
and disrupting blood
flow to one or more
lobes of the lung

Form of emboli
air
fat
amniotic fluid
 PULMONARY
An embolus blocking the
pulmonary artery and
disrupting blood flow to one
or more lobes of the lung

Causes
•Almost all pulmonary emboli
arise from deep vein
thrombosis (blood clot)
(DVT) in the lower extremities
• Air
• fat
• amniotic fluid
PULMONARY
Physiologic factors that contribute to
Deep vein thrombosis
Venous stasis,
Venous endothelial injury,
Hypercoagulability states
prolonged bed rest, trauma, surgery,
childbirth, fractures of the hip and femur, MI
and congestive heart failure
oral contraceptive, pregnancy, and hormone
replacement therapy
PULMONARY

Assessment Findings

Chest pain (pleuritic), sudden onset

Dyspnea
Tachypnea
Fever (low grade)
Apprehension
Cough (productive, blood-steaked)
Shock (massive)
PULMONARY

Diagnostics:
Pulmonary Angiography (CT
ANGIOGRAM)
Reveals location and extent of
embolism
Perfusion Lung Scan
determine pulmonary circulation
PULMONARY

Medical Management:
Anticoagulants
Thrombolytics
Dextran 70
Narcotics
Vasopressors if with shock

Surgery: Embolectomy
PULMONARY

Nursing Management:
Administer meds as ordered
Administer O2
Elevate HOB
Assist with Cough and DBE, turning
Hydration
Offer support and reassurance
COR
COR

Etiology: The most frequent

cause is severe COPD
Pulmonary Embolism
Pulmonary Vascular
Disease
COR

Diagnostics:
Radiologic exam: pulmonary trunk
and hilar vessels are enlarged
Echocardiography – enlarged right
ventricle
Cardiac cath.: pulmonary vascular
pressures
COR

Clinical Manifestations:
usually related to underlying lung disease - COPD.
with right ventricular failure:
edema of feet and legs
distended neck veins,
hepatomegaly
ascites
heart murmur
Headache, confusion, and somnolence
Increasing shortness of breath, wheezing, cough, and
fatigue
COR

Management:
Treatment of underlying lung disease
Long Term, low flow O2
Diuretics/ DIGITALIS
Pulmonary Vasodilators ( Nitroprusside,
Hydralazine)
Check ABG values
Check electrolyte levels: restrict Na intake if with
edema
COR

Nursing Management
Monitor respiratory status and provide adequate
ventilation
Administer O2
High or semi fowlers
Monitor ABGs
Assess breath sounds
Provide physical and emotional rest
ALTERATIONS
IN
GAS
TRANSPORT
 The circulatory system

The heart – which pumps the blood

The arterial system – which distributes
oxygenated blood to the tissue
The venous system – which collects
deoxygenated blood from the
tissues and returns it to the heart
The capillaries – where exchange
of gases, nutrients, and waste
occurs
 THE HEART
■
• a hollow, muscular
organ located in
the center of the
thorax
• weighs
approximately 300 The pumping
grams action of the heart is
• pumps blood to the accomplished by the
tissues, supplying rhythmic contraction
them with oxygen and relaxation of its
and other nutrients. muscular wall.
Layers of the heart

The heart is a four-

chambered pump

two atria (the

right and left
atrium)

two ventricles
( right and
left ventricle)
HEART VALVE Permits blood flow
in only one direction
2 Types
ATRIOVENTRICULAR
VALVES
Tricuspid valve
Mitral valve

SEMILUNAR VALVES
Aortic valve
Pulmonic valve
• 2 structures that maintain
valve closure?
Systemic & Pulmonary Circulation

• Pulmonary • Systemic
circulation circulation
- functions as - Functions as
low pressure high
system; pressure
MAP = 12 system;
mmHg MAP = 90
to100mmHg
SYSTEMIC & PULMONARY
CIRCULATION
Coronary Arteries The left and right
coronary arteries
and their branches
supply arterial blood
to the heart.

coronary arteries
are perfused during
diastole
increase in heart
rate shortens diastole and
can decrease
myocardial perfusion
 CONDUCTION SYSTEM
Sinoatrial Node

Atrioventricular
Node

AV bundle or
Bundle of His

Right & Left

Bundle Branch

Purkinje fiber
ELECTROPHYSIOLOGIC PROPERTIES

RACE
Rhythmicity
(Refractoriness)
Automaticity
Conductivity
Excitability
ELECTROPHYSIOLOGIC PROPERTIES

Rhythmicity
Myocardial
muscle are arranged
in an interconnected
manner (synctium)

coordinated contraction
and relaxation
regularity of impulse
transmission
 ELECTROPHYSIOLOGIC PROPERTIES

Automaticity

ability to initiate an
electrical impulse

SA node – dominant
pacemaker
60 – 100 impulse/min
 ELECTROPHYSIOLOGIC PROPERTIES

Conductivity
ability to
transmit an electrical
impulse from one
cell to another
ELECTROPHYSIOLOGIC PROPERTIES

Excitability
ability to respond to
an electrical impulse
 ELECTROPHYSIOLOGIC PROPERTIES

Absolute refractory period – heart cannot be restimulated

regardless of the strength of the electrical stimulus

Refractoriness
Protect hearts
from sustained
contraction
 Cardiac Cycle

used to described the

rhythmic pumping of
the heart

two major periods:

Systole - ventricles are
contracting
Diastole -when the
ventricles are relaxed
and filling
 Phases of Cardiac Cycle
A. Atrial Systole
atria contracts and forces blood to be ejected into relaxed
ventricles
B. Atrial Diastole
atria relaxes
C. Ventricular Systole first phase
ventricles contract making AV valves closed
D. Ventricular Systole second phase
pressure in the ventricles increases making the semilunar
valves open and blood is ejected.
E. Early Ventricular Diastole
semilunar valves closed. Blood flows to the relaxed atria.
F. Late Ventricular Diastole
all chambers are relaxed.
Physiology of cardiac conduction

Cardiac electrical activity is the result of the

movement of ions across the cell membrane

The electrical charges recorded within a single

cell is known as the action potential

A change in serum potassium affects the

normal electrical voltage of the cell

A change in the calcium concentration may alter

the contraction of the heart
Cardiac action potential
Depolarization
(electrical activation of the
cell); Contraction of
the myocardium follows

Repolarization (return
of the cell to its
resting state) this
corresponds to
relaxation of myocardial
muscle.
 In the resting state, cardiac muscle cells
are polarized, which means an electrical
difference exists
negatively charged inside
positively charged outside
of the cardiac cell membrane.
 CARDIAC OUTPUT

The volume of blood ejected by each

ventricle per minute

STROKE VOLUME
The volume of blood ejected by each
ventricle per beat
5 liters /minute
CO = HR x SV 70ml /beat
HR - 60 to 80 beats/min
 Cardiac reserve refers to the maximum
percentage of increase in cardiac output
that can be achieved above the normal
resting level.
300% to 100%

CARDIAC INDEX
The cardiac output divided by
body surface area
 FACTORS THAT DETERMINE
STROKE VOLUME
• PRELOAD
THE AMOUNT OF BLOOD THAT THE
HEART MUST PUMP WITH EACH BEAT
• AFTERLOAD
THE PRESSURE THAT THE HEART MUST
GENERATE TO MOVE BLOOD INTO
THE AORTA
• CONTRACTILITY
THE ABILITY OF HEART TO CHANGE ITS
FORCE OF CONTRACTION WITHOUT
CHANGING ITS RESTING LENGTH
end of diastole is the period when filling
volume in the ventricles is the highest
and the degree of stretch on the muscle
fibers is the greatest
Frank-Starling law of the heart

As the volume of blood

returning to the heart increases,
muscle fiber stretch also
increases,
resulting in stronger
contraction and a greater stroke
volume.
 SNS stimulation
- releases norepinephrine and epinephrine
causing vasoconstriction and increase heart rate
(cardioaccelerating center)
 PNS stimulation
- releases acetylcholine, causing decreased cardiac
contractility thereby reducing heart rate
(cardioinhibiting center)
 Chemoreceptors
- increases heart rate as a response to increased
CO2 and decreased O2 levels in the body
 Baroreceptors – specialized nerve cells (aortic/
internal carotid arteries) sensitive to change in BP
 Cardiac
Assessment
HEALTH HISTORY AND
CLINICAL MANIFESTATIONS

obtains the health history using a few

specific questions about the onset and severity
of chest discomfort, associated symptoms,
current medications, and allergies

observes the patient’s general

appearance and evaluates hemodynamic
status (heart rate and rhythm, BP)
 COMMON MANIFESTATIONS
OF HEART DISEASE

Chest pain is the most common manifestation

in patients with cardiac disease, and
is the second most common chief complaint
presenting to emergency departments

Other manifestations of heart disease may include

shortness of breath
palpitations
weakness,
fatigue, dizziness, syncope, or GI complaints.
 SIGN & SYMPTOMS
1. CHEST PAIN
W – Where is the pain? Does it radiate?
H – How does it feel?
A – Aggravating factor/Alleviating factors
that increase/relieve the pain?
T – Timing of pain: onset, duration,
frequency?
S – Severity of pain?
U – Useful data for associated symptoms
P – Perception of patient about problem
PHYSICAL ASSESSMENT

General Appearance and Cognition

patient’s level of distress
level of consciousness,and
thought processes

indication of the heart’s ability

to propel oxygen to the brain (cerebral
perfusion)
Inspection of the Skin
Skin color, temperature, and texture
• Pallor - anemia or decreased arterial perfusion
• Peripheral cyanosis – decreased flow rate of
blood to a particular area
• Central cyanosis - denotes serious cardiac
disorders
Temperature
cool and moist - in cardiogenic shock
diaphoresis is common during an acute MI.
Assess presence of edema
 BLOOD PRESSURE MEASUREMENT

PULSE PRESSURE
the difference between the systolic and
the diastolic pressures

normally is 30 to 40 mm Hg
Assessment of Arterial Pulses

PULSE RATE
PULSE RHYTHM
disturbances of rhythm (dysrhythmias) often
result in a pulse deficit

PULSE QUALITY
Scales to rate the strength of the pulse
0 pulse not palpable or absent
+1 weak, thready pulse; difficult to palpate;
obliterated with pressure
+2 diminished pulse; cannot be obliterated
+3 easy to palpate, full pulse; cannot be obliterated
+4 strong, bounding pulse; may be abnormal
Jugular Venous Pulsations

an estimate of
right-sided heart
function

an obvious distention of the veins with

the patient’s head elevated 45 to 90 degrees
indicates an abnormal increase in the volume
of the venous system
Heart Inspection and Palpation
Examination of the chest wall is performed
in the following areas
HEART AUSCULTATION
◼ S1 – 1st heart sound - associated with tricuspid and mitral closure;
lub sound
◼ S2 – heart sound - associated with aortic and pulmonic valve
closure; dub sound
◼ S3 – 3rd heart sound (ventricular gallop)
◼ - normal in children and young adults
- for older people signs of heart failure
◼ S4 – 4th heart sound (atrial gallop) – normal mostly on older adult;
sign of hypertension in adult
◼ Cardiac Murmurs
- turbulent sounds occuring between normal heart sounds
- sign of congenital heart disease, valvular defect
◼ Pericardial Friction Rub
- high- pitched scratchy sound heard during S1 and or S2 at the
apex (sign of pericarditis)
 CARDIOVASCULAR SYSTEM
ANATOMY AND PHYSIOLOGY_______________________

HEART
Location: mediastinum, apex lies on the diaphragm pointing to the left and the base lies just below the second rib
: two thirds of its mass is to the left of the midline of the body and one third to the right

Coverings of the heart______________________________________

PERICARDIUM
Fibrous pericardium – tough, loose-fitting, inextensible sac
Serous pericardium – parietal layer lies inside the fibrous
pericardium and visceral layer (epicardium) adheres to the
outside of the heart: pericardial space with pericardial fluid
separates the 2 layers

Function: provides protection against friction

Wall of the Heart – made up of 3 distinct layers

A. Epicardium – outer layer of the heart wall

B. Myocardium – thick, contractile middle
layer of heart wall: compresses the heart
cavities, and the blood within them, with
great force.
C. Endocardium – delicate inner layer of
endothelial tissue
Chambers of the heart – divided into 4 cavities separated by a septum
ATRIA – 2 superior “receiving chambers” myocardial wall of each
chamber is not very thick
VENTRICLES – 2 lower “pumping chambers”, great force must be
generated to pump the blood at a large distance: left ventricular
myocardium is thicker than the right

Valves of the Heart: mechanical devices that permit flow of blood in one
direction only
A. ATRIOVENTRICULAR (AV) VALVES
1. Tricuspid valve – right AV valve: attached to papillary
muscles by chordae tendineae
2. Biscuspid or Mitral Valve – similar in structure with
Tricuspid except only for 2 flaps

B. SEMILUNAR (SL) VALVES

1. Pulmonary Semi -lunar valves – valve at the entrance
of the pulmonary artery
2. Aortic Semi-lunar valve –at the entrance of the aorta

PULMONARY AND SYSTEMIC CIRCULATION

Pulmonary Circulation
- functions as low pressure system
- MAP = 12 mmHg
Systemic Circulation
- functions as high pressure system
MAP = 90-100 mmHg

__________________________________________________BLOOD SUPPLY OF HEART TISSUE

Coronary arteries – myocardial cells receive blood from the right and left coronary arteries
Coronary Veins
_____________________________________________________________________CONDUCTION SYSTEM:
special electrical cells generate and coordinate electrical impulses to myocardial cells

PROPERTIES (RACE)

RHYTHMICITY
Regularity of impulse transmission
AUTOMATICITY
Ability to initiate electrical impulses
CONDUCTIVITY
Ability to transmit electrical impulse from one cell to another
EXCITABILITY
Ability to respond to electrical stimuli

Phases of Cardiac Cycle_________________________________________________________

Cardiac
electrophysiology_________________________
__________

____________________CARDIAC OUTPUT
Amount of blood pumped by each ventricle per minute
The product of heart rate and stroke volume

STROKE VOLUME –volume of blood pumped by the

ventricle with each contraction (60-70 cc)

3 factors that affect stroke volume

Preload:
: the degree of stretch of the heart muscle at the end of
diastole
: the amount of blood that the heart must pump with
each beat

Afterload
:the pressure that the vetricular myocardium must
overcome to eject blood during contraction
: the pressure that the heart must generate in order to
move blood into the aorta

Contactility
: term used to denote the force generated by the given condition
:the ability of muscle cells to contract after receiving stimulus

Starling’s law
THE GREATER THE MYOCARDIAL CELLS ARE STRETCHED THE MORE FORCEFUL THE CONTRACTION
Regulation of the Cardiovascular System__________________________
 SNS stimulation
- releases norepinephrine and epinephrine by adrenal medulla, causing vasoconstriction
and increase heart rate (cardioaccelerating center)
 PNS stimulation
- releases acetylcholine, causing decreased cardiac contractility thereby reducing heart rate
(cardio inhibiting center)
 Chemoreceptors
- increases heart rate as a response to increased CO2 and decreased O2 levels in the body
 Baroreceptors
- influences blood pressure changes

Subjective
Cardiac Assessment 1. CHEST PAIN (WHAT’S UP)

W – Where is the pain? Does it radiate?

H – How does it feel?
A – Aggravating factor/Alleviating factors
2. Level of consciousness
that increase/relieve the pain?
3. Palpitations
T – Timing of pain: onset, duration,
4. Fatigue
frequency?
5. Paresthesia/Paralysis
S – Severity of pain?
6. Dyspnea
A. Exertional
U – Useful data for associated symptoms
B. Orthopnea
P – Perception of patient about problem
C. Paroxysmal Nocturnal Dyspnea

Objective
Inspection

Distended neck veins

4-point scale
Central Cyanosis for grading edema
Peripheral Cynosis
Clubbing of Nail beds

Palpation
Pulse
- bounding Auscultation
- thread st
• S1 – 1 heart sound
- irregular
- associated with tricuspid and mitral closure; lub sound
- pulsus alternans • S2 – heart sound
- thrill - associated with aortic and pulmonic valve closure; dup sound
Edema •
rd
S3 – 3 heart sound
- ventricular gallop
th
Percussion • S4 – 4 heart sound
Abnormal cardiac borders - atrial gallop
• Cardiac Murmurs
- turbulent sounds occuring between normal heart sounds
• Pericardial Friction Rub
- high- pitched scratchy sound heard during S1 and or S2 at the apex

Normal or physiologic splitting of S2 occurs during inspiration. It results from delayed closure of the pulmonic valve. Both pulmonic and
aortic components of S2 can be heard. Inspiration creates negative pressure in the thoracic cavity, pulling blood from the periphery into
the right side of the heart . Because of the transient augmentation in venous return, right ventricular volume increases and emptying is
delayed, delaying pulmonic valve closure. The ‘split second heart sound’ is best heard over the pulmonic area.
___________________________Coronary Artery Disease (CAD)
• is a condition in which the blood supply to the heart muscles is completely or partially blocked.
ARTERIOSCLEROSIS
• Chronic disease of the arterial
system characterized by abnormal
thickening & hardening of the
vessel walls
ATHEROSCLEROSIS
• A condition where patchy deposits
of fatty material develop in the
walls of arteries, leading to reduced
or blocked blood flow.

1. Nonmodifiable risk factors:

a. age
b. sex
c. race
d. genetics

2. Nonmodifiable risk factors:

H ypertension
O besity
P VD
E levated Serum cholesterol level
F emale (Menopause)
U p glucose – Diabetes Mellitus
L evels of Homocysteine elevated
S moking
S tress
S edentary life style

____________________________CAUSES
1. decreased blood supply
– atherosclerosis
– vasopasm
– thrombus, embolus
2. decreased oxygen in blood
– anemia
– carbon monoxide
3. Increased demand for blood
– Hypertension
– Valvular stenosis/ insufficiency
– Hyperthyroidism
– Hyperthermia
– Stress
ANGINA PECTORIS___________________________
Transient chest pain caused by insufficient blood flow to the myocardium resulting in myocardial ischemia.

• Precipitating Events (5 E’s)

– Exertion
TYPE DESCRIPTION
– Emotions
Stable angina predictable and consistent pain – Eating
that occurs on exertion and is
– Extremes of temperature
relieved by rest
– Exercise/Sexual activity
Unstable symptoms occur more frequently
angina and last longer than stable angina
Signs and Symptoms___________________
(preinfarction
or crescendo)
• Pain start in the center of the chest, but the
Intractable or Chronic, severe incapacitating
pain may spread to the left arm, neck, back,
refractory chest pain
angina throat, or jaw.
• numbness or a loss of feeling in the arms,
Variant angina pain at rest; thought to be caused
(Prinzmetal’s by coronary artery vasospasm shoulders, or wrists.
angina) • shortness of breath; pallor, diaphoresis, light-
headedness, nausea and vomiting.
Silent ischemia objective evidence of ischemia • Pain is relieved by rest or with the use of
(such as electrocardiographic
nitroglycerin
changes with a stress test), but
patient reports no symptoms • An episode usually lasts less than 20 min

Diagnostic Tests

• ECG: normal during rest or absence of an anginal

attack
• ST depression and T wave inversion only during
acute attacks
• Cardiac enzymes are normal
• Increased C reactive protein: inflammation of the
vascular endothelium
• CORONARY ANGIOGRAPHY – provides the most
accurate info. about the patency of the coronary
arteries
 CONGESTIVE HEART FAILURE________________________________________

• A general term to describe several types of cardiac dysfunction that result in inadequate
perfusion of tissues with vital blood—borne nutrients.

RISK FACTORS

R- enal disease
A- nemia
P- ulmonary embolism
I- nfection (myocarditis, Pericarditis)
D- elivery after pregnancy
F- orget to take the meds
A- rrhythmias
I- ischemia/infarction
L- ipid aggregation
U- ncontrolled hypertension
R- HD
E- ndocarditis

DESCRIPTION

CLASS I No symptoms noted with normal

activity

CLASS II Symptoms noted with normal

activity but subside with rest

CLASS III Symptoms noted with minimal

activity; may or may not be
symptom free at rest
CLASS IV Symptoms usually present at rest
and worsened at any type of
activity

Compensatory Mechanisms*

• Sympathetic Response
• Baroreceptor Reflex
• Frank-Starling Law
• Dilation & Hypertrophy of the Heart
• RAA System
• Release of ADH
FUNCTIONAL CLASSIFICATION OF HEART FAILURE
___________________
*read Pathophysiology by Porth
 LEFT SIDED HEART FAILURE_________
Occurs when left side of the heart is unable to pump the total volume of blood it receives from the right side of the heart

Pathophysiology

CLINICAL MANIFESTATIONS

• Dyspnea in the early

stages
• Decreases O2 saturation
• Increase RR
• Easy fatigability, weakness
and dizziness
• Orthopnea
• Auscultation reveals S3
gallop
• Pulsus alternans
• Paroxysmal Nocturnal
Dyspnea
• Cardiac asthma
• Acute pulmonary edema=
life-threatening since it may progress to
shock & death
 _________________________________________RIGHT SIDED HEART FAILURE
Impairs the ability to move deoxygenated blood from the systemic circulation into the pulmonary circulation

Etiology

• Persistent left sided heart failure

• Stenosis / Regurgitation of tricuspid or pulmonic valves
• Right ventricular infarction
• Acute / chronic pulmonary disease: COPD, severe pneumonia, pulmonary embolus
• Pulmonary hypertension (cor pulmonale)

Pathophysiology

Clinical Manifestation________________________
• Major manifestation: PERIPHERAL EDEMA
• Weight gain
• Hepatomegaly
• RUQ pain
• Splenomegaly
• Ascites
• Anorexia and abdominal discomfort
• JV distention
_____________________Diagnostic tests
• Chest x-ray
• Echocardiography
• Elevated SGPT
• Decrease CVP

Nursing Diagnosis Goals:

Decreased cardiac output 1. To monitor for reduced cardiac workload
Fluid Volume Excess 2. To maintain adequate fluid balance
Impaired Gas Exchange 3. To reduce myocardial workload
Ineffective Tissue Perfusion 4. To monitor for pulmonary edema
Risk for Activity Intolerance 5. To assess response to medical therapies
Risk for impaired skin integrity
Risk for Anxiety

Management_________

U- pright position
N- itrates
L- asix, dieuretics
O- xygen
A- minophylline
D- igoxin
F- luids decrease
A- fterload decrease (ace, beta, ca)
S- Na restriction
T-est (monitor diff electrolytes), SFF

Surgical Management

A. VENTRICULAR ASSIST DEVICE

Is a mechanical circulatory device that is
used to partially or completely replace the
function of the failing heart.

B. HEART TRANSPLANTATION

C. CARDIOMYOPLASTY
MYOCARDIAL INFARCTION___________________________________
o The formation of localized necrotic areas within the myocardium.
o Usually follows sudden coronary occlusion and the abrupt cessation of
blood and oxygen flow to the heart muscle.

Classifications:
• TRANSMURAL INFARCT
- from endocardium to epicardium
• SUBENDOCARDIAL INFARCT
- affects myocardium and endocardium
• INTRAMURAL INFARCT
- patchy area of the myocardium with longstanding angina pectoris

The 3 areas which develop in MI are as follows

Zone of injury – elevated ST segment
Zone of ischemia – T wave inversion
Zone of infarction – pathologic Q wave (permanent)
Pathophysiology
Myocardial Ischemia

Decrease blood supply to Decrease blood supply to cardiac

cardiac tissue for less than 20 tissue for more than 20 minutes
minutes
Release of
Angina Pectoris Myocardial necrosis
lysosomal enzymes

Anaerobic metabolism
Elevated
CPK-MB,
Hydrogen ions & lactic acid
Chest
Trop I
accumulation Pain

Acidosis

Altered cell
membrane integrity

Suppressed impulse Decreased myocardial

conduction contractility

Decreased left Increased in

ventricular function preload
ECG changes;
Dysrythmias

Decreased stroke
volume

increased HR;
SNS stimulation Increased
afterload

Further increase in
myocardial O2
demand
_________________________________ Manifestations

Diagnostic
Blood Chemistry
Increased WBC
Increased ESR
Cardiac Enzymes
ECG Changes

Cardiac Enzymes
Cardiac specific isoenzyme
Accurate indicator of myocardial damage
Elevated 4 hrs after
NV:
M- 50-325 mu/ml
F- 50-250 mu/ml

Myoglobin
Earliest enzyme to increase
Elevated 1-3 hrs after
Troponin
Protein found in the myocardium, regulates
the myocardial contractile process
Elevated 3-4 hrs after; duration is 3 weeks
Aspartate Aminotransferase (AST)
Formerly SGOT
Elevated level indicates tissue necrosis
Elavated 4-6 hrs after
Lactic Dehydrogenase (LDH)
__________________Medical Management Surgical Management
I V access/regulation Percutaneous transluminal coronary angioplasty
N arcotic analgesics (morphine) • Mechanical dilatation of the coronary vessel wall
P osition in Semi fowlers by compressing the atheromatous plaque
A spirin/ Anticoagulant (heparin, warfarin)
R est / relieve anxiety (diazepam)
C onverting enzyme inhibitor (ACE inhibitor –
captopril)
calcium channel blocker (nifedipine, verapamil)
T hrombolytics (streptokinase, urokinase & TPA)
I V beta blocker (propranolol, metoprolol, atenolol)
O xygen
N itrates (nitroglycerin)
S tool Softeners

Intravascular stenting
Maintains good luminal geometry after balloon deflation &
withdrawal
Done to prevent restenosis after PTCA
Risk of thrombus formation

Atherectomy
Invasive interventional procedure that involves the removal of the atheroma, or plaque, from a coronary artery
TRANSMYOCARDIAL LASER REVASCULARIZATION
Coronary artery bypass graft (CABG)
Main purpose is myocardial revascularization
Commonly used grafts:
-Saphenous vein
-Internal mammary artery

Open Heart Surgery

_____________________________Cardiac Rehabilitation
A process in which a person is restored to health &
maintains optimal functioning. TEACHING GUIDE IN RESUMPTION OF SEXUAL ACITVITY
Begins the moment a client is admitted to the hospital • CLUE: able to climb two flights of stairs without
Goals: dyspnea , chest pain and other abnormalities
To live as full, vital & productive life • Assume less fatiguing position ( non MI partner
Remain within the limits of the heart’s ability to respond on top)
to activity & stress • If both are MI patients: side lying
• Perform activity in a cool, familiar environment,
Teaching and Counseling early in the morning
• Discontinue smoking • Take nitroglycerine before sexual act
• Continued medical supervision • Refrain from sexual activity during a fatiguing
• Diet modification day, after eating a large meal
• Weight reduction • If any abnormalities occur, stop activity
• Progressive exercise
• Stress management
• Resume sexual activity – after 4-6 weeks
 Complications
A rrhythmias
A neurysm
B radycardia
B P lower
C ardiogenic shock
C ardiac tamponade
D ressler’s syndrome
E mbolism

_________________________________________KILLIP Classification System

 The is used in individuals with an acute myocardial infarction (heart attack), in order to risk stratify them.
 Individuals with a low Killip class are less likely to die within the first 30 days after their myocardial
infarction than individuals with a high Killip class.

Killip class I
- no clinical signs of heart failure
Killip class II
- with rales or crackles in the lungs, an S3 sound, and jugular vein distention
Killip class III
- with acute pulmonary edema

Killip class IV
- cardiogenic shock or hypotension & evidence of peripheral vasoconstriction
 CONGENITAL HEART DEFECTS

USUAL CAUSE: Failure of a heart structure to progress beyond an early stage of embryonic
development
 Maternal rubella
 Familial

CLASSIFICATION OF CONGENITAL HEART ANOMALIES

Classification Description Example

CYANOTIC  Occurs when blood is shunted from Tetralogy of Fallot
the venous to arterial system as a Transposition of the great arteries
result of abnormal communication
Tricuspid atresia
between the two
Pulmonary atresia
 Right-to-left shunt
Hypoplastic left heart syndrome
Persistent truncus arteriosus
ACYANOTIC
a. Left-to-right shunt Ventricular septal defect
Atrial septal defect
Patent ductus arteriosus
Atrioventricular septal defect
a. Obstructive Pulmonic stenosis
Aortic stenosis
Aortic coarctation

FOUR SPECIFIC CLASSIFICATIONS

1. Increased pulmonary blood flow
2. Obstruction to blood flow (out of the heart)
3. Mixed blood flow (oxygenated and deoxygenated blood mixing in the heart or great vessels)
4. Decreased pulmonary blood flow

DEFECTS WITH INCREASED PULMONARY BLOOD FLOW

 Involves blood flow from the left side of the heart (greater pressure) to the right side (less pressure)
through some abnormal opening or connection between the two systems or the great arteries.
 Defects:
o ASD
o VSD
o AVC (Atrioventricular canal)
o PDA
1. ATRIAL SEPTAL DEFECT
 Abnormal opening between the atria that causes an increased flow of oxygenated blood to the right side
of the heart
 Right atrial and ventricular enlargementoccur.
 Infant may be asymptomatic or may develop CHF.
 Signs and symptoms of decreased cardiac output may be present
Types
 ASD 1 (ostium primum): Opening is at the lower end of the septum.
 ASD 2 (ostium secundum): Opening is n ear the center of the septum.
 ASD 3 (sinus venosus defect): Opening is near the junction ofthe superior vena cava and the right atrium.

Assessment
o Asymptomatic
o Prone to RTI
o Dyspnea on mild exertion
o May develop CHF
o Feeding difficulties
o S/SX OF DECREASE CARDIAC OUTPUT
 Decreased peripheral pulses
 Exercise intolerance
 Feeding difficulties
 Hypotension
 Irritability, restlessness, lethargy
 Oliguria
 Pale, cool extremities
  Tachycardia
 Management:
o Nonsurgical treatment: The defect may be closed during a cardiac catheterization.
Surgical treatment: Open repair with cardiopulmonary bypass usually is performed before school
age.

2. VENTRICULAR SEPTAL DEFECT

 Abnormal opening between the right & left ventricles
 Many VSDs close spontaneously during the first year of life in children having small or moderate defects.
 A characteristic murmur is present.
 TYPES
o Low septum (smaller)
o High septum (bigger)
 Management:
o Nonsurgical: Cardiac Cath
o Surgical: Open repair

3. ATRIOVENTRICULAR CANAL
 The defect results from incomplete fusion of the endocardial cushions.
 The defect is the most common cardiac defect in Down syndrome.
 A characteristic murmur is present.
 The infant usually has mild to moderate CHF, with cyanosis increasing with crying.
 Signs and symptoms of decreased cardiac output may be present.
 Surgical treatment can include pulmonary artery banding for infants with severe symptoms (palliative) or
complete repair via cardiopulmonary bypass.
4. PATENT DUCTUS ARTERIOSUS
 Failure of fetal ductus arteriosus to close within the first weeks of life
 HR: mothers exposed to rubella during pregnancy
 Assessment:
o Machinery like murmur
o Asymptomatic
o s/sx of CHF
o Prominent radial pulses
o s/sx of decreased cardiac output
 Management:
 Medical: Indomethacin (Indocin) - a
prostaglandin inhibitor, may be administered
to close a patent ductus in prematureinfants
and some newborns.
 The defect may be closed during cardiac
catheterization or the defect may require
surgical management.
OBSTRUCTIVE DEFECTS
 Blood exiting a portion of the heart meets an area of anatomical narrowing (stenosis), causing obstruction
to blood flow.
 The location of narrowing is usually near the valve of the obstructive defect.
 Infants and children exhibit signs of CHF.
 Children with mild obstruction may be asymptomatic.
 Defects:
o Aortic stenosis
o Coarctation of the aorta
o Pulmonary stenosis

1. AORTIC STENOSIS
 Aortic stenosis is narrowing or stricture of the aortic
valve, causing resistance to blood flow in the left
ventricle, decreased cardiac output, left ventricular
hypertrophy, and pulmonary vascular congestion.
 Valvular stenosis is the most common type and usually
is caused by malformed cusps, resulting in a bicuspid
rather than a tricuspid valve, or fusion of the cusps.
 A characteristic murmur is present.
 Infants with severe defects demonstrate signs of
decreased cardiac output.
 Children show signs of exercise intolerance, chest pain,
and dizziness when standing for long periods of time.
 Nonsurgical treatment for valvular aortic stenosis is
done during cardiac catheterization to dilate the
narrowed valve.
 Surgical treatment for valvular aortic stenosis is aortic valvotomy
(palliative); a valve replacement may be required at a second
procedure.

2. COARCTATION OF AORTA
 Localized narrowing of aorta – near insertion of ductus
arteriosus
 Coarctation of the aorta is localized narrowing near the insertion
of the ductus arteriosus.
 The blood pressure is higher in the upper extremities than the lower extremities; bounding pulses in the
arms, weak or absent femoral pulses, and cool lower extremities may be present.
 Assessment:
o Absent femoral pulses – pathognomonic sign
o BP
 Higher in upper extremities – headache; epistaxis; pulses are rapid & bounding
  Lower in lower extremities – leg pains, cold feet, muscle spasms; pulses are weak,
delayed or absent
o Myocardial hypertrophy
 Management:
o Nonsurgical treatment is balloon angioplasty in children; restenosis can occur.
o Surgical:
 Mechanical ventilation and medications to improve cardiac output are often necessary before surgery.
 Resection of the coarcted portion with end-to-end anastomosis of the aorta or enlargement of the
constricted section using a graft may be required.
 Because the defect is outside the heart, cardiopulmonary bypass is not required and a thoracotomy
incision is used.

3. PULMONARY STENOSIS
 Pulmonary stenosis is narrowing at the entrance to the
pulmonary artery.
 Resistance to blood flow causes right ventricular
hypertrophy and decreased pulmonary blood flow; the
right ventricle may be hypoplastic.
 Pulmonary atresia is the extreme form of pulmonary
stenosis in that there is total fusion of the commissures
and no blood flows to the lungs.
 A characteristic murmur is present.
 The infant or child may be asymptomatic.
 Newborns with severe narrowing will be cyanotic.
 If pulmonary stenosis is severe, CHF occurs.
 Signs and symptoms of decreased cardiac output may
occur.
 Nonsurgical treatment is done during cardiac
catheterization to dilate the narrowed valve.
 Surgical treatment
 o In infants, transventricular (closed) valvotomy procedure.
o In children, pulmonary valvotomy with cardiopulmonary bypass.
DEFECTS WITH DECREASED PULMONARY BLOOD FLOW
• Obstructed pulmonary blood flow and an anatomical defect (ASD or VSD) between the right and left sides
of the heart are present.
• Pressure on the right side of the heart increases, exceeding pressure on the left side, which allows
desaturated blood to shunt right to left, causing desaturation in the left side of the heart and in the
systemic circulation.
• Typically hypoxemia and cyanosis appear.

1. TETRALOGY OF FALLOT

 The tetralogy of Fallot includes

four defects—VSD, pulmonary
stenosis, overriding aorta, and
right ventricular hypertrophy.
 If pulmonary vascular
resistance is higher than
systemic resistance, the shunt
is from right to left; if systemic
resistance is higher than
pulmonary resistance, the
shunt is left to right.

 Infants
o The infant may be acutely cyanotic at birth or may have mild cyanosis that progresses over the
first year of life as the pulmonic stenosis worsens.
o A characteristic murmur is present.
o Acute episodes of cyanosis and hypoxia (hypercyanotic spells), called blue spells or tet spells,
occur when the infant's oxygen requirements exceed the blood supply, such as during periods of
crying, feeding, or defecating.
 Children: With increasing cyanosis, squatting, clubbing of the fingers, and poor growth may occur.
o Squatting is a compensatory mechanism to facilitate increased return of blood flow to the heart
for oxygenation.
o Clubbing (an abnormal enlargement in the distal phalanges seen in the fingers) is symptomatic of
chronic hypoxia as peripheral circulation is diminished to allow oxygenation of vital organs and
tissues.
 Summary of Assessment Findings:
o Cyanosis
o Tet spells
o Clubbing of fingers
o Growth retardation
o Exertional dyspnea relieved by squatting
 o Polycythemia --- CVA
o DX: History; PE; Cardiac catheterization; angiography
 Management:
o Conservative: hydration, prevent infection, positioning; O2; morphine; Do not allow to cry for
long period of time
o Surgical treatment: Palliative shunt (Blalock-Taussig)
 The shunt increases pulmonary blood flow and increases oxygen saturation in infants
who cannot undergo primary repair.
 The shunt provides blood flow to the pulmonary arteries from the left or right
subclavian artery.
o Surgical treatment: Complete repair (Brock procedure)
 Complete repair usually is performed in the first year of life.
 The repair requires a median sternotomy and cardiopulmonary bypass.

2. TRICUSPID ATRESIA
 Tricuspid atresia is failure of the tricuspid valve to develop.
 No communication exists from the right atrium to the right ventricle.
 Blood flows through an ASD or a patent foramen ovale to the left side of the heart and through a VSD to
the right ventricle and out to the lungs.
 The defect often is associated with pulmonic stenosis and transposition of the great arteries.
 The defect results in complete mixing of unoxygenated and oxygenated blood in the left side of the heart,
resulting in systemic desaturation, pulmonary obstruction, and decreased pulmonary blood flow.
 Cyanosis, tachycardia, and dyspnea are seen in the newborn.
 Older children exhibit signs of chronic hypoxemia and clubbing.
 Surgical treatment
 o If the ASD is small, the defect
may be closed during cardiac
catheterization; otherwise,
surgery is needed.
o For the neonate whose
pulmonary blood flow
depends on the patency of
the ductus arteriosus, a
continuous infusion of
prostaglandin E1 is initiated
until surgery.

MIXED DEFECTS
 Fully saturated systemic blood flow
mixes with the desaturated blood flow,
causing a desaturation of the systemic blood flow.
 Pulmonary congestion occurs and cardiac output decreases.
 Signs of CHF are present; symptoms vary with the degree of desaturation.
 Defects:
o Hypoplastic left heart syndrome
o Total anomalous pulmonary venous connection
o Transposition of the great arteries or transposition of the great vessels
o Truncus arteriosus

1. HYPOPLASTIC LEFT HEART SYNDROME

 Underdevelopment of the left side of the
heart occurs, resulting in a hypoplastic left
ventricle and aortic atresia.
 Mild cyanosis and signs of CHF occur until
the ductus arteriosus closes; then
progressive deterioration with cyanosis
and decreased cardiac output are seen,
leading to cardiovascular collapse.
 The defect is fatal in the first few months
of life without intervention.
 Surgical treatment
o Surgical treatment is necessary;
transplantation in the newborn
period may be considered.
o In the preoperative period, the neonate requires mechanical ventilation and a continuous
infusion of prostaglandin E1 to maintain ductal patency, ensuring adequate systemic blood flow
2. COMPLETE TRANSPOSITION OF GREAT
ARTERIES OR GREAT VESSELS
 The pulmonary artery leaves the left
ventricle, the aorta exits from the right
ventricle
 The pulmonary artery leaves the left
ventricle, and the aorta exits from the
right ventricle.
 No communication exists between the
systemic and pulmonary circulation.
 Infants with minimal communication
are severely cyanotic and depressed at
birth.
 Infants with large septal defects or a
patent ductus arteriosus may be less
severely cyanotic, but may have
symptoms of CHF.
 Cardiomegaly is evident a few weeks
after birth.
 Nonsurgical treatment
o Prostaglandin E1 may be initiated to increase blood mixing temporarily if systemic and
pulmonary mixing are inadequate.
o Balloon atrial septostomy during cardiac catheterization may be performed to increase mixing
and to maintain cardiac output over a longer period.
 Surgical treatment: The arterial switch procedure reestablishes normal circulation with the left ventricle
acting as the systemic pump and creation of a new aorta.
3. TOTAL ANOMALOUS PULMONARY VENOUS CONNECTION
 The defect is a failure of the pulmonary veins
to join the left atrium.
 The defect results in mixed blood being
returned to the right atrium and shunted
from the right to the left through an ASD.
 The right side of the heart hypertrophies,
whereas the left side of the heart may remain
small.
 Signs and symptoms of CHF develop
 Cyanosis worsens with pulmonary vein
obstruction; once obstruction occurs, the
infant's condition deteriorates rapidly.
 Surgical treatment
o Corrective repair is performed in
early infancy.
o The pulmonary vein is anastomosed
to the left atrium, the ASD is closed,
and the anomalous pulmonary
venous connection is ligated.

4. TRUNCUS ARTERIOSUS
 Truncus arteriosus is failure of normal
septation and division of the embryonic
bulbar trunk into the pulmonary artery and
the aorta, resulting in a single vessel that
overrides both ventricles.
 Blood from both ventricles mixes in the
common great artery, causing desaturation
and hypoxemia.
 A characteristic murmur is present.
 The infant exhibits moderate to severe CHF
and variable cyanosis, poor growth, and
activity intolerance.
 Surgical treatment: Corrective surgical repair
is performed in the first few months of life.
INTERVENTIONS: CARDIOVASCULAR DEFECTS____________________
• Monitor for signs of a defect in the infant or child (as described with defects above).
• Monitor vital signs closely.
• Monitor respiratory status for the presence of nasal flaring, use of accessory muscles, and other signs of
impending respiratory distress and notify the physician if any changes occur.
• Auscultate breath sounds for crackles, rhonchi, or wheezes.
• If respiratory effort is increased, place the child in a reverse Trendelenburg position, elevating the head and
upper body, to decrease the work of breathing.
• Administer humidified oxygen as prescribed.
• Provide endotracheal tube and ventilator care as prescribed.
• Monitor & manage hypercyanotic spells
o Place the infant in a knee-chest position.
o Administer 100% oxygen by face mask.
o Administer morphine sulfate as prescribed.
o Administer fluids intravenously as prescribed
• Assess for signs of CHF, such as periorbital edema or dependent edema in the hands and feet.
• Assess peripheral pulses.
• Maintain strict fluid restriction if prescribed.
• Monitor intake and output, and notify the physician if a decrease in urine output occurs.
• Obtain daily weight.
• Provide adequate nutrition (high calorie requirements) as prescribed.
• Administer medications as prescribed.
• Keep the child as stress-free as possible.
• Plan interventions to allow maximal rest for the child.
• Prepare the child and parents for cardiac catheterization, if appropriate.

CARDIAC CATHETERIZATION________________________
• Discharge teaching
– Remove dressing; cover w/ band-aid for 2-3 days
– Keep site clean & dry
– Avoid tub baths for 2-3 days
– Child may return to school
– Diet as tolerated
– Administer medications
– Follow-up appointment

___________________________CARDIAC SURGERY
• Postoperative
– Monitor vital signs frequently, especially the temperature, and notify the physician if fever
occurs.
– Monitor for signs of sepsis, such as fever, chills, diaphoresis, lethargy, and altered levels of
consciousness.
– Maintain strict aseptic technique.
– Monitor lines, tubes, or catheters that are in place and monitor for signs and symptoms of
infection.
 – Assess for signs of discomfort, such as irritability, restlessness, changes in heart rate, respiratory
rate, and blood pressure.
– Administer pain medications as prescribed.
– Administer antibiotics and antipyretics as prescribed.
– Encourage rest periods.
– Facilitate parent-child contact as soon as possible.

• Home Care After Cardiac Surgery_____________________

– Omit play outside for several weeks.
– Avoid activities in which the child could fall, such as bike riding, for 2 to 4 weeks.
– Avoid crowds for 2 weeks after discharge.
– Follow a no-added salt diet if prescribed.
– Do not add any new foods to the infant's diet.
– Do not place creams, lotions, or powders on the incision until completely healed.
– The child may return to school the third week after discharge, starting with half-days.
– The child should not participate in physical education for 2 months.
– Instruct the parents to discipline the child normally.
– Instruct the parents about the importance of the 2-week follow-up.
– Avoid immunizations, invasive procedures, and dental visits for 2 months.
– Advise the parents regarding the importance of a dental visit every 6 months after age 3 years
and to inform the dentist of the cardiac problem so that antibiotics can be prescribed if
necessary.
– Instruct the parents to call the physician if coughing, tachypnea, cyanosis, vomiting, diarrhea,
anorexia, pain, or fever occur, or any swelling, redness, or drainage occurs at the site of the
incision.
 1. Acute stage
- History of strep infection
Infectious Disease - Subsequent involvement of connective tissues
of the Heart________________________ - Aschoff bodies
2. Recurrent stage
- Extension of the cardiac effects of the disease
RHEUMATIC FEVER 3. Chronic stage
Inflammatory autoimmune disease that affects the connective - Permanent deformity of the heart valves
tissues of the heart, joints, subcutaneous tissues, blood vessels of - Common cause of mitral valve stenosis
the CNS
Complication: RHD
Agent: GABHS

Risk Factors
• Age: 5-15 years old
• Crowding & poor hygiene
• Poor nutrition
• History of GAS infection Pathophysiology
• Genetics

Jones Criteria
1. Presence of 2 major signs
2. Presence of 1 major + 2 minor
3. Evidence of GABHS infection.

MAJOR MANIFESTATIONS_________________

Joints (Polyarthritis) MINOR MANIFESTATIONS

-painful & migratory, affects larger joints
Carditis I ncreased WBC
- Heart murmurs, cardiomegaly, CHF, T emperature elevated (Fever)
pericarditis E levated ESR / C – reactive protein
N odes (Subcutaneous Nodules) R aised or prolonged PR interval
- hard, painless nodules in the knees, I tself (previous history of rheumatic fever
wrist & elbows A rthralgia
E rythema marginatum
-maplike, macular lesions on the trunk
S ydenham/Chorea or St. Vitus dance
-CNS disorder; irregular, aimless, involuntary movement
Diagnostic tests:

• (+) throat culture

• ASO titer (>250 todd in adult; >333
todd in children
• Elevated streptococcal antibody titer
• Elevated WBC, ESR, C-reactive protein
• 2D-echo
• Jones Criteria

Management
– ↓ demand from weakened heart
• CBR
• Cluster care
• Modify lifestyle post discharge
– Prevent further cardiac damage
• Penicillin IM once a month x 3-5
yrs
• Steroids
– Safety precautions for chorea
– Joint pain management

INFECTIVE ENDOCARDITIS_________________________
• a relatively uncommon, life-threatening infection of the
endocardial surface of the heart, including the heart valves.
• FORMS:
– Subacute Bacterial Endocarditis (SBE) Endocarditis
– Acute Bacterial Endocarditis (ABE) - Inflammation of
– Native Valve endocarditis the endocardium
– Prosthetic valve endocarditis -
Bacterial
– Nonbacterial thrombotic endocarditis Non Bacterial

Risk factors

1.Most often bacterial but may be fungal or viral.

2. History of preexisting heart condition.
3. History of recent invasive procedures: minor surgery, dental
procedures, procedures involving the urinary tract.
 Pathophysiology

C
A

Clinical Features___________

1. Osler’s Nodes
2. Janeway’s Lesions
3. Petechiae
4. Splinter hemorrhage (fingernail)
5. Murmurs
_________________Diagnostics
MAJOR CRITERIA
1. History to identify site of entry.
1. Positive Blood Culture
2. Echocardiography
2. Evidence of endocardial involvment (+
3. Blood cultures
echocardiogram)
4. CBC
MINOR CRITERIA
5. ESR
1. Predisposition: Predisposing heart
6. DUKE Criteria
condition or injection drug use
2. Fever > 38 degrees Celsius
3. Vascular phenomena: Janeway lesions,
Nursing Diagnosis____________
conjunctival hemorrhage, intracranial
hemorrhage, major arterial emboli, septic
1. Hyperthermia
pumonary infarcts,
2. Decreased Cardiac Output
4. Immunologic phenomena:
3. Activity Intolerance
glomerulonephritis, Osler’s node, Roth’s
4. Deficient Knowledge
spots, Rheumatoid factor,
5. Microbiologic evidence: positive blood
culture not meeting major criterion
________________GOALS
1. Attainment of normal or baseline cardiac function
2. Performance of ADL without fatigue
3. Knowledge of therapeutic regimen

Treatment

A. IV antibiotic therapy for 4 to 6 weeks

B. Bed rest if high fever or evidence of cardiac damage is present
C. Prophylactic antibiotics for 3 to 5 years, especially in children with history of rheumatic fever or
congenital anomalies.
D. Surgical interventions for severe valvular damage.

E NSURE BED REST

N SAID
D OPPLER SCAN
O BSERVE EMBOLIZATION
C ULTURE OF BLOOD
A NTIBIOTIC REGIMEN
R HD PRECAUTION
D RUG FOR FEVER AND JOINT PAIN
I NTAKE AND OUTPUT MONITORING
U PHOLD GOOD ORAL HYGIENE
M ANAGE VALVULAR DEFECTS
 CARDIAC ENZYME ANALYSIS
• Creatine Kinase (CK is a catalyst for energy production
and is found in brain, myocardium, and skeletal muscle)
ISOENZYME
• (CK-MB): most specific enzyme in Acute M.I
• Accurate indicator.
- CK MM (skeletal muscle)
- CK BB (brain)

Myocardial Infarction
» Onset: 3 to 6 hrs.
» Peaks: 12 to 18 hrs.
» Returns to normal: 3 to 4 days
CARDIAC ENZYME ANALYSIS
• Aspartate Aminotransferase (AST)

• Elevated level indicates tissue necrosis.

• Myocardial Infarction
–Initial elevation: 4 to 6 hrs.
–Peaks: 4 to 36 hrs.
• Return to normal: 4 to 7 days
CARDIAC ENZYME ANALYSIS
• Lactic Dehydrogenase
LDH1 is higher than LDH2
“flipped pattern”; signifies myocardial
necrosis
• Elevation occurs 24 hours post MI and peak in 48
to 72 hours
 CARDIAC ENZYME ANALYSIS

Troponin (three component I.C, T)

Troponin I: contractile CHON found only in
cardiac muscles.
• Most specific laboratory test to detect MI.

Troponin C binds calcium and Troponin T binds I and C.

• Elevated Troponin T is as sensitive as Ck-MB for the
detection of myocardial injury.
• Useful for diagnosis after 4 to 6 hours and
4 to 7 days post MI
CARDIAC ENZYME ANALYSIS

Hydroxybutyrate Dehydrogenase (HBD)

– It is valuable in detecting “silent M.I.”
• because it remains elevated for a long period of
time, even after the other enzymes have returned
to normal.
– Range with Myocardial Infarction
• Onset: 10 to 12 hrs.
• Peaks: 48 to 72 hrs.
• Returns: 12 to 13 days
 LABORATORY TESTS
CARDIAC ENZYMES

ASPARTATE CREATINE KINASE LACTIC HYDROXYBUTYRATE TROPONIN T, I MYOGLOBIN

AMINOTRANS- (CK MB) DEHYDRO- DEHYDROGENASE AND C An O2 binding
FERASE (AST) a catalyst for GENASE (LDH) (HBD) contractile CHON found in
energy CHON found cardiac and
production only in skeletal muscle
cardiac
muscles

ELEVATED valuable in
means Accurate most sensitive detecting silent mi Most specific Valuable in
TISSUE NECROSIS indicator of to myocardial test for early
myocardial damage. myocardial detection
damage injury
 COMPLETE BLOOD COUNT

ELEVATED RBCs: suggests

inadequate oxygenation

ELEVATED WBCs: may indicate

infectious heart disease and
myocardial infarction
ERYTHROCYTE SEDIMENTATION RATE

Measurement of the rate at which RBCs settle out

of anticoagulated blood in an hour

Used as a gauge for evaluating progression

of inflammatory condition

During Inflammatory process

precipitate a rapid settling of the RBC

ELEVATED: infectious heart disease

 COAGULATION TESTS

Prothrombin time determination

Measure the time for clotting to occur after
thromboplastin and calcium are added to decalcified plasma

valuable in evaluating the effectiveness of Coumadin

Normal range is 11 to 16 seconds.

INTERNATIONAL NORMALIZED RATIO (INR)

 COAGULATION TESTS

Partial Thromboplastin Time (PTT)

measures the time required for clotting
to occur after a “partial thromboplastin reagent”
is added to blood plasma.
he best single screening test for disorders of coagulation

to evaluate the effectiveness of Heparin

Normal range is 60 to 70 secs
.
Activated Partial Thromboplastin Time (APTT). -most
specific test to evaluate effectiveness of Heparin.
Normal range is 30 to 45 secs.
 LABORATORY TESTS

• BLOOD UREA NITROGEN (BUN) 10-20 MG/DL

• DECREASED CARDIAC OUTPUT LEADS TO LOW RENAL

PERFUSION AND REDUCTION IN GFR. THE BUN LEVEL
BECOMES ELEVATED
 SERUM LIPID TESTS

BLOOD LIPIDS/LIPID PROFILE

TO ASSESS THE RISK OF DEVELOPING CORONARY ARTERY
DISEASE

SERUM CHOLESTEROL
• NORMAL: 150-250 MG/DL

TRIGLYCERIDES
• FASTING FOR 10-12 HRS PRIOR TO TEST
• NORMAL: 40-150 MG/DL

LIPOPROTEIN
• LDL: LESS THAN 130 MG/DL
• HDL: MEN 35-65 MG/DL FEMALE: 35-85 MG/DL
 SERUM ELECTROLYTE TESTS

SERUM ELECTROLYTES
Electrolytes affect cardiac contractility

Normal range
Na – 135 to 145
K+ - 3.5 to 5 meq
Ca -4.5 to 5.5
 SERUM ELECTROLYTE TESTS

SERUM SODIUM concentration reflects relative

fluid balance
Hyponatremia – fluid excess
Hypernatremia – fluid deficit
 SERUM ELECTROLYTE TESTS

SERUM POTASSIUM

Hypokalemia – cardiac irritability; digitalis toxicity

Hypekalemia – myocardial depression

Both can cause ventricular fibrillation/ cardiac

standstill
 SERUM ELECTROLYTE TESTS

SERUM CALCIUM – BLOOD COAGULABILITY and

neuromuscular activity
can cause dysrhythmias
C-Reactive Protein (CRP)
•CHON that is synthesized by the liver
& is not normally present in the blood
except when there is tissue trauma.

•Inflammatory markers predictor of

future coronary events in seemingly
healthy person
Homocysteine
•Amino acid produced by body as a
by product of consuming meat

•linked to the development of

atherosclerosis

•Associated with genetic factors &

diet low in folic acid, vitamin B6 &
vitamin B12..
Brain (B-Type) Natriuretic
Peptide (BNP)
• neurohormones

primarily secreted from the ventricles in

response to increase preload

• Blood marker for identifying

and treating congestive heart
failure (CHF)
 LABORATORY TESTS

• URINALYSIS

• ALBUMINURIA- seen in pts. with hypertension or diabetes

• MYOGLOBINURIA – supports diagnosis of MI
•
 INVASIVE HEMODYNAMIC MONITORING

CENTRAL VENOUS PRESSURE (CVP)

• Refers to the measurement of the
pressure within the vena cava, the right
atrium and venous return
• Requires the threading of a catheter into
a large central vein (subclavian, internal
or external jugular, median basilic, or
femoral).
CENTRAL
VENOUS
PRESSURE
(CVP)
Catheter placement is
confirmed through CXR

The O level of the

manometer must be
placed at the right,
midaxillary line, 4th ICS,
the approximate level of
the right atrium when in
supine position
• The phlebostatic axis is located at the fourth intercostal space right
midaxillary. This approximates the location of the right atrium.
Normal CVP pressure
3 to 8 mmHg (5-12 cm H2O)
elevated CVP- increase in blood volume
decreased CVP- decrease in blood volume
Measuring CVP
a. The zero point on the transducer
needs to be at the level of the right atrium.
b. The client needs to be supine, with the
head of the bed at 45 degrees.
c. The client needs to be relaxed; coughing
or straining, will cause false increases in the
readings.

Complication: air embolism, infection

 Nursing Responsibilities

• Inspect site daily for signs of infection

• Practice strict asepsis. Cleanse catheter

insertion site and change sterile
dressings daily
 PULMONARY ARTERY PRESSURE MONITORING

tool used to assess ventricular function;

diagnose the etiology of shock and evaluate
the response to medical intervention

SWAN GANZ CATHETER ( a balloon-

tipped flow directed; 4-lumen catheter)
inserted via antecubital vein into the right
side of the heart and is floated into the
pulmonary artery
1st lumen- terminates in
the right atrium which
measures CVP, fluid
infusion and venous
access for blood samples
2nd lumen – terminates in
the Pulmonary Artery
measures the PA
systolic pressure, diastolic
pressure, and mean
pressure
3rd lumen – for inflation
and deflation of balloon (
1-1.5 cc)
4th lumen – is the
thermistor port, measure
cardiac output
PULMONARY ARTERY PRESSURE MONITORING

Normal range:
• PAP: 20-30 mmHg
• PCWP: 8-13 mmHg

• PCWP reading above 25 suggests

impending pulmonary edema
Nursing responsibilities:
• Inflate balloon only for PCWP readings,
deflate between readings
• Assess Insertion site; culture site every
48 hrs
• Complications: infection, pulmonary
artery rupture, pulmonary embolism,
dysrhythmias
Cardiac catheterization
TEE
 CARDIAC CATHETERIZATION

• An invasive test involves the

insertion of a catheter into the heart
and surrounding vessels guided by
fluoroscopy
 to obtains
information about
the structure
and performance
of the heart
chambers
and valves and the
coronary
circulation
 NURSING RESPONSIBILITES:
PRE PROCEDURE
• Provide psychosocial support and obtain informed consent
• Assess for allergy to seafood and iodine
• Obtain baseline VS, NPO for 6-8 hours
• Obtain height and weight, encourage to void, assess
distal pulses
 NURSING RESPONSIBILITES

PRE PROCEDURE
• Cardiac monitoring
• Inform pt: may fell warm or flushing sensation
(contrast medium)
• “fluttering” sensation OR palpitations may
be felt as the catheter enters the heart
chambers
• Encourage client to cough to clear the contrast
agent from the artery
POST PROCEDURE
. Monitor VS, ECG , peripheral pulses
• Assess presence of hematoma at insertion site
• Apply pressure dressing, small sand bag over the
puncture site
• Maintain strict bed rest for 6 to 12 hours as
prescribed; however, the client may turn from side to
side.
• Monitor extremities for color, temperature. and tingling
sensation
• Increase Oral Fluid Intake
POST PROCEDURE
• Keep extremity extended for 4 to 6 hours, as
prescribed, keeping the leg straight to prevent
arterial occlusion.
• If the antecubital vessel was used, immobilize the
arm with an armboard.
• Provides a higher quality picture than
regular echocardiogram. The throat is
anesthetized & the esophageal scope is
inserted.

Nursing Interventions:
1. Maintain NPO status for 8 hours before test.
2. Check for gag reflex before client resumes
oral intake of fluids
 Electrocardiographic Studies
 ECG
 Continuous ECG monitoring
 Hardwire
 telemetry
 Holter Monitoring

 Cardio stressTests
 Radiographic Cardiac Tests
 CXR
 CT Scan
 MRI
 Echocardiogram
 graphical recording of the
electrical activities of the
heart.
It is recorded on a rhythm strip
using ECG machine
 useful for detecting
cardiac dysrhythmias,
 location and extent of
myocardial infarction, and
 evaluation of the
effectiveness of cardiac
medications.
Pre-procedure:
 Explain the purpose of the test.
 Patient will not experience
electrocution or shock
 Remove all metal objects
 Wash the skin to reduce skin oil
 Instruct patient to lie still, breathe
normally and refrain from talking
ECG PAPER or STRIP
ECG WAVEFORMS
COMPONENTS  P wave
 PR interval
 QRS complex
 ST Segment
 T wave
 QT INTERVAL
 J POINT
 U wave
P WAVE
 P WAVE
 Represents ATRIAL DEPOLARIZATION.
 Usually rounded and upright
PR Interval
 PR Interval

 Represents the time it takes an impulse to travel from

the atria through the AV node, bundle of his , bundle
branches to the purkinje fibers.
 0.12 - 0.20 sec
QRS COMPLEX
 QRS COMPLEX

 Represents ventricular depolarization

 consists of 3 waveforms. The Q,R,and S wave
ST SEGMENT
 ST SEGMENT

 Represents the end of ventricular depolarization and

beginning of ventricular repolarization
 Extends from the end of S wave to the Beginning of T
wave
 Duration is not measured
T WAVE
 T WAVE

 Represents repolarization of ventricles.

 <5mm in standard leads
 Usually upright
QT interval
 QT interval

 The time required for ventricular depolarization and

Repolarization takes place.

 Duration varies from age, sex and heart rate. But

usually 0.36 to 0.44 sec.
 ER pattern – early repolarization

Benign variation The point at

Hypothermia which the QRS
Vagal stimulation
complex meets
the ST segment
 U waves are thought to represent
repolarization of the
papillary muscles or Purkinje fibers.
Interpretation
Prominent U – often seen in hypokalemia
may be present in hypercalcemia, thyrotoxicosis,
or exposure to digitalis, epinephrine,
An inverted U wave may represent myocardial ischemia
or left ventricular volume overload
normally be seen in younger, athletic individuals
 Obtaining an ECG

1. place electrodes in standard

positions on the chest wall
and extremities.
2. attached to cable wire
which are connected to ECG
machine

The standard 12-lead ECG is the most commonly used tool to

diagnose dysrhythmias
Electrode placement
 Standard Location of Chest Leads

 V1: 4th ICS at right sternal

border
 V2: 4th ICS at left sternal
border
 V3: midway between V2
& V4
 V4: 5th ICS on LMCL
 V5: LAAL at same level
asV4
 V6: LMAL at same level
as V4
 Sinus Rhythm (SR)
 Normal P, QRS, T wave
 Heart rate: 56 – 99 bpm
 P – QRS ratio: 1 is to 1
 Rhythm: regular
 1. Identify the rhythm ( R – R interval)

PAPER & PENCIL METHOD

place a straight edge of a paper along the strip.
Then identify the Peak of 2 consecutive R-wave and make a dot on the paper.
Then compare.

R R R R R R

Regular = SINUS
Irregular = Identify the arrhythmia
 DETERMINING THE RATE

 Times Ten ( 6sec method)

Obtain a 6 second strip then count the no. of P
waves (Atrial rate) or R waves (Ventricular rate)
within the 6-second strip then multiply by 10. The
product is the rate.
Measurement of Rate
 Formula 1:____________300__________
# big squares between R-R

 Formula 2: ___________1500_________
# small squares between R-R
 is standard for patients who are at
high risk for dysrhythmias.

Two techniques:
hardwire monitoring
telemetry
Hardwire monitoring
 is composed of 3-5
electrodes, a lead cable, &
a bedside monitor
TELEMETRY
a battery –operated
transmitter that transmit
radio waves to a bank of
monitors

Nursing Responsibilities:
 Clean the skin with
soap and water
 change electrodes
every 24-48 hrs
 Assess skin irritation
 HOLTER MONITORING

 is a portable device for continuously monitoring

various electrical activity of the cardiovascular
system for at least 24 hours
(small tape recorder)

Nursing Responsibilities:
Assesses the activities which precipitate dysrhythmias and
the time of the day the patient experiences them
Instruct patient to keep a diary of activities
Avoid operating heavy machinery, electric shavers, hair
dryers, bathing or showering.
 CARDIAC
STRESS TESTING
Exercise stress test,
Pharmacologic stress test
Mental or emotional stress test
noninvasive ways to evaluate
the response of the cardiovascular
system to stress.
 A. EXERCISE STRESS TEST

 patient walks on a
treadmill or
pedals a
stationary bicycle
 ECG is monitored
during exercise ;
lasts 6-12 mins
 A. EXERCISE STRESS TEST

PATIENT TEACHING:
Avoid tea, coffee, smoking and alcohol on the
day of the test
Fast for 4 hors prior to test
Wear loose fitting clothes ad low heeled rubber
shoes
I report chest pain, SOB, dizziness
 B.PHARMACOLOGIC STRESS
TESTING
Physically disabled or deconditioned patients

2 vasodilating agents
dipyridamole (Persantine) and adenosine
(Adenocard), (mimic the effects of exercise by
maximally dilating the coronary arteries)

 Dobutamine (Dobutrex)
a synthetic sympathomimetic, increases
heart rate, myocardial contractility, and BP
 B.PHARMACOLOGIC STRESS
TESTING
Nursing Interventions:
1. NPO 4H before the test
2. NO CAFFEINE containing foods and
beverages
3. Instruct on common side effects-
FLUSHING OR NAUSEA
 CHEST X RAY
 To determine overall size and
configuration of the heart and
size of the cardiac chambers

Patient Teachings:
 Remove brassiere, practice
holding breath, may use lead
shield if pregnant
 Strong magnetic field and radio waves to detect and define
difference between healthy and diseased tissues

NURSING RESPONSIBILITES:
Secure consent
Assess for claustrophobia
remain still during the procedure
A loud knocking noise is heard in the MRI unit
Clients with metal items, artificial pacemakers,
 it provide cross sectional images of the chest, heart
and great vessels
patient is on a table while scanner rotates around him
Nursing Interventions:
patient must lie still
an IV line may be inserted in with contrast medium
(check allergy, NPO)
Assess for pregnancy, claustrophobia
 MYOCARDIAL SCINTIGRAPHY/MYOCARDIAL
PERFUSION IMAGING

MOST COMON TESTS INCLUDE: THALIUM IMAGING,

MULTIGATED BLOOD POOL IMAGING (MUGA)

injection of radioactive isotopes via catheter. As the isotope

is absorbed by the myocardium, photons are emitted. External
gamma camera will produce image showing myocardial
function, motion and perfusion.
 MUGA Scanning
(multiple-gated acquisition)
to study left ventricular function and wall motion of the
heart
by injecting the patient's red cells with radioactive
technetium-99m to form an image of the blood pool
within the heart
using an ECG, gamma camera, and computer.

Patient must lie still during the scan.

NURSING RESPONSIBILITES:
Assess for pregnancy. Test involves radiation exposure

Stress test may be done simultaneously

Light meal to prevent nausea and stomach cramping

during exercise
2D ECHOCARDIOGRAPHY
Uses ultrasound to assess cardiac structure and mobility in 2
dimensional format
No special preparation is required
Painless and takes approx. 30-60 mins

Nursing Intervention:
Client has to remain still, in supine position slightly
turned to the left side with head of bed elevated 15-20
degrees
ALTERATIONS
IN
GAS
TRANSPORT
 Coronary artery disease
(CAD)
• is a condition in which the blood supply to the
heart muscles is completely or partially
blocked.
Is a narrowing or obstruction of one or more
coronary arteries as a result of
atherosclerosis
Causes:
1. Decreased blood 3. Increased demand for
supply blood
– Atherosclerosis
– Vasospasm – Hyperthyroidism
– Thrombus, embolus – Hyperthermia
2. Decreased oxygen in – Stress
blood
– Anemia
– Carbon monoxide
Nonmodifiable risk factors:
a. age
b. sex - male
c. race -
d. genetics
2. Modifiable risk factors:
• Hypertension
• Hyperlipidemia
• Diabetes Mellitus
• Smoking

– elevated levels of Homocysteine

– Stress
– Sedentary life style
– obesity
CORONARY ARTERY DISEASE
Narrowing of the artery

Decreases myocardial perfusion

Ischemia and anaerobic metabolism
Classic Sign of CAD
ANGINA PECTORIS
Transient chest pain caused
by insufficient blood flow to
the myocardium resulting in
myocardial ischemia.
ANGINA PECTORIS
•Precipitating Events
– Exertion/physical stress
– Emotional stress
– Eating
– Extremes of
temperature
– Sexual activity
ANGINA PECTORIS
TYPE DESCRIPTION
predictable and consistent pain that occurs on
Stable angina
exertion and is relieved by rest
Unstable angina
symptoms occur more frequently and last longer than
(preinfarction or
stable angina
crescendo)
Intractable or
Chronic, severe incapacitating chest pain
refractory angina
Variant angina
pain at rest; thought to be caused by coronary artery
(Prinzmetal’s
vasospasm
angina)
objective evidence of ischemia (such as
Silent ischemia electrocardiographic changes with a stress test), but
patient reports no symptoms
 Signs and Symptoms
• Chest Pain relieved by rest or
with the use of nitroglycerin
• An episode usually lasts less than
20 min
• Pain may spread to the left arm,
neck, back, throat, or jaw.
• shortness of breath; diaphoresis,
light-headedness, nausea and
vomiting.
DIAGNOSTICS:
• ECG - ST depression and T wave inversion
only during acute attacks
• C reactive protein: inflammation of the
vascular endothelium
• Cardiac Catheterization – provides the most
accurate information about the patency of
the coronary arteries
 MEDICAL MANAGEMENT
• Control of risk factor
• GOAL • Oxygen therapy
– To decrease the
oxygen demand
• Pharmacologic therapy
of the Nitroglycerin
myocardium and Beta-adrenergic
to increase
blocking agent
oxygen supply
Calcium channel
blockers
Antiplatelet
ACUTE CORONARY SYNDROMES
▪ is an umbrella term that covers a spectrum of clinical
presentations; common pathology is a ruptured plaque
within a coronary artery leading to thrombosis and flow
limitation.
ACUTE CORONARY SYNDROMES
1. Unstable Angina
• a syndrome where a patient develops worsening of angina
symptoms such that angina occurs on increasingly less
exertion, or at rest
• generally narrowed but not completely occluded giving
symptoms of ischemia without myocardial infarction.
• not associated with a rise in cardiac markers such as
Troponin, but ECG changes such as ST segment
depression or T-wave inversion can sometimes be seen.
ACUTE CORONARY SYNDROMES
2. Non ST Elevation Myocardial Infarction (NSTEMI)
• generally had prolonged chest pain at rest.
Sometimes pain can come on with exertion but not be
relieved by rest or nitrates
• rise in cardiac markers such as Troponin, indicating
that there has been myocardial damage
• ECG changes can be quite variable in NSTEMI
• some cases the ECG can be normal, and in other
cases, either ST segment depression or T-wave
inversion can be seen
• occluded small branch or occlusion of distal small
vessels.
 ACUTE CORONARY SYNDROMES

3. ST Elevation Myocardial Infarction (STEMI)

• is characterized by ECG change
• present with prolonged chest pain at rest and cardiac markers
such as Troponin are elevated
• an important ECG change is elevation of the ST segment.
This needs to be at least 1mm of ST elevation in two or more
• the areas of ST elevation on the ECG can be used to
identify which region of the heart is affected
• generally one of the main coronary arteries that is affected.
MYOCARDIAL INFARCTION
 MYOCARDIAL INFARCTION
o The formation of localized necrotic areas
within the myocardium.
o Usually follows sudden coronary
occlusion and the abrupt cessation of blood
and oxygen flow to the heart muscle.
severe ischemia
(> 20 - 40 minutes)

IRREVERSIBLE cellular damage

and necrosis of the myocardium.
 CLASSIFICATION OF MYOCARDIAL
INFARCTION
Classifications:
• TRANSMURAL INFARCT
endocardium to epicardium
• SUBENDOCARDIAL INFARCT
myocardium and endocardium
• INTRAMURAL INFARCT
- patchy area of the myocardium with
longstanding angina pectoris
PATHOPHYSIOLOGY
of
MYOCARDIAL
INFARCTION
 SIGNS &
yspnea SYMPTOMS

nxiety
Ausea & vomiting
Hest pain
Levation in temp.
AIN/PalLor
rrythmia
Cute pulmonary edema

iaphoresis

hock
 Diagnostic Tests

⚫ECG
ECG Changes in MI
 Cardiac Enzymes

CK-MB
⚫ Cardiac specific isoenzyme
⚫ Accurate indicator of myocardial damage
⚫ Elevated 4 hrs after
⚫ NV:
⚫ M- 50-325 mu/ml
⚫ F- 50-250 mu/ml
 Cardiac Enzymes
Myoglobin
⚫ Earliest enzyme to increase
⚫ Elevated 1-3 hrs after

Troponin
⚫ Protein found in the myocardium, regulates
the myocardial contractile process
⚫ Elevated 3-4 hrs after; duration is 3 weeks
 Cardiac Enzymes

Aspartate Aminotransferase (AST)

⚫ Elevated level indicates tissue necrosis
⚫ Elavated 4-6 hrs after

Lactic Dehydrogenase (LDH)

flipped pattern
 MEDICAL MANAGEMENT
I V access/regulation
N arcotic analgesics (morphine)
P osition in Semi fowlers
A spirin/ Anticoagulant (heparin, warfarin)
R est / relieve anxiety (diazepam)
C onverting enzyme inhibitor (ACE inhibitor – captopril)
calcium channel blocker (nifedipine, verapamil)
T hrombolytics (streptokinase, urokinase & TPA)
I V beta blocker (propranolol, metoprolol, atenolol)
O xygen
N itrates (nitroglycerin)
S tool Softeners
SURGICAL
MANAGEMENT
 1. PERCUTANEOUS TRANSLUMINAL
CORONARY ANGIOPLASTY
• Mechanical dilatation of the coronary
vessel wall by compressing the
atheromatous plaque
INTRAVASCULAR
STENTING • Maintains good
luminal
geometry after
balloon
deflation &
withdrawal
• Done to prevent
restenosis after
PTCA
• Risk of
thrombus
formation
2. ATHERECTOMY
•Invasive procedure that
involves the removal of the
atheroma, or plaque, from a
coronary artery

3. TRANSMYOCARDIAL LASER
REVASCULARIZATION
4. CORONARY ARTERY BYPASS
GRAFT (CABG)

• Main purpose is
myocardial
revascularization
• Commonly used
grafts:
– Saphenous vein
– Internal
mammary artery
Cardiac Rehabilitation
• A process in which a
person is restored to
health & maintains
optimal functioning.
• Goals:
– To live as full, vital &
productive life
– Remain within the
limits of the heart’s
ability to respond to
activity & stress
Teaching & Counseling
• Discontinue smoking
• Continued medical supervision
• Diet modification
• Weight reduction
• Progressive exercise
• Stress management
• Resume sexual activity – after 4-6 weeks
 TEACHING GUIDE IN RESUMPTION OF
SEXUAL ACITVITY
• CLUE: able to climb two flights of stairs without
dyspnea , chest pain and other abnormalities
• Assume less fatiguing position ( non MI partner on
top)
• If both are MI patients: side lying
• Perform activity in a cool, familiar environment, early
in the morning
• Take nitroglycerine before sexual act
• Refrain from sexual activity during a fatiguing day,
after eating a large meal
• If any abnormalities occur, stop activity
COMPLICATIONS
A rrhythmias
A neurysm
C ardiogenic shock
C ardiac tamponade
C ongestive heart failure
D ressler’s syndrome
E mbolism
 CLASSIFICATION
Killip class I
- no clinical signs of heart failure
Killip class II
- with rales or crackles in the lungs, an S3
sound, and jugular vein distention
Killip class III
- with acute pulmonary edema
Killip class IV
- cardiogenic shock or hypotension &
evidence of peripheral vasoconstriction
• is the inability of the heart to
pump a sufficient amount of oxygen to meet
the metabolic needs of the body.
MNEMONICS:
R- enal disease
A- nemia
P- ulmonary embolism
I- nfection (myocarditis, Pericarditis)
D- elivery after pregnancy
F- orget to take the meds
A- rrhythmias
I- ischemia/infarction
L- ipid aggregation
U- ncontrolled hypertension
R- HD
E- ndocarditis
 FUNCTIONAL CLASSIFICATION
OF HEART FAILURE
DESCRIPTION

CLASS I No symptoms noted with normal

activity

CLASS II Symptoms noted with normal activity

but subside with rest

CLASS III Symptoms noted with minimal activity;

may or may not be symptom free at
rest
CLASS IV Symptoms usually present at rest and
worsened at any type of activity
Due to decrease in cardiac output
• Occurs when left side of the heart is
unable to pump the total volume of blood it
receives from the right side of the heart

• Common cause- is MYOCARDIAL

INFARCTION
 Backward effects

volume & end-diastolic

Emptying of LV vol. in LA
pressure in LV

Transudation of fluid from capillaries volume in pulmonary capillary bed

to interstitial spaces of alveoli

Fluid in Bronchoconstriction
Rapid filling of alveolar spaces alveoli s/s: Wheezing (Cardiac Asthma)

s/s:dyspnea,dec.O2 sat,
Pulmonary Edema Shock
Increased RR, death
Orthopnea, PND
 Cardiac output Perfusion of tissues BLD flow to kidneys
of the body and glands

s/s:Pulsus alternans s/s: easy fatigability,

Weakness, dizziness

Secretion of Na & Reabsorption of Na & H2O

H20-retaining hormones Vasoconstriction

Total blood vol &

ECF volume Increased systemic BP

s/s: S3 gallop
• Dyspnea in the early • Pulsus alternans
stages • Paroxysmal Nocturnal
• Decreases O2 saturation Dyspnea
• Increase RR • Cardiac asthma
• Easy fatigability, • Acute pulmonary
weakness and dizziness edema= life-threatening
• Orthopnea since it may progress
to shock & death
• Auscultation reveals S3
gallop
• Impairs the ability to move deoxygenated
blood from the systemic circulation into the
pulmonary circulation

• Blood goes back to the systemic

circulation

• Systemic circulation is congested

(backward effect); output to lungs is
decrease (forward effect)
• Persistent left sided heart failure
• Stenosis / Regurgitation of tricuspid or
pulmonic valves
• Right ventricular infarction
• Acute / chronic pulmonary disease: COPD,
severe pneumonia, pulmonary embolus
 Weakened heart muscle, restrict
blood flow to the LUNGS
(Increase residual volume)

Increases pressure in the great

veins and distensible organs

Inc. pressure in -Decrease systemic blood

capillary vessel Jugular vein
distention flow & pressure
= dependent
peripheral = dec. tissue perfusion to
edema organs such as the kidneys
Inc. pressure in Hepatomegaly ,
Spleenomegaly -SNS stimulation , Inc. blood
peritoneal vessels
volume & vasoconstriction
= ascites
• Major manifestation: PERIPHERAL
EDEMA
• Weight gain
• Hepatomegaly
• RUQ pain
• Splenomegaly
• Ascites
• Anorexia and abdominal discomfort
• JV distention
 Pitting edema

JVD
• Chest x-ray
• Echocardiography
• Elevated SGPT
• Decrease CVP
1. Decreased cardiac output
2. Fluid Volume Excess
3. Impaired Gas Exchange
4. Ineffective Tissue Perfusion
5. Risk for Activity Intolerance
6. Risk for impaired skin integrity
7. Risk for Anxiety
Goals:
1. To monitor for reduced cardiac workload
2. To maintain adequate fluid balance
3. To reduce myocardial workload
4. To monitor for pulmonary edema
5. To assess response to medical therapies
U- pright position
N- itrates
L- asix, dieuretics
O- xygen
A- minophylline
D- igoxin
F- luids decrease
A- fterload decrease (ace, beta, ca)
S- Na restriction
T-est (monitor diff electrolytes), SFF
VENTRICULAR
ASSIST DEVICE
• Is a mechanical
circulatory
device that is
used to partially
or completely
replace the
function of the
failing heart.
• HEART
TRANSPLANTATION

• CARDIOMYOPLASTY
VALVULAR
HEART
DISEASES
 Types of Valvular Disease
• Stenosis
– The valve leaflets become
thickened with scar tissue
and become stenotic.
– These valves cannot open
fully, causing obstruction
of blood flow.
• Regurgitation
– Caused by scarring and
retraction of the leaflets
– Allows blood to move back
through the valve when it
should be closed.
Stenotic
valvular defects
difficulty in
emptying itself
through the
narrow orifice ;
therefore, it
dilates and
hypertrophies.
Regurgitant valves

permit backflow of
blood

increased work
demands
on the chamber
ejecting to maintain
adequate output
 Disorders

•Mitral Stenosis
•Mitral Regurgitation
•Aortic Regurgitation
•Aortic Stenosis
Aortic valve stenosis Mitral regurgitation

Mitral valve stenosis Aortic regurgitation

CAUSES

Inflammation - Rheumatic endocarditis is a

common cause
Congenital defects
Trauma
Ischemic heart disease
Diagnosis
Cardiac auscultation - murmur
Transesophageal Echocardiography (TEE)
create an image of the internal
structures of the heart
Cardiac catheterization
• Assessment:

– Murmurs
– Fatigue, weakness
– Dyspnea, cough, orthopnea, nocturnal dyspnea
– Palpitations, chest pain, dizziness
– Jugular vein distention
– Corrigan’s pulse,

A pulse that is forceful and then suddenly

collapses. It is usually found in patients with aortic
regurgitation,

caused by the large stroke volume and rapid run off of

blood back into the left ventricle.
Management:
–Prophylactic antibiotic therapy
–Digitalis
–Diuretics
–Antidysrhythmics
–Vasodilators
–Anticoagulant
–Low-sodium diet
•Management:
•Percutaneous balloon
valvuloplasty
• a balloon-tipped
catheter is inserted,
causing a cracking
of the calcified
commissures and
enlargement of the
valve orifice.
•Surgical
–Valvuloplasty
•Closed commissurotomy
•Open commissurotomy

is the procedure
performed to separate
the fused leaflets
Annuloplasty
repair of the valve annulus; is
useful for the treatment of valvular
regurgitation.

two annuloplasty techniques

1. uses an annuloplasty ring
2. tacking the valve leaflets to the atrium with sutures to
tighten the annulus
A
Chordoplasty
repair of the chordae tendineae
 Valve replacement
Mechanical Tissue or
prosthetics BiologicValves
• They are durable • Xenografts,
• Thromboembolism Homografts,
• Anticoagulant Autografts
therapy • Long-term
anticogulant
therapy may not
be indicated
INFECTIOUS
DISORDERS
of the
HEART
RHEUMATIC FEVER
•Inflammatory autoimmune
disease that affects the
connective tissues of the heart,
joints, subcutaneous tissues,
blood vessels of the CNS
• Complication: RHD

•`Agent: GABHS
RISK FACTORS:
•Age: 5-15 years old
•Crowding & poor hygiene
•Poor nutrition
•History of GAS infection
•Genetics
 STAGES
1. Acute stage
- History of strep infection
- Subsequent involvement of connective tissues
• Aschoff bodies (a localized area of tissue necrosis surrounded
by immune cells)
2. Recurrent stage
- Extension of the cardiac effects of the disease
3. Chronic stage
- Permanent
deformity of the
heart valves
mitral valve
stenosis
 PATHOPHYSIOLOGY
Inflammatory changes in the
connective tissues

Valvular structure becomes red swollen;

small vegetative lesions on the valve
leaflets

Fibrous scar tissue

Contraction of the Shortening of the

valve leaflets chordae tendinae

Fusion of the valve leaflets

JONES CRITERIA
1. Presence of 2 major signs
2. Presence of 1 major + 2
minor
3. Evidence of GABHS
infection.
MAJOR MANIFESTATIONS:
J oints (Polyarthritis)
- painful & migratory, affects larger joints
Carditis
- heart murmurs, cardiomegaly, CHF, pericarditis
N odes (Subcutaneous Nodules)
- hard, painless nodules in the knees, wrist &
elbows
E rythema marginatum
- maplike, macular lesions on the trunk
S ydenham/Chorea or St. Vitus dance
- CNS disorder; irregular, aimless, involuntary
movement
MINOR MANIFESTATIONS:
I ncreased WBC
T emperature elevated (Fever)
E levated ESR / C – reactive protein
R aised or prolonged PR interval
I tself (previous history of rheumatic
fever
A rthralgia
 DIAGNOSTIC TEST:
• (+) throat culture
• ASO titer (>250 todd in adult; >333 todd in children
• Elevated streptococcal antibody titer
• Elevated WBC, ESR, C-reactive protein
• 2D-echo
• Jones Criteria
 MANAGEMENT:
•↓ demand from weakened heart
• CBR
• Clustercare
• Modify lifestyle post discharge
• Prevent further cardiac damage
• Penicillin IM once a month x 3-5 yrs
• Steroids
• Safety precautions for chorea
• Joint pain management
inflammation of the endocardium

•Non-infective
•Infective
• a relatively uncommon, life-threatening
infection of the endocardial surface of
the heart, including the heart valves.

• FORMS:
– Subacute Bacterial Endocarditis (SBE)
– Acute Bacterial Endocarditis (ABE)
– Native Valve endocarditis
– Prosthetic valve endocarditis
– Nonbacterial thrombotic endocarditis
Etiology
Virus, fungal Etiology:
• Staphylococcus
aureus
RISK FACTORS • Streptococci
• HACEK
History of preexisting organisms
heart condition (Haemophilus,
History of recent invasive Actinobacillus,
procedures: Cardiobacterium,
minor surgery, dental Eikenella,
procedures involving the Kingella)
urinary tract.
 Two Factors : Infective
Infective
Endocarditis

• 1. damage
endotheleal
surface
• 2. portal of entry
by the organism
 High
Turbulent blood flow
Altitude
(valvular
Cold dysfunction)
Exposure

Stress
Endothelial
SLE, damage
RHD Cardiac
Catheterization

Development of Thrombi

Nonbacterial Thrombotic
Endocarditis
 Genitourinary
Hemodialysis
instrumentation

Dental procedure IV drug abuse

Skin Infection Cardiac Surgery

Pathogen Entry into bloodstream

BACTEREMIA
 Bacterial infiltration of platelet-fibrin
thrombi

Colonization on endocardial surfaces

Adherence of more
Formation of more fibrin
platelets

Grow of vegetation Right-sided

Left-sided Heart heart
embolization embolization

INFECTIVE
ENDOCARDITIS
 Local valve damage

Infiltration of supporting
structures

Sepsis Heart Failure Heart Block

CLINICAL MANIFESTATION
OSLER NODES
REDDISH TENDER LESIONS ( ON THE
PADS OF FINGERS, HANDS AND TOES

Janeway’s lesion

osler’s node
Janeway lesions (nontender hemorrhagic
lesions) on the fingers, toes, nose, or
earlobes
Murmurs
Petecchiae
Splinter hemorrhage
(fingernail)
Roth’s spots

Hemorrhages with pale centers

in the fundi of the eyes
Diagnostics:
1. History to identify site of entry.
2. Echocardiography
3. Blood cultures
4. CBC
5. ESR
6. DUKES Criteria
MAJOR CRITERIA
1. Positive Blood Culture (HACEK)
2. Evidence of endocardial involvment (+ echocardiogram)

MINOR CRITERIA
1. Predisposition: Predisposing heart condition or injection
drug use
2. Fever > 38 degrees Celsius
3. Vascular phenomena: Janeway lesions, conjunctival
hemorrhage, intracranial hemorrhage, major arterial
emboli, septic pumonary infarcts,
4. Immunologic phenomena: glomerulonephritis, Osler’s
node, Roth’s spots, Rheumatoid factor,
5. Microbiologic evidence: positive blood culture not meeting
major criterion
1. Hyperthermia
2. Decreased Cardiac Output
3. Activity Intolerance
4. Deficient Knowledge
GOALS:
1. Attainment of normal or baseline cardiac
function
2. Performance of ADL without fatigue
3. Knowledge of therapeutic regimen
Treatment:
A. IV antibiotic therapy for 4 to 6
weeks
B. Bed rest if high fever or evidence
of cardiac damage is present
C. Prophylactic antibiotics for 3 to 5
years, especially in children with
history of rheumatic fever or
congenital anomalies.
D. Surgical interventions for severe
valvular damage.
E NSURE BED REST
N SAID nursing
D OPPLER SCAN
O BSERVE EMBOLIZATION
C ULTURE OF BLOOD
A NTIBIOTIC REGIMEN
R HD PRECAUTION
D RUG FOR FEVER AND JOINT PAIN
I NTAKE AND OUTPUT MONITORING
U PHOLD GOOD ORAL HYGIENE
M ANAGE VALVULAR DEFECTS
CONGENITAL
HEART
DEFECTS
 CONGENITAL HEART DEFECTS
ACYANOTIC CYANOTIC

Increased Decreased
Obstruction Mixed
pulmonary pulmonary
to blood flow blood flow
blood flow blood flow

TGV
ASD COA
TOF TAPVC
VSD AORTIC STENOSIS
TRICUSPID TRUNCUS
PDA PULMONARY
ATRESIA ARTERIOSU
AV canal STENOSIS
HLHS
DEFECTS WITH INCREASED
PULMONARY BLOOD FLOW
Involves blood flow from
the left side of the heart
(greater pressure) to the
right side (less pressure)

Increases pulmonary blood flow

Decrease systemic blood flow
 ATRIAL SEPTAL DEFECT
• Abnormal opening
between the atria
that causes an
increased flow of
oxygenated blood
to the right side of
the heart
 ATRIAL SEPTAL DEFECT

• Assessment • MGT:
– Asymptomatic Nonsurgical:
– Prone to RTI Cardiac Catheterization
– Dyspnea on mild Surgical:
exertion Open heart surgery
– May develop CHF
– Feeding difficulties
 VENTRICULAR SEPTAL
DEFECT
• Abnormal opening
between the right &
left ventricles
• MGT
Nonsurgical:
Cardiac Catheterization
Surgical:
Open repair
 ATRIOVENTRICULAR CANAL
• The defect
results from
incomplete
fusion of the
endocardial
cushions.
• Most common
cardiac defect in
Down syndrome.
 ATRIOVENTRICULAR CANAL

• A characteristic murmur is present.

• The infant usually has mild to moderate CHF,
with cyanosis increasing with crying.
• Signs and symptoms of decreased cardiac
output may be present.
 ATRIOVENTRICULAR CANAL
• Surgical treatment
Pulmonary artery banding
for infants with severe
symptoms (palliative)
Complete repair via
cardiopulmonary bypass.
to reduce excessive pulmonary Safe placement of a pulmonary
blood flow and protect artery band: (A) encircling the
the pulmonary vasculature from aortopulmonary trunk,
hypertrophy and irreversible (B) encircling the aorta,
pulmonary hypertension. and (C) completing the pulmonary
artery band at the final location.
 PATENT DUCTUS ARTERIOSUS

• Failure of fetal ductus

arteriosus to close within
the first weeks of life
• HR: mothers exposed to
rubella during pregnancy
• Assessment:
– Machinery like murmur
– Asymptomatic
– s/sx of CHF
– s/sx of decreased
cardiac output
 PATENT DUCTUS
ARTERIOSUS

• MGT:
– Medical: Indomethacin (Indocin)
• works by stimulating the muscles inside the PDA to
constrict
– PDA Ligation
OBSTRUCTIVE DEFECTS

Blood exiting a portion of

the heart meets an area
of anatomical narrowing
(stenosis), causing
obstruction to blood flow.
 AORTIC STENOSIS
• narrowing or stricture of the aortic valve, causing
resistance to blood flow in the left ventricle,
decreased cardiac output, left ventricular
hypertrophy, and pulmonary vascular
congestion.
• VALVULAR STENOSIS
– most common type
– caused by malformed cusps, resulting in a bicuspid
rather than a tricuspid valve, or fusion of the cusps.
 AORTIC STENOSIS
• A characteristic murmur is present.
• Infants with severe defects demonstrate signs of
decreased cardiac output.
• Children show signs of exercise intolerance,
chest pain, and dizziness when standing for long
periods of time.
 AORTIC STENOSIS
• Nonsurgical treatment
– Done during cardiac
catheterization to dilate the
narrowed valve.
• Surgical treatment
– Aortic valvotomy (palliative)
– A valve replacement may be
required at a second
procedure.
 COARCTATION OF AORTA
• Localized narrowing of aorta
• Assessment:
– Absent femoral pulses – pathognomonic sign
– BP
• Higher in upper extremities – headache; epistaxis;
pulses are rapid & bounding
• Lower in lower extremities – leg pains, cold feet,
muscle spasms; pulses are weak, delayed or absent
– Myocardial hypertrophy
 COARCTATION OF AORTA

• MGT:
– Nonsurgical: balloon angioplasty
– Surgical:
• Resection of the coarcted portion with end-to-end
anastomosis of the aorta
 PULMONARY STENOSIS
• Narrowing at the
entrance to the
pulmonary artery.
• Resistance to blood
flow causes right
ventricular
hypertrophy and
decreased
pulmonary blood
flow
 PULMONARY STENOSIS
• A characteristic murmur is present.
• The infant or child may be asymptomatic.
• Newborns with severe narrowing will be
cyanotic.
• If pulmonary stenosis is severe, CHF occurs.
• Signs and symptoms of decreased cardiac
output may occur.
 PULMONARY STENOSIS
• Nonsurgical treatment
– Done during cardiac
catheterization to dilate the
narrowed valve.
• Surgical treatment
– Infants: closed valvotomy
procedure.
– Children: pulmonary valvotomy
with cardiopulmonary bypass.
 DEFECTS WITH
DECREASED PULMONARY
BLOOD FLOW
• Pressure on the right side of the heart
increases, exceeding pressure on the left side,
which allows desaturated blood to shunt right
to left, causing decrease pulmonary blood flow
• Typically hypoxemia and cyanosis appear.
• Anatomical defect (ASD or VSD) between the
right and left sides of the heart are present.
 TETRALOGY OF FALLOT
• Four defects:
– Pulmonary stenosis
– VSD
– Overriding of the
aorta
– Right ventricular
hypertrophy
 TETRALOGY OF FALLOT
• Assessment:
– Cyanosis
– Tet spells
– Clubbing of fingers
– Growth retardation
– Exertional dyspnea relieved by squatting
– Polycythemia
 TETRALOGY OF FALLOT

TeT Spell
Cyanosis
Hypercyanotic
Tet Spells

The child assumed squatting to increase

systemic vascular resistance and to encourage
increased pulmonary blood flow; infants may be
more comfortable in a knee chest position
 TETRALOGY OF FALLOT
• DX: History; PE; Cardiac catheterization; angiography
• MGT:
– Conservative: hydration, prevent infection,
positioning; O2; morphine; Do not allow to cry for
long period of time
– Surgical:
• Palliative: Blalock-Taussig
• Corrective: Brock procedure
– entails an incision into the right ventricular
chamber and the cutting of the stenosed
pulmonary valve or the removal of obstructing
tissue in the outflow tract of the right ventricle.
 TRICUSPID ATRESIA
• Failure of the
tricuspid valve to
develop.
• No communication
exists from the
right atrium to the
right ventricle.
 TRICUSPID ATRESIA

• Cyanosis, tachycardia, and dyspnea are seen in the

newborn.
• Older children exhibit signs of chronic hypoxemia and
clubbing.
 TRICUSPID ATRESIA
• Treatment
– Neonate - whose pulmonary blood flow
depends on the patency of the ductus
arteriosus, a continuous infusion of
prostaglandin E1 is initiated until surgery.
– Atrial septostomy
– Fontan procedure (connects superior vena
cava to the pulmonary)
 MIXED DEFECTS
•Fully saturated systemic blood
flow mixes with the desaturated
blood flow, causing a
desaturation of the systemic
blood flow.
•Pulmonary congestion occurs
and cardiac output decreases.
 HYPOPLASTIC LEFT HEART
SYNDROME
• Underdevelopment of the
left side of the heart
occurs, resulting in a
hypoplastic left ventricle
and aortic atresia.
• Progressive deterioration
with cyanosis and
decreased cardiac output
are seen, leading to
cardiovascular collapse.
 HYPOPLASTIC LEFT HEART
SYNDROME
• The defect is fatal in the first few months of life
without intervention.

• Surgical treatment
– Surgical treatment is necessary; transplantation in the
newborn period may be considered.
– Preoperative period:
• Mechanical ventilation
• Continuous infusion of prostaglandin E1
 COMPLETE TRANSPOSITION OF
GREAT VESSELS
• the aorta is
connected to the
right ventricle, and
the pulmonary artery
is connected to the
left ventricle
• Assessment:
– Cyanosis
– Cardiomegaly
COMPLETE TRANSPOSITION OF
GREAT VESSELS
• MGT:
– Nonsurgical:
• Prostaglandin E1 – increase blood mixing
temporarily
• Balloon atrial septostomy
– Surgical:
• Arterial switch procedure
Aorta is switched with pulmonary artery
 TOTAL ANOMALOUS PULMONARY
VENOUS CONNECTION
• There is a failure of the
pulmonary veins to join the left
atrium.
• The defect results in mixed
blood being returned to the
right atrium and shunted from
the right to the left through an
ASD.
• The right side of the heart
hypertrophies, whereas the left
side of the heart may remain
small.
 TOTAL ANOMALOUS PULMONARY
VENOUS CONNECTION

• Signs and symptoms of CHF develop

• Cyanosis worsens with pulmonary vein
obstruction
• Once obstruction occurs, the infant's condition
deteriorates rapidly.
 TOTAL ANOMALOUS PULMONARY
VENOUS CONNECTION

• Surgical treatment
– Corrective repair is performed in early
infancy.
– The pulmonary vein is anastomosed to
the left atrium, the ASD is closed, and
the anomalous pulmonary venous
connection is ligated.
• Failure of normal TRUNCUS ARTERIOSUS
septation and division of
the embryonic bulbar
trunk into the pulmonary
artery and the aorta,
resulting in a single
vessel
• Blood from both
ventricles mixes in the
common great artery,
causing desaturation
and hypoxemia.
 TRUNCUS ARTERIOSUS
• A characteristic murmur is
present.
• The infant exhibits moderate
to severe CHF and variable
cyanosis, poor growth, and
activity intolerance.
 TRUNCUS ARTERIOSUS
Surgical treatment:
• Close the hole between the two
ventricles, often with a patch
• Implant a tube (conduit) and valve to
connect the right ventricle with the upper
portion of the pulmonary artery — creating
a new, complete pulmonary artery
• Reconstruct the single large vessel and
aorta to create a new, complete aorta
 Blood
• the average human has 5 litres of
blood
• a transporting fluid
• carries vital substances to all parts of
the body
 BLOOD
• Delivery of nutrients
– Oxygen
– Food
– Vitamins
• Removal of wastes
– Carbon dioxide
– Nitrogenous wastes
– Cellular toxins
• Repair of its conduit
• Protection against invading microorganisms
• Multiple cellular & acellular elements
 HEMATOLOGY
• Red Blood Cells-Oxygen & CO2
transport
• White Blood Cells-Protection versus
microorganisms
• Coagulation/platelets-Maintenance of
vascular integrity
blood plasma

plasma (55%)
red blood cells
(5-6-million /ml)

white blood cells

(5000/ml)
platelets
Plasma
liquid part of blood

plasma transports:-
• soluble food
molecules
• waste products
• hormones
• antibodies
Red blood cells
(RBCs)

• transports oxygen
• Also carry some
CO2
Red Blood Cells

• 45% of blood volume

• Life Span: 120 days
• Function: O2 transport
• Membrane – flexible
• Composed
predominantly of
hemoglobin
 Characteristics of Red blood cells:

1) biconcave shape 2) no nucleus

→ extra space inside

3) contain hemoglobin
→ the oxygen
carrying molecule
increases the → 250million
surface area so molecules / cell
more oxygen can be
carried
Hemoglobin
• gives red blood
cells their color
• can carry up to 4
molecules of O2
• associates and
dissociates with
O2
• contains iron
 release of BM stimulated to
Decrease in
erythropoietin by increase production
Oxygen
the kidneys of RBCs
 Factors necessary for
erythropoiesis
• 1. Erythropoietin
• 2. Iron
• 3. Vitamin B12
(cyanocobalamin)
• 4. Folic Acid (folate)
• 5. Ascorbic acid (Vitamin C)
• 6. Pyridoxine (Vitamin B6)
• 7. Amino acids
Assessment

HEALTH HISTORY
(weakness, fatigue,
generalized malaise,
dyspnea, pallor, ulceration,
mouth sores, anxiety,
increased risk for infection)
Assessment

MANIFESTATIONS
 TissueHypoxia – can give rise to
angina, night cramps, fatigue,
weakness & dyspnea
 Brain hypoxia – results in headache,
faintness & dim vision
 Redistribution of blood from
cutaneous tissues or a lack of Hb
causes pallor of the skin or mucous
membranes, conjuctiva & nail beds
Assessment
 Compensation w/ an ↑ Cardiac
Output - tachycardia &
palpitations
 Changes in blood viscosity may
result in a flow-type systolic
murmur
 W/ pre-existing heart disease—
ventricular hypertrophy and high-
output heart failure may develop
Assessment
 Diffusebone pain & sternal
tenderness may develop d/t
accelerated erythropoiesis
 In hemolytic anemia,
accompanied by jaundice
 In aplastic anemia, petechiae
& bleeding as result of
reduced platelet function.
Assessment
 CHECK FOR HEMORRHAGIC
TENDENCIES:
 PETECHIAE
 ECCHYMOSES
 BLEEDING IN THE
CONJUNCTIVA
Assessment
 INSPECTION AND PALPATION IN IPPA
 MUCOUS MEMBRANE
 Pallor
 Cyanosis (bluish discoloration of the
skin; decreased O2 in cells)
 Redness (polycythemia)
 Jaundice, petechiae, ecchymosis
 glossitis
Assessment
 INSPECTION AND PALPATION IN IPPA

PALPATION
Splenomegaly
Hepatomegaly
Lymphadenopathy
Diagnostic exams

COMPLETE BLOOD COUNT

(CBC)
includes RBC count,
Hemoglobin, hematocrit,
RBC indices, WBC with or
without differential count,
and platelet count
 Red Blood Cells
Normal Values
RBC Parameters Normal Values

Hematocrit
Females 35-47%
Males 40-52%
Hemoglobin
Females 12.0-16.0 gm/dl
Males 13.5-17.5 gm/dl

MCV 80-100 fl
Reticulocyte Count 0.2-2.0%
Diagnostic exams

 RBC indices
 used to help diagnose the cause of anemia.
 Average red blood cell size (MCV) or mean
corpuscular volume
 N: 80 to 100 femtoliter
 Hemoglobin amount per red blood cell (MCH) or
mean corpuscular hemoglobin
 N: 27 to 31 picograms/cell
 The amount of hemoglobin relative to the size of the
cell (hemoglobin concentration) per red blood cell
(MCHC)
or Mean corpuscular hemoglobin concentration:
 32 to 36 grams/deciliter
Diagnostic exams

PERIPHERAL BLOOD SMEAR –

determines variations and
abnormalities in RBC,
leukocytes and platelets
Cells of normal size –
NORMOCYTES
Cells of normal color –
NORMOCHROMIC
 Reticulocyte Count

• Young RBC that still contains a small

amount of RNA
• 1/120th of RBC normally
• valuable in the evaluation of all patients
with anemia as it is a simple measure of
production
Diagnostic exams

COAGULATION SCREENING
TEST
Platelet count
Protime (PT) – 11-16 sec
Bleeding time (1-9 min)
Partial Thromboplastin time
(PTT) – 60-70 sec
Diagnostic exams

BONE MARROW ASPIRATION

AND BIOPSY
Checks and identify most
blood dyscracias (aplastic
anemia, leukemia, etc)
Taken from the posterior iliac
crest (sternum – alternative
site)
posterior
iliac crest
sternum – alternative site)
Diagnostic exams

PRE PROCEDURE
Prepare and explain the
purpose and what to expect
Inform that there will be pain
during the procedure
Secure and verify informed
consent
Sedation as ordered
Diagnostic exams

POST PROCEDURE
Apply pressure dressing or
/and sand bags
Educate to observe site for
bleeding
Analgesics (mild) may be
given
RED BLOOD CELL
DISTURBANCES
 ANEMIA

▪ one of the most common blood disorders

▪ an abnormally low hemoglobin level,

number of circulating red blood cells, or
both, resulting in diminishedoxygen-carrying
capacity of the blood.

▪ as a results from excessive blood loss or

destruction of red blood cells or from
deficient red blood cell production because
of a lack of nutritional elements or bone
marrow failure.
Classification of Anemias
physiologic approach

1. Blood loss anemia

▪ results from excessive
loss
2. Hemolytic anemia
▪ increased destruction
3. Hypoproliferative anemia
▪ impaired production of
red blood cells
 Iron Deficiency Anemia - microcytic hypochromic anemia

▪ most common type of anemia in all age group

CAUSES
▪ Excessive menstrual bleeding
▪ GI bleeding (most common pathologic cause)
▪ Poor Intake/Absorption
▪ Milk formula for baby
▪ Inflammatory bowel disease
▪ Increased Need
▪ Early childhood and adolescence (growth
spurts)
▪ Pregnancy (extra 3.8 mg/day over baseline)
▪ Lactation
 Insufficient Without IRON Impaired
dietary intake of absorption of
IRON IRON
Blood Loss HEMOGLOBIN Increased
concentration in the demands for
RBC production
RBC

Chronic, hypochromic, microcytic RBCs

Cells unable to oxygenate the
body tissues adequately
HYPOXIA

CLINICAL MANIFESTATIONS:
 Clinical manifestation

▪ Pallor
▪ Weakness and fatigue
▪ Tachycardia
▪ Shortness of Breath
▪ Koilonychia –brittle spoon shape nails
▪ Cheilosis
Plummer – Vinson syndrome
▪ Glossitis triad symptoms of iron
deficiency anemia, dysphagia
▪ Pica – a craving for unusual substances and esophageal web
 Diagnostic Test

Serum iron
Serum ferritin –a protein helps to store iron
Transferrin level – carries iron in the blood
Total iron-binding capacity – measures transferrin level
Common side effects of oral iron
Treatment preparations
Dietary intake of iron rich food ▪ Nausea
Oral or parenteral iron supplement
▪ Gastric discomfort
▪ Constipation
▪ Diarrhea
NURSING MGT:
ADMINISTER WITH ORANGE JUICE AS VITAMIN C
ANTACIDS WILL DECREASE IRON ABSORPTION
PROVIDE DIETARY TEACHING REGARDING FOOD HIGH
IN IRON
➢ FOOD SOURCES HIGH IN IRON:
▪ ORGAN MEATS (E.G., BEEF OR CALF’S LIVER, CHICKEN LIVER),
OTHER MEATS,
▪ BEANS (E.G., BLACK, PINTO, AND GARBANZO), LEAFY GREEN
VEGETABLES, RAISINS, AND MOLASSES)
 Cobalamin (Vitamin B )-Deficiency Anemia
12

Vitamin B12
➢ is essential for the synthesis of DNA
➢ deficiency may cause , nuclear maturation and cell
division, especially of the rapidly proliferating red cells
➢ deficiency may also prevent fatty acids from being
incorporated into neuronal lipids; which may predispose to
myelin breakdown and production of the neurologic
complications of vitamin B12 deficiency.
CAUSE
➢ strict vegetarians who avoid all dairy products as well as
meat and fish.
 Cobalamin (Vitamin B )-Deficiency Anemia
12

➢ Vitamin B12 must bound to

intrinsic factor, a protein
secreted by the gastric parietal
cells to be absorbed in the
distal elium.
 Folic Acid Deficiency - macrocytic anemia

▪ Folic acid is also required for DNA synthesis and red cell
maturation, and its deficiency produces the same type of red cell
changes that occur in vitamin B12 deficiency anemia, but the
neurologic manifestations are not present
CAUSES
▪ Malnutrition or Inadequate folate intake
▪ Malabsorption syndrome - intestinal disorders
▪ Drugs -barbiturates, phenytoin, and oral contraceptives.
▪ Pregnancy – increases the needs of folic acid, nausea, poor diet
 Folic acid therapy

▪ Folate therapeutics:
▪ Also, as folic acid, 5mg tablets.
▪ Usually in multivitamin preparations
▪ Recommended natural folate sources:
▪ Green vegetables, Nuts, Cereals, Fruits and meat
 Pernicious Anemia

A decrease in red blood cells due to

failure to absorb dietary B12 because of the
absence of intrinsic factor
CAUSES
▪ as result of an autoimmune disease that
destroys the parietal cells of the stomach
(hereditary atrophic gastritis)
▪ gastrectomy, ileal resection, and
malabsorption syndromes in which vitamin
B12 and other vitamin B compounds are
poorly absorbed.
 without
Cobalamin/B12
GI manifestations: Production of
Wt. loss, anorexia,
N/V, abd’l MYELIN on
DNA synthesis distention, nerves greatly
steatorrhea,
and cell BEEFY, red affected
replication is inflammed
impaired
tongue NEUROLOGIC
disorders
RBC precursors do not
divide normally
Paresthesia,
LARGE & POORLY poor gait,
memory loss,
FUNCTIONING RBC cognitive
MACROCYTIC CELL problems &
depressions
Manifestations of Anemia
DIAGNOSTIC TEST
abnormally low vitamin B12 serum level

SCHILLING TEST

MEASURES the absorption of orally administered radioactive VitB12

before and after parenteral injection of INTRINSIC FACTOR
To determine cause of Vitamin B12 deficiency
✓ Collect 24-hour urine specimen
✓ NORMAL == increased Vit. B12 in urine
✓ (+) Pernicious Anemia = decreased excretion of Vit B12 in the
urine
SCHILLING TEST
Medical management:
Drug therapy: Vit, B12 injections: monthly
maintenance
NURSING MGT:
Avoid highly seasoned, coarse, or very
hot food if with mouth sores
Mouth care before and after meals
Provide dietary instruction
Emphasize importance of lifelong vitamin
B12 therapy
 APLASTIC ANEMIA - normochromic, normocytic anemia

▪ rare disease caused by a decrease in or

damage to marrow stem cells
▪ Stem cell damage is caused by the body’s
T cells mediating an inappropriate attack
against the bone marrow, resulting in bone
marrow aplasia
▪ aplasia - markedly reduced hematopoiesis
▪ severe anemia, significant neutropenia
and thrombocytopenia (pancytopenia)
Aplastic Anemia

Causes
▪ acquired or, rarely, congenital, are idiopathic (most
cases)
▪ Viral infections and pregnancy can trigger it
▪ Drugs, Chemicals, Radiation damage
▪ Paint remover, dry-cleaning solution
 Aplastic Anemia: Signs and Symptoms

▪ Anemia
▪ Pallor, fatigue, dyspnea

▪ Thrombocytopenia
▪ bruises, petechiae
▪ serious bleeding

▪ Neutropenia
▪ Infections
PANCYTOPENIA – severe anemia, significant neutropenia and
thrombocytopenia
▪ Other: lymphadenopathies, splenomegaly, retinal
hemorrhages are common.
Diagnostic Findings
1. CBC reveals pancytopenia
2. A bone marrow aspirate -hypoplastic or aplastic marrow replaced with fat.

Treatment
▪ Hematopoietic stem cell transplant (HSCT)
▪ Immunosuppressive therapy: antithymocyte globulin (ATG)
and cyclosporine or androgens
▪ Supportive therapy
▪ transfusionsof PRBCs and platelets
▪ Infection aggressively treated
NURSING MANAGEMENT:
Administer blood transfusions
Monitor for signs of infection and provide care
to minimize risk
Monitor for signs of bleeding
Encourage high protein and high vitamin diet
to help reduce incidence of infection
 Hemolytic Anemia
Characterized by the
1. Premature destruction of red cells
2. Retention in the body iron and other
products of hemoglobindestruction;
(bilirubin)
3. Increase erythropoiesis
 Hereditary spherocytosis

▪ transmitted as an autosomal
dominant trait; the most common
inherited disorder of the red cell
membrane
▪ 1/5000 in northern European
populations
▪ a deficiency of membrane
proteins( spectrin and ankyrin)
that leads to gradual loss of the
membrane surface, resulting in a
tight sphere instead of a concave loss of membrane results to loss of
disk deformability; RBC is susceptible to destruction
as it passes through the venous sinuses of the
splenic circulation
Hereditary spherocytosis

Spherocytes are
red blood cells that are
almost spherical in shape.
They have no area of
central pallor like a normal
red blood cell.
Hereditary spherocytosis

▪ Clinical features: ▪ Treatment

▪ clinical severity varies ▪ most patients do not need
▪ most have mild to moderate anemia treatment
▪ splenomegaly, cholelithiasis, jaundice ▪ splenectomy
may occur ▪ counsel patient and family
about inheritance
▪ Laboratory features
▪ hemolytic anemia with spherocytes
▪ osmotic fragility test (saline solution)
▪ negative direct antiglobulin Test
Glucose-6-Phosphate Dehydrogenase Deficiency

▪ The G-6-PD gene produces an enzyme

within the erythrocyte that is essential for
membrane stability.
▪ inherited as X-linked defects
▪ some patients have inherited an enzyme
that is so defective that they have a chronic
hemolytic anemia
▪ RBC hemolyze during infection and oxidant
drugs(antimalarial drugs, aspirin, sulfadiazine,
nitrofurantoin)
▪ oxidative damage to red cells leads to Heinz Acute hemolysis in G6PD deficiency
body formation (degraded hemoglobin) (arrows indicate “blister cells,” and
arrowheads irregularly contracted cells).
▪ ingestion of fava beans, menthol, tonic water,
and some Chinese herbs.
 G6PD deficiency
Clinical Manifestations
▪ asymptomatic, normal hemoglobin
levels and reticulocyte counts
Exposure to an offending medication
or substance:
▪ pallor,
▪ Jaundice
▪ hemoglobinuria
▪ reticulocyte count increases
▪ stains of the peripheral blood may
then disclose Heinz bodies
▪ Laboratory diagnosis
▪ Peripheral stain of Heinz bodies
▪ Quantitative assay of G-6-PD
▪ Treatment
▪ Arrest the source and stop the
offending medication
▪ Transfusion - severe hemolytic state
(Mediterranean variety of G-6-PD
deficiency)
 Nursing Management

▪ Educated patient and family about the

disease and given a list of medications and
substances to avoid
➢ seek advice before taking any new
medication or supplement. An excellent
▪ Patients should be instructed to wear Medic-
Alert bracelets
▪ Genetic counseling may be indicated
 SICKLE CELL ANEMIA

A severe hemolytic anemia due to

inheritance of sickle hemoglobin gene(Hbs).
➢ most common inherited disorder in US
autosomal recessive pattern
➢ occurs when a person inherits
two abnormal genes (one from each parent)
that cause their RBCs to change shape.
SICKLE CELL ANEMIA
SICKLE CELL ANEMIA

when O2 is released, the

shape of the RBCs change from
round & pliable to crescent
shaped, rigid, & inflexible
local hypoxia & continued
sickling lead to plugging of the
vessels
SICKLE CELL ANEMIA

▪ sickled RBCs live for 6-20 days

causing hemolytic anemia
▪ 6 mos or less – (-) symptoms due
levels of fetal hemoglobin
▪ death occurs in early adulthood
due to occlusion or infection
SICKLE CELL ANEMIA
Hbs
(Valine substitutes normal Glutamic Acid)

exposure to low pH, low Oxygen tension

sickling of RBCs

Hemolysis vascular obstruction vaso- oclussive crisis

S/Sx: anemia

jaundice hypoxia

infarct
 FACTORS RELATED TO SICKLING:

➢ HbS acquires a crystal-like formation when exposed to

➢Cold
low oxygen tension.
➢ Stress ➢ The following factors could predispose an oxygen level in
venous blood that can be low enough to cause sickling
➢ Exertion ❖ consequently, the erythrocyte containing HbS loses its
round, pliable, biconcave disc shape and becomes
➢ Infection
dehydrated, rigid, and sickle shaped
➢ Hypoxia ➢ The sickling process takes time; if the erythrocyte is again
exposed to adequate amounts of oxygen before the
➢ Acidosis membrane becomes too rigid (e.g., when it travels through
the pulmonary circulation), it can revert to a normal shape.
➢ Dehydration
❖ For this reason, the “sickling crises” are intermittent.
Sickle cell anemia – clinical features

▪ The clinical
manifestations
primarily occur as a
result of obstruction
caused by sickled red
blood cells and
increased red blood
cell destruction
➢ delayed growth &
development
➢ Pain: due to vaso-
occlusive crisis
➢ Jaundice: due to
hemolysis
➢ Priapism: result in
impotence ( 6-12%)
Sickle cell anemia – clinical features

➢Dactylitis ( hand
foot syndrome);
- symmetrical soft
tissue swelling of the
hands & feet without
obvious trauma
Sickle cell anemia – clinical features

Leg ulcers
 DIAGNOSTIC TESTS:

1. CBC – anemia

2. Sickle Cell test-

deoxygenation of a
drop of blood on a slide
Sickledex
➢a drop of bld from a
fingerstick is mixed w/
solution
➢mixture turns cloudy if
(+) HgbS
 DIAGNOSTIC TESTS

3. Hemoglobin
electrophoresis – a test to
measures the different
types of hemoglobin
4. Prenatal: DNA of fetus via
amniocentesis
 Hemoglobins in normal adults
Types of hemoglobin

HbA HbF HbA2

98% ~1% <3.5%

 MEDICAL MANAGEMENT

➢Penicillin – prophylaxis @ 3mos-5 yrs

➢ Routine vaccination
➢ Blood transfusion
➢ Hydroxyurea – increase Hgb F synthesis
➢Stem cell transplant
 NURSING INTERVENTIONS

➢Hydration
➢Avoid tight clothing; may impair circulation
➢Keep wounds dry & clean
➢CBR
➢Keep arms & legs from becoming cold
➢decrease emotional stress
➢provide good skin care
➢test siblings for presence of sickle cell
trait
 SICKLE CELL CRISIS
1. Acute Vaso-occlusive Crisis
▪ most common type
▪ crescent-shaped RBCs clump
together; agglutination causes
blockage of small blood vessels
▪ tissue hypoxia, inflammation, and
necrosis
 SICKLE CELL CRISIS

2. Sequestration Crisis
▪ sickled cells block outflow tract resulting in
sudden & massive collection of sickled cells into
an organ
▪ the common organs involved in sequestration
are the liver and spleen, more seriously, the
lungs.
▪ Splenic sequestration may lead to hypovolemia
▪ Lung sequestration may lead to acute chest
syndrome, pulmonary hypertension
SICKLE CELL CRISIS

3. Aplastic Crisis
▪ results from infection with the
human parvovirus.
▪ hemoglobin level falls rapidly, and
the marrow cannot compensate,
as evidenced by an absence of
reticulocytes
Medical Management
➢ Hematopoietic Stem Cell Transplant
➢ Pharmacologic Therapy
▪ Hydroxyurea is a chemotherapy agent that is effective in increasing fetal
hemoglobin
▪ Daily folic acid replacements to maintain or increased erythropoiesis from
hemolysis
▪ Antibiotics – to treat Infections
▪ Pneumococcal infection - common in children.
▪ Staphylococcus aureus - In adults
▪ Corticosteroid
▪ Pneumococcal and annual influenza vaccinations.
➢ Incentive spirometry - decreases the incidence of pulmonary complications
significantly
➢ Hydration (carefully monitored as fluid overload can develop quickly)
➢ RBC Transfusions reverse the hypoxia
▪ chelation therapy - Iron overload is most likely with frequent transfusion
▪ supported with corticosteroids (prednisone), and possibly intravenous
immunoglobulin (IVIG) and erythropoietin (epoetin alfa [Epogen]).
Supportive Therapy
❖ Pain management is a significant issue
Acute pain is caused by vaso-occlusive crisis, and is the most common reason for
hospitalization
▪ Use of medication to relieve acute pain
▪ Aspirin is very useful in diminishing mild to moderate pain; it also diminishes inflammation and
potential thrombosis (due to its ability to decrease platelet adhesion).
▪ NSAIDs are useful for moderate pain or in combination with opioid analgesics
▪ Parenteral opioids
▪ Patient-controlled analgesia
▪ Nonpharmacologic approaches to pain management are crucial in this setting
▪ physical and occupational therapy,
▪ physiotherapy (including the use of heat, massage, and exercise)
▪ cognitive and behavioral intervention (including distraction, relaxation, and motivational
therapy)
▪ support groups.
▪ Adequate hydration is important during
Thalassemia

▪ a group of hereditary anemias characterized

by hypochromia and extreme microcytosis
▪ are associated with defective synthesis of
hemoglobin; the production of one or more
globulin chains within the hemoglobin
molecule is reduced
▪ the imbalance in the configuration of the
hemoglobin causes it to precipitate, thus consists of two different proteins(globulin),
increases the rigidity of the erythrocytes an alpha and a beta chain
resulting to the premature destruction
Thalassemias are classified into two major groups

1. Alpha-thalassemias - reduced alpha chain

synthesis
▪ occur mainly in people from Asia and the Middle
East,
2. Beta-thalassemias - reduced beta chain synthesis
▪ are most prevalent in people from Mediterranean
regions
 Classification & Terminology of Thalassemia

Thalassemia minor – asymptomatic silent carrier

• Normal /
Thalassemia trait – produces mild microcytic anemia • Silent carrier - /
Thalassemia intermedia – manifest splenomegaly, • Minor -/-
moderate to severe anemia
--/
Thalassemia major – severe anemia, requires • Hb H disease --/-
transfusion to sustain life
▪ Alpha thalassemia major - Barts hydrops fetalis • Barts hydrops fetalis --/--
▪ Beta thalassemia major – Cooley anemia
Other symptoms are
failure to thrive, frequent infections,
diarrhea, splenomegaly, hepatomegaly
jaundice, fatigue, shortness of
breath, bone deformities, growth failure

Beta thalassemia major

Male 18 years
Thalassemia beta major or Cooley’s anemia
Management

▪ Haematopoietic stem cell transplantation

(HSCT) -offers a chance of cure
▪ Regular Transfusion of PRBCs
▪ Regular iron chelation therapy can reduce
the complications of iron overload and
prolong the life of these patients
POLYCYTHEMIA

Gk polys (many) , kytos(cells), haima(blood)

▪ refers to an increased volume of RBCs.
▪ It is used when the hematocrit is elevated (more
than 55% in males, more than 50% in females)
Classification of Polycythemia

1. Primary polycythemia, also called

polycythemia vera - is a proliferative
disorder
2. Secondary polycythemia is caused by
excessive production of erythropoietin this
may occur in response to a reduced
amount of oxygen, which acts as a
hypoxic stimulus,
PRIMARY POLYCYTHEMIA
- result of an abnormality of the bone
marrow;
- classified as a myeloproliferative
disease
- JAK2 gene (janus kinase 2)mutation
SECONDARY POLYCYTHEMIA - is caused by
excessive production of erythropoietin in response to a
reduced amount of oxygen, which acts as a hypoxic
stimulus (pathologic/ non-pathologic condition) such
as:
▪ Obstructive sleep apnea (OSA)
▪ Chronic obstructive pulmonary disease (COPD)
▪ Cyanotic heart disease
▪ neoplasms (e.g., renal cell carcinoma) that stimulate
▪ erythropoietin production,
▪ Living at a high altitude or exposure to low levels of
carbon monoxide
 CLINICAL MANIFESTATION

Headache, dizziness, paresthesia, blurred vision

Angina, claudication, thrombosis
Generalized pruritus –histamine release due to increase in basophils
Erythromelalgia – a burning sensation in fingers and toes
Ruddy red-colored complexion of face
 DIAGNOSIS

▪ CBC - hemoglobin
▪ Hematocrit male>55 %; female>50%
▪ Erythropoietin level
▪ BMA – stem cell hyperplasia
 TREATMENT

▪ Phlebotomy – removes 300ml-500ml of blood

▪ Aspirin – anticoagulant
▪ Pruritus – antihistamines
▪ Treat underlying condition
hydroxyurea to supress bone marrow function
 HEMOPHILIA

▪ Refers to a group of bleeding

disorders resulting from a deficiency
of specific coagulation proteins
▪ most common types
1. hemophilia A or classic hemophilia
- factor VIII deficiency
2. hemophilia B or Christmas disease
- factor IX deficiency
 Assessment
▪ 1. Abnormal bleeding in response to trauma or surgery
▪ 2. Epistaxis (nosebleeds)
▪ 3. Joint bleeding causing pain, tenderness, swelling, and
limited range of motion
▪ 4. Tendency to bruise easily
Primary treatment is replacement of the missing clotting
factor
Nursing mgt
1.Prepare to administer replacement factors as prescribed.
2. Assess neurological status and monitor hematuria.
3. Control joint bleeding by immobilization, elevation, and the
application of ice
4. Apply pressure (15 minutes) for superficial bleeding.
PERIPHERAL VASCULAR DISEASE (PVD) IS A SLOW AND
PROGRESSIVE CIRCULATION DISORDER CAUSED BY
NARROWING, BLOCKAGE, OR SPASMS IN A
BLOOD VESSEL.
PVD MAY INVOLVE DISEASE IN ANY OF THE
BLOOD VESSELS OUTSIDE OF THE HEART INCLUDING
THE ARTERIES, VEINS, OR LYMPHATIC VESSELS.
 VASC ULAR

DIAGNOSTIC TESTS
 Doppler Ultrasound Flow Studies

- used to detect the blood flow in vessels when pulses cannot

be reliably palpated
- a handheld continuous wave(CW) Doppler ultrasound
device which emits a continuous signal through the
patient’s tissues
- signals are reflected by (“echo off”) the moving blood cells
- signal is then transmitted to a loudspeaker or headphones,
where it can be heard for interpretation
 Doppler Ultrasound Flow Studies
To evaluate the lower extremities
a. the patient is placed in the supine position with the head
of the bed elevated 20 to 30 degrees
b. the legs are externally rotated, if possible, to permit
adequate access to the medial malleolus.
c. Acoustic gel is applied to the patient’s skin to permit
uniform transmission of the ultrasound wave.
d. The tip of the Doppler transducer is positioned at a 45-
to 60-degree angle over the expected location of the
artery and angled slowly to identify arterial blood flow.
e. Excessive pressure is avoided because severely diseased
arteries can collapse with even a minimal pressure
 Doppler Ultrasound Flow Studies
Doppler is more useful as a clinical tool when
combined with ankle blood pressures, which are
used to determine the ankle-brachial index (ABI)
Ankle-brachial index (ABI)
- is the ratio of the systolic blood
pressure in the ankle to the systolic
blood pressure in the arm
- is an objective indicator of arterial
disease that allows to quantify the
degree of stenosis.
- with increasing degrees of arterial
narrowing, there is a progressive
decrease in systolic pressure distal
to the involved sites.
Steps on ABI
1. The patient rest in a supine position
for approximately 5 minutes.
2. An appropriatel sized blood pressure
cuff (typically, a 10-cm cuff) is applied
to the patient’s ankle above the
malleolus.
3. The systolic pressures, are obtained
in both ankles, while listening to the
Doppler signal at each artery.
To calculate ABI
The highest ankle systolic pressure for
each foot is divided by the higher of the
two brachial systolic pressures
In general, systolic pressure in the ankle
of a healthy person is the same or slightly
higher than the brachial systolic pressure

ABI of about 1.0 - no arterial insufficiency

ABI of 0.90 to 0.50- mild to moderate
insufficiency; patients with
claudication
ABI of less than 0.50 -ischemic rest pain
ABI of 0.40 or less - patients with severe
ischemia or tissue loss
 DUPLEX ULTRASONOGRAPHY

➢ involves B-mode grayscale imaging of the tissue, organs, and

blood vessels (arterial and venous) and permits estimation of
velocity changes by use of a pulsed Doppler
➢ may be used to determine the level and extent of venous
disease as well as chronicity of the disease.
➢ Using B mode and Doppler, it is possible to image and assess
blood flow, evaluate flow of the distal vessels, locate the
disease (stenosis versus occlusion), and determine anatomic
morphology and the hemodynamic significance of plaque
causing stenosis
➢ noninvasive and usually requires no patient preparation
➢ standard for diagnosing lower extremity venous thrombosis
DUPLEX SCAN
EXERCISE TESTING
➢ used to determine how long a patient can
walk and to measure the ankle systolic
blood pressure in response to walking
➢ the patient walks on a treadmill at 1.5
mph with a 12% incline for a maximum of
5 minutes, or the test can be modified to
walking a set distance in a hallway
➢ A normal response to the test is little or
no drop in ankle systolic pressure after
exercise
➢ in a patient with true vascular
claudication, the ankle pressure drops.
COMPUTED TOMOGRAPHY SCAN

PROVIDES CROSS SECTIONAL IMAGES OF SOFT

TISSUE AND CAN IDENTIFY THE AREA OF VOLUME CHANGES
TO AN EXTREMITY

In multidetector-computed
tomography (MDCT), a spiral CT
scanner and rapid intravenous
(IV)infusion of contrast agent are
used to image very thin sections of
the target area, and the results are
configured in three dimensions so
that the image can be rotated and
viewed from multiple angles.
COMPUTED TOMOGRAPHY SCAN
NURSING INTERVENTIONS:
▪ NPO, IF WITH CONTRAST MEDIUM
▪ ASSESS TO IODINE AND SEAFOODS
ALLERGY
▪ ASSESS FOR CLAUSTROPHOBIA
▪ INSTRUCT TO REMAIN STILL
DURING THE ENTIRE PROCEDURE
▪ SEDATE IF UNABLE TO REMAIN
STILL
 MAGNETIC RESONANCE IMAGING
PERFORMED WITH A STANDARD MRI SCANNER BUT CAN
SPECIFICALLY ISOLATE THE BLOOD VESSELS; DOES NOT USE A
CONTRAST AGENT

-
 ANGIOGRAPHY
▪ An arteriogram produced by
angiography
▪ to confirm the diagnosis of occlusive
arterial disease when surgery is
considered.
▪ a radiopaque contrast agent directly
injected into the arterial system to
visualize the vessels.
▪ location of a vascular obstruction or an
aneurysm and the collateral
circulation can be demonstrated

❖ Magnetic resonance angiography (MRA) is

performed with a standard magnetic resonance
imaging (MRI) scanner and special software
programmed to isolate the blood vessels.
 Contrast Phlebography (Venography)
▪ involves injecting a radiopaque contrast agent into the
venous system
▪ Injection of the contrast agent may cause brief but
painful inflammation of the vein
▪ test is generally performed if the patient is to undergo
thrombolytic therapy;

-
 D DIMER
a product of fibrinolysis, is
elevated in venous
thromboembolism .

-
Peripheral vascular disease (PVD) is a
slow and progressive
circulation disorder caused by
narrowing, blockage, or spasms in a
blood vessel.
PVD may involve disease in any
of the blood vessels outside of the heart
including the arteries, veins, or
lymphatic vessels.
-
 HYPERTENSION

as a systolic blood pressure (SBP) of 140 mm Hg

or higher or a diastolic blood pressure
(DBP) of 90 mm Hg or higher, based on the
average of two or more accurate blood pressure
measurements taken 1 to 4 weeks apart by a
-
healthcare provider

(American Society of Hypertension (ASH)

and the International Society of Hypertension (ISH)
 :
:
:
:
-
 1. ESSENTIAL/IDIOPATHIC/PRIMARY
HYPERTENSION
No known cause
ACCOUNTS FOR 90% TO 95 % OF ALL
CASES OF HYPERTENSION
Risk factors
a. Aging
b. Family history
-
c. Black race, with higher
prevalence in males

Classification of Hypertension
2. SECONDARY HYPERTENSION
cause of hypertension can identified
occurs as a result of other disorders or
conditions.

a. Cardiovascular disorders
b. Renal disorders
-
c. Endocrine system disorders
d. Pregnancy
e. Medications (e.g., estrogens)

classification of hypertension
 LABILE HYPERTENSION -
Is intermittently elevated BP

RESISTANT
HYPERTENSION -
Hypertension that does not
respond to usual treatment

-
WHITE COAT
HYPERTENSION -
Elevation of BP only during
clinic visits

classification of hypertension
 HYPERTENSIVE CRISIS -
Situation that requires
immediate blood pressure
lowering (within 1 hr, systolic
pressure more than 240 and
diastolic more than 120
mmHg)

classification of hypertension
 HYPERTENSIVE CRISIS
A. HYPERTENSIVE EMERGENCY
is a situation in which blood pressure
must be lowered immediately (not necessarily to less than
140/90 mm Hg) to halt or prevent damage to the target organs.

associated conditions:
acute myocardial infarction, dissecting aortic aneurysm, and
intracranial hemorrhage.
-

Mgt: fast acting IV vasodilators, intensive care setting

.
 HYPERTENSIVE CRISIS

B. Hypertensive Urgency
a situation in which blood pressure must be lowered
within a few hours to prevent damage to target
organs

Mgt: PO antihypertensive meds

-

.
RACE
African Americans –had highest prevalence of
hypertension in the world and tend to develop
hypertension at younger ages than white
AGE
32.6% of the adults in the United States have
hypertension, and the prevalence increases
significantly as people get older
GENDER
more common in younger men compared with
younger women
Family History - pattern of heredity is unclear whether a
single gene or multiple genes are involved
 is supported by the fact that hypertension is seen
most frequently among persons with a family history
of hypertension
Insulin resistance and hyperinsulinemia
Metabolic disturbances - type 2 diabetes,
hyperlipidemias, and obesity
Lifestyle Factor
High Salt Intake.- causes an elevation in blood volume, increases the
sensitivity of cardiovascular or renal mechanisms to adrenergic; influences
some other mechanism such as the renin-angiotensin-aldosterone mechanism
 Excess Alcohol Consumption
 Low levels of dietary potassium
 Stress
 is thought to reside with the kidney and its role
regulating vascular volume through salt and water
elimination;
the renin angiotensin- aldosterone system
through its effects on blood vessel tone, regulation of
renal blood flow
and the sympathetic nervous system, which
regulates the tone of the resistance vessels.
CLINICAL
MANIFESTIONS:
May reveal no
abnormalities other than
high BP; asymptomatic

Left ventricular
hypertrophy
Occipital headache
Epistaxis
Blurred vision
Nape pain
Dizziness
Papilledema
Retinopathy
DIAGNOSTIC EXAMS

2D ECHO
Renal Function Studies
Lipid Profile
 L—Limit salt and alcohol.
I—Include daily potassium, calcium, and
magnesium.
F—Fight fat and cholesterol.
E—Exercise regularly.
S—Stress management.
T—Try to quit smoking.
Y—Your medications are to be taken daily.
L—Lose weight.
- E—End-stage complications will be avoided!

DASH DIET

hypertension LIFESTYLE modification

 A chronic occlusive arterial disease
that may affect the abdominal
aorta or the lower extremities.
- Common among men ages 50-60
Caused by atherosclerosis
Risk factors: hypertension, DM,
cigarette smoking, hyperlipidemia
 Risk factors

accumulation of atherosclerotic plaques

thickening of intima and media of arterial

wall

arteries narrow
s/s: hair loss on extremities,
diminished perfusion paresthesia, pallor,
Pulselessness, Poikilothermia
progressive oxygen deprivation (tissue
ischemia)

aerobic to anaerobic metabolism s/s: pain, leg cramps

atrophy of tissue, poor healing capacity, s/s: paralysis, ulceration,
infection and tissue necrosis gangrene
CLINICAL MANIFESTATIONS
6 Ps Paralysis
Pain Pulselessness
Paresthesia Pallor Ulceration & gangrene
Hair loss on extremities
Poikilothermia (coolness)
 Diagnostics

Doppler USD
Treadmill testing
provide objective measurement of
claudication
-
Serum Triglycerides: elevated
 Medical management

Vasodilators = isoxsuprine HCL

Antihyperlipidemics = Simvastatin
Pain relievers
Anti-coagulants
-
Anti platelet - Pentoxyfylline (Trental) improves
oxygenated blood supply by reducing blood
viscosity and increses RBC flexibility
Cilostazol (Pletaal) = inhibits platelet
aggregation
 Surgical Management

Vascular grafting/ by pass grafts to

reroute blood around the stenosis or
-
occlusion
ENDARTERECTOMY: an incision is made
into the artery and the atheromatous
obstruction is removed.
AMPUTATION
 Nursing Management
Risk modification
Skin and foot care
Low fat Low cholesterol diet
Daily walking program
Promote tissue perfusion:
-
Maintain warm environmental temperature
Avoid pressure on affected extremity, use padding
for support
Avoid chilling and exposure to cold
Wear comfortable well fitted pair of shoes
 Acute, inflammatory disorder
affecting the medium/smaller
arteries and veins of the lower extremities.
- Disease is idiopathic;
high incidence among smokers
Affects men ages 25-40
cause: Heavy cigarette smoking, autoimmune response

irritation and inflammation of the small & medium-

sized arteries and veins

Polymorphonuclear lukocytes infiltrate the walls

thrombus develops in vascular lumen

occlude and obliterate the portions of the small

vessels

decrease blood flow to the feet

and leg

development of
ischemic pain

if left untreated lead to

ulceration and gangrene
 Intermittent Claudication
A muscular, cramp-type pain in the
extremities
caused by the inability of the arterial
system to provide adequate
blood flow to the tissues in the face of
increased demands for nutrients
-
during exercise.
Cold sensitivity
Decreased or absent peripheral
pulses
Ulceration and gangrene
 Diagnostics:
same with ASO but no increase in
triglycerides
-
 Medical management
similar with ASO.
Only really effective treatment is
cessation of smoking
Nursing management
- Prepare client for surgery.
Teach on: drug regimen, avoiding
trauma to affected extremity,
maintain warmth and importance
of cessation of smoking
It is the localized, irreversible dilation of an
artery secondary to an alteration in the integrity
of its wall
MOST COMMON CAUSE:
atherosclerosis
possible congenital weakness

RISK factors: genetic predisposition, smoking,

hypertension
Affects men 4 times than women, common
among Caucasians, elderly
CLASSIFICATION

FUSIFORM – involves out

pouching on both sides of the
artery
SACCULAR - one side only
DISSECTING – separation or tear
in the tunica intima & media,
medial layer is weak and blood
enters into it

BERRY – brain aneurysm

MOST COMMON
TYPE: ABDOMINAL
AORTIC ANEURYSM
(AAA)
characteristic
manifestation is
PULSATILE MASS
WITH A SYSTOLIC
BRUIT OVER THE
AORTA OVER THE
ABDOMEN
ESPECIALLY WHEN
LYING DOWN.
OTHER CLINICAL
MANIFESTATIONS:
Can be asymptomatic
Lower abdominal pain
Hypertension
Low back pain

Complication:
RUPTURE OF ANUERYSM

Diagnostics: to confirm,
determine size & location
Abdominal USD & CT scan
Arteriography
 cause: atherosclerosis, hereditary

weakens the artery

wall loss of elasticity in the artery

increase force of blood flow

increase tension in the vessel wall

abnormal dilatation of blood

vessel
Surgical Management:
Open surgical repair:
resecting the vessel and
sewing a bypass graft in
place
Endovascular grafting:
placement and attachment
of a sutureless aortic graft
prosthesis across an
aneurysm.

Nursing management:
NO abdominal palapation
NO bending, straining
BP monitoring
Encourage compliance with
anti hypertensive meds
Intemittent episode of arterial spasms.

Most frequently involving the fingers

Cause is unknown

Common among women ages 15-40

Aggravated by emotional stress,
smoking, and cold sensitivity
Clinical manifestations:

Pallor (vasoconstriction) –
cyanosis (pooling of
deoxygenated blood
during vasospasm) ----
rubor (increased blood
flow)
Numbness, tingling,
swelling, and coldness of
affected part (bilateral)

Diagnostics: Allen’s test

 factor: cold exposure, emotional events

vasospasm of digital artery

diminished blood supply s/s: pallor to cyanosis, a

(tissue ischemia) sensation of cold, changes
in sensory perception, such
as numbness and tingling.
Tissue Hypoxia
s/s: intense
blood vessels reopen and redness,
if progress: vessels remain constricted throbbing,
hyperemia occurs
paresthesia

severe decrease blood flow

return to normal color
tissue necrosis and
gangrene
Medical management:

Ca Channel blockers
to relieve vasospasm
NSAIDs
Surgical management:
AMPUTATION
Avoid exposure to cold
Importance of Stopping
smoking
Need to use gloves when
Client Teaching handling cold objects/
frozen objects
Avoid stress (emotional)
Avoid triggering factors
-
Thrombosis is an abnormal
condition in w/c a clot (thrombus)
develops within the blood vessels
saphenous veins - superficial
Femoral vein - DVT

Risk factors: smoking

Venous stasis
Vessel Wall Injury
Hypercoagulability of the blood
RISK FACTORS:
ENDOTHELIAL DAMAGE:
TRAUMA, SURGERY, CENTRAL
VENOUS CATHETERS
VENOUS STASIS:
IMMOBILIZATION, OBESITY,
VARICOSITIES, SPINAL CORD
INJURY
OTHERS:
CANCER, PREGNANCY,
POLYCYTHEMIA
CM:
Calf pain
(+) Homan’s sign
Warmth
Tenderness
Edema
 injury to the vessel

triggers the haemostatic process

platelets adhere to the damaged

endothelium

platelets aggregate

protective factors that inhibit this may be unable

to reach due to venous stasis

thrombus is formed and persist as unorganised fibrin

thrombus may dislodged to

circulation
 Venous Thromboembolism
› Deep vein thrombosis (DVT) and
pulmonary embolism (PE) collectively
make up the condition called .
https://youtu.be/gYm9MBZFaic
https://youtu.be/pHddAMauvFk
Diagnostics:
Doppler Ultrasound
Duplex Scan
Nursing Management
Bed rest
Avoid prolonged sitting,
standing
Warm moist packs
Walking
Elevation
Elastic compression stocking
Maintain ideal body weight
Measure thigh and calves once
a day
Prominent, abnormally
dilated, dark and tortuous
veins, usually affecting the
lower extremities.
Common among women,
30 to 50 years of age
 cause

increased venous pressure and pooling of the blood

veins enlarged and valves stretched

blood flow is reversed

increased in venous pressure and distension

increased in capillary hydrostatic pressure

fluid and pigment leak out with discoloration

s/s: leg edema,
sluggish circulation dilated tortuous
vein, heaviness on
tissue hypoxia affected extremity

cell death and venous stasis ulcers

 CM: Dilated
purplish tortuous
veins
Leg pain (dull,
aching)
Leg edema
Heaviness in the legs
DIAGNOSTICS
Medical-surgical management:

Sclerotherapy: involves
injection of a sclerosing
agent (Na murrhate)
Vein ligation
It is also sometimes called phlebectomy.
Ligation refers to the surgical tying off of a large vein
in the leg called the greater saphenous vein, while
Stripping refers to the removal of this vein through
incisions in the groin area or behind the knee
NURSING MANAGEMENT:
Post vein ligation and stripping: bed rest for 24 hrs.
then walking every 2 hrs. for 5 to 10 mins.
Elastic compression stockings
Assist in exercises
Elevate foot of the bed
Avoid prolonged sitting and standing
Monitor peripheral pulses
Post sclerotherapy: burning sensation is normal for 1 to
2 days, elastic compression stocking are applied for 5
days, to be removed by physician, walking exercises to
dilute the sclerosing agent
Vascular Disorders Prevention

Venous Thromboembolism - Deep vein ○ Identification of risk factors and preventive

thrombosis and pulmonary embolism make up the measures
condition
○ Compression stockings and devices, early
● Frequently not diagnosed because often ambulation, leg exercises
clinically silent
○ LMWH as ordered
● Common in patients post-op
○ Lifestyle changes - weight loss, smoking cessation
Risk factors and regular exercise

○ Endothelial damage Medical Management

○ Venous stasis ○ GOAL: prevent thrombus from growing and

fragmenting
○ Altered coagulation
○ Anticoagulant therapy and ultrasonic-assisted
Patho
thrombolytic therapy
○ Virchow Triad > phlebitis > formation of
○ Pharmacologic Therapy
thrombus (phlebothrombosis)
■ Unfractionated heparin, low-molecular
Clinical Manifestations
weight heparin, oral anticoagulants, factor Xa and
○ Non-specific except phlegmasia cerulea dolens direct thrombin inhibitors, thrombolytic therapy

○ Sudden venous hypertension ○ Endovascular management

○ Deep veins ■ Anticoags and thrombolytics are C/I

■ Edema and swelling, warm, deep veins ■ Thrombectomy, ultrasound-assisted

appear more prominent thrombolysis, balloon angioplasty

■ Tenderness Nursing Management

○ Superficial veins ○ Assessing and monitoring anticoagulant therapy

■ Tenderness, redness, warmth ○ Monitoring and managing potential

complications
Diagnostic Exams
■ Bleeding, thrombocytopenia, drug
○ Careful assessment of lower extremities interactions

■ Feeling of heaviness, functional impairment, ○ Providing comfort

ankle engorgement, edema, areas of tenderness
○ Providing compression therapy
○ Homan Sign is not reliable for DVT
 ■ Stockings Prevention

■ External compression devices and wraps ○ Avoid activities or clothing that cause venous
stasis
■ Intermittent pneumatic compression
devices Medical Management

○ Positioning the body and encouraging exercise ○ Exercises and changing position

○ Promoting home, community-based, and ○ Graduated compression stockings

transition care
○ Weight reduction
Varicose Veins - Abnormally dilated, tortuous,
○ Surgical treatment
superficial veins caused by incompetent venous
valves ■ Ligation and stripping
- Common in the lower extremities but can occur ■ Thermal ablation
elsewhere
■ Sclerotherapy
- Common in people whose occupations require
prolonged standing Management

- Hereditary weakness of the vein wall contribute ○ Promoting comfort and understanding
however rare before puberty,
○ Promoting home, community-based, and
- Pregnancy transitional care

Patho Arterial Disorders

○ Reflux of venous blood > venous stasis > Peripheral Arterial Occlusive Disease - Blockage or
accumulation of venous blood > vein distention narrowing of an artery in the legs. Symptoms are
dependent on the affected artery and how severe
Clinical Manifestations the blockage
○ IF PRESENT: Dull aches, muscle cramps, increased - Occurs most often in men and common cause of
muscle fatigue in lower legs, ankle edema, and a disability
feeling of heaviness of legs, nocturnal cramps
- Legs are most frequently affected
○ If deep veins are involved, signs and
symptoms of chronic venous insufficiency (edema, Clinical Manifestations
pain, pigmentation, and ulcerations)
○ Intermittent claudication*
Diagnostic Exams
○ Rest pain - critical ischemia
○ Duplex ultrasound scan*
Diagnostic Exams
○ Venography, CT venography
○ History and assessment
 ○ Continuous-wave doppler, ABI, treadmill ○ Imaging Studies
testing for claudication, duplex ultrasonography
Thoracic Aortic Aneurysm
Management
○ Clinical Manifestations
○ Exercise (walking) program, unsupervised
■ Depends on how rapidly aneurysm dilates
walking exercise programs
and how pulsating mass affects surrounding
○ Exercise + weight reduction + smoking structures
cessation
■ Pain* - during supine
○ Pentoxifylline and cilostazol, antiplatelets,
statins ■ Dyspnea, cough, stridor, hoarseness or
aphonia, dysphagia
○ Endovascular management
Abdominal Aortic Aneurysm
■ Balloon angioplasty, stent, stent graft,
○ Clinical Manifestations
atherectomy
■ Only 40% are symptomatic
Surgical Management
■ “Feel their heart beating in their abdomen
■ For severe/disabling claudication
when lying down”
■ Endarterectomy, bypass grafts
■ Systolic bruit
Nursing Management
■ Signs of impending rupture
○ Nursing care of the postoperative patient
● Severe back or abdominal pain
■ Maintaining circulation
■ Signs of rupturing aneurysm
■ Monitoring and managing potential
complications ● Constant intense back pain, falling BP,
decreasing hematocrit
■ Home care
■ Rupture to peritoneal cavity
Aortic Aneurysm - Weakened area in the upper part
● FATAL - hematomas in lower thorax
of the aorta

- Commonly caused by atherosclerosis Medical Management

- morbidity and mortality rates ○ Controlling blood pressure and risk factors

○ Sodium nitroprusside
Risk Factors

○ : Men, race (caucasian), age (65yo and above), ○ Surgery - to repair aneurysm and restore
genetics, tobacco use, hypertension vascular continuity with a vascular graft, stents

Diagnostic Exam
 ○ Cerebrospinal fluid drainage to improve spinal ○ Calcium-channel blockers, sympathectomy
perfusion
○ Avoidance to cold and measure to improve
Nursing Management circulation for acrocyanosis

○ Pre OP and post OP care Nursing Management

○ Post implantation syndrome - fever, ○ Avoid stress, cold

leukocytosis, thrombocytopenia
○ Education about complications that are
Raynaud’s and Buerger’s uncommon, side effects of medications

Raynaud Phenomenon - Intermittent arteriolar ○ Avoid nicotine

vasoconstriction that results in coldness, pain, and
pallor of the fingertips or toes Buerger’s Disease

- Primary or Idiopathic and Secondary Raynaud’s Thromboangiitis Obliterans - medium vessel

○ SLE, RA, trauma, obstructive arterial lesions
- Triggered by emotions or sensitivity to cold
Risk Factors
○ Women, Age (<30)
vasculitis
- Segmental thrombosing inflammation
- Strongly associated with heavy tobacco use
- Moderate-to-severe claudication that quickly
progress to critical limb ischemia

● Acrocyanosis - variant Risk Factors

● Variable prognosis - some slowly improve, some ○ 20-40 yo male

become progressively worse, others no change
○ Indian, korean, japanese
Clinical Manifestations
○ Tobacco use
○ Pallor due to sudden vasoconstriction

○ Cyanosis and hyperemia

○ White - Blue - Red with numbness, tingling, and

burning pain

○ Bilateral and symmetric involving toes and

fingers

○ Acrocyanosis differs by persistence of skin

color changes, symmetry and non paroxysmal

Medical Management

○ Avoiding stimuli that provoke vasoconstriction Clinical Manifestations

 ○ Distal extremity ischemia (claudication, pain
at rest, ischemic ulcers, gangrene)
○ Thrombophlebitis, paresthesia, impaired
distal pulses
○ Ulcerations, gangrene (auto-amputations)
Diagnostic Exams
○ Arteriography on all 4 limbs (unaffected first)
○ Echo, CT angiography
Medical Management
○ Smoking cessation
○ Pharmacologic therapy not effective
○ amputations
Hypertension - SBP 140< and DBP 90< on two or
more accurate measurements taken 1 to 4 weeks
apart.
- N: <120/80; 120/80 to 139/89 as preHTN;
140/90< as HTN
- preHTN = at risk of HTN; slight increases in BP also
has increased risks of other comorbids
○ preHTN = lifestyle changes
○ HTN S1 = lifestyle changes + medications
○ HTN S2 = same but more frequent consultations
- Primary hypertension = unidentified cause
- Secondary hypertension = identifiable cause
- Pregnancy = preeclampsia
- “Silent killer”
- Sign and risk factor
Risk Factors
○ Race, Gender, Age, Family History
○ Alcohol intake, obesity, high salt diet,
sedentary lifestyle, tobacco use, stress
○ CKD, renal artery stenosis,
hyperaldosteronism, pheochromocytoma, sleep
apnea, pregnancy, cardiovascular conditions
Pathophysiology
○ Contraction of the heart > pressure transfer
from heart muscle to the blood > blood exerts the
same pressure to the blood vessels
○ Increase in cardiac output or increase in
peripheral resistance > increase in pressure
Clinical Manifestations
○ Elevated blood pressure alone
○ Retinal changes, vascular damage, left
ventricular hypertrophy
○ Heart failure, nocturia, TIA or CVA
Diagnostics Exams
○ Routine: UA, blood chemistry, ECG
○ Echo
○ Add: creatinine clearance, renin level, urine
test, 24-hour urine protein
○ Risk factor assessment
Medical Management
○ GOAL: prevent complications by maintaining
BP
○ Lifestyle modifications
○ Pharmacologic Therapy
 ■ Decrease peripheral resistance, blood Complications
volume, and strength & rate of contraction
○ Heart failure, paresthesias, delirium
■ Calcium-channel blocker + thiazide (60<)
Medical Management
■ ACEi and ARB (<60)
○ GOAL: correct and control the cause of anemia
■ Small dosage and simplest treatment
Hypoproliferative Anemias
Red Blood Cell Disturbances
○ Iron-deficiency Anemia
Anemias - Strictly defined as a decrease in red
blood cell mass ○ Aplastic Anemia

- Reflects the presence of fewer than the normal Hemolytic Anemia

number of erythrocytes within the circulation ○ Sickle-cell Anemia
- Amount of oxygen delivered to the body tissues is Hypoproliferative Anemias
diminished
Iron-Deficiency Anemia
- Not a specific disease state but a sign of an
underlying disorder ○ Intake of iron is inadequate for hemoglobin
synthesis
Classification
○ Depleted stored iron, supply iron to BM is
○ Erythrocyte production defect inadequate
○ Erythrocyte destruction ○ Most common type of anemia
○ Loss of erythrocyte ○ Diet (low iron intake, vegetarian) or blood
loss (GI), iron malabsorption
Clinical Manifestations
○ Clinical manifestations: general anemia +
○ Influenced by rapidity of development (more
rapid, more severe), chronicity (generally smooth, red tongue, brittle and ridged nails, angular
asymptomatic), metabolic requirements of the body cheilosis
(activities produce more symptoms), concurrent Diagnostic Exams:
disorders or disabilities, complications that
produced anemia (diseases involving oxygenation) Bone Marrow Aspiration, same as general anemia

Diagnostic Exams Medical Management:

○ CBC - Hgb, Hct, reticulocyte count, RBC count investigate cause of anemia

○ Iron studies + vitamin B12 and folate levels, ■ Oral iron supplementation
haptoglobin and erythropoietin levels
■ IV administration for poor absorption
○ Bone marrow aspiration
Nursing Management - Mechanism of erythrocyte destruction varies but
share certain laboratory features
■ Preventive education
○ High reticulocyte count, unconjugated
● Diet - foods to eat and avoid (vit C, intake hemoglobin; low haptoglobin
with food, tablets and enteric-coated caps, antacids
and dairy products) - Sickle cell disease, thalassemia, thalassemia major,
G-6-PD deficiency, hereditary spherocytosi
Aplastic Anemia
Sickle Cell Disease - Inheritance of sickle
○ Decrease in or damage to marrow stem cells, hemoglobin (HbS) gene which causes the
damage to microenvironment within the marrow, hemoglobin molecule to be defective
and replacement of the marrow with fat
- Erythrocyte containing HbS loses its round shape
○ T-cells mediating an attack to the bone and becomes sickle-shaped
marrow
- Low oxygen levels promote the change however
○ Idiopathic can be reversed if the cell is not too rigid yet
Clinical Manifestations - “Intermittent sickle crises”
■ Insidious onset - Sickle cell anemia is the most severe form of sickle
■ Severe anemia, neutropenia, cell disease
thrombocytopenia - Sickle cells can adhere to the small blood vessels
Diagnostic Exams: Clinical Manifestations
CBC and Bone Marrow Aspiration ■ Anemia, jaundice, enlargement of bones of the
Medical Management face and skull

■ Immunosuppressive therapy ■ Tachycardia, cardiac murmurs, cardiomegaly,

dysrhythmia, heart failure
■ Corticosteroids, but not for long-term
■ Thrombosis: spleen, lungs, and CNS
■ Supportive therapy
■ Sickle cell crisis
Nursing Management
● Vaso-occlusive crisis - most common and very
■ Careful assessment for signs of bleeding and painful
infection
● Aplastic crisis - hgb falls rapidly
■ Monitoring side effects of therapies
● Sequestration crisis - pooling of sickle cells in
Hemolytic Anemias - Erythrocytes have a shorter organs
life span, creation of premature RBCs called
reticulocytes Diagnostic Exams
■ Low Hct, sickled cells on smear; high WBC and
platelets
■ Hemoglobin electrophoresis
Medical Management
■ Hematopoietic Stem Cell Transplant
■ Pharmacologic Therapy
● Hydroxyurea, folic acid replacements,
hydration, corticosteroids
■ Transfusion Therapy
■ Supportive Therapy
Thalassemia - Group of hereditary anemias
characterized by hypochroma, extreme
microcytosis, hemolysis, and variable degrees of
anemia
- Defective synthesis of hemoglobin > reduction of
globulin chain production within hemoglobin >
imbalance of configuration of hemoglobin >
increased rigidity and premature destruction
- Alpha or Beta thalassemia
Alpha thalassemia
■ Milder and can be asymptomatic
■ Erythrocytes are extremely microcytic but
anemia is mild
Beta thalassemia
■ Mild forms have microcytosis and mild anemia
■ Severe = thalassemia major/Cooley’s anemia and types, recovery may not occur
can be fatal for the first few years of life
■ Hematopoietic stem cell transplantation can cure ■ G-6-PD deficiency screening test
but when not possible, transfusion of PRBCs and
iron chelation
Thalassemia Major
■ Severe anemia, marked hemolysis, ineffective
erythropoiesis
○ Regular chelation reduced complications of iron
overload
○ Long-term survivors of beta thalassemia may
experience neurologic complications
○ Death is often due to heart failure
Glucose-6-Phosphate Dehydrogenase Deficiency -
G-6-PD gene produces an enzyme within the
erythrocyte essential for membrane stability
- Hemolysis when the erythrocytes are stressed by
certain situations
- X-linked defect
- Oxidant drugs trigger hemolysis
- Severe hemolytic episode after ingestion of fava
beans, menthol, tonic water, and some chinese
herbs
Clinical Manifestations
■ Asymptomatic and normal Hgb levels,
reticulocyte count most of the time
■ Days after exposure to medication or
substance: pallor, jaundice, hemoglobinuria,
increased reticulocyte, symptoms of hemolysis
■ “Heinz bodies”
■ Hemolysis is often mild but in more severe
Diagnostic Exams
Medical Management
 ■ Arrest the source
■ Transfusion only in severe hemolytic state
Nursing Management
■ Education about the disease, list of medications
and substances to avoid
■ Seek advice prior to any treatment
■ Hemolysis treatment for hemolytic episodes
■ Medic-alert bracelets
Polycythemia - Refers to an increased volume of
RBCs
- Hematocrit is significantly elevated
- Primary and Secondary Polycythemia
Primary Polycythemia or Polycythemia vera
○ Proliferative disorder of the myeloid stem
cells
○ Hypercelllular bone marrow resulting to
elevated erythrocytes*, leukocytes, and
thrombocytes
○ Bone marrow may become fibrotic > inability
to produce many cells = “burnt out phase” >
metaplasia or AML
○ Death results from thrombosis, hemorrhage,
and rarely evolution to AML
○ Diagnosis: elevated Hgb JAK2 gene (+),
decreased serum erythropoietin
Clinical Manifestations
■ Ruddy complexion, splenomegaly
■ Symptoms from increased blood volume
(headache, dizziness, tinnitus, fatigue, paresthesias, Respiratory Centers
blurred vision)
■ Symptoms from increased blood viscosity (angina,
claudication, dyspnea, thrombophlebitis, elevated
BP
■ Elevated uric acid (gout, renal stone)
■ Pruritus, erythromelalgia
Medical Management
■ GOAL: reduce risk of thrombosis without
increasing risk of bleeding, and reduce risk of
evolution
■ Low-dose aspirin*, hydroxyurea, phlebotomy
■ Aggressive management of atherosclerosis
(anti HTN and antihyperlipidemic)
■ Allopurinol
■ anagrelide, interferon alfa-2b
Nursing Management
■ Symptom management
■ Monitoring progression and complications
Secondary Polycythemia - Excessive production of
erythropoietin
- Response to reduced amount of oxygen, “hypoxic
stimulus”, from hemoglobinopathies, or from
neoplasms > all increase erythropoietin production
Medical Management
■ If mild, not necessary
■ Treating the primary condition first
■ Therapeutic phlebotomy
Neural Regulation
 a. Medulla Oblongata - inspiration center
expiratory center
➢responsible for the cyclic pattern of breathing
b. Pons of the brainstem
➢modifies the output of the medullary centers.
apnuestic center - prevent medullary inspiratory
neurons from switching off, creating a prolonged,
gasping inspiration.
pneumotaxic center - shorten inspiratory time and
increasing respiratory rate.
Chemoreceptors
- Initiate periodic sighing and yawning
3. Juxtacapillary or J receptors - are located in the
alveolar wall, close to the pulmonary capillaries:
thought to sense lung congestion
Peripheral Proprioceptors
■ Proprioceptors in muscles, tendons, and joints
and pain receptors in muscles and skin send
stimulatory signals to the medullary respiratory
center
■ Proprioceptors in joints and tendons may be
important in initiating and maintaining increased
ventilation at the beginning of exercise

➢Monitor blood levels of carbon dioxide, oxygen HYPOTHALAMUS - Modifies the output from the
and pH medulla

Central chemoreceptor(medulla) - increase in CO2 Emotions:

and H+ -Anger = increase RR
Peripheral (carotid and aortic bodies) - decrease in -Fright = gasp
PaO2 (decreases to about 60 mm Hg)
CEREBRAL CORTEX -Enables us to voluntarily
• The primary stimulus for breathing in healthy change breathing rate or rhythm
individuals is arterial CO2
-Talking, singing
• The secondary stimulus for breathing in healthy
individuals is arterial hypoxemia, which is not
clinically significant until PaO2 is less than 60 mm
Hg

Lung Receptors

Three Types

1. Stretch receptors

Hering –Breurer reflexes – baroreceptors in lung

tissue detect stretching and send impulses to the
medulla to depress the inspiratory center

2. Irritant receptors - stimulated by noxious gases,

cigarette smoke, inhaled dust, and cold air
PRIMARY INDICATORS OF RESPIRATORY
DISORDERS
1. DYSPNEA - difficult or labored breathing
shortness of breath
TYPES
a. Exertional
b. Orthopnea
c. Paroxysmal nocturnal dypsnea
2. COUGH - results from irritation of the mucous
membranes anywhere in the respiratory tract
Evaluate character of cough
• Dry - URTI,
• Severe changing - carcinoma
Time of cough
• Am – bronchitis
• Pm - asthma
3. SPUTUM PRODUCTION - is the reaction of the
lungs to any constantly recurring irritant.
Thick yellow - bacterial infection
Rust-colored sputum – pneumonia
Thin, mucoid sputum - viral bronchitis.
A gradual increase of sputum – chronic bronchitis
Pink-tinged mucoid sputum - lung tumor.
Profuse, frothy, pink material - pulmonary edema.
Foul-smelling sputum - lung abscess
4. CHEST PAIN - Chest pain associated with
pulmonary conditions may be sharp, stabbing, and
intermittent, or it may be dull, aching, and
persistent.
- Chest pain may occur with pneumonia,pulmonary
embolism with lung infarction, and pleurisy
5. WHEEZING - is often the major finding in a
patient with Bronchoconstriction or airway
narrowing.
6. CLUBBING OF THE FINGERS - a sign of lung
disease found in patients with chronic hypoxic
conditions
7. HEMOPTYSIS - expectoration of blood from the
respiratory tract
The most common causes are:
• Pulmonary infection
• Carcinoma of the lung
- Blood from the lung is usually bright red, frothy,
and mixed with sputum
8. CYANOSIS - a bluish coloring of the skin, is a very
late indicator of hypoxia
- Cyanosis appears when there is 5 g/dL of
unoxygenated hemoglobin
Acentral cyanosis –tongue and lips decrease in
oxygen tension in the blood.
Peripheral cyanosis – due to decreased blood flow
to a certain area of the body
-vasoconstriction from exposure to cold
-nail bed, earlobe
Oxygenation - Cardio
Joshua P Coronel, RN, MN
 Heart
Failure
Clinical syndrome resulting from
structural or functional cardiac
disorders that impair the ability
of the ventricles to fill or eject
blood
 Heart Failure

● Fluid overload and decreased tissue perfusion from

inadequate cardiac output
● Impaired contraction or filling of the heart leads to
pulmonary or systemic congestion
● Reversible but most often chronic and progressive
● GOAL: prevent episode of acute decompensated
heart failure
 Heart Failure

● Chronic Heart Failure

○ Increases with age; most common reason for hospitalization for
people older than 65 years old
● 2 Major Types
○ Systolic Heart Failure - alteration in ventricular contraction
○ Diastolic Heart Failure - difficulty for the ventricle to fill
● Ejection Fraction (EF) in Echo determines HF
○ Reduced EF is a hallmark for systolic HF however severity is
classified according to symptoms
Heart Failure
 Heart Failure

● Etiology
○ Myocardial dysfunction
● Risk Factors
○ Non modifiable - Family History, Age, Sex, Race
○ Modifiable - atherosclerosis, hypertension, cardiac arrhythmias,
systemic infection, diet (excessive water and sodium),
myocardial ischemia, valvular disease,
○ Cardiorenal syndrome
 Heart Failure - Pathophysiology
Structural Cardiac
Insufficiency

Decreased perfusion to Disruption of circulatory Decreased cardiac output

kidneys homeostasis Decreased blood pressure

Conversion of
Kidneys release renin angiotensinogen to Activation of baroreceptors
angiotensin I

Conversion of angiotensin I Angiotensin I circulates to SNS release epinephrine

to angiotensin II the lungs and norepinephrine

Release of aldosterone
Sodium and fluid retention Systemic vasoconstriction
from adrenal cortex

Increase in preload and

afterload
 Heart Failure - Pathophysiology
Increase in preload and Increased stress in
Increased cardiac workload
afterload ventricular wall

BNP

Ventricular hypertrophy Ventricular dilation Decreased Contractility

Myocardial apoptosis Myocardial fibrosis begins Heart Failure

Back to disruption of 1. Imaging (Echo¹, Ecg,

homeostasis Xray)
2. Labs (BNP*, S. elec, BUN,
Creatinine, Liver function
test)
 (L) Heart Failure - Pathophysiology
Gradual increase in
Heart Increased vascular Increase in
systemic blood
Failure resistance ventricular pressure
volume

Increase pulmonary Decreased blood Decreased blood

Increase atrial
vein volume and flow from pulmonary flow from left atrium
pressure and volume
pressure vein to left atrium to left ventricle

Leakage of fluids
from pulmonary
Pulmonary Decreased perfusion
capillaries to
Interstitial Edema to organs
pulmonary tissues
and alveoli
Weak peripheral
Oliguria, Nocturia Re-activation of the pulses
Signs of pulmonary congestion
Indigestion RAAS Fatigue
(dyspnea, progressive and worsening
Dizziness, Lightheadedness, Insomnia
cough, crackles, orthopnea,
confusion, restlessness,
paroxysmal nocturnal dyspnea) &
anxiety
difficulty sleeping
Cool, clammy, pale skin Left-Sided Heart
Failure
Decreased oxygen saturation levels
 (R) Heart Failure - Pathophysiology
Failure to eject and
accommodate Backflow of blood
Increased systemic Increased venous
Heart Failure blood of the left to the venous
blood volume pressure
atrium and system
ventricle

Continuous
backflow of blood Backflow to the
Anorexia, nausea,
at the right side of abdomen
abdominal pain
the heart

Venous Increased venous

Increased pressure Engorgement of Backflow to the
engorgement and pressure in
in portal veins liver liver
stasis abdomen

Leakage of fluids to
Backflow to the Bipedal
the abdominal
lower extremities edema
cavity

Further increase in
Respiratory Increased pressure Right-Sided Heart
Ascites systemic venous
Distress on diaphragm Failure
pressure
 Heart Failure

● Clinical Manifestations
○ LSHF - pulmonary signs and symptoms
○ RSHF - systemic signs and symptoms
● Diagnostic Exams
○ Echocardiogram - EF
○ BNP
○ Chest Xray and ECG
○ Serum electrolytes, BUN, creatinine, liver function tests, TSH, CBC,
UA
● Medical Management
○ GOAL: relieve patient symptoms
○ ACE inhibitors, Angiotensin receptor blockers, hydralazine, ISDN,
Beta-blockers, Diuretics, Digitalis*
○ IV Infusions - inotropes
 Heart Failure

● Medications for Diastolic Function

○ Treatment of underlying cause - HTN and ischemic heart disease
● Other medications
○ Anticoagulants, antiarrhythmic drugs, antihyperlipidemic drugs
○ AVOID NSAIDs
● Therapies
○ Nutritional therapy - low salt, limit fluid intake
○ Oxygen therapy
● Other Interventions
○ Surgical approaches for underlying cause
○ Cardiac Resynchronization Therapy - pacemaker
○ Hemodialysis
 Infectious
Disease of the
Heart
 Rheumatic
Endocarditis

Develops after a group A

beta-hemolytic streptococcal
pharyngitis
 Rheumatic Endocarditis

● Rheumatic fever proceeds to rheumatic heart

disease - new heart murmur, cardiomegaly,
pericarditis, and heart failure
● Treatment of “strep” throat with antibiotics
● RF: malnutrition, overcrowding, poor hygiene, lower
socioeconomic status
● Rheumatic fever - preventable. Treat streptococcal
pharyngitis
● More common in children
 Infective
Endocarditis

Microbial infection of the

endothelial surface of the heart
 Infective Endocarditis
● Develops with prosthetic heart valves, cardiac
devices, or structural cardiac defects
● More common in older adults
● RF: degenerative or calcific valve lesions, reduced
immunologic response, and metabolic alterations
associated with aging.
● Staph endocarditis of the R side of heart are common
among IV drug abusers
● Hospital-acquired - patients with debilitating disease
or indwelling catheters; hemodialysis or prolonged IV
or antibiotic therapy; immunosuppressive
medications or corticosteroids
 Endocarditis - Pathophysiology
Invasion of
microorganisms in the
endocardium

Accumulation of fibrin and

Injury of the endocardium
platelets

Platelets, fibrin, blood cells Clot in the endocardium

Microorganisms invade the
and microorganisms expands and is covered by
clot and lesion
vegetates another clot

Embolus formation

Erosion of endocardium Microorganism is concealed

Inflammatory Process
into underlying tissues from host defenses

Endocarditis
 Endocarditis
● Clinical Manifestations
○ Fever - intermittent or absent
○ Heart murmur - absent initially but develops eventually
○ Cluster of petechiae, osler nodules, janeway lesions, roth spots,
splinter hemorrhages
○ Headache, cerebral ischemia, stroke d/t embolism
○ Heart failure
● Diagnostic Exams
○ Blood culture - 2 sets*
○ CBC - elevated WBC, ESR, CRP
○ Echo
 Endocarditis
● Prevention
○ Antibiotic prophylaxis, good oral hygiene,
○ No IUDs
○ IV catheters and surgical procedures
● Medical Management
○ GOAL: eradicate invading organisms
○ Antimicrobial agents through parenteral
○ Surgery - if not responding to treatment or with prosthetic heart
valves
● Nursing Management
○ Meds, fluids, resting periods (symptomatic approach)
○ Management of infection - infection control
○ Education, emotional support, and coping strategies
Valvular Heart
Diseases
 Mitral
Stenosis

Obstruction to blood flowing

from the left atrium into the left
ventricle
 Mitral Stenosis
● Most often caused by rheumatic endocarditis
● RF: rheumatic endocarditis
● Patho
○ Infection > inflammation > valve thickening > narrowing of
passage
○ 1/3 to 1/2 decrease in opening for symptoms to occur
● CM:
○ Exertional dyspnea, fatigue, activity intolerance, cough, wheezing
○ Hemoptysis, palpitations, orthopnea, paroxysmal nocturnal
dyspnea, repeated respi infections
● Diagnostic Exams
○ Echo*
○ ECG, stress test, cardiac catheterization with angiography
 Mitral Stenosis
● Prevention
○ Minimizing risks and treatment of bacterial infections
○ Antibiotic prophylaxis
● Medical Management
○ Anticoagulants, cardioversion for AF, beta-blockers,
calcium-channel blockers, digoxin
○ “Treating heart failure”
○ Surgical treatment - valvuloplasty
 Aortic
Stenosis

Narrowing of the orifice between

the left ventricle and aorta
 Aortic Stenosis
● Degenerative calcifications - proliferative and
inflammatory changes through the years
● RF: Age; diabetes, hypercholesterolemia,
hypertension, smoking, elevated LDL, rheumatic
endocarditis
● Patho: Infection > inflammation > calcification (years)
● Clinical Manifestations
○ “Asymptomatic”
○ Exertional dyspnea, increased pulmonary venous pressure,
orthopnea,
○ Decreased perfusion - dizziness , syncope, angina pectoris,
 Aortic Stenosis
● Diagnostic Exams
○ Echo, cardiac MRI, CT scan
○ ECG, left sided heart catheterization
● Prevention
○ Control of risk factors
● Medical Management
○ Treatment of underlying cause/comorbids
○ Surgical replacement of aortic valve
● Nursing Management
○ Education on diagnosis, progressive nature, and treatment,
bacterium and valves, relief of symptoms thru comorbids,
○ Weight gain reporting and planning of activities
 Oxygenation -
Vascular/H ema
Joshua P Coronel, RN, MN
Table of Contents

Vascular Disorders Red Blood Cell Disturbances

01 Deep vein thrombosis 03 Iron deficiency anemia
Phlebitis Aplastic anemia
Varicose veins Hemolytic anemia
Sickle-cell anemia
Hereditary spherocytosis
Arterial Disorders
02
G6PD
Peripheral Arterial Disease Thalassemia
Reynaud’s syndrome Polycythemia
Buerguer’s disease Hemophilia
Aortic aneurysm
Hypertension
 01
Vascular
Disorders
 Venous
Thromboembolism
Deep vein thrombosis and pulmonary
embolism make up the condition called
Venous Thromboembolism
Venous Thromboembolism
● Frequently not diagnosed because often clinically
silent
● Common in patients post-op
● Risk factors
○ Endothelial damage
○ Venous stasis
○ Altered coagulation
● Patho
○ Virchow Triad > phlebitis > formation of
thrombus (phlebothrombosis)
Venous Thromboembolism
● Clinical Manifestations
○ Non-specific except phlegmasia cerulea
dolens
○ Sudden venous hypertension
○ Deep veins
■ Edema and swelling, warm, deep veins
appear more prominent
■ Tenderness
○ Superficial veins
■ Tenderness, redness, warmth
Venous Thromboembolism
● Diagnostic Exams
○ Careful assessment of lower extremities
■ Feeling of heaviness, functional
impairment, ankle engorgement, edema,
areas of tenderness
○ Homan Sign is not reliable for DVT
● Prevention
○ Identification of risk factors and preventive
measures
○ Compression stockings and devices, early
ambulation, leg exercises
○ LMWH as ordered
○ Lifestyle changes - weight loss, smoking
cessation and regular exercise
Venous Thromboembolism
● Medical Management
○ GOAL: prevent thrombus from growing and
fragmenting
○ Anticoagulant therapy and ultrasonic-assisted
thrombolytic therapy
○ Pharmacologic Therapy
■ Unfractionated heparin, low-molecular
weight heparin, oral anticoagulants,
factor Xa and direct thrombin inhibitors,
Thrombolytic therapy
○ Endovascular management
■ Anticoags and thrombolytics are C/I
■ Thrombectomy, ultrasound-assisted
thrombolysis, balloon angioplasty
Venous Thromboembolism
● Nursing Management
○ Assessing and monitoring anticoagulant
therapy
○ Monitoring and managing potential
complications
■ Bleeding, thrombocytopenia, drug
interactions
○ Providing comfort
○ Providing compression therapy
■ Stockings
■ External compression devices and wraps
■ Intermittent pneumatic compression
devices
Venous Thromboembolism
● Nursing Management
○ Positioning the body and encouraging
exercise
○ Promoting home, community-based, and
transition care
Varicose Veins
Abnormally dilated, tortuous, superficial veins
caused by incompetent venous valves
Varicose Veins
● Common in the lower extremities but can occur
elsewhere
● Common in people whose occupations require
prolonged standing
● Hereditary weakness of the vein wall contribute
however rare before puberty,
● Pregnancy
● Patho
○ Reflux of venous blood > venous stasis >
accumulation of venous blood > vein distention
Varicose Veins
● Clinical Manifestations
○ IF PRESENT: Dull aches, muscle cramps, increased
muscle fatigue in lower legs, ankle edema, and a
feeling of heaviness of legs, nocturnal cramps
○ If deep veins are involved, signs and symptoms of
chronic venous insufficiency (edema, pain,
pigmentation, and ulcerations)
● Diagnostic Exams
○ Duplex ultrasound scan*
○ Venography, CT venography
Varicose Veins
● Prevention
○ Avoid activities or clothing that cause venous stasis
● Medical Management
○ Exercises and changing position
○ Graduated compression stockings
○ Weight reduction
○ Surgical treatment
■ Ligation and stripping
■ Thermal ablation
■ Sclerotherapy
Varicose Veins
● Nursing Management
○ Promoting comfort and understanding
○ Promoting home, community-based, and
transitional care
 02
Arterial
Disorders
Peripheral Arterial
Occlusive Disease
Blockage or narrowing of an artery in the
legs. Symptoms are dependent on the
affected artery and how severe the blockage
Peripheral Arterial Occlusive Disease
● Occurs most often in men and common cause of
disability
● Legs are most frequently affected
● Clinical Manifestations
○ Intermittent claudication*
○ Rest pain - critical ischemia
● Diagnostic Exams
○ History and assessment
○ Continuous-wave doppler, ABI, treadmill testing for
claudication, duplex ultrasonography
Peripheral Arterial Occlusive Disease
● Medical Management
○ Exercise (walking) program, unsupervised walking
exercise programs
○ Exercise + weight reduction + smoking cessation
○ Pentoxifylline and cilostazol, antiplatelets, statins
○ Endovascular management
■ Balloon angioplasty, stent, stent graft,
atherectomy
○ Surgical Management
■ For severe/disabling claudication
■ Endarterectomy, bypass grafts
Peripheral Arterial Occlusive Disease
● Nursing Management
○ Nursing care of the postoperative patient
■ Maintaining circulation
■ Monitoring and managing potential
complications
■ Home care
Aortic Aneurysm
Weakened area in the upper part of the aorta
Aortic Aneurysms
● Commonly caused by atherosclerosis
● High morbidity and mortality rates
● Risk Factors
○ : Men, race (caucasian), age (65yo and above),
genetics, tobacco use, hypertension
● Diagnostic Exam
○ Imaging Studies
Aortic Aneurysm
● Thoracic Aortic Aneurysm
○ Clinical Manifestations
■ Depends on how rapidly aneurysm dilates and
how pulsating mass affects surrounding
structures
■ Pain* - during supine
■ Dyspnea, cough, stridor, hoarseness or
aphonia, dysphagia
Aortic Aneurysm
● Abdominal Aortic Aneurysm
○ Clinical Manifestations
■ Only 40% are symptomatic
■ “Feel their heart beating in their abdomen
when lying down”
■ Systolic bruit
■ Signs of impending rupture
● Severe back or abdominal pain
■ Signs of rupturing aneurysm
● Constant intense back pain, falling BP,
decreasing hematocrit
■ Rupture to peritoneal cavity
● FATAL - hematomas in lower thorax
Aortic Aneurysm
● Medical Management
○ Controlling blood pressure and risk factors
○ Sodium nitroprusside
○ Surgery - to repair aneurysm and restore vascular
continuity with a vascular graft, stents
○ Cerebrospinal fluid drainage to improve spinal
perfusion
● Nursing Management
○ Pre OP and post OP care
○ Post implantation syndrome - fever, leukocytosis,
thrombocytopenia
Raynaud’s and
Buerger’s
Raynaud Phenomenon
● Intermittent arteriolar vasoconstriction that results in
coldness, pain, and pallor of the fingertips or toes
● Primary or Idiopathic and Secondary Raynaud’s
○ SLE, RA, trauma, obstructive arterial lesions
● Triggered by emotions or sensitivity to cold
● Risk Factors
○ Women, Age (<30)
● Acrocyanosis - variant
● Variable prognosis - some slowly improve, some
become progressively worse, others no change
Raynaud Phenomenon
● Clinical Manifestations
○ Pallor due to sudden vasoconstriction
○ Cyanosis and hyperemia
○ White - Blue - Red with numbness, tingling, and
burning pain
○ Bilateral and symmetric involving toes and fingers
○ Acrocyanosis differs by persistence of skin color
changes, symmetry and non paroxysmal
● Medical Management
○ Avoiding stimuli that provoke vasoconstriction
○ Calcium-channel blockers, sympathectomy
○ Avoidance to cold and measure to improve
circulation for acrocyanosis
Raynaud Phenomenon
● Nursing Management
○ Avoid stress, cold
○ Education about complications that are
uncommon, side effects of medications
○ Avoid nicotine
Buerger’s Disease
● Thromboangiitis Obliterans - medium vessel vasculitis
● Segmental thrombosing inflammation
● Strongly associated with heavy tobacco use
● Moderate-to-severe claudication that quickly progress
to critical limb ischemia
● Risk Factors
○ 20-40 yo male
○ Indian, korean, japanese
○ Tobacco use
Buerger’s Disease
Immunologic
phenomenon

ischemia
Injury to
blood vessel
Decreased
blood flow to
Inflammation affected area

Thrombus Obstruction in
formation the vessel
Buerger’s Disease
● Clinical Manifestations
○ Distal extremity ischemia (claudication, pain at rest,
ischemic ulcers, gangrene)
○ Thrombophlebitis, paresthesia, impaired distal
pulses
○ Ulcerations, gangrene (auto-amputations)
● Diagnostic Exams
○ Arteriography on all 4 limbs (unaffected first)
○ Echo, CT angiography
● Medical Management
○ Smoking cessation
○ Pharmacologic therapy not effective
○ amputations
Hypertension
SBP 140< and DBP 90< on two or more
accurate measurements taken 1 to 4 weeks
apart.
Hypertension

● N: <120/80; 120/80 to 139/89 as preHTN; 140/90< as

HTN
● preHTN = at risk of HTN; slight increases in BP also has
increased risks of other comorbids
○ preHTN = lifestyle changes
○ HTN S1 = lifestyle changes + medications
○ HTN S2 = same but more frequent consultations
● Primary hypertension = unidentified cause
● Secondary hypertension = identifiable cause
Hypertension
Hypertension
● Pregnancy = preeclampsia
● “Silent killer”
● Sign and risk factor
● Risk Factors
○ Race, Gender, Age, Family History
○ Alcohol intake, obesity, high salt diet, sedentary
lifestyle, tobacco use, stress
○ CKD, renal artery stenosis, hyperaldosteronism,
pheochromocytoma, sleep apnea, pregnancy,
cardiovascular conditions
Hypertension
● Pathophysiology
○ Contraction of the heart > pressure transfer from
heart muscle to the blood > blood exerts the same
pressure to the blood vessels
○ Increase in cardiac output or increase in peripheral
resistance > increase in pressure
● Clinical Manifestations
○ Elevated blood pressure alone
○ Retinal changes, vascular damage, left ventricular
hypertrophy
○ Heart failure, nocturia, TIA or CVA
Hypertension
● Diagnostics Exams
○ Routine: UA, blood chemistry, ECG
○ Echo
○ Add: creatinine clearance, renin level, urine test,
24-hour urine protein
○ Risk factor assessment
● Medical Management
○ GOAL: prevent complications by maintaining BP
○ Lifestyle modifications
○ Pharmacologic Therapy
■ Decrease peripheral resistance, blood volume,
and strength & rate of contraction
■ Calcium-channel blocker + thiazide (60<)
■ ACEi and ARB (<60)
■ Small dosage and simplest treatment
 03
Red Blood Cell
Disturbances
 Anemias
Strictly defined as a decrease in red blood cell
mass
Anemia
● Reflects the presence of fewer than the normal number
of erythrocytes within the circulation
● Amount of oxygen delivered to the body tissues is
diminished
● Not a specific disease state but a sign of an underlying
disorder
● Classification
○ Erythrocyte production defect
○ Erythrocyte destruction
○ Loss of erythrocyte
Anemia
● Clinical Manifestations
○ Influenced by rapidity of development (more rapid,
more severe), chronicity (generally asymptomatic),
metabolic requirements of the body (activities
produce more symptoms), concurrent disorders or
disabilities, complications that produced anemia
(diseases involving oxygenation)
● Diagnostic Exams
○ CBC - Hgb, Hct, reticulocyte count, RBC count
○ Iron studies + vitamin B12 and folate levels,
haptoglobin and erythropoietin levels
○ Bone marrow aspiration
Anemia
● Complications
○ Heart failure, paresthesias, delirium
● Medical Management
○ GOAL: correct and control the cause of anemia
● Hypoproliferative Anemias
○ Iron-deficiency Anemia
○ Aplastic Anemia
● Hemolytic Anemia
○ Sickle-cell Anemia
Hypoproliferative Anemias
● Iron-Deficiency Anemia
○ Intake of iron is inadequate for hemoglobin
synthesis
○ Depleted stored iron, supply iron to BM is
inadequate
○ Most common type of anemia
○ Diet (low iron intake, vegetarian) or blood loss (GI),
iron malabsorption
○ Clinical manifestations: general anemia + smooth,
red tongue, brittle and ridged nails, angular
cheilosis
Hypoproliferative Anemias
● Iron-Deficiency Anemia
○ Diagnostic Exams: Bone Marrow Aspiration, same
as general anemia
○ Medical Management: investigate cause of anemia
■ Oral iron supplementation
■ IV administration for poor absorption
○ Nursing Management
■ Preventive education
● Diet - foods to eat and avoid (vit C, intake
with food, tablets and enteric-coated
caps, antacids and dairy products)
Hypoproliferative Anemias
● Aplastic Anemia
○ Decrease in or damage to marrow stem cells,
damage to microenvironment within the marrow,
and replacement of the marrow with fat
○ T-cells mediating an attack to the bone marrow
○ Idiopathic
○ Clinical Manifestations
■ Insidious onset
■ Severe anemia, neutropenia,
thrombocytopenia
○ Diagnostic Exams: CBC and Bone Marrow
Aspiration
Hypoproliferative Anemias
● Aplastic Anemia
○ Medical Management
■ Immunosuppressive therapy
■ Corticosteroids, but not for long-term
■ Supportive therapy
○ Nursing Management
■ Careful assessment for signs of bleeding and
infection
■ Monitoring side effects of therapies
H emolytic Anemias
● Erythrocytes have a shorter life span, creation of
premature RBCs called reticulocytes
● Mechanism of erythrocyte destruction varies but share
certain laboratory features
○ High reticulocyte count, unconjugated hemoglobin;
low haptoglobin
● Sickle cell disease, thalassemia, thalassemia major,
G-6-PD deficiency, hereditary spherocytosi
H emolytic Anemias
● Sickle Cell Disease
○ Inheritance of sickle hemoglobin (HbS) gene which
causes the hemoglobin molecule to be defective
○ Erythrocyte containing HbS loses its round shape
and becomes sickle-shaped
○ Low oxygen levels promote the change however
can be reversed if the cell is not too rigid yet
○ “Intermittent sickle crises”
○ Sickle cell anemia is the most severe form of sickle
cell disease
○ Sickle cells can adhere to the small blood vessels
H emolytic Anemias
● Sickle Cell Disease
○ Clinical Manifestations
■ Anemia, jaundice, enlargement of bones of the
face and skull
■ Tachycardia, cardiac murmurs, cardiomegaly,
dysrhythmia, heart failure
■ Thrombosis: spleen, lungs, and CNS
■ Sickle cell crisis
● Vaso-occlusive crisis - most common and
very painful
● Aplastic crisis - hgb falls rapidly
● Sequestration crisis - pooling of sickle
cells in organs
H emolytic Anemias
● Sickle Cell Disease
○ Diagnostic Exams
■ Low Hct, sickled cells on smear; high WBC and
platelets
■ Hemoglobin electrophoresis
○ Medical Management
■ Hematopoietic Stem Cell Transplant
■ Pharmacologic Therapy
● Hydroxyurea, folic acid replacements,
hydration, corticosteroids
■ Transfusion Therapy
■ Supportive Therapy
H emolytic Anemias
● Thalassemia
○ Group of hereditary anemias characterized by
hypochroma, extreme microcytosis, hemolysis, and
variable degrees of anemia
○ Defective synthesis of hemoglobin > reduction of
globulin chain production within hemoglobin >
imbalance of configuration of hemoglobin >
increased rigidity and premature destruction
○ Alpha or Beta thalassemia
H emolytic Anemias
● Thalassemia
○ Alpha thalassemia
■ Milder and can be asymptomatic
■ Erythrocytes are extremely microcytic but
anemia is mild
○ Beta thalassemia
■ Mild forms have microcytosis and mild anemia
■ Severe = thalassemia major/Cooley’s anemia
and can be fatal for the first few years of life
■ Hematopoietic stem cell transplantation can
cure but when not possible, transfusion of
PRBCs and iron chelation
H emolytic Anemias
● Thalassemia
○ Thalassemia Major
■ Severe anemia, marked hemolysis, ineffective
erythropoiesis
○ Regular chelation reduced complications of iron
overload
○ Long-term survivors of beta thalassemia may
experience neurologic complications
○ Death is often due to heart failure
H emolytic Anemias
● Glucose-6-Phosphate Dehydrogenase Deficiency
○ G-6-PD gene produces an enzyme within the
erythrocyte essential for membrane stability
○ Hemolysis when the erythrocytes are stressed by
certain situations
○ X-linked defect
○ Oxidant drugs trigger hemolysis
○ Severe hemolytic episode after ingestion of fava
beans, menthol, tonic water, and some chinese
herbs
H emolytic Anemias
● Glucose-6-Phosphate Dehydrogenase Deficiency
○ Clinical Manifestations
■ Asymptomatic and normal Hgb levels,
reticulocyte count most of the time
■ Days after exposure to medication or
substance: pallor, jaundice, hemoglobinuria,
increased reticulocyte, symptoms of hemolysis
■ “Heinz bodies”
■ Hemolysis is often mild but in more severe
types, recovery may not occur
H emolytic Anemias
● Glucose-6-Phosphate Dehydrogenase Deficiency
○ Diagnostic Exams
■ G-6-PD deficiency screening test
○ Medical Management
■ Arrest the source
■ Transfusion only in severe hemolytic state
○ Nursing Management
■ Education about the disease, list of
medications and substances to avoid
■ Seek advice prior to any treatment
■ Hemolysis treatment for hemolytic episodes
■ Medic-alert bracelets
Polycythemia
Refers to an increased volume of RBCs
Polycythemia
● Hematocrit is significantly elevated
● Primary and Secondary Polycythemia
● Primary Polycythemia or Polycythemia vera
○ Proliferative disorder of the myeloid stem cells
○ Hypercelllular bone marrow resulting to elevated
erythrocytes*, leukocytes, and thrombocytes
○ Bone marrow may become fibrotic > inability to
produce many cells = “burnt out phase” >
metaplasia or AML
○ Death results from thrombosis, hemorrhage, and
rarely evolution to AML
○ Diagnosis: elevated Hgb JAK2 gene (+), decreased
serum erythropoietin
Polycythemia
● Primary Polycythemia or Polycythemia vera
○ Clinical Manifestations
■ Ruddy complexion, splenomegaly
■ Symptoms from increased blood volume
(headache, dizziness, tinnitus, fatigue,
paresthesias, blurred vision)
■ Symptoms from increased blood viscosity
(angina, claudication, dyspnea,
thrombophlebitis, elevated BP
■ Elevated uric acid (gout, renal stone)
■ Pruritus, erythromelalgia
Polycythemia
● Primary Polycythemia or Polycythemia vera
○ Medical Management
■ GOAL: reduce risk of thrombosis without
increasing risk of bleeding, and reduce risk of
evolution
■ Low-dose aspirin*, hydroxyurea, phlebotomy
■ Aggressive management of atherosclerosis
(anti HTN and antihyperlipidemic)
■ Allopurinol
■ anagrelide, interferon alfa-2b
○ Nursing Management
■ Symptom management
■ Monitoring progression and complications
Polycythemia
● Secondary Polycythemia
○ Excessive production of erythropoietin
○ Response to reduced amount of oxygen, “hypoxic
stimulus”, from hemoglobinopathies, or from
neoplasms > all increase erythropoietin production
○ Medical Management
■ If mild, not necessary
■ Treating the primary condition first
■ Therapeutic phlebotomy
 1

Cancer Carcinoma in Situ- Neoplasm which remains

A disease process whereby cells proliferate confined on the site of origin.
abnormally, ignoring-regulating signals in the
environment surrounding cells. Cellular Adaptive Process:

Estimated New Cancer Cases, Both Sexes in US 1. Hyperplasia

(2020) American CA Society:
1. Digestive System 2. Metaplasia
2. Genital System
3. Breast 3. Dysplasia
4. Respiratory System
5. Urinary System 4. Anaplasia
6. Skin
7. Lymphoma
8. Leukemia Contact Inhibition
9. Endocrine System - cessation of growth ones the cell comes in
10. Oral Cavity & Pharynx contact with another cell. It switches off cell
growth by blocking the synthesis of DNA, RNA &
Definition of Terms: CHON.
Aberrant Cellular Growth It is an alteration in
the normal cellular growth Types of cells according to their ability to
undergo regeneration:
Apoptosis 1. Labile
2. Stable
Cyst- A closed sac having a distinct membrane 3. Permanent or Fixed
and developing abnormally
Secondary Prevention- Early Detection of CA
Metastasis- It is the spread of cancer cells A. Health history and PE
B. Screening Methods
Neoplasm - Greek: NEO “new” Plasia “growth 1. Mammography
of tissue ; A mass of new tissue that grows
independently of its surrounding structures Pap Smear

Carcinoma - A specific form of CA or malignant Prostate exam

tumor arising from epithelial cells.
Digital rectal exam
Tumor- It is a lump, mass, or swelling or
enlargement 2. Self-care practices
Breast Self Exam
Sarcoma
Testicular exam
Oncogenes Tumor - genes that promote cell
proliferation and are capable of triggering 4. Sigmoidoscopy and
cancerous characteristics
Fecal occult blood test
Oncology - The field or study of cancer
Diagnostic Tools in Detecting Cancer
Proto-oncogenes - These are benign forms of A. Laboratory Tests
oncogenes necessary for some normal cellular 1. CBC /Differential count
functions, especially growth and development.

Differentiation – extent to w/c tissue cells

resemble normal cells Serum Electroyles
Ca – increase, bone metastasis
Progression- Na – Decrease, Bronchogenic CA
K – decrease, Liver CA
Neoplastic Progression
2. Tumor Markers or proteins associated with
specific cancer
 2

1. Serum prostate- specific antigen (PSA) C. Electrosurgery

D. Cryosurgery
2. Alpha-fetoCHON (AFP) E. Chemosurgery
F. Laser Surgery
3. Cancinoembryonic Antigen (CEA) G. Stereotactic Radiosurgery

B. Cytologic Examination Other forms of Surgery:

Ex: Papanicolaou Test (PapSmear) 1. Prophylactic

2. Palliative

3. Reconstructive

Nursing Management in Cancer Surgery

C. Oncologic Imaging
1. Complete a thorough pre-operative
1. Radiographs/ X-ray
assessment .
Chest X-ray
2. Provide education and emotional
Mammograms
support.
CT Scan/MRI
3. Communicate frequently with the
2. Positron Emission Tomography (PET)
health team members .
3. Biopsy
4. Assess the patient’s responses to the
surgery and monitor possible
complications.
D. Invasive diagnostic techniques
5. Provide comfort.
 Biopsy
6. Initiate as early as possible plans for
 Cyst aspiration
discharge, follow-up and home care and
 Cystoscopy
treatment to ensure continuity of care.
7. Patients and family are encouraged to
use community resources such as the
Philippine Cancer Society.
Management of Patient with Neoplastic
Diseases
Goals:
1. cure
2. control
3. palliation

A. SURGERY
* Diagnostic Surgery

3 methods:
a. Excisional biopsy

b. Incisional biopsy

c. Needle biopsy

* Surgery as Primary Treatment

Goal: TO remove the entire tumor or as much
as possible and any involved surrounding tissue,
including regional lymph nodes.
2 Common Procedures:
1. Local incision
2. Wide or Radical Excision

New Approaches: SURGERY AS PRIMARY

TREATMENT
A. Video
B. Salvage surgery
CHEMOTHERAPY c.Alkyl sulfonates (bisulfan)
d.Triazines (decarbazine)
It is a systemic intervention:
e.Ethylenimines (thiotepa)
-disease is widespread
Ex: Cisplatin, Chlorambucil, Cyclophosphamide,
-The risk of undetectable disease is high
Bisulfan
-The tumor cannot be resected and is resistant
to radiation therapy
2.Antimetabolites

GOALS:
Phase-specific, working best in the S phase and
-
having little effect in G0.
-
Subclasses:
- a.Folic Acid Analogues (Methotrexate)
2 Types of Chemotherapy: b.Pyrimidine analogues (5-flourouracil)
c.Cystocine arabinoside (ARA-C)
1. Adjuvant chemotherapy Purine analogues (6-Mercaptopurine)
It is started after initial treatment with either
surgery or radiation therapy. 3.Cytotoxic Antibiotics

2. Neoadjuvant Chemotherapy Derived from various species of

Refers to the preoperative use of and are generally too toxic to be used as
chemotherapy to reduce the bulk and lower the antibacterial agents.
stage of a tumor
Action:
•Disrupt DNA replication and RNA transcription.
(cell cycle non-specific)
•
Classes of Antineoplastic Drugs:

1.Alkylating Agents •

Non-phase specific and basically act on

performed nucleic acids by creating defects in
tumor DNA. They cause cross-linking of DNA Examples:
strands, which can permanently interfere with Actinomycin D
replication and transcription Doxorubucin
Bleomysin
Common adverse effects:
Mithramycin
-acute myelogenous leukemia
Mitomycin-C
-Irreversible infertility
-Nephrotoxicity
4.Plant Alkaloids
-Hemorrhagic cystitis
There are 2 main groups extracted from plant
sources:
5 Subclasses:
a.Nitrogen mustards (mechlorethamine) A. Vinca Alkaloids
b.Nitrosoureas (carmustine) - Vincristine
 - Vinblastin 5.Hirsutism

Action: Phase-specific acting during mitosis. B. Hormone antagonists

They bind to a specific protein that promotes
chromosome migration during mitosis and Work with hormone-binding tumors,
serves as a conduit for neurotransmitter
transport along axons.
Examples:
Toxicity: 1.Tamoxifen – competes with estradiol
a.Depression of deep tendon reflexes receptors in breast tumors.
b.Paresthesias 2.Diethystilbestrol – competes with hormone
Motor weakness receptors in endometrial and prostate tumors
d.Cranial nerve disruptions 3.Anti-androgen (Flutamide) and Luteinizing
e.Paralytic ileus hormone – releasing hormone block
testosterone synthesis in prostate cancer.

6.Miscellaneous Agents
B.Etoposide
Eposin, Etopophos, Vepesid, VP-16
Eg. Cisplatin (Alkylating agent)
An organic drug containing platinum and
Action: It inhibits the enzyme topoisomerase II,
chlorine atoms; most active in the G1 subphase.
which aids in DNA unwinding, and by doing so
causes DNA strands to break.
These platinum complexes react by binding to
Acts in all phases of the cell cycle, causing
and causing cross-linking of DNA,
breaks in DNA and metaphase arrest.

Toxicity: Toxic effect:

1.Bone marrow suppression
2.Nausea and vomiting
3.Hypotension

5. Hormone and Hormone Antagonists

A. Corticosteroids

Phase-specific (G1); acts by binding to specific

intracellular receptors, repressing transcription
of memory RNA

Side Effects:
1.Impaired healing
2.Hyperglycemia
3.Hypertension
4.Osteoporosis
Other Therapeutic Modalities Two types:
Ductal Carcinoma in Situ (DCIS)
A. Immunotherapy
Lobular Carcinoma in Situ (LCIS)
Using Biologic Response Therapy
B. Invasive Carcinoma
- arises from the intermediate ducts of
the breast
B. Photodynamic Therapy

Phototherapy/ photoradiation/ Seven types:

photochemotherapy Infiltrating Ductal Carcinoma
Infiltrating Lobular Carcinoma
Medullary Carcinoma
Mucinous Cancer
Tubular Ductal Carcinoma
– an intravenous dose of
Inflammatory Carcinoma
photosensitizing compound, which is selectively
Paget’s Disease
retained in higher concentrations of malignant
tissue.

Etiology
Cause is unknown.
C. Bone Marrow Transplant
Although genetic, hormonal or biochemical
factors are likely to be involved, 70% of women
with breast CA had no known risk factors.

D. Hormone Therapy Precipitating factors:

Reproductive history
Radiation exposure
lifestyle

Because steroid hormones are powerful drivers Predisposing factors:

of gene expression in certain cancer cells, Gender
changing the levels or activity of certain Race
hormones can cause certain cancers to cease Age
growing, or even undergo cell death. Family history
Medical history
Menstrual history
Breast cancer
TYPES: Men – risk factors:
A. Carcinoma in Situ A 1st degree male or female relative with
- characterized by the proliferation of breast cancer
malignant cells within the , Variations in BRCA2 gene
without invasion into the surrounding tissue. Klinefelter’s syndrome
Exposure to ionizing radiation
Signs & Symptoms:
Small, hard painless lump in breast
Non-tender & fixed lesions
Lesions are hard with irregular borders rather
than encapsulated and smooth
Nipple discharge
Change in size & shape of breast
Dimpling, pulling, or retractions
Peau d’ orange skin
Persistent skin rash near nipple area
Flaking or eruption near the nipple

Diagnostic Exams:

Imaging Studies:

Specimen examinations:

Breast conserving procedures:

Axillary lymph node dissection

Breast reconstruction:
Transverse Rectus Abdominis Muscle Flap

Latissimus Dorsi Muscle Free Flap

BRAIN TUMOR
Groups of Tumors
}Arising from the coverings of the
brain (meningioma)
}Arising from the cranial nerves
(acoustic neuroma/vestibular
schwannoma)
}Originating from brain tissue
(gliomas)
}Metastatic Tumors
Incidence
}Cause is Unknown
}Metastatic CA is the most
CA in the brain
}25% of people with CA
develop brain metz
Types of Tumors

● Malignant - cancerous = infiltrating

● Benign - non-infiltrating (encapsulated)
❖ Gliomas (60%)
Glioblastoma - worst, aggressive & malignant
Astrocytoma (70%)- doesn’t spread outside brain tissue
❖ Meningioma - usually benign
➢ Metastatic carcinoma (35%)
- areas: skin, lung, breast, prostate
 SIGNS & SYMPTOMS
}Result from enlarging mass which compresses brain structures

}Depend on type of tumor, location, & degree of invasion

}May be localized or systemic

Increased ICP due to cerebral
edema

}Classic Signs:
}Headache – aggravated by
straining
}Vomiting – irritation of vagal
centers in medulla
}Papilledema – present in 70% of
patients
Cushing’s Triad

Physiological nervous system response to increased ICP, usually seen in

terminal stages of acute head injury (ABI) & may indicate imminent brain
herniation.

★ Hypertension
★ Bradycardia
★ Irregular respirations
Personality changes
Focal deficits in motor, sensory, & cranial nerve function
Diagnostic Tests

➔ CT scan
➔ MRI
➔ Cerebral Angiography
➔ Electroencephalogram
➔ CSF studies (cytology)
Management
1.Craniotomy – remove tumor whenever possible
2.Radiation & ChemoTx – may follow surgery; also for inaccessible &
metastatic tumors
3.Watch for wound breakdown & ICP
4.Drug Tx – hyperosmotic agents, steroids, & diuretics to manage increased
ICP
Nursing Management
}VS/NVS monitoring
}Watch for increased ICP
}Administer meds as ordered
}Supportive care for neuro deficits
}Pre – op care/ Chemo Care
}Psychological support
}Document seizure activity
}Watch for Pupillary dilatation & loss of light reflex
Two types: Adenocarcinoma and Squamous cell
carcinoma

● Squamous cell carcinoma- develops from squamous

epithelial cells; and is the most common form of
cervical cancer
● Adenocarcinoma- develops from Columnar epithelial
cells.
 ETIOLOGY

Precipitating Factors
Sexual History- Women who had sexual intercourse at an early age
(17 y.o) women -Multiple sexual partners ;Smoking
HPV- Humanpapilloma virus
HIV- Human immunodeficiency virus; damages the body’s immune
system
Diet- Low fruits and vegetables
Immunosuppression
Predisposing Factors
Age (35-55 y.o)
Race (Black women: African-american)
Low socioeconomic status
Signs and Symptoms
Initial symptoms includes:
Post-coital bleeding
Irregular vaginal bleeding or spotting between
periods or after menopause
Malodorous discharge
Late symptoms include:
Bleeding becomes more constant and
accompanied by pain that radiates to buttocks and
legs
Weight loss
Anemia
Fever
PAP TEST (Pap smear)- most commonly used for
diagnosing cervical cancer.
Colposcopy- involves the use of a special binocular
microscope that is called a colposcope and similar to a
Pap smear).
Pelvic exam-
Endocervical curettage- scraping the mucus
membrane of the endocervical canal (passageway
between cervix and uterus) to obtain a small tissue
sample.
HPV Vaccine
Cervical Conization
Hysterectomy –
Cryosurgery –
Laser Surgery –
Radiotherapy-
Chemotherapy-
Nursing Diagnosis:
Acute Pain related to disease process
Deficient fluid volume related to excessive
bleeding
Anxiety related to threat of death
Risk for imbalanced body temperature related to
presence of invading pathogens
Risk for Constipation related to tumor obstruction
NURSING INTERVENTIONS
Assess vital signs, including temperature, pulse,
respiration and blood pressure.
Obtain client’s assessment of pain to include
location, characteristics, onset, duration,
frequency, and intensity; use pain scale for
evaluating
Identify client’s perception of the threat
represented by the situation
Observe behaviors that can point to client’s level
of anxiety
Observed for discharges from the vagina and note
for its odor, color, and amount
Encourage client to express feelings about the current condition
Be available to client for listening
Help the patient seek information on stage of cancer, treatment
options.
Provide comfort measures such as quiet environment, and calm
activities
Administer analgesics as prescribed by the doctor
Provide adequate fluid intake including high-fiber foods.
Encourage client to comply well with treatment regimen
Explain the importance of life-long follow up regardless of
treatments to determine the response to treatment and to detect
spread of cancer.
Provide privacy for patient.
 LEUKEMIA
}A group of malignant disorders
affecting the blood and blood-forming
tissues of the bone marrow, lymph
system, and spleen.
}Neoplasm derived from lymphoid or
myeloid cells primarily affecting the
bone marrow and peripheral blood.
 Bone Marrow- flexible
tissue found in the hallow
interior of bones
Types:
a.Red marrow- consisting
mainly of myeloid tissue
(RBC, platelets, most WBC)
b.Yellow
marrow- fat cells and
some WBC develop in YM
 NORMAL BLOOD CELLS
1. WBC- infection
Granulocytes- neutrophil, eosinophil, basophil
Agranulocytes- lymphocytes, monocytes,
macrophages

2. RBC - carry oxygen

3. Platelets – clotting factors
CHARACTERISTICS
}Replacement if BM with
malignant, immature WBC
}Appearance of abnormal,
immature WBCs in peripheral
circulation
}General infiltration of cells
into liver, spleen & LNs
throughout the body
 ETIOLOGY
L-eukemia virus: HTLV-1
E-spraying of pesticides
U-se of chloramphenicol
K-apamilya
E-xposure to benzene
M-ay Down Syndrome
I-onizing radiation
A-lkYlating agents
Classifications of Leukemia:
1. ACUTE LYMPHOCYTIC
LEUKEMIA
}Mostly lymphoblast present in BM
}Age of onset is less than 15 years
old
2. ACUTE MYELOGENOUS
LEUKEMIA
}Mostly myeloblast
}Age of onset is between 15-39 years
old
3. CHRONIC MYELOGENOUS
LEUKEMIA
}Mostly granulocyte present in BM
}Age of onset is after 50 years old
4. CHRONIC LYMPHOCYTIC
LEUKEMIA
}Mostly lymphocytes present in BM
}Age of onset is after 50 years old.
 Clinical Manifestations
1.Anemia
2.Thrombocytopenia
3.Leukopenia
4.Chloromas
5.Gum infiltration
6.Hepatosplenomegaly
7.Bone pain
8.Anorexia
9.Petechiae
A rare form of cancer
with a high mortality
rate
90% arise from the liver
parenchymal cells
(hepatoma)
Some originate from the
intrahepatic bile duct
(cholangioma)
 A-lcoholic beverages
L-iver cirrhosis
C-igarette smoking
O-verexposure to
aflatoxin
H-epatitis B,C,D &
Schistosomiasis
O-ncogenic foods
Aspergillus flavus - mold L-iver toxins( vinyl
chloride, arsenic)
◦ Hepatocellular CA
◦ Cholangiocellular CA
Abdominal mass, RUQ
pain, jaundice, anemia

CA signs: weight loss,

fatigue, anorexia

Portal hypertension,
ascites, esophageal
varices which may rupture
and cause hemorrhage
 ⦿ AFP (alpha-feto protein)
⦿ Serum Bilirubin 0.3 to 1.9 ⦿ Liver scan, USD, CT,
mg/dL
MRI, PET scan
⦿ Alkaline Phosphatase
⦿ SGOT/ AST ⦿ Needle biopsy
⦿ SGPT/ ALT ⦿ Increased Serum
⦿ LDH Ammonia
⦿ Increase WBC, low RBC ⦿ Serum Crea, BUN
⦿ Hypoglycemia
⦿ Hypercholesterolemia
⦿ Hepatojugular reflux sign
⦿ Serum albumin (3.4-5.4 g/dl)
1. SURGERY
◦ Treatment of choice when
confined to one lobe; not for
pt with cirrhosis (SUBTOTAL
HEPATECTOMY)

-TYPES OF SURGERY
B. LOBECTOMY
C. CRYOSURGERY
D. LIVER TRANSPLANT
2. Chemotherapy
◦ adjuvant prior to surgery

3. Radiation Therapy
◦ for unresectable tumors, palliative so NO significant change in
survival rate.

4. Transcatheter chemoembolization
 A.Non-small cell Lung Cancer

o Squamous cell carcinoma

o Large cell carcinoma
o Adenocarcinoma
B.Small cell carcinomas
Precipitating Factors:

Carcinogens
Tobacco smoke
Secondhand(passive) smoke
Occupational exposures
Dietary deficits
Air Pollution
Ionizing Radiation
 Predisposing Factors:
•Gender
•Genetics
•Race
Cough or chronic cough
Dyspnea
Hemoptysis of blood
Chest or shoulder pain
Fever
Chest pain or tightness
Cardiac tamponade
Weakness
Anorexia
Weight loss
Primary Tumors:
T0 – no evidence of primary tumor
TX – tumor can’t be measured
Tis - Carcinoma in situ
T1 - tumor <3cms w/o invasion
T2 – tumor > 3.0 cm in diameter, or a tumor of
any size that invades the visceral pleura
T3 - tumor of any size with direct extension into
an adjacent structure, such as chest wall
T4 – tumor of any size w/ invasion to distal sites
like esophagus or opposite lung
Lymph Node Involvement:
N0 - no demonstrable metastasis to regional lymph
nodes
N1- metastasis to nodes in the peribronchial and/or
ipsilateral hilar region
N2 - ipsilateral mediastinal &/or subcarinal LN
N3 - metastasis to contralateral mediastinal or hilar
lymph nodes, supraclavicular LN
Metastasis:
M0 - no distant metz
M1- distant metastasis, such as to scalene or
contralateral hilar lymph nodes, brain, and lungs
Diagnostic Exams:
Fiberoptic Bronchoscopy
Low Dose Helical Computed Tomography
Endoscopy with Esophageal Ultrasound
Mediastinoscopy
Papanicolau test of the sputum
Diagnostic Exams:
Low Dose Helical Computed
Tomography
Nursing Diagnosis:

Chronic pain r/t to pressure of tumor on

surrounding structures and erosion of tissues.
Ineffective airway clearance r/t increase amount of
secretions
Impaired breathing pattern r/t compression of
bronchus
Risk for infection r/t immunosuppression
Fatigue r/t decreased oxygen supply to the body
secondary to anemia.
 TREATMEN T PHASE
Client undergoing Thoracic Surgery
1.
2.
 9. Administer pain medications as ordered
10. Position client as indicated by phase of
recovery and surgical procedure
a.Non-operative side-lying position may be used
until consciousness is regained
b.Semi-Fowler’s position is recommended once vital
signs are stable
c.Avoid positioning client on operative side. If a
wedge resection has been performed
d.Avoid complete lateral positioning after
pneumonectomy
11. Gently turn the client every 1 to 2 hours
unless contraindicated
12. Avoid traction on chest tubes while changing
client position. Check for kinking or compression
of tubing
13. Begin passive ROM exercises of the arm
and shoulder on the affected side 4 hours
after recovery from anesthesia
14. Encourage client to use arm on affected
side in daily activities
is a type of lymphoma, which is
a cancer originating from white blood
cells called lymphocytes. 
 characterized by the orderly spread of
disease from one lymph node group to
another and by the development
of systemic symptoms with advanced
disease.
The disease occurrence shows two
peaks: the first in young
adulthood (age 15–35) and the
second in those over 55 years old.
RISK FACTORS:
Sex: male
Ages: 15–40 and over 55
Family history
History of infectious mononucleosis or
infection with Epstein-Barr virus, a causative
agent of mononucleosis
Weakened immune system, including
infection with HIV or the presence of AIDS
Prolonged use of human growth hormone
Exposure to exotoxins, such as Agent Orange
Fatigue
Fever and chills that come and go
Itching all over the body that cannot be
explained
Loss of appetite
Soaking night sweats
Painless swelling of the lymph nodes in the
neck, armpits, or groin (swollen glands)
Weight loss that cannot be explained
Coughing, chest pains, or breathing problems
Pain or feeling of fullness below the ribs
Pain in lymph nodes after drinking alcohol
Skin blushing or flushing
Blood chem
CBC
Lymph node biopsy
BM aspiration & biopsy
CT scan
PET scan
Stage I & II – no lymphoma outside of lymph
nodes, or lymphoma in only 1area outside of
lymph nodes
Stage III & IV – lymphoma is in more than 1
organ of the body outside of lymph nodes
Stages I and II
local radiation therapy, chemotherapy, or
combination
Stages III
 chemotherapy alone or a combination of
radiation therapy and chemotherapy.
Stage IV (extensive disease)
most often treated with chemotherapy alone.

Tumor marker = Lactic dehydrogenase

✔ High-dose chemotherapy
✔ Autologous BMT
Steps:
1. Collection
2. Processing
3. Cryopreservation
4. Chemotherapy
5. Reinfusion
Additional treatments depend on other
symptoms. They may include:
Transfusion of blood products, such as
platelets or red blood cells, to fight low
platelet counts and anemia
Antibiotics to fight infection, especially if a
fever occurs
OVARIAN CANCER
 A CANCEROUS GROWTH arising from
the OVARY

Symptoms are frequently non specific early on

and may include:
❖ Bloating/ abdominal distension

❖ pelvic pain,

❖ difficulty eating and

❖ urinary frequency, and are easily confused

with other illnesses.
Sources/sites:

surface (epithelium) of the ovary

 fallopian tube 
egg cells (germ cell tumor) 

Other symptoms:
✔ Back pain

✔ Constipation

✔ Urinary urgency

✔ Pelvic pain

✔ Vaginal bleeding

✔ Weight loss
Etiology - Unknown

Risk factors:
❖  Older women
❖ Genetics
❖ Infertile women
❖ Endometriosis
❖  postmenopausal estrogen
replacement therapy
DIAGNOSIS
 physical examination 
CA 125
TVS
surgery to inspect the abdominal cavity,
take biopsies
Management
CHEMOTHERAPY
SURGERY
RADIATION
❖ The 2nd leading cause of
death in males
❖ 80% of cases diagnosed
after age 80
❖ Fertility is not a factor

PROSTATE CANCER
 RISK
FACTORS
Increasing Age
African – Americans

High Fat Diet : lowest

incidence in Japanese

Genetics : 8x more risk if 1st

& 2nd degree
relatives are affected
Signs & Symptoms
Asymptomatic in early stages

Urinary symptoms: frequency, dribbling,

retention, obstruction, hematuria, cystitis

Bone metastases results in hip pain,

back ache, weight loss, perineal & rectal
discomfort
DRE Diagnosis
Biopsy
T-R USD
PSA – may be (+) in BPH
& prostatitis - 0 to 4
ng/ml
ACID PHOSPHATASE –
increased in 2/3 of pt; more
predictive of metz

ALKALINE PHOSPHATASE +
Bone Scan = metz
P Omegranate juice
MANAGEMEN
R
O
Adiation: BrachytherapyT
ST
rchiectomy/cryoablation

A
Surgery: Radical Prostatectomy

TE eletherapy

nalgesics

he use of chemotherapy

-hormal therapy YAN

Hormone Therapy:
Luteinizing hormone-releasing hormone
agonists (LHRH agonists.)

Anti-androgens - Flutamide

❖ Etoposide - Plant Alkaloid

External beam
radiation
Brachytherapy
placement of about 100
small "seeds" containing
radioactive material (such
as iodine-125 or
palladium-103) with a
needle through the skin of
the perineum

Pomegranate juice (under

study)
 Nursing Problems
Altered urinary elimination
Pain
Sexual dysfunction / Body Image disturbance
Urinary retention
Altered role performance
The CELL
 THE CELL CYCLE
Divided into two periods –
I. Mitosis (M) Phase, which includes nuclear division (mitosis) and cell
division (cytokinesis)
II. Interphase, part of the cell cycle which is not contained in M phase
 INTERPHASE PERIOD
• The cell grows, accumulating nutrients needed for mitosis and duplicating its DNA.
Interval or Steps:
• G – gap
• M – the interval separating Mitosis
• S – synthesis
Gap 1 (G1) – cells increase in size & produce RNA
Synthesis – DNA replication occurs
Gap 2 (G2) – cells grow & getting ready for mitosis
Gap 0 (G0) – resting phase where the cell has left the cycle
and has stopped dividing
 Other factors which contribute to the development
of CA

✔ Immunologic Defects
✔ Age
✔ Gender
✔ Heredity
✔ Poverty
✔ Stress
✔ Lifestyle Practices
a. Smoking
b. Nutrition
c. Obesity
d. Sexual and reproductive factors
 Comparison between Normal and Malignant Cell

Characteristics Normal Malignant

1. Mitotic Division Leads to 2 daughter cells Leads to multiple daughter cells

2. Appearance Homogenous in size, Larger & grows more rapidly than

shape & growth normal, heterogeneous
Cohesive, forms regular
Not cohesive, irregular pattern of
patterns of expansion
expansion
Uniform in size to nucleus
Well differentiated Larger, more prominent nucleus

Lack of pattern in organization

Characteristics Normal
3. Growth pattern Do not invade adjacent
tissue
Proliferation in response
to specific stimuli
Grows in ideal condition
Cell birth is equal to cell
death
Stable cell membranes
Constant predictable
growth rate
Cannot grow out of
specific environment
Malignant
Invade adjacent tissue
Proliferation in response to
abnormal stimuli
Grows in adverse condition
Cell birth exceeds cell death
Loss of control as a result of cell
membrane change
Erratic growth rate
Able to break of cells that migrate
through blood stream/ lymphatic
channels
Characteristics Normal Malignant
4. Functions Have specific designated No useful purpose
purpose
Contribute to overall Parasitic
well-being of host
Functions in specific
predetermined manner No normal function, causes damage
instead

5. Others Chromosomes remain

constant throughout cell Chromosome aberration occur as
division cells matures
Cannot invade, erode or
spread Invades, erode and spreads
Have own blood supply
 Classification of Neoplasm is based on Tissue of Origin

“OMA” – means tumor; usually attached to a term for a parent tissue of the tumor
Example: “aden” (gland) + oma = Adenoma

❖when one or more parent tissue enters into the formation of

neoplasm, the names of a tumor are even more descriptive
Example:
Adenomyoma – benign neoplasm that contains both glandular & myoma
cells

3 Most Common Benign Tumors:

1. Fibroma
- grows anywhere in the body
-encapsulated, harmless tumor & may not cause
symptoms unless they press on a bone or nerves.
2. Lipoma
very common benign tumor (adipose tissue);
poorly encapsulated; may put pressure on
surrounding tissue as they expand

3. Leiomyoma
smooth myoma in origin; rarely become
malignant (1% of cause)
 Malignant Tumors:

Carcinoma – origin in epithelial tissue

Sarcoma – mesenchymal origin (blood vessels, lymphatics, nerves)

Examples of Malignant Tumors:

1. Carcinoma in Situ – neoplasm of epithelial tissue that remains confined to the site of origin
2. Malignant Fibrosarcomas – may originate from benign fibromas
3. Bronchogenic Carcinoma - 90% of all cases of lung CA; usually develops in lower trachea and
lower bronchi

• Adeno – glandular tissue

• Angio – blood vessels
• Basal cells – epithelium, mainly sun exposed area
• Embryonal – gonads
• Lympho – lymphoid tissue
• Melano – pigmented cells of epithelium
• Myo- muscles
• Osteo - bone
CHEMOTHERAPY
 Chemotherapeutic administration
1. Oral route
2. Intramuscular or Subcutaneous injection
3. Intravenous – most common, provides better absorption
Risk: Infection & Phlebitis

Management: IV administration
1. Smallest needle gauge
2. Aseptic technique
3. Monitor IV site frequently
4. Change IV fluid q4hrs

4. Central Venous Catheter Infusion

-A.K.A. “Central Line”; peripherally inserted central catheter line goes
into the arm & runs all the way to a large vein near the heart.
- A thin tube (port) with 1 or 2 discs on one end places on the chest, just
under the collarbone.
 Risk: Central Venous Catheter Infusion
-Infection
-Catheter clot
-Sepsis
-Needle malposition

✔ Management:
a. Aseptic technique
b. Monitor site daily
c. Flush catheter daily/ between use
d. Assess for signs of infection
5. Venous Access Device (VADs)
- for prolonged infusion
Risk: infection
infiltration from malposition

6. Intra-arterial Route
- delivers agents directly to tumor in high concentration while
decrease drug systemic toxic effect.

Risk: infection
bleeding at catheter site
clotting at site

Management:
1.dressing change daily and assess infection
2. Irrigate/flush catheter
3. Avoid kinks in tubing
 7. Intraperitoneal
- used for ovarian and colon CA
- high concentration of agents delivered to peritoneal cavity via catheter,
then drain

Chemotherapy Safety Guidelines

1. Obtain special training
2. Wear: gloves
disposable, closed, long-sleeved gown

3. Label prepared drugs appropriately

4. Double bag drugs prepared – transport
5. Clean any accidental spill
6. Dispose all used materials appropriately
7. Dispose all syringes and needles intact
Side Effects of Chemo and Nursing Management
1. GI System
a. Nausea and Vomiting

- antiemetics 4-6 hrs before initiated

- Withhold fluids/foods 4-6 hours before

- Support food preferences
- Small frequent feeding/ meals – Calories and CHON

b. Diarrhea due to toxicity

- antidiarrheal
- everyday perieneal care
- Monitor K, Na, & CL level
✔Constipation due to drug affecting nerve endings of GIT (ex.Vincristine- Vinka
alkaloids)
-increase fiber and fluids
-Have stool softeners

c. Stomatitis
- good oral hygiene
- rinse with lidocaine before meals
- cleansing rinse with plain water or dilute a water-soluble lubricant
after meal
- petroleum jelly to cracked lips
- avoid spicy and acidic foods
2. Hematologic System
1. Thrombocytopenia
Platelet ( below 150T –300T)

a. Avoid bumping/bruising skin

- shorter life span
b. Protect from physical injury
c. Avoid aspirin product
d. Avoid IM injection
e. Monitor blood count
f. Assess/teach bleeding tendencies

2. Leukopenia (below 5T-10T)

a. Careful handwashing technique/aseptic technique

b. Reverse isolation
c. Assess for respiratory infection
d. Avoid crowds or people with infection
 Anemia
a. Adequate rest
b. Monitor hgb and hct count
c. Oxygen PRN

3. Intergumentary System
1. Alopecia (2-3 wks)
- temporary
- support and encouragement
- wear wig

2. Leukopenia
3. Anemia
4. Renal System
Direct damage to kidney (excretion)
- frequent voiding
- increase oral fluid intake
- Allopurinol (Zyloprim) to prevent uric acid formation

5. Reproductive System
- infertility/mutagenic damage to chromosomes
- banking sperm

6. Neurologic System (due to repeated use of vincristine)

- hearing loss
- paralytic ileus
- loss of tendon reflex
RADIATION
THERAPY
Precautionary measures for Radiation TXT
1. Place patient in a private room.
2. Place a sign on the patient’s door and on the patient’s chart indicating that
the patient is receiving internal radiation therapy.
3. Observe principles of time and distance.
4. Check all linens, bedpans and emesis basin routinely to see if the sealed
source has been accidentally lost from the tissue.

Radiation Txt Sign

5. If sealed source is dislodged, but has not fallen out of the
patient’s body, notify the x-ray radiation department at
once.
If fallen out, do not pick it up with bare hands. Use forceps
and place it in a lead container.

6. Most patients are placed on bed rest and instructed to

remain in certain positions so that the emanations from
the element will reach the correct area.
7. Visitors will spend limited time in the room to 30 minutes daily, seeing that visitors
maintain a 6-foot distance from the radiation source.
8. Prohibit visits by children or pregnant visitors.

Special precautions – Patient receiving internal radiation therapy from an

unsealed source:
1. Observed the principles of time, distance and shielding for radiation protection.
2. Wear gloves when handling bedpans, bed linens and patient’s clothes.
3. Dispose of urine, feces and vomitus according to policy.
4. Handle dressings with forceps and dispose of them according to policy.
5. Follow hospital procedure for disposal of patient’s bed linens and clothing.
Common Side Effects of Radiation Therapy

External Radiation
Head and Neck
-irritation of oral mucous membranes with oral pain
and risk of infection.
-Loss of taste.
-Irritation of the pharynx and esophagus with
nausea and indigestion.
-Increase intracranial pressure.

Chest

- Inflammation of lung tissue with increase susceptibility to infection.

Abdomen
- nausea, vomiting, diarrhea, anorexia

Pelvis
- diarrhea, cystitis, sexual dysfunction, Urethral and rectal
stenosis

General Side Effects:

SKIN: change in texture and/or color, moist desquamation(rare);
alopecia
BLOOD: bone marrow depression with leucopenia, anemia and
thrombocytopenia.
Depressed Immune Function
Fatigue
Internal Radiation
General Effects:
1. Elevated temperature.
2. Cervical implant: Urinary frequency, diarrhea, nausea,
vomiting and anorexia.
3. Head and Neck: mucositis, oral pain and risk for
infection, anorexia.;
 Skin Care Treatment
1. Apply the special skin care lotion four times a day, starting immediately.
2. Do not wash off treatment markings. Tatoos, if done, are permanent.
3. Keep skin clean and dry. Expose the skin to air as much as possible.
4. Protect the skin in the treatment area from the sun and cold by using scarves, hats
or other clothing.
5. Cornstarch may be used for dry, itchy skin.
6. Irritated skin, a different lotion may be needed.
7. Bathing – clear water and pat dry. Use mild soap.
8. Clothing: wear soft, loose cotton clothing over the treatment area.
9. Shampooing – use baby shampoo.
10. Shaving – use electric razors.
11. Do not rub or scratch the skin in the treatment area.
12. Do not use lotions or creams not approved by the doctor.
13. Do not use deodorants, perfumes or make-up in the treatment area.
14. Do not use ice packs or heating pads
15. Do not use tape in the treatment area.
Lead Apron PPE

Dosimeter badge
 Post Removal of Source (Internal Radiation for
Cervix)
1. Betadine douche
2. Enema – to prevent constipation
3. Out of bed – may ambulate
4. Avoid direct sunlight
5. May use vaginal cream (hypoallergenic)

•May resume Sexual intercourse within 7-10 days

PAIN in Cancer
Psychological Causes:

depends on the client’s perceived

Causes:
threat.
1.Bone marrow destruction
1.Fear or anxiety generated
2.Obstruction of an organ from the effects
3.Compression of peripheral nerves
2.Loss or threat of loss
4.Infiltration or distention of tissue
3.Frustration
5.Inflammation, infection and
necrosis
 Assessment:

1.Severity and duration

2.What, when and where pain occurs

3.Understand as client views it

4.Nature of the disease

5.Probable life expectancy

6.Temperament and psychological state

7.Occupational, economic, educational background

8.Vital sign

a. Low to moderate pain and superficial in origin (sympathetic)

- Increase BP, PR, RR and muscle tension

b. Severe pain or visceral in origin (parasympathetic)

- decrease BP, PR, N/V, weakness

9.Behavior as indicator of pain -

-Posture

-Gesture

-Daily activities

Medication Management:

1.Acetaminophen, ASA, NSAIDs (mild pain)

2.Opioids – CODEINE

added to regimen as pain increases

3.Intraspinal Morphine Administration

- an implantable infusion pump delivers a continual supply of opiate to the epidural or subarachnoid
space
 Surgical Management:

1.Nerve blocks

involves interruption of nerve

pathways some place along the path
of transmission from periphery to
brain.

2. Non invasive Modalities

•Transcutaneous Nerve Stimulation

(TENS)

electrical stimulation of the skin

surface over a painful area
Stage Tumors Surgery Chemo Tx Radiation

0 Cis TM or lumpectomy Tamoxifen For lumpectomy

I Tumors are < 2 cm BCT or MRM Considered for all For BCT
in diameter & invasive tumors
confined to breast

II Tumors are < 5 cm, BCT or MRM Regimen depends For BCT
or smaller with on tumor size &
mobile axillary nodal status
lymph node
involvement

TM-Total BCT- breast

Mastectomy conservation
treatment
IIIa Tumors are > 5 MRM Post-op & To chest wall
cm, possible & possibly
accompanied pre-op axillae after
by enlarged MRM
axilllary lymph
nodes fixed to
one another or
to adjacent
tissue
IIIb More advanced MRM Post-op & To chest wall &
lesions w/ possibly pre-op possibly axillae
sattelite nodules, after MRM
fixation to the
skin or chest
wall, ulceration,
edema, or w/

IV All tumors w/ Possibly To control To control

distant mets lumpectomy or progression progression
mRM and/or palliation and/or palliation
Treatment:
A.Medical Mgt.
1.)Chemotherapy : combination therapy
ØDoxorubicin (Adriamycin)
ØCyclophosphamide (Cytoxan)
ØMethotrexate
Ø5-fluorouracil
2.) Hormonal therapy:
üAndrogens: fluorymesterone (Halotestin)
üEstrogens: diethylstilbestrol ( DES)
üAntihormonal agents: Tamoxifen
3. Radiation therapy
- typically begins about 6 wks after the surgery to allow the incision to heal
Treatment:
B. Surgical mgt.

1.Breast-conserving procedures 6. Breast Reconstruction

oLumpectomy oTissue Expanders
oWide excision oTransverse Rectus Abdominis Muscle
oPartial mastectomy Flap
oSegmental mastectomy oLatissimus Dorsi Muscle Free Flap
oQuadrantectomy oNipple-Areola Reconstruction
2. Axillary lymph node dissection
3. Total Mastectomy
4. Modified Radical Mastectomy
5. Radical Mastectomy
Nursing management
Diagnostic Phase:
1.Minimize uncertainty
2.Prevent disease advancement
3.Protect emotional well-being
4.Establish trusting communication
Adjuvant Therapy Phase:
1.Develop a supportive network
2.Minimize adverse physical outcomes
3.Manage stress
4.Understand family members’ responses
Ongoing Recovery Phase:
1.Maintain association with professionals
2.Maintain positive outlook
3.Redefine self and partner
4.Cultivate ongoing support
Preoperative Nursing Intervention:
1.Explain breast CA, correct misconceptions, and treatment options.
2.Reduce fear
3.Reduce anxiety
4.Improve coping ability
5.Promote decision-making ability
 Postoperative Nursing Intervention:
1.Relieve pain and discomfort
2.Maintain skin integrity
3.Prevent infection, injury
4.Promote positive adjustment & coping
5.Monitor drainage; monitor bleeding
COLORECTAL
CANCER
 Incidence
The American Cancer Society’s estimates for number of
colorectal cancer cases in the U.S. for 2020 are:
ü104,610 new cases of colon cancer
ü43,340 new cases of rectal cancer

Etiology
- unknown
Precipitating Predisposing
-diet -age
-geographic location -hereditary
-socioeconomic factor
-religion
-inflammatory bowel
Disease (IBD)
-tobacco use
Affected part Clin. Manifestation
Cecum no noticeable alterations
in bowel habits
Ascending colon same, fatigue, palpitation,
unexplained iron deficiency
anemia, melena
Transverse abdominal cramping, diarrhrea
Descending constipation,perforation,”apple
core” radiograph results
Affected part Clin. Manifestations
Rectosigmoid hematochezia, narrowing
of the caliber of the stool,
unexplained anemia,
abdominal distention, feeling of incomplete
evacuation after a bowel movement,
alternating constipation/diarrhea
 DIAGNOSTIC EXAM
}Stool occult blood test
}DRE
}Barium enema
}Flexible sigmoidoscopy
}Colonoscopy

MEDICAL MANAGEMENT
-IV, blood components- bleeding
-Radiation
-chemotherapy
 SURGICAL
MANAGEMENT
1.Segmental resection with
anastomosis
2.Abdominoperineal
resection with permanent
sigmoid colonostomy
3. Temporary colostomy
4. Permanent colostomy
NURSING MANAGEMENT:
1.If client submits himself to surgery,
prepare him.
2.Record intake and output.
3.Monitor increasing abdominal
distention and loss of bowel sounds.
(Gastric decompression)
4.Monitor IV fluids and serum
electrolytes.
5.Assess skin turgor, dry mucous
membrane and concentrated urine.
Protecting the skin around the stoma (American Cancer Society)

The skin around your stoma should always look the same as skin anywhere else on your abdomen. But ostomy output can
make this skin tender or sore. Here are some ways to help keep your skin healthy:

Use the right size pouch and skin barrier opening. An opening that’s too small can cut or injure the stoma and may
cause it to swell. If the opening is too large, output could get to and irritate the skin. In both cases, change the pouch or skin
barrier and replace it with one that fits well.

Change the pouching system regularly to avoid leaks and skin irritation. It's important to have a regular schedule for
changing your pouch. Don't wait for leaks or other signs of problems, such as itching and burning.

Be careful when pulling the pouching system away from the skin and don't remove it more than once a day unless
there’s a problem. Remove the skin barrier gently by pushing your skin away from the sticky barrier rather than pulling the
barrier away from the skin.
Clean the skin around the stoma with water. Dry the skin completely before putting on the skin barrier or pouch.

Watch for sensitivities and allergies to the adhesive, skin barrier, paste, tape, or pouch material. They can develop
after weeks, months, or even years of using a product because you can become sensitized over time. If your skin is
irritated only where the plastic pouch touches it, you might try a pouch cover or a different brand of pouch. A stoma
nurse can offer ideas if needed. Pouch covers are available from supply manufacturers, or you can make your own.
You may have to test different products to see how your skin reacts to them.
BONE TUMOR
❖ A neoplastic growth of tissue in bone. Abnormal
growths found in the bone can be either benign
(noncancerous) or malignant (cancerous).
Bone Tumor
Classification:
1.Primary Tumors
Benign-neoplastic,deve
lopmental, traumatic,
infectious, or
inflammatory in
etiology
Eg. Osteoma,
Osteoblastoma
Primary Tumors
Malignant
Eg. osteosarcoma, chondrosarcoma, Ewing's
sarcoma
2. Secondary tumors
➢ include metastatic tumors which have spread from
other organs, such as carcinomas of the breast,
lung, and prostate.

Manifestations:
★ Pain
★ Pathologic fracture
TREATMENT:
❏ CHEMOTHERAPY
❏ RADIATION THERAPY

MEDICATIONS:
ØNonhormonal bisphosphonates
Ø Metastron (strontium-89 chloride )
SURGICAL TREATMENT:
➔ AMPUTATION
Prognosis
The outlook depends on the type of tumor
Benign = good prognosis
Malignant but no metz = may achieve cure
Cure rate =depends on type of CA, location, size,
and other factors
UTERINE CANCER
 CANCER OF THE
ENDOMETRIUM
The most common
gynecologic CA
Usually AdenoCA

✔Endometritis
✔Endometriosis
RISK FACTORS
 RISK FACTORS
Cumulative exposure to
estrogen; but OCP in
combi preps decrease risk
by 50%
Familial tendency
✔ DM, HPN, gallbladder
disease
✔ Ovarian neoplasms
=decrease sex hormone –
binding globulin
Tamoxifen
Obesity – most
important risk factor
Increases estrogen
production & bio
availability in muscle &
adipose
Overweight by up to
22.7% = 3x more risk
>22.7% = 9x more risk
SI
GN
S
&
SY Abdomino Uterine
–pelvic pain enlargement
M
PT
O
M
Pre - & Post –
S
menopausal bleeding –
HALLMARK

Constitutional CA signs
 Annual PE/ Gyne Exam

Biopsy

Pap Smear – 50% of patients with

abnormal results

Schiller’s test (Lugol’s test) – cervical

tissue staining; CA cells resist the stain

MRI or CTscan – evaluates myometrial

invasion & LN involvement

CA 125 - >40 U/ml

DIAGNOSTIC TEST
U-se of chemotherapy
T-ake hormonal agents
E-mphasize follow-up care
R-adiation:
External/Intracavitary
U-tmost psychosocial
support
S-urgery: TAH/TAHBSO
Pathology of Infection
Gemshe M. Santos, RN

https://poweredtemplate.com/03757/0/index.html
Terminologies
⁕ Host – any organism capable of supporting
the nutritional and physical growth of
another organism.
⁕ Infection - the presence and multiplication
of a living organism on or in the host.
⁕ Normal flora – harmless bacteria living in a
host
⁕ Commensalism – an interaction between the
host and the commensal bacteria.
⁕ Mutualism – an infection in which the
microorganism and the host derive benefits
from the interaction.
Terminologies

⁕ Infectious disease – a pathologic process in

response to an infection.
⁕ Virulence – the disease-producing potential of
the microorganism
⁕ Pathogens – group of microorganism
⁕ Saprophytes - harmless free-living
organisms that grow on decaying organic
material.
⁕ Opportunistic pathogens – capable of
producing an infectious disease.
What is Infection?
✓is the colonization of a host by microbial
species. Infecting microbes seek to use the
host’s resources to reproduce, often resulting
in disease. Infections are considered to be
caused by microscopic organisms like viruses,
prions, bacteria and viroid though larger
organisms like macro parasites and fungi can
also infect.
Classification of Infection

I. EXTENT of INVOLVEMENT:
a. LOCAL - limited to one locality
of the body

b. FOCAL - a local infection from

which the organism spread to
other parts of the body

c. SYSTEMIC - infectious agent is

spread throughout the body
II. LENGTH OF INFECTION PROCESS:

a. Acute
- rapid onset, short course
- immediate immune response

b. Chronic
- gradual onset/ longer
- delayed immune response
III. ETIOLOGY
a. Primary
- develops after initial exposure to antigen

b. Secondary / Opportunistic
- develops when antigens take advantage of
the weakened defense resulting from
primary infection
- develops when host defenses are
diminished because of disease process or
therapeutic modalities
STAGES OF INFECTIOUS PROCESS:

1. Incubation - Entry of microorganisms into the body to

the onset of signs and symptoms
2. Prodromal - Onset of non-specific signs and symptoms
to the appearance of specific signs and symptoms
3. Acute - Specific signs and symptoms develop and
becomes evident
4. Convalescent - Signs and symptoms start to abate
until the client returns to normal state of health.
5. Resolution - Normal state of health and total
elimination of pathogens
FACTORS AFFECTING INFECTIOUS PROCESS:

1. Force of infection: Epidemiologic Triangle consist of 3

components
❖ Host - any organism that harbors and provides
nourishment for another organism.
❖ Agent - intrinsic property of microorganism to survive
and multiply in the environment to produce disease.
❖ Environment - it is the sum total of all external
conditions and influences that affect the development of
an organism which can be biological, social or physical.

2. Force of Resistance: Immunity (see separate

discussion on immunity)
CHAIN OF INFECTION
1. Pathogenic microorganism/ causative
(infectious)agent
❖ Microorganism that causes infection such as
bacteria, virus, fungi and parasites.
❖ There must be a sufficient dose of the organism that
has enough amount and concentration to cause
infection.
CHAIN OF INFECTION
2. Reservoir
❖ Place where the microorganism lives, such as in humans, animals, in
soils, food, plants, air or water
❖ It includes humans, animals and the environment
❖ The reservoir may or may not be the source from which an agent is
transferred to a host
❖ The reservoir must meet the needs of the pathogen to survive and
multiply
❖ The natural habitat of the organism where it resides and multiply
3. Portal of Exit
▪ The portal of exit is the path by which the pathogen leaves its host.
▪ It usually corresponds to the site where the pathogen is localized.
▪ These are the following mode of escape from the reservoir:
❖ Respiratory tract (most common in human)
❖ Gastrointestinal tract
❖ Genitourinary tract
❖ Open lesions
❖ Mechanical escape
(bites of insect)
❖ Blood
•
4. Mode of transmission
▪ An infectious agent may be transmitted from its natural reservoir to a
susceptible host in different ways.
▪ The mode of transmission is the weakest link in the chain of infection
▪ There are different modes of transmission:

❖ Vertical - Maternal to fetal transmission (crossing

the placental barrier or via vaginal route)
❖ Horizontal - It can be direct or indirect or through
break in the skin integrity

a. Direct contact
❏ Occurs through skin to skin contact, kissing, and sexual
intercourse
❏ Also refers to contact with soil or vegetation harboring
infectious microorganism
❏ A droplet spread is considered to be a direct contact which
refers to sprays with relatively large short-range aerosols
produced by coughing, sneezing or even talking.
b. Indirect contact
➔ Airborne
◆ Occurs when infectious agents are carried by dust or droplet
nuclei suspended in the air.
◆ Airborne dust includes materials that have settled on surfaces
and becomes suspended by air currents as well as infectious
particles blown from the soil by the wind
➔ Vehicle-borne
◆ It includes food, water, biologic products (blood) and fomites
(inanimate objects such as bedding, handkerchief or scalpels)
◆ A vehicle may passively carry a pathogen- as food or water
may carry a virus.
◆ The vehicle may provide an environment in which the agent
grows, multiplies or produces toxins.
➔Vector-borne (mechanical or biologic)
◆ Mosquitoes, fleas or ticks may carry an infectious agent through
purely mechanical means or may support growth or changes in the
agent
◆ In biologic transmission, the causative agent undergoes maturation
in an intermediate host before it can be transmitted to humans

c. Break in the Skin Integrity

❏Intact skin is the first line of defense against
infection
❏A breaking the skin integrity may result in
infection.
5. Portal of Entry
▪ This how the microorganism enters the host
▪ Refers to the manner in which a pathogen enters a susceptible
host
▪ The portal of entry must provide access to tissues in which the
pathogen can multiply or a toxin can act
5. Portal of Entry
▪ Often, infectious agents use the same portal that they used to exit
the source host in entering a new host.
▪ In a fecal-oral route, the agent leaves the source host in feces
and are carried on inadequately washed hands to a vehicle such
as food, water, or utensils and enter a new host through the
mouth.
6. Susceptible Host
▪ The final link in the chain of infection
▪ Susceptibility of the host depends on genetic or constitutional
factors, specific immunity and nonspecific factors that affect an
individual’s ability to resist infection or to limit pathogenicity
▪ An individual’s genetic makeup may either increase or decrease
susceptibility
▪ Specific immunity refers to protective antibodies that are
directed against a specific agent such as antibodies that may
develop in response to infection, vaccines or toxoids or may be
acquired by transplacental transfer from mother to fetus or by
injection of antitoxin or immunoglobulin
6. Susceptible Host
▪ Nonspecific factors that defend against infection include the skin,
mucus membrane, gastric acid, cilia in the respiratory tract, the
cough reflex and nonspecific immune response
▪ Factors that may increase susceptibility to infection by disrupting
host defenses are:
❖ Malnutrition
❖ Alcoholism
❖ Disease
❖ Therapy that impairs the nonspecific immune response
- END -
Immunology and
Inflammatory
INTRODUCTION
Objectives:
❖Recall the basic components and major functions of the immune system;
❖Compare the structure and functions of the primary and secondary
lymphatic organs and tissues;
❖To identify other component of Immune System that aids in Immune
response
Review on Anatomy and
Physiology of the Immune
/Lymphatic System
Immune System
➢Comprises CELLS & MOLECULES
➢Functions as the body’s defense mechanism against invasion

“Immunity”
➢Refers to the body’s specific protective response to an invading
foreign agent or organism.
Lymphatic System
“major part of immune system”

Primary functions of Lymphatic System

1.Draining excess interstitial fluids
2.Transporting dietary lipids
3.Carrying out immune responses
Component of Lymphatic System
1. LYMPH :
✓Means LIMF =“ CLEAR WATER” in Latin
✓The fluid that flows inside Lymphatic vessels and lymph nodes ( whole
lymphatic system) after it passes through the interstitial space.

❑ The major difference between interstitial fluid and lymph is location:

Interstitial fluid is found between cells, and lymph is located within
lymphatic vessels and lymphatic tissue.
Lymph Formation
*As protein concentration in interstitial
spaces increases, its pressure increases.

*Increasing pressure forces tissue fluid

into lymphatic capillaries.

*Lymph formation prevents accumulation

of excess tissue fluid (i.e. prevents edema)
Component of Lymphatic System
2. Lymphatic Vessel
➢A pathway of lymph which resemble small veins in structure but have thinner walls and more
valves.
➢At intervals along the lymphatic vessels, lymph flows through lymph nodes, encapsulated bean
shaped organs consisting of masses of B cells and T cells.

Location:
• In the skin, lymphatic vessels lie in the subcutaneous tissue and generally follow the same
route as veins.
• Lymphatic vessels of the viscera generally follow arteries, forming plexuses (networks) around
them.
Component of Lymphatic System
3. Lymph nodes
4. Lymphatic Organs
Lymphatic Pathways
lymphatic capillaries

afferent lymphatic vessels

LYMPH NODES
lymph nodes

efferent lymphatic vessels

 LYMPHATIC TRUNK

two collecting ducts

COLLECTING DUCTS (2)

subclavian
SUBCLAVIANveins
VEIN
CVS
Organs of Lymphatic System
Based on the Functions:

1.Primary Lymphatic Organs

• Bone Marrow
• Thymus

2.Secondary Lymphatic Organs

• Lymph Nodes
• Lymph Nodules
◦ Tonsils
◦ Peyer’s Patches
• Spleen
I. Primary Lymphatic Organ

A. Bone Marrow - WBC

(Leukocytes)
◦ Found in medullary cavities of LONG
BONES & spaces of SPONGY Bone
B Cells – mature in bone marrow
T Cells migrate going to Thymus.
I. Primary Lymphatic Organ
B. Thymus
➢bilobed organ (mediastinum
between sternum & aorta)

Lobule – Outer cortex

➢Large number of T cells

Central medulla
➢widely scattered, more mature T cells
Thymus Gland
Cells in the THYMUS are:
Thymic stromal cell
✓Thymic cortical epithelial cells
✓Thymic medullary epithelial cells
✓Dendritic cells

Cells of hematopoietic origin

✓Developing T-cells = thymocytes
FUNCTIONS:
❖Immature T cells migrates

❖The epithelial cells secrete a hormone called thymosin

❖The site of maturation of T cells

II. Secondary Lymphatic Organs

A. Lymph Nodes
❑containing large numbers of leukocytes
❑mammary glands, axillae & groin

Functions: to filter lymph

serve as a center for the production of PHAGOCYTES
B. Lymph Nodules
small, localized collection of lymphoid tissue, usually located
in the loose connective tissue beneath wet epithelial
(covering or lining) membranes, as in the digestive system,
respiratory system, and urinary bladder.

It differs from lymph nodes in that it is much smaller and

does not have a well-defined connective-tissue capsule as a
boundary. It also does not function as a filter, because it is
not located along a lymphatic vessel.
◦ Tonsils
◦ Peyer’s Patches
C. Spleen
is located in the upper left portion of
the abdominal cavity (behind
stomach).

Contains 2 types of tissue:

a. White pulp = contains lymphocytes
& macrophages
b. Red pulp = site for old and injured
RBC’s to be destroyed
 Functions of Spleen
❖ Removal and destruction of foreign particles and worn blood cells from
blood.
❖ Stores and releases blood during hemorrhage.
❖ Site of B cell proliferation into plasma cells.
❖ Storage of platelets, 1/3 of body supply
❖ Production of cells during fetal life
Other Component of Immune System
WBC “Leukocytes”
➢are cells of the immune system involved in defending the body against both
infectious disease and foreign materials
Basic Types of Leukocytes
A. Phagocytes
➢Cells that “chew up” invading organism
B. Lymphocytes
➢ cells that allow the body to remember and recognize previous invaders and help the
body destroy them.
A. Phagocytic Cells
Types of Phagocytic Cells

I. Granulocytes
◦ Neutrophils
◦ Eosinophils
◦ Basophils

II. Agranulocytes
◦ Monocytes
◦ Lymphocytes
I- Granulocytes
Neutrophils
➢62%
➢primarily fights BACTERIA, small particles
➢1st to arrive at the site of invasion
Eosinophils
➢2.3%
➢PARASITIC Worm
➢ Involve also in hypersensitivity response
Basophils
➢ 0.3 - 0.5% of WBC (.4%)
➢releases histamine, bradykinin, serotonin, leukotrienes in acute
hypersensitivity reaction.
II – AGRANULOCYTES
a. Monocytes
✓mature into macrophages when in
the body tissues or dendritic cell

❑Macrophages
✓Mature forms of blood monocytes
✓General scavenger cells of the body
✓Process & present antigen to specific
lymphocytes
II – AGRANULOCYTES
❑Dendritic cells
✓Together with macrophages, present
antigen to T cells
✓Found in lymphoid tissues and other
body areas where antigen enters the
body

✓They act as messengers between the

innate and the adaptive immune
systems.
B. Lymphocytes
represents 25 – 35% of blood leukocytes
➢involved in cellular and humoral immunity

3 Kinds of Lymphocytes
1. B lymphocytes - mature in the bone marrow and then enter the circulation.
2. T lymphocytes - move from the bone marrow to the thymus, where they mature into several
kinds of cells capable of different functions.
3. Natural killer cells / NK cells
• not identifiable as either T cells or B cells
• non specific effector cells that can kill tumor and virus infected cells
-End-
 IMMUNOLOGIC
DEFENSES
(Part 1)

&
INFLAMMATORY
RESPONSE
Gemshe M. Santos, RN

https://poweredtemplate.com/10098/0/index.html
Specific Objectives

❖ To identify the 2 types of Immunologic Defenses mainly

the Non Specific Defense and Specific Defense
❖ To know about the types of Non Specific Defenses and
it’s mechanism.
❖ To understand the Inflammatory Response as Non
specific Defenses, the Injury and Wound Healing
❖ Overview of Specific Defenses as part of the
Immunologic Defenses.
 WHAT IS IMMUNOLOGIC
DEFENSES?

❖Individuals have defenses that protect

the body from infection.

❖These defenses can be categorized as

nonspecific and specific.
 TYPES OF IMMUNOLOGIC
DEFENSES
1. Non specific resistance or Innate
Defenses

bodily defenses that protect a person

against all microorganisms, regardless of
prior exposure.
It includes anatomic and physiological
barriers and the inflammatory response.
1. NON SPECIFIC RESISTANCE

Types of Non Specific Resistance

A. External defenses/ 1st line of defense
B. Internal defenses/ 2nd line of defense

Mechanisms of Non Specific Resistance

A. Physical/mechanical barriers
B. Chemical barriers
 1ST LINE OF
DEFENSE/EXTERNAL DEFENSE
A.Physical Barriers:
➢ provides physical barriers to invaders

❖ Skin – A thick layer of dead cells in the epidermis provides

a physical barrier to viruses, bacteria, and microbes. As the
epidermis sheds, microbes are removed

❖ Mucous membranes – Mucous membranes produce

mucus to trap microbes so they cannot spread to the rest of
the body

❖ Hair – Hair within the nose filters microbes, dust, and

pollutants from the air to prevent them from invading the
body
A.Physical Barriers:
❖ Cilia – Cilia lines the upper respiratory tract and traps
and propels inhaled debris to the throat so it can exit the
body more quickly

❖ Urine – Urine flushes microbes out of the body

via the urethra
❖ Defecation and vomiting – The body expels
microorganisms via bowel movements and vomit.
B. Chemical Barriers:
❖ Lysozyme – Lysozyme is an enzyme produced in
tears, sweat, and saliva that breaks down cell walls and
acts as an antibiotic by killing bacteria
❖ Gastric juice – Acids in the stomach destroy bacteria
and toxins
❖ Saliva – Saliva dilutes the number of microorganisms in
the body and washes the teeth and mouth
❖ Acidity – Skin acidity inhibits bacterial growth
❖ Sebum – Unsaturated fatty acids known as sebum
provide a protective film on the skin and inhibits growth
❖ Hyaluronic acid – A gelatinous substance, hyaluronic
acid slows the spread of microorganisms that can harm
the body
 2nd LINE OF
DEFENSE/INTERNAL DEFENSE
A. ANTIMICROBIAL PROTEINS
❖ Interferons - released by host cells in response to the
presence of pathogens (viruses, bacteria, parasites or tumor
cells)
❖ Complement - refers to a group of least 20 plasma proteins
that normally circulate in the blood in an inactive state. Its
activation unleashes chemical mediators that amplify virtually
all aspects of inflammatory process

❖ Transferrin - iron-binding CHONs that inhibit the growth of

certain bacteria by reducing the amount of available iron
 2nd LINE OF
DEFENSE/INTERNAL DEFENSE

B. NATURAL KILLER CELLS

Kills a wide variety infectious microbes and certain tumor cells

Ways:
1. Release of perforins - chemicals inserted
into plasma membrane à leaky
2. Release molecules that may cause
apoptosis
 2nd LINE OF
DEFENSE/INTERNAL DEFENSE

C. PHAGOCYTES
➢ Phagocytic cells ingest and destroy microbes that pass
into body tissues

Phases of Phagocytosis:
CHEMOTAXIS: Chemically stimulated
movement of phagocytes to a site of damage

ADHERENCE: Attachment of the phagocyte to

the microbe or other foreign material
Phases of Phagocytosis:

INGESTION: Process of engulfing the

microbes and forms a vesicle

DIGESTION: Phagosome + lysosome-

microbe-containing vesicle fuses with a
lysosome which breaks down the molecule
into simpler components.

KILLING: Release of lysozyme, other digestive

enzymes, lethal oxidants
 2nd LINE OF
DEFENSE/INTERNAL DEFENSE
D. FEVER
➢ inhibits bacterial growth and increase the rate
of tissue repair when an infection is present in
the body

Effects:
❖Intensify interferon
❖Inhibits microbial growth
❖Speeds up body reactions
 2nd LINE OF
DEFENSE/INTERNAL DEFENSE
E. INFLAMMATION

➢ is a localized response in the tissue that

occurs when tissues are damaged or in
response to other stimuli. Inflammation occurs
when white blood cells flood an area of
invasion by microbes. The response includes
swelling, redness, heat, and pain
Stages of Inflammatory Response:
➢ The inflammatory response is a major function of the natural
(nonspecific or innate) immune system elicited in response to tissue
injury or invading organisms.
➢ Inflammation represents the response of body tissue to immune
reactions, injury, or ischemic damage.

I. Vasodilation & Increased Blood vessel permeability

A. Substances:
❖ Histamine
❖ Kinins (polypeptide) - inactive precursor, kininogens and affects
some nerve endings
❖ Prostaglandins (lipids) - released by damaged cells, stimulates
emigration, intensifies histamine and kinins; Intensify and prolong
pain.
❖ Leukotrienes (LTs)- chemotactic agent
❖ Complement - stimulate release of Histamines and chemotactic
agent
I. Vasodilation & Increased Blood vessel permeability

B. Chemical mediators assist this response

by:
• minimizing blood loss,
• walling off the invading organism
• activating phagocytes
• promoting formation of fibrous scar tissue and
regeneration of injured tissue
Stages of Inflammatory Response:

II. Emigration of Phagocytes

✓ Within an hour after, phagocytes appear on the

scene
✓ Neutrophils begin to squeeze through the wall
of the blood vessel called Emigration
✓ Monocytes follow neutrophils
Stages of Inflammatory Response:

III. Tissue Repair

❖ When tissues are injured during infection or following toxic or

mechanical injury, an inflammatory response is induced in
response to damage-associated molecular patterns (DAMPs)
and pathogen-associated molecular patterns (PAMPs) released
by dead and dying cells and invading organisms. These
molecular triggers induce a complex inflammatory response that
is characterized by the recruitment, proliferation, and activation of
a variety of immune cells including neutrophils, macrophages,
NK cells, B cells, T cells, fibroblasts and endothelial cells that
together make up the cellular response that orchestrates tissue
repair.
 Main Features of Inflammatory
Response

1. Vasodilation
2. Increase vascular permeability
3. Cellular Infiltration
4. Changes in Biosynthetic Profile of Organs
5. Activation of the Immune System
Classic Response to Inflammation

5 Cardinal Signs: PRISH

• P – pain (dolor)
• R – redness (rubor)
• I – immobility (functio laesa)
• S – swelling (tumor)
• H – heat (calor)
I. Acute Inflammation
A. VASCULAR RESPONSE:

✓Increase blood flow to the local

area
✓Mobilize the transport cells to the
area
✓Initiate healing
B. CELLULAR RESPONSE

Key players in Tissue:

1. Leukocyte [WBC] (granulocyte-
neutrophils)
a. Emigration of Phagocytes
❖Margination
❖Diapedesis

2. Erythrocyte [RBC]
a. Leak to tissue → hemorrhage
B. CELLULAR RESPONSE

Key players in Vessel:

1. Fibrinogen
2. Fibronectin
3. Platelets
4. RBC – “rouleau”
WBC Function in Cellular Response

• Destroying infective organism

• Remove damage cell
• Releasing more inflammatory
mediators
✓ control further inflammation
✓ healing
Chemical mediators assist this
response by:

✓ minimizing blood loss,

✓ walling off the invading organism,
✓ activating phagocytes,
✓ and promoting formation of fibrous scar
tissue and regeneration of injured tissue
Other Effects of Inflammation

1. Production of acute phase proteins

(Ex: complement)
2. Fever → pyrogens acting on
hypothalamus
3. Systemic immunity → lymphocyte
activation (peripheral lymphoid tissues)
VASCULAR PHASE
CELLULAR PHASE
Local Manifestations of Inflammation
Serous exudates
– watery fluids
– result from plasma entering the inflammatory
site

• Hemorrhagic exudates
- severe tissue injury
- damage to blood vessels
- leakage of red cells from capillaries.
Fibrinous exudates
- contain fibrinogen
- form a blood clot

Membranous or
pseudomembranous exudates
-develop on mucous membrane
surfaces
- composed of necrotic cells
enmeshed in a fibropurulent
exudate.
• Purulent or suppurative exudate -
contains pus, which is composed of
degraded white blood cells, proteins,
and tissue debris
• Abscesses
- typically have a central necrotic core
containing purulent exudates
surrounded by a layer of neutrophils.
Ulceration

- Refers to a site of
inflammation where an
epithelial surface (e.g., skin
or gastrointestinal
epithelium) has become
necrotic and eroded, often
with associated
subepithelial inflammation.
II. CHRONIC INFLAMMATION

CELLULAR RESPONSE
• If the damage is sufficiently severe, a chronic
cellular response may follow over the next few
days.
• A characteristic of this phase of inflammation is
the appearance of a mononuclear cell infiltrate
composed of
1.Macrophages -- involved in microbial killing, in
clearing up cellular and tissue debris, and they also
seem to be very important in remodeling the tissues.
2. Lymphocyte
III. FLUID EXUDATION
- Most active: 24 hours after injury
or invasion.

- Fibrinogen is converted into thick

network of fibrin threads to clot
isolates the invading microbes
and their toxins.

Exudative Component:
It involves movement of
1. Plasma fluid
2. Immunoglobulins
IV. Healing: Reconstruction & Maturation

1. Reconstruction
Begins once the inflamed
area is cleaned and
debrided, producing new
cells to fill in the space left
by the injury.

2. Maturation
Scar tissue is remodeled,
capillaries contract,
structure and function of
damaged tissue is restored.
ABBERANT TO HEALING
✓ May cause complications, deformity and decrease function
of the injured tissue results from abnormality in healing
mechanisms.

1) Exuberant granulations and keloids

Keloids- excessive, bulging, tumorous scars that extend
beyond the confines of the original wound and seldom
regress.
2. Excessive Contracture
✓ wound that continues to contract
after closure and produces
disfiguring scar or disability.

3. Adhesion
✓ Exudates cause scar tissue to
bind or adhere to adjacent
surfaces
4. DEHISCINCE AND EVISCERATION
❖ Dehiscence (wound separation)- a surface
disruption that results in the bursting open of
a previously closed wound
❖ Evisceration – refers to internal organs
moving through a dehiscence
Wound Healing

• Primary objective is to fill the gap

created by tissue destruction and
restore the structural continuity of the
injured part

• Depending on the extent of tissue loss,

wound closure and healing occur by
primary or secondary intention.
Phases of Wound Healing
A. Inflammatory Response
Signs & Symptoms
✓ pain
✓ warmth
✓ swelling
✓ palpable tenderness
✓ limitation in joint or muscle range of motion

Focus of Care
✓ decrease pain and swelling
✓ prevent chronic inflammation
✓ maintain mobility and strength in adjacent areas while
injured areas are rested
B. Proliferative Phase

• Begins 2-3 days of injury and may last

as long as 8weeks
• Focus on building of new tissues to fill
the wound space
• Key cells: Fibroblast- connective tissue
that synthesize and secretes collagen
and intercellular elements needed for
wound healing
• Final component : epithelialization
Signs & Symptoms
✓ less warmth and swelling
✓ palpable tenderness decreases
✓ pain felt with tissue resistance or stretch of the
tissue

Focus of Care
✓ range of motion exercises
✓ joint mobilization
✓ scar mobilization to produce a mobile scar
✓ light loads to promote tissue remodel
C. Remodeling

• Begins approximately 3 weeks after

injury and can continue for 6 months or
longer
• Simultaneous synthesis of collagen by
fibroblast result to the architecture of
the scar becomes reoriented to
increase tensile strength of wound
Signs & Symptoms
✓ Improved range of motion and strength

Focus of Care
✓ stretching
✓ active contraction
✓ resistive loads
2. Specific Resistance
to Diseases
This system relies on antigens, which
are specific substances found in
foreign microbes.
Most antigens are proteins that serve
as the stimulus to produce an immune
response.
- END -
Immunologic Defense (part 2)
and
Immune Response
Gemshe M. Santos, RN

https://poweredtemplate.com/07141/0/index.html
Specific Objectives:
▪ To review the Non Specific Defenses
▪ To review the Specific Defense and know the
Immune Cells.
▪ To know about the Antigens and Specific
Antibody
▪ To learn about the types of Immunity and it's sub
type.
▪ To understand the Immune response and it’s
classification.
▪ To educate about Nursing responsibility in
vaccination
Let’s recall...

Non specific resistance or Innate Defenses

bodily defenses that protect a person against all microorganisms, regardless of prior
exposure.
It includes anatomic and physiological barriers and the inflammatory response

Types of Immunity:
1. Natural (Innate) Immunity - also called in born/inherent
immunity
A. Physical barrier: Skin and Mucous membrane
B. Chemical barrier substance produced by the body cellular barrier: Saliva

Note:
Natural ( Innate) Immunity uses Non specific/ Innate Defenses in the form of
Physical and Chemical barrier externally( first line of defense) whereas releasing of
Antimicrobial proteins and NK cells, Activates Inflammatory response and promotes
phagocytoses, internally (2nd line of defense).
Let’s recall…

Specific Resistance/ Adaptive Defenses

This system relies on antigens, which are specific substances found in
foreign microbes.
Most antigens are proteins that serve as the stimulus to produce an
immune response.

Types of Immunity:
2. Acquired (Adaptive) Immunity
-Consists of immunological responses that are not present at birth but
acquired throughout life.
-Developed after exposure to the disease and immunization

Note:
Acquired ( Adaptive) Immunity uses Specific Resistance/Adaptive
defenses against pathogens through Antigen Presenting Cell that activates
the B lymphocytes and T lymphocytes.
In Bone Marrow, Hematopoiesis happen forming to RBC and
WBC ( leukocytes). Hematopoiesis starts with Multipotent
hematopoietic cells that develops in different cell type. Some
becomes Myeloid Progenitor cell ( Cells in Innate Defense)
and others are Lymphoid progenitor cells ( Cells in Adaptive
defense). Lymphoid progenitor cell becomes lymphoid cells
which are the NK cell (Innate Defense Cell), B cells and T
cells ( Main Cells in Adaptive Defense).
Immune Cells of Non Specific Defenses
A. B-cells or B lymphocytes:
❖ Cells that derived from the bone marrow important for producing a
humoral immune response.

❖ Lymphocyte cells that are important in producing circulating

antibodies that are programmed to produce one specific antibody.
On encountering a specific antigen, B cells stimulate production of
plasma cells, the site of antibody production. The result is the
outpouring of antibodies for the purpose of destroying and removing
the antigens.
Immune Cells of Non Specific Defenses
B. T-cells or T lymphocytes:

❖ Cells that derived from the thymus

❖ Lymphocyte cells that can cause graft rejection, kill foreign cells, or
suppress production of antibodies
❖ T cells, or T lymphocytes, assist the B cells. T cells secrete substances
that direct the flow of cell activity, destroy target cells, and stimulate the
macrophages. The macrophages present the antigens to the T cells
and initiate the immune response. They also digest antigens and assist
in removing cells and other debris. Unlike a specific antibody, a T cell
does not bind free antigens.
C. Maturation of T and B cells

❖Lymphocytes originate from stem cells

in the bone marrow. B lymphocytes
mature in the bone marrow before
entering the bloodstream, whereas T
lymphocytes mature in the thymus,
where they also differentiate into cells
with various functions
ANTIGEN
• Any substance capable of exciting the immune
system and provoking an immune response
• Examples of common antigens
– Foreign proteins
– Nucleic acids
– Large carbohydrates
– Some lipids
– Pollen grains
– Microorganisms
Functional properties of Antigen
• Immunogenicity
- is the ability to stimulate proliferation of
specific lymphocytes and antibody
• Reactivity
- is the ability to react or activate
lymphocytes and the antibody by
immunogenic reaction
SELF ANTIGENS
• Our immune cells do not attack our own
proteins
• Our cells in another person’s body can
trigger an immune response because
they are foreign
– Restricts donors for transplants
Antigen Presenting Cells (APC)

Functions:
- to engulf antigens and present
fragments of them, like signal flags, on
their own surfaces where they can be
recognized by T cells
PROCESSING OF ANTIGENS
Exogenous Antigen
➢ Bacteria and toxins, worm parasites, pollen, dust,
viruses
▪ Antigen Presenting Cells (APC)
- Process Exogenous Antigens:
• Macrophages, B cells, Dendritic cell

Endogenous Antigen
✓ Foreign antigens that are synthesized within a
body cell
✓ Viral Proteins , abnormal Proteins
✓ Antigen fragment- MHC I complex
Antibody
• Also called “Ig” or immuno
globulins or gamma globulins

• Proteins produced by plasma

cells in response to foreign
antigens.
ANTIBODY CLASSES

5 Types of
Immunnoglobulins
1.Ig G
2.Ig A
3.Ig M
4.Ig E
5.Ig D
Immunoglobulin G (Ig G)
✓ 80% Present in tissues and serum
✓ Major role in bloodborne and tissue infections
✓ Crosses the placenta
✓ Enhances phagocytosis
Immunoglobulin A (Ig A)

✓ 10-15 % Sweat, tears, mucus,

breastmilk, GI secretions
✓ Tends to decrease during
stress
✓ Helps prevent attachment of
antigen to epithelial cells
surface
Immunoglobulin M (Ig M)
✓ 5-10 %
✓ Limited to vascular system
✓ First Immunoglobulin produced in
response to bacterial & viral infxn
✓ Agglutinating agent and activates
complement
 Immunoglobulin E (Ig E)
Ig E
✓ 0-1 %
✓ Present in serum
✓ Involved in allergic and hypersensitivity rxn
✓ Help defense against parasites
Immunoglobulin D (Ig D)

✓ Location: B Lymphocytes
✓ Receptors on B lymphocytes
✓ Total: 0.2%

• Functions mainly as an antigen receptor on

B cells that have not been exposed to
antigens.
• It has been shown to activate basophils and
mast cells to produce antimicrobial factors.
Classificatio % Characteristics
n
IgG 75 Found in all body fluids
Responsible for newborn protection
Major antiviral, antitoxin, and antibacterial
antibodies
IgA 15 Predominant in body’s secretion such as saliva,
nasal secretions, breast milk, sweat and respi,
GI, GU secretions
Protects mucous membranes
IgM 10 Usually found in vascular system
Dominant activity in primary or initial immune
response
Forms natural antibodies such as for ABO
blood antigen
IgD 0.2 Action not known, may affect B cell maturation

IgE 0.004 Binds to mast cells and basophils, involved in

allergic reaction and parasitis infection
 ANTIBODY FUNCTION

• Antibodies inactivate antigens in a number

of ways
– Complement fixation
– Neutralization
– Agglutination
– Precipitation
During Action of Antibody

1. Neutralizing
2. Immobilizing bacteria
3. Agglutinating and precipitating Ag
4. Activating complement system
5. Enhancing phagocytosis
Types of Antigen-antibody Reaction
Types of Antigen-Antibody Reaction
✓ The immunologic defenses are developed by the
body of the person being defended.

✓ Is a temporary type of immunity transmitted from

one source that has developed immunity through
previous disease or immunization.
✓ Always temporary, lasting a few weeks to a few
months
❑ Antibodies from another source eventually
breakdown
The person has recovered from a disease and now has
antibodies and memory cells specific for that pathogen.

Result of the vaccine that stimulated production of

antibodies and memory cells.
Antibodies from the mother are transferred to the
baby across the placenta or in milk

Antibodies produced by another person are

injected or infused
 Acquisition of immunity Development Duration

Active a. Natural - exposed to develops long term;

often lifetime
antigens, by having the disease slowly;
ex. Chickenpox protective
levels reached
in a few weeks
b. Artificial – immunization develops Several years;
extended
with antigen slowly;
protection
ex. Vaccines, toxoids protective with
levels reached “booster”
in a few weeks doses

Temporary,
Passive a. Natural – transplacental immediate several
and colostrum transfer from
months
mother to child
ex. Breastfeeding

immediate Temporary,
b. Artificial – ready made several weeks
antibodies
ex. HTIG
Nursing Responsibilities in Vaccination
Vaccines can protect one’s health and the health of the community.
Efficacy and safety of vaccines can be enhanced by using education,
enforcement and engineering in which a nurse or health care provider
plays a key role.

This includes the following:

▪ Proper storage and handling of vaccines
▪ Never administer vaccines later than expiration date
▪ Administer vaccines within prescribed time periods
following reconstitution
▪ Administer immunization following the protocol in right
administration of medicine
Nursing Responsibilities in Vaccination

▪ Record vaccine and administration information in the

patient’s record
▪ Never mix vaccines in the same syringe unless approved for
mixing by the FDA
▪ Infuse proper aseptic technique and infection control
▪ Screen patients for contraindication and precautions
▪ Prepare to manage vaccine side effects
▪ Report suspected side effects of vaccine to authority
▪ Provide health teaching regarding schedules of
immunization activity
▪ Discuss common side effects of vaccine with patient or
guardian
 IMMUNE RESPONSE
✓ Is how your body recognizes and defends itself
against bacteria, viruses, and substances that
appear foreign and harmful.

Stages of Immune response:

❖ RECOGNITION STAGE
▪ Body accomplishes recognition using lymph nodes and
lymphocytes for surveillance
▪ Continuously discharge small lymphocytes into the
bloodstream.
▪ Macrophages, neutrophils & complement help
 Stages of Immune response
❖ PROLIFERATION STAGE
▪ the sensitized lymphocyte stimulates some of the
resident dormant T and B lymphocytes to enlarge,
divide, and proliferate.
▪ T lymphocytes differentiate into cytotoxic (or killer) T
cells, whereas B lymphocytes produce and release
antibodies.

❖ RESPONSE STAGE
▪ Actual humoral and cell-mediated immune
response

❖ EFFECTOR STAGE
▪ total destruction of the invading microbes or the
complete neutralization of the toxin
 IMMUNE RESPONSE
I. Humoral immunity (Antibody-Mediated
Immunity) Immune Response
Transformation of B cells to plasma cells
Dominated by B lymphocytes

Works mainly against:

▪ Antigens dissolved in body fluids
▪ Extracellular pathogen (bacteria)
 I. Humoral immunity (Antibody-Mediated
Immunity) Immune Response

❖ B lymphocytes with specific receptors bind to a specific antigen.

The binding event activates the lymphocyte to undergo clonal
selection. A large number of clones are produced (primary
humoral response)

❖ Most B cells become plasma cells produce antibodies to destroy

antigens, activity lasts for four or five day. Some B cells become
long-lived memory cells (secondary humoral response)

Secondary humoral response:

Memory cells are long-lived
A second exposure causes a rapid response
The secondary response is stronger and longer lasting
II. Cell – Mediated Immunity
• Dominated by T lymphocytes
• Needs the signal of TCR and APC for immune
response to occur
• Particularly effective against: cells attacking
cells.
✓ intracellular pathogen (parasites, fungi, viruses)
✓ some cancer cells
✓ foreign tissue transplant
• Often termed as delayed hypersensitivity
T lymphocytes
– on exposure to antigen, proliferate and
differentiate into:
❖Helper T cells -activated upon recognition of
antigen & stimulates the rest of immune response
❖Suppressor T cells- has the ability to decrease
B cell production, thereby keeping immune
response at the level compatible with health
 ❖Memory T cells- responsible for recognizing
antigens from previous exposure and mounting
an immune response
▪ Are programmed to recognize the original
invading antigen

❖Cytotoxic T cells/T8 cells- attach the antigen

directly by altering the cell membrane and
causing cell lysis (disintegration) and releasing
cytolytic enzymes & cytokines
▪ Perforin and lymphotoxin
❖
Comparison of Humoral Immunity &
Cell Mediated Immunity
Characteristics Humoral Cell Mediated
Immunity Immunity

Cells Involved B Lymphocytes T Lymphocytes,

macrophages

Products Antibodies Sensitized T Cells,

cytokines

Memory Cells Present Present

Protection Bacteria
Viruses (extracellular)
Fungus
Viruses (Intracellular)
Respiratory & Chronic infectious agents
Gastrointestinal pathogens Tumor Cells

Examples Anaphylactic Shock

Atopic diseases
Tuberculosis
Fungal Infections
Transfusion reaction Contact dermatitis
Bacterial infections Graft rejection
Destruction of Cancer Cells
 DIFFERENCES BETWEEN
T-CELL & B-CELLS

PROPERTIES B-CELL T-CELL

ORIGIN BONE MARROW THYMUS

POSITION OUTSIDE LYMPH INTERIOR OF LYMPH

NODE NODE
CAN CONNECT TO Ag CAN ONLY CONNECT TO
CONNECTIONS RIGHT ON THE SURFACE VIRUS Ag ON THE
OF VIRUS & BACTERIA OUTSIDE OF INFECTED
CELL

LIFE SPAN SHORT LONG

 PROPERTIES B CELL T CELL

SURFACE ANTIBODY PRESENT ABSENT

SECRETIONS ANTIBODIES LYMPHOKINES

FORM KILLER, HELPER

FORMATION PLASMA CELL & & SUPRESSOR CELL
MEMORY CELL
MOVEMENT TO PLASMA CELL DO NOT LYMPHOBLAST MOVE
INFECTION SITE MOVE TO SITE OF TO THE SITE OF
INFECTION INFECTION

BLOOD 20% OF LYMPHOCYTE 80% OF LYMPHOCYTE

 PROPERTIES B CELL T CELL

FUNCTIONS FIGHTS VIRUS & INCLUDES FUNGI

BACTERIA

NO INHIBITORY SUPRESSOR CELL

EFFECT INHIBIT

DO NOT REACT KILLER CELL AGAINST

AGAINST TRANSPLANT TRANSPLANT &
& CANCER CELL CANCER CELL

HUMORAL OR Ab CELL MEDIATED

MEDIATED IMMUNE IMMUNE SYSTEM
SYSTEM
III. Complement System (innate
immunity)

✓ promotes inflammatory process

✓ The complement system consists of a number of small
proteins found in the blood

Major effects:
a. Cytolysis – lysis and destruction of cell membranes of body
cells or pathogens
b. Opsonization – targeting of the antigen so it can be easily
engulfed and digested by the macrophages and other
phagocytic cells
c. Chemotaxis – chemical attraction of neutrophils and
phagocytic cells to the antigen
d. Anaphylaxis – activation of mast cells and basophils
Cytokines
• Regulatory proteins that are produced during all phases of
an immune response

• Molecules that form a communication link between immune

cells & other tissues & organs of the body

a. Interleukin 1 / IL-1 : mediator of the inflammatory response

b. Interleukin 2 / IL – 2 : necessary for the proliferation and function

of helper T, cytotoxic T, B cells, & NK cells

c. Interferons / IFNs : protect neighboring cells from invasion by

intracellular parasites, including viruses, rickettsia, malarial
parasites and other organisms
_ END _
ASSESSMENT &
DIAGNOSTIC
EXAM
GEMSHE M. SANTOS, RN
Health History
Physical Examination

A.

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Physical Examination

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Physical Examination

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Physical Examination

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Physical Examination

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Physical Examination
G.

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❖
❖
COMMON DIAGNOSTIC EXAMINATION

autoimmune diseases
immune deficiencies blood disorders.
COMMON DIAGNOSTIC EXAMINATION
COMMON DIAGNOSTIC EXAMINATION

bone marrow disease cancer.

●
▪
▪
COMMON DIAGNOSTIC EXAMINATION

❖
▪
▪
▪
▪
❖
❏
❏
❏
COMMON DIAGNOSTIC EXAMINATION

▪
COMMON DIAGNOSTIC EXAMINATION

▪
OTHER TEST:

❖ Enzyme-linked Immunosorbent Assay (ELISA)

❖ Western blot

❖ CD4 and CD8 cell counts

❖ P24 antigen test

❖ Polymerase chain reaction (PCR)

❖ Phagocytic Cell Function Tests

- END-
https://poweredtemplate.com/coronavirus-3d-rendering-presentation-73052/

ALTERATION IN THE
IMMUNE RESPONSE
Gemshe M. Santos, RN
 Specific Objectives
• To know about the Different types of Immunologic disorder/
Immune Aberrations.
• To define the Immune Deficiency
• To focus in different classification of Immune Deficiency
• To be educated about the rare disorders and their sign and
symptoms

Note: This presentation is focus only Immune deficiency and it’s type.
Other types of Immunologic Disorder will be present differently.

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Immunologic Disorder
4 Primary Immune Aberrations:
I. Immune deficiency
II. Autoimmune Disorder
III. Allergy and Hypersensitivity
IV. Gammopathy
 Immunologic Disorder
What is Immune Deficiency?

✓ Abnormality in one or more branches of the immune system that

renders a person susceptible to diseases normally prevented by
an intact immune system
✓ may be caused by a defect or deficiency in phagocytic cells, B
lymphocytes, T lymphocytes, or the complement system.

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 2 Classification of Immunodeficiency:
1. Primary immune deficiency:
Congenital or inherited

2. Secondary immune deficiency:

Acquired later in life

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Primary Immune Deficiency
10 warning signs of Immune Deficiency:
1. 8 or more ear infections within 1 year
2. 2 or more sinus infections within 1 year
3. 2 or more antibiotics with little effects
4. 2 or more pneumonias in a year
5. Poor growth
 10 warning signs of Immune Deficiency:
6. Recurrent deep skin/ organ abscesses
7. Persistent thrush in mouth/ skin in a year
8. Need for intravenous antibiotics to clear infection
9. 2/more deep-seated infections
▪ (meningitis, cellulitis or sepsis)
10. A history of primary immune deficiency

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PRIMARY IMMUNODEFICIENCY
Other Symptoms:

✓ Frequent or unusual
infections
✓ prolonged diarrhea
✓ poor childhood growth
CHARACTERISTIC:

❖ Rare disorders with genetic origins

❖ Seen primarily in infants and young children.
❖ Symptoms usually develop early in life
❖ Seldom survive to adulthood
❖ May involve one or more components of the
immune system.
 1. Primary Immune Deficiency
Types of Inherited B- Cell Deficiencies

1st type:
✓ Lack of differentiation of B-cell (precursors into mature B cells)
✓ Plasma cell are lacking – leads to complete lack of antibody
production

2nd type
✓ Results from a lack of differentiation of B cells into plasma cells.
✓ Diminished antibody production called hypogammaglobulinemia,
is a frequently occurring immunodeficiency

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Inherited B- Cell Deficiencies
I. Antibody / B cells Immunodeficiency
A. X – Agammaglobulinemia (Bruton’s disease)
B. Hypogammaglobulinemia
C. Selective: IgA, IgM, IgG deficiency – lack of both
serum and secretory IgA
Inherited B- Cell Deficiencies
A. X – linked Agammaglobulinemia
✓ First immunodeficiency to be identified.
✓ Also known as Bruton Type Agammaglobulinemia
X – linked Infantile Agammaglobulinemia, or Congenital
Agammaglobulinemia.

❖ Bruton’s disease or Congenital Agammaglobulinemia

❖ Defect on maturation of B cells
❖ X – Linked inheritance – in about 6 mos. of age of a child (Ig
G is depleted)
Clinical Features
✓ Spleen, lymph nodes, tonsils, adenoids, Peyer’s patches
decrease in size or absent in individuals
✓ Ig G depleted
✓ Serious enteroviral infections
✓ Chronic pulmonary disease
✓ Skin disease
✓ Inflammatory bowel disease
▪ (UC and Chron’s disease)
✓ CNS complications
NOTE: T-lymphocytes elevated
Inherited B- Cell Deficiencies
B. Hypogammaglobulinemia
✓ Also known as Common Variable Immunodeficiency (CVID)
✓ Term that encompasses variety of defects (ranging from IgA
def.to panhypo-globulinemia)

• Defects ranging from immunoglobulin A (IgA) deficiency, in

which only the plasma cells that produce IgA are lacking,
to the other extreme, in which there is severe
panhypoglobulinemia (general lack of immunoglobulins
in the blood).
✓ Common in adult; all gender; occur in second decade of life(15-
35yo)
Clinical Features
✓ Growth Retardation
✓ Abnormalities in lymphoid tissues and
organs
✓ Skin and mucus membrane abnormalities
✓ Ear, nose, throat abnormalities.
✓ Pulmonary/ Cardiovascular / Neurologic
abnormalities
Other Manifestations:
Common sites are:
1. Inner ear: Otitis media
2. Sinuses: Sinusitis , rhinitis
3. Lower respiratory tract: Pneumonia, Bronchitis
4. meninges: Meningitis
5. Blood stream: Sepsis

❑ Diagnosis and treatment is similar to X-linked

Agammaglobulinemia
Diagnostic Tests
✓ Low, IgG : 200 mg/ dl,
✓ IgA, IgM, IgD, and IgE :
low or absent.
✓ White blood cell counts:
are normal,
✓ B – lymphocytes,:
absent
✓ T – cell responses:
Normal
Normal Level in Adult
IgA 80-350 mg/dl
IgG 620-1400 mg/dl

IgM 45-250 mg/dl

IgD .3-3 mg/dl
IgE .002-2 mg/dl
Treatment:
Goal: Maintain Ig G at 500mg/dl
❖ There is no cure for X – linked
Agammaglobulinemia

❖ Gammaglobulin Replacement therapy:

❖ IV Immunoglobulin G
• Dose of 300 mg/ kg every three weeks, or
more monthly ( life long maintenance)
Prognosis
❖ Without gammaglobulin treatment, these
patients may die from infections at an early age.
C. Selective IgA Deficiency
❖It is the total absence or severe
deficiency of IgA.
❖Blood serum levels for IgA
deficient persons are usually
found to be 7 mg/ dl
❖Usually asymptomatic.
Diagnostic:
✓ Ig A: 7 mg/dl or less

Treatment:
✓ No Cure
✓ Ig A Replacement
✓ Palliative: immunosuppressive therapy,
Antibiotics
Prognosis:
✓ Many persons with selective IgA deficiency live their
full life span without any problems.
Primary Immune Deficiency
II. T cell Immunodeficiency
✓ Defects in T cells lead to opportunistic infections. Most
primary T-cell immunodeficiencies are genetic in origin.
✓ Because the T cells play a regulatory role in immune
system function, the loss of T-cell function is usually
accompanied by some loss of B-cell activity
a. Hodgkin's disease ( See separate discussion/ Cancer Concept)
b. Di George’s Syndrome
c. Chronic Mucocutaneous Candidiasis
II. T cell Immunodeficiency
Di George’s Syndrome/ Thymic Hypoplasia

✓ A syndrome caused by the

deletion of a small piece
of chromosome 22
✓ Causing underdeveloped
thymus gland
Manifestations:
“CATCH”
C – cardiac abnormality
A – abnormal facies
T – thymic aplasia
C – cleft palate
H – hypoparathyroidism/
hypocalcemia
II. T cell Immunodeficiency
Chronic Mucocutaneous Candidiasis
✓ An autosomal recessive inheritance affecting the
thymus and endocrine glands.
✓ It is characterized by chronic infections with
Candida that are limited to mucosal surfaces, skin
& nails. However, it can also be associated with
other types of infections, such as Human
Papilloma Virus (HPV)
 Manifestations:
▪ Candida infection
▪ Nails may be markedly
thickened, fragmented, and
discolored
▪ Skin are hyperkeratotic

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Manifestations:
Lymphocyte count (Normal Value-: 16-45%)
✓ Less than 16%

MEDICAL/SURGICAL MNGT:
✓ P. carinii prophylaxis
✓ Management of hypocalcemia
✓ Treatment for CHF to pateints with
congenital disease.
✓ Administration of human leukocyte antigen
III. Combined B & T cell Immunodeficiency
A. Wiskott-Aldrich syndrome (WAS)

✓ X-linked recessive disease accompanied by

thrombocytopenia (low platelet count), eczema and bloody
diarrhea (secondary to the thrombocytopenia).

✓ It is also sometimes called the eczema-thrombocytopenia-

immunodeficiency syndrome in keeping with Aldrich's
original description in 1954
III. Combined B & T cell Immunodeficiency
B. Ataxia – telangiectasia
✓ Loss of muscle coordination and blood vessel dilation
✓ Also known as “Louis-Bar Syndrome”
✓ Autosomal recessive disorder
✓ With accompanying IgA, IgG, IgE deficiencies
✓ With cerebral ataxia, telangiectasis, recurrent infections
of the lungs and sinuses and increased incidence of
cancer.
Hallmark Signs:
❖ Ataxia – uncoordinated muscle
movement
❖ Telangiectasia – vascular lesions
caused by dilated blood vessels
❖ Usually appears in the first 4
years of life
❖ On 2nd decade of life – mental
retardation, lung disease and
physical disability becomes severe.
Medical Management

✓ Antimicrobial therapy
✓ Postural drainage and physical therapy for
lung conditions
✓ Transplantation of fetal thymus tissue and
IVIG administration.
IV. SEVERE COMBINED IMMUNODEFICIENCY
✓ “Bubble Boy Disease”,"Alymphocytosis," "Glanzmann–
Riniker syndrome," "Severe mixed immunodeficiency
syndrome," and "Thymic alymphoplasia
✓ is a genetic disorder in which both "arms" (B cells and T
cells ) of the adaptive immune system are impaired due
to a defect in one of several possible genes.
✓ Equates to an almost absent immune system

Characteristics:
- Lymphoid aplasia
- Thymic dysplasia.
• David Phillip Vetter (September 21,
1971 – February 22, 1984)

▪ He became famous for living in a sterile

environment. He was born without a
working immune system called Severe
combined immunodeficiency or (SCID),
even the most benign germ would kill
him.
8/29/2020 Designed by PoweredTemplate.com 35
Manifestations
✓ Onset of symptoms occurs within the first 3
months.
✓ Pneumonia and other respiratory infections
✓ Diarrhea
✓ Poor growth and development
✓ Vomiting
✓ Fever
✓ Skin rash
Medical Management
▪ IV I G administration
An ideal donor is an HLA- sibling
(HLA-human leukocye antigen)

Surgical Management
▪ Stem cell transplant
▪ Bone marrow transplant
▪ Thymus gland transplantation
IV. SEVERE COMBINED IMMUNODEFICIENCY

SWISS TYPE AGAMMAGLOBULINEMIA

❖ Affected children have lymphopenia
❖ Thymus is always hypoplastic or absent
.
❖ Lymph nodes are not visible
❖ Lymph nodes in tonsils, gut and appendix are hypoplastic
❖ Most die on the first year of life
IV. Phagocytic Cell Disorder

Characteristics:
- Increase incidence of bacterial and fungal infections
- Recurrent furunculosis
- Cutaneous abscesses
- Bronchitis, pneumonia
- Chronic otitis media and sinusitis
V. Phagocytic Cell Disorder
Hyperimmunoglobulinemia (formerly known as Job
syndrome)
✓ White blood cells cannot produce an inflammatory response to
the skin infections
✓ This results in deep-seated cold abscesses that lack the classic
signs and symptoms of inflammation (redness, heat, and pain).
V. Phagocytic Cell Disorder
Hyperimmunoglobulinemia (formerly known as Job
syndrome)
Clinical Features:
✓ May be asymptomatic
✓ Severe neutropenia
✓ Accompanied by deep and painful mouth ulcers,
gingivitis, stomatitis, and cellulitis
V. Phagocytic Cell Disorder
Chronic granulomatous disease
✓ produces recurrent or persistent infections of the soft
tissues, lungs, and other organs
✓ these are resistant to aggressive treatment with antibiotics

Characteristics:
▪ Excessive inflammation even when there is not an infection
▪ Diarrhea
▪ Bladder & kidney problems
MANAGEMENT:

P : rophylactic antibiotic
R : aw foods should be AVOIDED
O: PV/ live virus vaccines should be AVOIDED
T : each frequent handwashing
E : xercise
C: ontagious diseases should be avoided.
T : herapy – Bone marrow transplantation; IVIG
SECONDARY IMMUNODEFIENCY
❖ Secondary Immunodeficiencies are more common than
primary immunodeficiencies and frequently occur as a result of
underlying disease processes or from the treatment of these
diseases.
Common Causes: ✓ Certain viruses
✓ Malnutrition ✓ Exposure to immunotoxic medications
✓ Chronic stress and chemicals
✓ Burns ✓ Self-administration of recreational drugs
✓ Certain autoimmune disorders and alcohol.

❏ AIDS, the most common secondary immunodeficiency disorder. Patients

with secondary immunodeficiencies have immunosuppression and are often
referred to as immunocompromised hosts.
-END-
SECONDARY IMMUNODEFICIENCY
Gemshe M. Santos, RN
Acquired immunodeficiency
syndrome
 Human Immunodeficiency Virus ( HIV )

✓ is a Retrovirus that selectively attacks the CD4 + T lymphocytes, the immune

cell responsible for orchestrating and coordinating the immune response to
Infection.
✓ Major types: HIV1 & HIV2
✓ Incubation Period: 10 years

• H - Human: because this virus can only infect human beings.

• I - Immuno-deficiency: because the effect of the virus is to create a

deficiency, a failure to work properly, within the body's immune system.

• V - Virus: because this organism is a virus, which means one of its

characteristics is that it is incapable of reproducing by itself. It reproduces by
taking over the machinery of the human cell.
Transmission

3 Mode of transmission:
1. SEXUAL CONTACT
▪ Vaginal and anal sexual intercourse, oral
sex (1-3%)
(Cunnilingus-oral stimulation of vulva/clitoris,
fellatio- oral stimulation of penis)
Sources: Semen/Sharing Uncleaned Sex toys

2. IV DRUG USERS/BLOOD
▪ Needle sharing/ Blood transfusion

3. VERTICAL TRANSMISSION
PERINATAL
▪ During labor, delivery & breast feeding Infected
mother in the utero/ through intrapartum
inoculation/ breastfeeding
4 Requisite of Successful HIV Transmission:

▪ E = exit
▪ S = sufficient
▪ S = survive
▪ E = enter
Pathogenesis
Life Cycle of HIV
Life Cycle of HIV
1. Free HIV
2. HIV attaches to CD4 receptor site
3. Reverse transcriptase
4. HIV DNA penetrates T-cell nucleus
5. DNA replicates HIV virus using protease
6. Assembly of new HIV virus
7. Accumulation of viral RNA
8. Cell Death
 Acquired Immunodeficiency Syndrome (AIDS)

✓ Is an infectious disease of the immune system

caused by the retrovirus HIV-1.
✓ HIV/AIDS

❖ A - Acquired: because it's a condition one must acquire or

get infected with; not something transmitted through the
genes
❖ I - Immune: because it affects the body's immune system, the
part of the body which usually works to fight off germs such
as bacteria and viruses
❖ D - Deficiency: because it makes the immune system
deficient (makes it not work properly)
❖ S -Syndrome: because someone with AIDS may experience
a wide range of different diseases and opportunistic
infections.
Seroconversion
✓The point at which an infected
person converts to from being
negative for the presence of
HIV antibodies in the blood to
being positive

Window period
✓Time after infection and before
seroconversion
CLASSIFICATION OF HIV INFECTION:
 CD4 cells
• 650-1200 cells/mm3: competent
immune system

• 500-200 cells/mm3: suppressed

immune system

• <200 cells/mm3: AIDS!!!!!!!!!!!

(according to CDC)
 VIRAL LOAD

▪ <10,000 (low risk)

▪ 10,000-100,000 (moderate risk)
▪ 100,000> (high risk)
 Diagnostic: 3 conditions

1. Presence of HIV
2. T4 cell count is
below 200 (CD4)
3. Presence of 1 or
more of AIDS
specified conditions
 CDC Classification System for HIV
Infection

• Cat A= >500 cells/ul

• Cat B= 200- 499 cell/ul
• Cat C=< 200 cells/ul.
Clinical Categories: According to Clinical Manifestation

Manifestations
1.) CATEGORY A
– Includes person who are asymptomatic or
have persistent generalized
lymphadenopathies.

Primary HIV infection

– Fever, myalgias, night sweats, fatigue, sore
throat, GI problems, lymphadenopathies,
rashes, headache
Sign & Symptoms of Acute HIV Infection:

▪ Fever
▪ Fatigue
▪ Rash
▪ Headache
▪ Lymphadenopathy
▪ Pharyngitis
▪ Arthralgia
▪ Myalgias
▪ Night sweats
▪ GI problems: diarrhea
▪ Aseptic meningitis
▪ Oral and genital ulcers
 Clinical Categories: According to Clinical Manifestation

2.) CATEGORY B
✓ Persons with symptoms of immune
deficiency not serious enough to be
AIDS defining
✓ Median time is 10 years
✓ CD4 count falls gradually from the
normal range
Clinical Categories: According to Clinical Manifestation

3.) CATEGORY C
✓ Includes AIDS defining illness
✓ Patients have OPPORTUNISTIC
INFECTIONS
 AIDS DEFINING CONDITIONS:

• Opportunistic infections:
– Pneumocystis carinii
pneumonia (PCP)
– Candidiasis
– Cytomegalovirus
– Herpes simplex
– Mycobacterium avium
complex (MAC)
– Mycobacterium tuberculosis
– Recurrent pneumonia
– Histoplasmosis
 OPPORTUNISTIC INFECTIONS:
• 1. Pneumocystis Carinii
Pneumonia (PCP)

• The alveoli becomes filled

with foamy, protein rich
fluid that impairs gas
exchange.

• S&Sx: Mild cough, fever,

sob, weight loss.
 OPPORTUNISTIC INFECTIONS:

2. Mycobacterium tuberculosis

3. AIDS dementia complex

– Is a syndrome of cognitive and
motor dysfunction.
– Sx: Impairment in attention,
concentration and Slowing of
mental speed, agility, apathetic
behavior.
 OPPORTUNISTIC INFECTIONS:

4. Kaposi’s sarcoma
✓ Is a malignancy of the
endothelial cells that line
small blood vessel
✓ lesions are nodules or
blotches that may be red,
purple, brown, or black,
and are usually papular
OPPORTUNISTIC INFECTIONS:
HIV wasting syndrome
Caused by anorexia, metabolic abnormalities,
endocrine dysfunction, malabsorption and
cytokine dysregulation.
OPPORTUNISTIC INFECTIONS:
Gynecologic:
❖ Recurrent vaginal candidiasis,
❖ genital ulcer disease
❖ venereal warts
 DIAGNOSIS:

1. ELISA ( Enzyme Linked

Immunosorbent Assay)
2. Western Blot assay
(confirmatory)
3. Orasure- saliva
4. CD4 cell count
5. Polymerase chain reaction
(PCR)
 DIAGNOSIS:
ELISA & Western blot
• With (+) result
• Antibodies to HIV are present in blood
• HIV is PROBABLY active
• Despite HIV infection, client does not
necessary have AIDS
• Client is NOT IMMUNE to AIDS.
5 MEANS OF HIV PREVENTION

A = abstain from sex

B = be faithful
C = correct & consistent use of condom
D = do not use illegal drugs/share needles
E = educate yourself
HEALTH TEACHINGS FOCUSES ON:

❖ Promote Good Nutrition

❖ Promote Self Care
❖ Provide Counseling
 Other Management with AIDS:

✓ Identification of persons at risk

✓ Obtaining a complete, accurate sexual history is
important
✓ Identify if IV drug user
✓ Check for other risk factors
✓ With high risk for HIV/AIDS- counsel about
significant of testing and necessity for follow-up.
✓ Educational and Counseling strategies with AIDS.
.
 Guidelines for care of the person with HIV/AIDS:

✓ Prevent infection
✓ Wash hands frequently
✓ Use gentle soap; avoid bar soap that may
irritate skin.
✓ Provide for daily showering/ basin bath; avoid
tub bath if rashes are present.
 Guidelines for care of the person with HIV/AIDS:

• Use separate washcloth for lesions

• Use soft toothbrush, nonabrasive
toothpaste.
• Prevent skin breakdown
• Elevate and support areas of
edema
• Observe surgical site and IV
insertion sites daily for signs of
infection.
• Change dressings (if any) daily.
Guidelines for care of the person with HIV/AIDS:

• Avoid eating fresh fruits /

vegetables; uncooked/ “rare”
foods.
• Carry out infection control
measures according to
institution’s policy
• Administer prescribed
antibiotics, IV fluids/
antipyretics.
• Encourage increase OFI.
• Monitor daily I and O records
Guidelines for care of the person with HIV/AIDS:
.

• Weigh patient daily

• Instruct patient in deep breathing coughing
exercise- to PX: Atelectasis and fever
• Modify alterations with body temperature:
TSB, DBE, and Coughing
 PREGNANCY AND AIDS

• Zidovudine (AZT)- recommended for

prevention of maternal fetal HIV transmission
and administer AFTER 14 WEEKS AOG with
PO medicine; IVTT DURING LABOR; and to
the NEONATE post birth for 6 weeks.
• Nevirapine – reverse transcriptase inhibitor
 Post Partum Period

✓ Monitor for signs of infection

✓ Place mother in isolation if mother
is immunosuppressed.
✓ RESTRICT BREASTFEEDING!
✓ Infant/ neonate is seen by
physician at birth, 1 week, 2
weeks, 1 month, 2 month, and 4
months of life.
 CHILD WITH AIDS

• PCP prophylaxis 1-12 months

• (need for additional prophylaxis is
determined by CD4 counts)

• Immunizations.
– Ensure administration of
pneumococcal and influenza
vaccines. : prevents
streptococcal infection
– AVOID VARICELLA VACCINE
 Health teachings

1. Discard unused refrigerated

formula and food for 24⁰.
2. Change diapers frequently, clean
up spills with BLEACH solution
(10:1) ratio.
3. Provide high CHON, high calorie
diet; monitor weight daily.
4. Avoid exposing the child to other
illnesses.
 MEDICATIONS (Antiretroviral)

GOAL:
1. To suppress infection,
prolonging life.
2. To treat opportunistic
infection.
3. Effectiveness: monitored
by viral load count, CD4
cell counts (↑500)
• Nucleoside reverse transcriptase inhibitors
(NRTI) / nucleoside analogs
blocking the elongation of the DNA

e.g. Zidovudine (AZT, Retrovir), Didanosine

(DDI, Videx), Zalcitabine (DDC, HIVID)

• Protease inhibitors (protease- is a viral

enzyme) bind to the protease enzyme and inhibit its action
e.g. Ritonavir (Norvir), Indinavir (Crixivan)
• Non nucleoside reverse transcriptase inhibitors (NNRTI)
e.g. Nevirapine (Viramune), Delavirdine (Rescriptor)

• Others: Interferons: Alpha interferons, gamma-interferons

• Receive pneumococcal, influenza, hepatitis B, vaccines

• To prevent PCP/ the CD4 ↓200= Trimethoprim-

sulfamethoxazole (Pentamidine)
- END -
HYPERSENSITIVITY DISORDER
Gemshe M. Santos, R.N
 HYPERSENSITIVITY
❑refers to excessive, undesirable reactions
produced by the normal immune system.
❑is any heightened immune response to an
antigen
Chemical mediators
Primary Mediators
(Preformed and found in mast cells
or basophils)
1. Histamine (preformed in mast
cells)
2. Eosinophil chemotactic factor of
anaphylaxis (ECF-A)
(preformed in mast cells)
3. Platelet-activating factor (PAF)
(requires synthesis by mast
cells, neutrophils, and
macrophages)
4. Prostaglandins (chemically
derived from arachidonic acid;
require synthesis by cells)
Basophil kallikrein (preformed in
mast cells)
Action
1. Vasodilation
Smooth muscle contraction, increased
vascular permeability, increased
mucus secretions
2. Attracts eosinophils
Smooth muscle contraction
3. Incites platelets to aggregate and
release serotonin and histamine
4. D and F series →bronchoconstriction
E series →bronchodilation
D, E, and F series →vasodilation
Frees bradykinin, which causes
bronchoconstriction, vasodilation, and
nerve stimulation
Chemical mediators Action

Secondary Mediators
(Inactive precursors formed or
released in response to primary
mediators)

1. Bradykinin (derived from 1. Smooth muscle contraction,

precursor kininogen) increased vascular permeability,
stimulates pain receptors,
increased mucus production

2. Serotonin (preformed in 2. Smooth muscle contraction,

platelets) increased vascular permeability

3. Heparin (preformed in mast 3. Anticoagulant

cells)
4. Leukotrienes (derived from 4. Smooth muscle contraction,
arachidonic acid and activated by increased vascular permeability
mast cell degranulation) C, D, and
E or slow-reacting substance of
anaphylaxis (SRS-A)
Classification
• Type I – IgE mediated hypersensitivity

• Type II – Cytotoxic hypersensitivity

• Type III – Immune complex hypersensitivity

• Type IV – Delayed hypersensitivity

Type 1 Hypersensitivity
▪ Immediate hypersensitivity is
mediated by IgE.

Primary Cellular Component

• Mast cell
• Basophils
HYPERSENSITIVITY
• Allergy=damaging immune
response by the body to a
substance

• The antigen causes the

allergy is ALLERGEN
Type I Hypersensitivity
▪ Commonly called “allergic reactions”
▪ Systemic or anaphylactic reactions
▪ Local or atopic reactions (genetic)
 Rhinitis (hay fever)
 Food allergies
 Bronchial asthma
 Hives
 Atopic dermatitis
• SENSITIZATION STAGE: No
Signs & Symptoms

Antigen invades the body

Stimulates B lymphocytes

Plasma cells produce IgE

IgE attaches to mast cells in the

body tissue
• SUBSEQUENT RESPONSE:

More of the same allergens invade

the body

Allergens bind to the sensitized mast

cell

Degranulation of mast cell

Triggers release of chemical

mediators

Vasodilation; increase permeability;

smooth muscle spasm
 A. Anaphylaxis
▪ Most severe form of type 1
▪ Caused by common
allergens
▪ S& Sx: Itching, apprehension,
anasarca, circumoral edema,
wheezing, dyspnea, signs of
vascular collapse of shock
▪ Can lead to DEATH
Types:

1. Local (atopic) 2. Anaphylactic

reaction shock
Ex: urticaria (hives); - systemic, life
allergic rhinitis; threatening
food allergies;
bronchial asthma
Management
• AIRWAY is maintained
by ET or tracheostomy
as necessary
• IV fluids
• Vasopressors
▪ Give
EPINEPHRINE
1:1,000 solution,
0.3-0.5 ml sq/IM

▪ Antihistamine:
Benadryl IVTT

▪ Hydrocortisone
IVTT
Prevention
• Identification of high risk
person
• Patient education with
allergens if known
• Desensitization
B. Urticaria & Angioedema
• Urticaria usually
caused by food
allergen: eggs, fish,
nuts, seafoods,
meds.
• S& Sx: pruritic
lesions with pale,
pink wheal on an
erythematous
background
❖Angioedema – form of urticaria but
.
involves subcutaneous tissue rather
than skin

❖S& Sx: hives, swollen lips, periorbital

edema

❖Management: Epinephrine,
Antihistamine, Corticosteroids
C. Atopic Allergy
✓Less severe form type 1
✓Common forms: Hay fever, atopic
dermatitis
✓Called “atopic” since majority of
population do not react to antigens
✓Reacts to pollen, fungal spores,
house dust, feathers
TYPE II CYTOTOXIC HYPERSENSITIVITY
REACTION

• IgG or IgM antibodies directed

against target antigens on the
surface cells or other tissue
components
Ex:
- Mismatched BT reactions
- Hemolytic disease of the
newborn due to ABO or Rh
incompatibility
- Certain drug reactions
• Primary Cellular Component:
✓ Ig M
✓ Ig G
✓ Complement System
 TYPE II CYTOTOXIC
HYPERSENSITIVITY REACTION
Antigen attached to foreign cell or tissue

Plasma cells produce IgG or IgM

Antibodies bind to tissue specific

antigens

Stimulate complement activation

Destruction of target cells by lysis,

phagocytosis or activation of killer
cells
TYPE II: DISORDERS

• Autoimmune hemolytic anemia

• Rheumatic heart disease
• Thrombocytopenia
• Erythroblastosis fetalis
• Goodpasture's syndrome
• Graves' disease
• Myasthenia gravis
TYPE III IMMUNE COMPLEX MEDIATED
HYPERSENSITIVITY REACTION

• Mediated by the formation of

insoluble antigen-antibody
complexes that activates
complement.
• Complexes are deposited in tissues
or vascular endothelium, as a result,
there is an increase in vascular
permeability and tissue injury.
• Primary Cellular Component:
✓Ig G,
✓Ig M,
✓Ig A
✓Complements
✓Neutrophils
 TYPE III IMMUNE COMPLEX MEDIATED
HYPERSENSITIVITY REACTION
Antigen invades body

Binds to antibody in the circulation

Antigen-antibody complexes are formed

Deposited in the membrane of

vessel walls & other tissues

Activates complement system

Enhanced Release of chemical Cell lysis

opsonization mediators

Tissue Damage
 a. Serum Sickness
❖Develops 1 -3 wks after
administration of large amounts of
foreign serum (horse antitetanus
toxin)
❖s/s: fever, urticaria, rash,
lymphadenopathy
❖Immune complexes can
accumulate in the glomerulus,
blood vessels and joints
TYPE III: DISORDERS
• Serum Sickness
• Rheumatoid Arthritis
• Post Streptococcal
Glomerulonephritis
• Membranous Nephropathy
• Reactive arthritis
• Lupus Nephritis
• SLE
Type IV Delayed Hypersensitivity
Reactions
• Cell-mediated: sensitized T cells attack
antigen
• Develops 24 to 72 hours after exposure to
antigens
• Primary Cell Component: T-lymphocyte
• Delayed-type hypersensitivity
– A. Tuberculin test
– B. Allergic contact dermatitis
– C. Hypersensitivity pneumonitis
– D. Tissue / Graft transplant rejection
 Delayed hypersensitivity reactions

Clinic
Reac
al
Type tion Histology Antigen and site
appear
time
ance
lymphocytes,
followed by
48-72 eczem epidermal ( organic chemicals,
Contact macrophages;
hr a poison ivy, heavy metals, etc.)
edema of
epidermis

local lymphocytes,
48-72 intradermal (tuberculin,
Tuberculin indurati monocytes,
hr lepromin,etc.)
on macrophages

macrophages,
persistent antigen or foreign
21-28 hardeni epitheloid and
Granuloma body presence (tuberculosis,
days ng giant cells,
leprosy, etc.)
fibrosis
PPD test
Contact dermatitis
Types of Transplant Rejection
Types description treatment

Hyperacute Occurs within minutes to Transplant can’t be

hours, days after transplant saved

Acute Occurs days to months Increase

After transplant, with signs of immunesuppression
inflammation & impaired by meds
organ function

Chronic Occurs 4 months to years NONE, loss of graft

after gradual deterioration of will occur, requiring
organ function retransplant
 TYPE IV: DISORDERS
• Contact dermatitis
• Mantoux test
• Chronic transplant rejection
• Multiple sclerosis
• Celiac disease
• Hashimoto's thyroiditis
DELAYED HYPERSENSITIVITY
• SJS
• Lyell’s Syndrome/TEN
ETIOLOGY:
SIGNS AND SYMPTOMS

✓Cough
✓Fatigue
✓Fever and Chills
✓Headache
✓Muscle and joint pain
✓Sore throat
MANAGEMENT
✓ Fluid Replacement
✓Wound Care
✓Eye Care
✓Pain Medication
✓Antihistamine
✓Antibiotics
✓Topical Steroids
✓Immunoglobulin intravenous
✓Skin Grafting
HYPERSENSITIVITY REACTIONS
RHEUMATIC
DISEASE
COMMON SITE:
✓Skeletal muscles,
✓bones,
✓cartilage,
✓ligaments,
✓tendons, and
✓joints
CLASSIFICATION:
1. MONOARTICULAR
- affects a single joint
2. POLYARTICULAR
- affects multiple joints

FURTHER CLASSIFICATION:
1. Inflammatory
2. Noninflammatory
 Rheumatoid Arthritis

• Rheumatoid arthritis (RA) is a systemic

inflammatory disease that affects 0.3%
to 1.5% of the population, with women
affected two to three times more
frequently than men.
• Peak: 40-60y.o.
• Onset: 30-50y.o.
• Pannus-proliferation of newly formed
synovial tissue infiltrated with
inflammatory cells
 Pathogenesis
Predisposing factors:
• Hereditary
• An aberrant type of immune response leading
to destruction of joint architecture.
• Rheumatoid factor
• Location of inflammation: blood, synovial
joint, synovial membrane
 Manifestations
• Fatigue
• anorexia
• weight loss
• generalized aching and stiffness
(30mins – several hours)
• Subluxation of joints
• Swan neck deformity ( hyperextension
of PIP joint and partial flexion of DIP)
• Boutonniere deformity
• Bulge sign
• Genu valgus
• Joint contractures
• Baker’s cyst
• Increase ESR
• Rheumatoid nodules :
ulna
• Ulcerations of lower
extremities
 Diagnostics
• Physical exam
• Rf test
• Presence of 4 major criteria
• Anti–cyclic citrullinated peptide (CCP)
antibodies
• Synovial fluid analysis
 Treatment
Symptom control:
• Regulating activity by pacing,
establishing priorities, and setting
realistic goals
• long-term adherence to the prescribed
treatment modalities
• Proper posture, positioning,body
mechanics, and the use of supportive
shoes
 Treatment
• ROM
• Goals of pharmacologic therapy:
– Reduce pain, decrease inflammation,
maintain or restore joint function, and
prevent bone and cartilage destruction.
• NSAIDS and ASA
– celecoxib, rofecoxib, and valdecoxib
 Treatment
• Disease modifying antirheumatic drugs
(DMARDs) include:
– gold salts, hydroxychloroquine,
sulfasalazine, methotrexate, and
azathioprine.
 Treatment
Methotrexate
– most potent: effect can be seen in 1 month
– interfere with purine metabolism, leading to
the release of adenosine, a potent anti
inflammatory compound
Corticosteroids
Antirheumatic drugs
Leflunomide, Etanercept, Infliximab, and
adalimumab
 Surgical Treatment
• Synovectomy
• Tenosynovectomy
• Arthroplasty
• Arthrodesis
-End-
ACUTE GLOMERULONEPHRITIS
Glomerulonephritis

is an inflammation of the glomeruli which result from

an antigen-antibody reaction produced from an
infection elsewhere in the body. This disorder which
is caused by an immunological reaction may result in
proliferative and vinflammatory changes within the
glomerular structure.
RISK FACTORS:

▪ Immunological or autoimmune diseases

▪ Group A beta-hemolytic streptococcal infection (GABHS)
▪ History of pharyngitis or tonsillitis 2 to 3 weeks before
symptoms
SIGNS AND SYMPTOMS:

▪ Hematuria ▪ Headache
▪ Dark, smoky, cola-colored ▪ Chills and fever
or red-brown urine ▪ Fatigue and weakness
▪ Proteinuria, frothy urine ▪ Nausea and vomiting
▪ Elevated urine specific ▪ Edema in the face
gravity periorbital area and feet
▪ Low urine pH ▪ Elevated Blood Pressure
▪ Oliguria to anuria
DIAGNOSTIC TESTS:
▪ Urinalysis
✓ (+) Hematuria and proteinuria - most important indicator of
glomerular injury.
✓ (+) Casts, elevated specific gravity, low pH
✓ Elevated BUN and Creatinine
▪ Positive antibody response test for streptococcus
▪ Elevated Erythropoietin Sedimentation Rate
▪ Hyponatremia
▪ Hypophosphatemia
▪ Hyperkalemia
MEDICAL MANAGEMENT:

▪ Antimicrobial / antibiotics – Penicillin,

Erythromycin, Cephalexin
▪ Diuretics
▪ Corticosteroids
▪ Calcium channel blockers
▪ Vasodilators
▪ Fluid and electrolytes balance
NURSING INTERVENTION
▪ Monitor Vital Signs including the NVS
▪ Monitor weight of patient daily
▪ Dietary restriction of sodium and protein
▪ Limit fluid intake
▪ Carbohydrates are given liberally to provide energy and reduce the
catabolism of protein
▪ Provide skin care
▪ Observe for complications like renal failure, cardiac failure and
hypertensive encephalopathy
▪ Monitor urinalysis, BUN and creatinine levels
▪ Promote rest and regular activity when hematuria and proteinuria resolves
-END-
Autoimmune
Disorder
AUTOIMMUNITY
➢production of antibodies against
the tissues of your own body

EFFECTS/CAUSES:
✓Failure to display self antigens
✓Presence of genetic abnormalities
(idiopathic)
✓Self reactive clones of T-cells & B-
cells
 LUPUS ERYTHEMATOSUS

❖collection of autoimmune diseases,

in which the human immune
system becomes hyperactive and
attacks normal, healthy tissues.
 LUPUS ERYTHEMATOSUS

Lupus – “wolf”
Erythematosus – reddened

CLASSIFICATION
Discoid Lupus Erythematosus
Drug-induced Lupus Erythematosus
Neonatal Lupus Erythematosus
Systemic Lupus Erythematosus(SLE)
 Classifications of Lupus:
I. Discoid lupus Erythematosus
DLE (Discoid Lupus Erythematosus)

3 DIVISION:

✓localized
✓generalized
✓childhood discoid lupus
erythematosus
II. Drug-induced Lupus Erythematosus
III. Neonatal lupus Erythematosus
 IV. Systemic Lupus Erythematosus
(SLE)

an autoimmune
disorder , non
contagious, chronic,
progressive
inflammatory disease
of the connective
tissue
cause is UNKNOWN
Risk Factors

Genetic Abnormality

Viral Infection

Medications
 Signs and symptoms

Arthritis (initial
manifestation) to
arthralgia
Weakness, fever, fatigue,
weight loss
Photosensitivity from the
sun
Butterfly rash / malar rash
Skin lesions
CHARACTERISTIC OF SKIN LESIONS:

✓ margins are bright red

✓ may extend beyond the hairline
✓ may occur in the exposed part of the
neck
✓ may spread to the mucous membranes
and other tissues of the body
✓ do not ulcerate, but cause
degeneration and atrophy of tissues
involved
 Systemic involvement of
other organs

Lupus Nephritis
Pleuritis
Pericarditis
Peritonitis
Neuritis
Anemia
Raynaud’s phenomenon
 Idiopathic loss of self-
tolerance

Auto-antibody
formation

Immune complex
deposition

Musculosk
eletal CARDIO-
system SKIN LUNGS KIDNEY CNS
VASCULAR

Arthralgi Malar •Nephroti

PLATELET
c
a, RBC rash •Pericarditis syndrome
arthritis
•Pleural
Hair •Nephritis
Effusion •Renal
Loss Failure
DIAGNOSTIC CRITERIA

Serositis – Pleuritis or pericarditis or

peritonitis

Oral ulcers

Arthritis

Photosensitivity
DIAGNOSTIC CRITERIA
Blood
Renal disorder
Antinuclear antibody
Immunologic disorder
Neurologic disorder

Malar rash
Discoid rash
DIAGNOSTIC EXAMS:

• Medical history
• Complete physical exam
• Laboratory tests:
✓ CBC
✓ ESR
✓ U/A
✓ BLOOD CHEMISTRIES
✓ COMPLEMENT LEVELS
❖ Anti nuclear antibodies/ANA or ANF
✓ The ANA test measures the pattern and amount of
autoantibody which can attack the body's tissues as
if they were foreign material.

❖Anti-extractable nuclear antigen (Anti-

ENA)
❖ Extractable nuclear antigens
❖ Anti-smith and anti-double stranded
DNA (dsdna)
❖Anti cardiolipin antibodies
❖Skin biopsy
❖Kidney biopsy
TREATMENT
NSAIDs
Antimicrobials
Corticosteroids
Immunosuppressive
Alternative therapies
✓ special diet
✓ nutritional supplement
✓ fish oils
✓ ointments and creams
✓ chiropractics
✓ sunscreens
✓ exercise and rest
✓ stress reduction
✓ family planning
✓ yearly influenza and
pneumococcal
vaccination
What to Avoid:

▪ Aromatic amines present in cleaning

agents and hair dyes
▪ Silicone and silica dust
▪ Alfalfa sprouts due to their high L-
canavanine content
▪ Hydrazines found in some mushrooms
and in tobacco smoke
▪ Tartrazines found as preservatives in
food dyes
▪ Ultraviolet light
▪ Excess alcohol
 Medications

Anti-inflammatory analgesics – NSAIDs

and Aspirin
Antimalarial drug : Hydroxychloroquine
(Plaquenil)
Corticosteroids (Prednisone) in high doses
Topical Corticosteroids
Cytotoxic Agents or Antineoplastic
 Other management

Kidney dialysis
Total hip replacement
Plasmapheresis
Plasmapheresis
Dialysis
-END-
GAMMOPATHY
MACROGLOBULINEMIA

the presence of increased levels

of macroglobulins in the
circulating blood
there is diffuse infiltration of bone
marrow and also, in many cases, of
the spleen, liver, or lymph nodes
 HODGKIN’S DISEASE

▪ is a type of lymphoma, which is

a cancer originating from white blood
cells called lymphocytes
▪ is characterized by the orderly spread
of disease from one lymph node group
to another and by the development
of systemic symptoms with advanced
disease
 MULTIPLE MYELOMA

A malignant disease of the most

mature form of B lymphocyte,
the plasma cell.
Proliferation of plasma cell from
BM into the hard bone tissue
causing erosion of the bone
Unknown cause
EFFECTS OF PROLIFERATION
OF PLASMA CELLS:
❑Interfere w/ normal production of
blood cells
✓ leukopenia
✓ anemia
✓ thrombocytopenia
❑May cause soft tissue masses/lytic
lesions
✓ plasmacytomas
 Risk Factors

Chronic immune stimulation

Autoimmune disorders
Exposure to ionizing radiation
Occupational exposure to
pesticides or herbicides
Classic Triad

Plasmacytosis
Lytic bone lesion
(plasmacytomas)
M. protein or Bence Jones Protein
 SIGNS & SYMPTOMS
 Characterized by widespread bone
destruction
 Bone pain (back ribs)
 Anemia
 Hypercalcemia (constipation, thirst,
altered mental status, dehydration,
confusion and coma)
 Increase uric acid
 Splenomegaly
 Frequent recurring of infections
 Spontaneous pathologic fractures
 Blood viscosity (due to increase IgA)
 COMPLICATIONS

bone pain
hypercalcemia
renal failure
spinal cord compression
immunosuppression*
 CRAB
CRAB:
C = Calcium (elevated)
R = Renal failue
A = Anemia
B = Bone lesions
 DIAGNOSTIC TEST

Bone Marrow biopsy

X-ray of bone
(+) Bence Jones
protein in the urine :
urine electrophoresis
(+) M protein : serum
protein
electrophoresis
 Management

 Prevent Infection
 Chemotherapy:
 Vincristine (Oncovin)
Cyclophosphamide
(Cytoxan)
 Dexamethasone
(Decadron)
 Thalidomide
 BM transplant
 Ambulation & Adequate
hydration
 Management
Meds shown to strengthen bone,
controlling bone pain and bone fracture:
by diminishing osteoclast activating
factor (biphosphonates)
✓ Pamidronate (Aredia)
✓ Zoledronic Acid (Zometa)
Thalidomide (Thalomid) : a sedative
having antimyeloma effect.
✓ Inhibits cytokines (Vascular endothelial growth
factor), IL-6 and tumor necrosis factor.
✓ Side Effect: fatigue, dizziness, constipation,
rash and peripheral neuropathy
Bone Marrow Transplant
 Nursing Management

▪ Administer NSAIDS combined with opioid

analgesic as ordered
▪ Educate patients for activity restrictions such
as lifting of heavy objects
▪ Use of braces to support the spinal column
▪ Maintaining mobility and hydration
▪ Instruct patient in infection prevention
measures
-END-
Kawasaki
Disease
Description

• Kawasaki Disease, also known as Kawasaki Syndrome or Mucocutaneous

Lymph Node Syndrome. It is a rare childhood illness that affects the blood
vessels and it causes inflammation in the walls of medium-size arteries throughout
the body. Kawasaki Disease a form of systemic vasculitis identified as an acute
febrile illness with multiple systems affected in which the most common cause of
acquired heart disease in children.

• ETIOLOGY: Unknown / Idiopathic

RISK FACTORS:

▪ Age - children 5 years old or younger

▪ Sex - boys are 1.5 X more likely to get it than
girls
▪ Ethnicity - Asian descent
STAGES OF KAWASAKI DISEASE:
Stage 1 - Acute Febrile Phase (First 10 days)
▪ Client is irritable and appears severely ill
▪ High spiking temperature of 40-degree Celsius for 5 days or more
▪ Oropharyngeal erythema and red dry lips
▪ Erythema and edema of hands and feet, desquamation of palms and soles
▪ Erythematous generalized rashes
▪ Cervical lymphadenopathy greater than 0.6 inch
▪ Pericarditis, myocarditis, cardiomegaly, pleural effusion and heart failure
STAGES OF KAWASAKI DISEASE:

Stage 2 - Subacute Phase (Day 11 to 25)

▪ Acute symptoms of stage 1 subside as temperature returns to normal
but still the client remains irritable and anorexic
▪ Dry, cracked lips with fissures
▪ Desquamation of toes and fingers
▪ Coronary thrombus, aneurysm, myocardial infarction and heart failure
▪ Thrombocytosis peaks at 2 weeks
STAGES OF KAWASAKI DISEASE:

Stage 3 - Convalescent Phase (Day 40 to 70)

▪ Client appears to well
▪ Transverse grooves of fingers and toenails
▪ Coronary thrombosis, aneurysm may occur
Clinical Manifestations
▪ High fever that persist for 5 or more ▪ Swollen hands and feet
days ▪ Vasculitis – Definitive sign
▪ Conjunctivitis, bloodshot eyes ▪ Loss of appetite
▪ Rashes on torso and groin ▪ Nausea and vomiting
▪ Adenopathy, swollen lymph nodes ▪ Abdominal pain
▪ Strawberry tongue ▪ Joint pain
▪ Bright red, swollen lips ▪ Temporary hearing loss
Diagnostic Tests:
▪ CBC - decrease hemoglobin and RBC
▪ Increased platelet count - 2nd to 4th week
▪ Transient elevation of IgM, IgG
▪ Elevated ESR, CRP, alpha1 antitrypsin
▪ Moderately elevated Liver Enzymes
▪ Low HDL and high Triglycerides
▪ Urinalysis - (+) protein and leukocytes
▪ ECG, Cardiac Catheterization and Angiocardiography
▪ Serum CK-MB
Medical Management
• The principal goal of treatment for Kawasaki Disease is to prevent coronary
artery disease and to relieve symptoms.
▪ Full dose of Intravenous Immunoglobulin (IVIG)
▪ Aspirin therapy
▪ Analgesics / Antipyretics
▪ Thrombolytic therapy
▪ Anti-inflammatory Drugs – Ibuprofen, Naproxen
▪ Plasma exchange
Nursing Management
▪ Closely monitor the vital signs of the client
▪ Observe ECG or telemetry for changes in rhythm
▪ Administer antipyretic and analgesic as ordered
▪ Maintain bedrest during the acute stage and provide assistance with care
▪ Encourage adequate fluid intake if not contraindicated
▪ Monitor and plan the gradual increase in the level of activity of the client
▪ Note and report occurrence of slow pulse, hypotension, decreased level of
sensorium, numbness and hyperreflexia
-END_
PELVIC
INFLAMMATORY
DISEASE
Description
• Pelvic inflammatory disease (PID) is an infection of the female
reproductive organs. Several different types of bacteria can cause PID,
including the same bacteria that cause the sexually transmitted diseases.
PID can become extremely dangerous even life threatening if the infection
spreads to the blood.

Etiologic Agent:
• Most cases of PID are polymicrobial, but these are the common pathogens:
▪ N. gonorrhoeae
▪ Chlamydia
Risk Factor:
▪ Having sex under the age of 25 years old
▪ Having multiple partners
▪ Having sex without any protection such as condoms
▪ Recently having an in
▪ Intrauterine device (IUD) inserted
▪ Douching
▪ Having history of pelvic inflammatory disorders
Clinical Manifestations
Some women with PID don’t have symptoms, they are called
asymptomatic until infection becomes severe.

▪ Pain in the lower abdomen - most ▪ Irregular bleeding

common symptom ▪ Increased or foul- smelling vaginal
▪ Pain in the pelvic area discharges
▪ Fever – temperature above 38⁰C ▪ Tiredness
▪ Painful sex ▪ Vomiting
▪ Painful urination ▪ Fainting
Diagnostics Tests
▪ Pelvic examination
▪Cervical culture
▪Urine test
▪Pelvic ultrasound
▪Endometrial biopsy
▪Laparoscopy
Medical and Nursing Management
Treatment of PID addresses the relief of acute symptoms, eradication of current infection and minimizes
the risk of long term sequelae. It includes empirical broad-spectrum antibiotics to cover the full
complement of common causes. These are the common brand-named antibiotics:

▪ Azithromycin
Long Term Complication of PID:
▪ Cephalosporin
▪ Infertility
▪ Ceftriaxone
▪ Doxycycline
▪ Ectopic pregnancy
▪ Clindamycin ▪ Chronic pelvic pain
▪ Metronidazole ▪ Tubo-ovarian abscess
▪ Unasyn
▪ Probenecid
Prevention:
▪ Teach client to practice safe sex
▪ Screen for sexually transmitted infections
▪ Avoid douches
▪ Teach client to wipe from front to back after using bathroom
-END-
BENIGN
PROSTATIC
HYPERTROPHY
Description

• Benign prostatic hypertrophy (BPH) is also known as benign

prostatic hyperplasia, and is characterized by proliferation of the
cellular elements of the prostate.

Risk Factors:
▪ Aging process
▪ Hormonal imbalance (estrogen, androgen)
Clinical Manifestations
Signs and Symptoms:
• Urinary frequency ▪ Incomplete bladder emptying
▪ Urinary urgency ▪ Straining
▪ Nocturia ▪ Decreased force of urine stream
▪ Hesitancy ▪ Dribbling
Diagnostic Tests

▪ Digital rectal examination ▪ Blood urea nitrogen (BUN)

▪ Urinalysis ▪ Ultrasonography
▪ Urine culture ▪ Endoscopy of the lower urinary
▪ Prostate-specific antigen tract
(PSA) ▪ Cystoscopy
▪ Serum electrolytes ▪ Renal biopsy
Medical Management
▪ Pharmacologic management:
• Terazosin (Hytrin) – A1-adrenergic receptor blocker.Relaxes
bladder sphincter.
• Finasteride (Proscar) – Inhibits 5-alpha red. Reduction of
glandular hyperplasia
▪ Balloon dilation – To relax smooth muscle of the bladder neck
and prostate
▪ Immediate catheterization
▪ Watchful waiting – To monitor disease progression
Surgical management:

• TURP (Transurethral Resection of the Prostate)

• Open prostatectomy
• Transurethral incision of the prostate (TUIP)
• Transurethral microwave therapy (TUMT)
• Transurethral needle ablation of the prostate (TUNA)
• Prostatic stents
• Laparoscopic prostatectomy
Complications:

▪ Urinary tract infections ▪ Hydroureter

▪ Urinary stones ▪ Hydronephrosis
▪ Kidney damage ▪ Bladder neck strictures post TUR
▪ Bleeding in the urinary tract ▪ Retrograde ejaculation
▪ A sudden inability to void ▪ Epididymitis
Nursing Management Post-Operative:

▪ Increase oral intake of client ▪ Teach Kegel’s exercises

▪ Maintain patency of continuous bladder ▪ Avoid giving client anticholinergic
irrigation (cystoclysis) agents
▪ Practice asepsis ▪ Instruct client to avoid the following
▪ Use sterile saline to prevent water after discharge:
intoxication ▪ Vigorous exercises
▪ Prevent thrombophlebitis ▪ Heavy lifting
▪ Monitor for bleeding ▪ Straining
▪ Post removal of catheter- observe for ▪ Prolonged sitting and standing
urinary retention ▪ Crossing the legs
-END-
14.CORONAVIRUS INFECTION

14.1 Middle East Respiratory Syndrome (MERS-CoV)

Middle East Respiratory Syndrome (MERS) is a viral respiratory illness and was
reported in Saudi Arabia in 2012 and has spread to several other countries including
the United States. Most people infected with MER-CoV developed severe acute
respiratory illness.

Etiologic Agent: MERS-Coronavirus

Mode of Transmission: Close contact with infected person

Incubation Period: 5 to 6 days, but can range from 2 to 14 days

Signs and Symptoms:

▪ Fever ▪ Shortness of breath ● Nausea and vomiting
▪ Cough ▪ Diarrhea

Diagnosis:
▪ Polymerase chain reaction (PCR) – CONFIRMATORY TEST ( used to detect viral
RNA)
▪ ELISA – SCREENING TEST used to detect the presence and concentration of
specific antibodies that bind to a viral protein.

Medical Management:
▪ Currently no vaccine is available to treat MERS-CoV
▪ Treatment is supportive and based on a person’s clinical condition.

Prevention:
▪ Wash hands often with soap and water for 20 seconds or use alcohol-based
sanitizers
▪ Cover nose and mouth with tissue when coughing or sneezing, then throw tissue in
the trash.
▪ Avoid touching the eyes, nose and mouth with unwashed hands.
▪ Avoid personal contact such as kissing or sharing cups or eating utensils with sick
people.
▪ Clean and disinfect frequently touched surfaces such as doorknobs and toys
14.2 Severe Acute Respiratory Syndrome (SARS)

SARS or Severe Acute Respiratory Syndrome is a serious, potentially life-

threatening viral infection caused by the Coronaviridae family, the SARS-associated
coronavirus (SARS-CoV). Initially began in the Guangdong province of southern
China. SARS is characterized by a phase of cytokine storms with various chemokines
and cytokines being elevated.

Signs and Symptoms:

The clinical course of SARS generally follows a typical pattern. Stage 1 is a flu like
prodrome that begins 2-7 days after incubation, lasts 3-7 days, and is characterized by
the following:
▪ Fever 38 ⁰C ▪ Chills ● anorexia
▪ Fatigue ▪ Myalgias
▪ Headaches ▪ Malaise

Less common features include the following:

▪ Sputum ▪ Coryza ▪ Dizziness
production ▪ Nausea and ▪ Diarrhea
▪ Sore throat vomiting

Stage 2 is the lower respiratory tract phase and is characterized by:

▪ Dry cough ▪ Progressive ▪ Respiratory failure
▪ Dyspnea hypoxemia in many that requires
cases mechanical
ventilation
Diagnostic test:

▪ Pulse oximetry ▪ Mild hyponatremia and hypokalemia

▪ Blood cultures
▪ Sputum gram stain and culture
▪ Viral respiratory pathogen test -
influenza A and B viruses and
respiratory syncytial virus
▪ Legionella and pneumococcal
urinary antigen test
▪ WBC- decreased
▪ Elevated lactate dehydrogenase alanine
aminotransferase and hepatic
transaminase
▪ Elevated creatine kinase level
▪ Serum antibodies to SARS-CoV in
single serum specimen
▪ RT-PCR (reverse transcriptase
polymerase chain reaction)
▪ Chest radiograph - interstitial infiltrates

Medical Management:

No definitive medication protocol specific to SARS has been developed, although various
treatment regimens have been tried.

▪ Corticosteroid neutralizes virus activity in vitro and in

▪ Antiviral agents (Ribavirin)
▪ Protease inhibitors (Lopinavir,
Ritonavir)
▪ Interferon
▪ Monoclonal antibodies -
emergency prophylaxis,
vivo
▪ Intravenous immunoglobulin (IVIG)
▪ Nitric oxide
▪ Glycyrrhizin - inhibits vitro replication of
the virus
▪ Vaccine - phase 1 clinical trial 2004
15. INFLUENZA

15.1 Swine Flu (H1N1)

H1N1 influenza, referred to as swine flu, is a highly contagious respiratory disease in

pigs that can be transmitted to humans.

Etiologic Agent: Influenza A virus subtype H1N1

Mode of transmission: close and direct contact with infected person

Incubation Period: ranges from 1 to 4 days with an average of 2 days up to 7 days

Signs and Symptoms:

▪ Cough ▪ Stuffy or runny ▪ Headaches
▪ Fever nose ▪ Chills
▪ Sore throat ▪ Body ache ▪ Fatigue

Diagnostic Test:
▪ PCR
▪ Rapid antigen or antibody immunoassays
▪ Viral culture

Medical and Treatment Management:

▪ Antipyretic ▪ Isolation
▪ Analgesics ▪ Vaccination – Influenza virus
▪ Increased fluid consumption vaccine trivalent (Fluzone,
▪ Bedrest Flucelvax)
▪ Antiviral agents (Oseltamivir/ ▪ Influenza virus quadrivalent (Afluria
Zanamivir) Quadrivalent, Fluarix)

Prevention and Precaution:

▪ Seek medical care if suspected with H1N1

▪ Isolate patient immediately in a negative-pressure air handling
▪ Wash hands frequently
▪ Wear face mask
▪ Social distancing or avoid large gatherings
▪ Routine cleaning and disinfection
▪ Pre-exposure prophylaxis
15.2 EBOLA VIRUS

Ebola Hemorrhagic Fever is a rare and deadly disease caused by infection with one
of the Ebola virus’s strains. Ebola can cause disease in humans and nonhuman
primates.

Etiologic Agent: Ebola Virus

Mode of transmission: Direct contact with blood or bloody fluids, objects of a person
infected with ebola and infected animals.

Incubation Period: 2 to 21 days after exposure to Ebola, but the average is 8 to 10 days.

Signs and Symptoms:

▪ Fever ▪ Weakness ▪ Abdominal pain
▪ Severe ▪ Fatigue ▪ Unexplained
headache ▪ Diarrhea hemorrhage
▪ Muscle pain ▪ Vomiting

Diagnostic Test:
Within a few days after symptoms begin:
Antigen-capture enzyme-linked immunosorbent assay (ELISA) testing
Igm ELISA
Polymerase chain reaction (PCR)
Virus isolation

Later in disease course or after recovery

IgM and IgG antibodies

Retrospectively in deceased patients

Immunohistochemistry testing
PCR
Virus isolation

Medical Management
▪ Symptoms of Ebola and complications are treated as they appear
▪ Provide intravenous fluids and balancing electrolytes in the body
▪ Maintain oxygen status and blood pressure
▪ Treat other infections if they occur.
▪ ERVEBO – First US FDA approved vaccine December 2019

Prevention:
▪ Practice careful hygiene
▪ Do not handle items that may have come in contact with an infected person’s blood or
body fluids
▪ Isolate patients with Ebola from other patients.
▪ Practice proper infection control and sterilization measures
▪ Wear appropriate personal protective equipment
▪ Notify health officials if had direct contact with blood or body fluids of a person who is
sick with Ebola
NCM 112- CARE OF CLIENTS WITH PROBLEMS IN CELLULAR
ABERRATIONS

By:

JOSEPHINE B. MAGNO, RN, MN

BEHAVIORAL OBJECTIVES:
⚫ Distinguish terms related to the concept;
⚫ illustrate the normal structure and function of the cell;
⚫ differentiate phases of cellular mitosis;
⚫ validate changes that occur in cancerous cells and their functional significance;
⚫ compare the normal cell from the malignant cell;
⚫ outline factors that contribute to cancer development;
⚫ categorize the different stages of cancer development;
⚫ contrast between benign and malignant tumor;
⚫ cite method for naming and classifying tumors;
⚫ validate the clinical manifestations of cancer;
⚫ propose the significance of health education and preventive care in lowering the
incidence of cancer;
⚫ organize ways of preventing cancer;
⚫ recommend the importance of identifying the different laboratory examinations and
the corresponding nursing management;
⚫ appraise the roles of surgery, chemotherapy, and radiation in treating cancer;
⚫ prioritize the nursing needs of clients according to the type of therapy received;
⚫ illustrate other treatment modalities in treating cancer;
⚫ describe briefly the cancer involving the specific site or organ in the body; and
⚫ formulate common nursing diagnoses and collaborative problems of patients with
cancer.
⚫ apply nursing process in formulating care plan for client with cancer.
Cancer
- a disease process whereby cells proliferate abnormally, ignoring-regulating signals in
the environment surrounding cells.

DEFINITION OF TERMS:
Aberrant Cellular Growth- it is an alteration in the normal cellular growth which occurs
when the cells escape the normal control in growth and differentiation.

Apoptosis – programmed cellular death.

Cyst- a closed sac having a distinct membrane and developing abnormally in a body
cavity or structure

Metastasis- it is the spread of cancer cells from the primary tumor to distant sites.

Neoplasm- Greek: NEO “new” Plasia “growth of tissue

- an abnormal mass of tissue that serves no useful purpose and may harm the
host organism.
- a mass of new tissue that grows independently of its surrounding structures
and has no physiologic purpose.

Carcinoma- a specific form of cancer or malignant tumor arising from epithelial cells.
( In Greek "Epi" means, "on, upon," and "Theli" meaning "tissue.“)

Tumor- it is a lump, mass, or swelling or enlargement; solid neoplasm

Sarcoma- a malignant tumor arising from non-epithelial tissue.

Oncogenes -inducing genes; genes that promote cell proliferation and are capable of
triggering cancerous characteristics

Oncology- the field or study of cancer; a medical specialty that deals with the
diagnosis, treatment and study of cancer.

Proto-oncogenes- these are benign forms of oncogenes necessary for some normal
cellular functions, especially growth and development.

Tumor suppressor gene- genes which inhibit cell division and survival.
 Proto-oncogene appear to be normal genes

Behavior may be altered due to

Incorporation of retrovirus Mutation of physical or chemical carcinogen

Transformation

Oncogene

Differentiation – extent to which tissue cells resemble normal cells

- it can be well differentiated or poorly differentiated

Progression – phenomenon by which malignancies attain their function slowly.

Neoplastic Progression- worsening of the cell’s biological potential, with the

passage of time neoplasm becomes more malignant.

Carcinoma in Situ- neoplasm which remains confined on the site of origin.

The CELL- is the basic structural and functional unit of living organisms.

Parts of the cell:

1. Cell Membrane- is a fragile, transparent barrier that contains the cell contents and
separates them from the surrounding environment.

2. Cytosol- is a semitransparent fluid that suspends the other elements. Water,

nutrients and variety of other solutes are dissolved in cytosol.

3. Nucleus- considered the “control center” of the cell. It is a large oval body near the
center of the cell which contains DNA. Plays central role in heredity.

4. Ribosomes- are tiny, bilobed, dark bodies made of proteins and one variety of RNA
called ribosomal RNA. The actual site of protein synthesis in the cell occurs in
ribosomes. Some ribosomes float free in the cytoplasm, where they manufacture
proteins that function in the cytoplasm. Others attach to membranes.
5. Endoplasmic Reticulum- serves as a minicirculatory system for the cell because it
provides a network of channels for carrying substances from one part of the cell to
another.

⚫ Rough Endoplasmic Reticulum- it has ribosomes, it is especially abundant in

cells that make and export proteins.
⚫ Smooth Endoplasmic Reticulum- has no ribosomes, it functions in lipid
metabolism and detoxification of drugs and pesticides.

6. Golgi Complex- its major function is to modify and package proteins, sent to it by the
rough ER via transport vesicles.

7. Lysosomes- are considered “suicide sacs”, function as the cell’s demolition sites.

8. Mitochondria- it is the powerhouse of the cell, it releases energy for cell functions.

9. Flagella and cilia- are structures that aid in locomotion and help move fluids across
the surface of tissue cells.

The Cell Cycle:

-is the series of changes a cell goes through from the time it is formed until it divides.

Divided into 2 periods:

1. M Phase- which includes nuclear division (mitosis) and cell division (cytokinesis)

Phases of Mitotic Cell Division:

⚫ Prophase
⚫ Metaphase
⚫ Anaphase
⚫ Telophase
⚫ Cytokinesis
2. Interphase- part of the cell cycle which is not contained in M phase

Interphase divided into three periods

Interval or Steps
G – gap
M – the interval separating Mitosis
S - synthesis

⚫ Step IA: G0 -interval in which the cell is at rest from cell division.

⚫ Step IB: G1- the cell grows physically larger, copies organelles and makes the
molecular building blocks it will need in later steps.

⚫ Step II: S- the cell synthesizes a complete copy of the DNA in its nucleus.

⚫ Step III: G2- the cell grows more and begins to recognize its contents in preparation
for mitosis.
＊Cell growth and reproduction are the most fundamental of all living functions.

Cellular Adaptive Process:

Differentiation
- cells are transformed into different and more specialized cell types as they
proliferate from a single stem cell

It determines:
What cell will look like?
How it will function?
How long will it live?

1. Hyperplasia- increase in the number of cells of a tissue; most often associated

with periods of rapid body growth.

2. Metaplasia- it is the conversion of one type of mature cell into another type of
cell.

3. Dysplasia- bizarre cell growth resulting in cells that differ in size, shape, or
arrangement from other cells of the same type of tissue.

4. Anaplasia- cells that lack normal cellular characteristics and differ in shape and
organization with respect to their cells of origin; usually, anaplastic cells are
malignant.
 DEFINITION
OF OTHER TERMS

ATROPHY

Decrease in cell size

HYPERPLASIA

Increase in the number of cells

METAPLASIA

Substitution of one cell with other type

HYPERTHROPHY

Increase in cell size

 DYSPLASIA

Deranged cell growth

Cellular Changes:

Contact Inhibition- ceasation of growth ones the cell comes in contact with another cell.
It switches off cell growth by blocking the synthesis of DNA, RNA and CHON.

Cell Proliferation – is well regulated, process by which multiply and bear offspring

Types of cells according to their ability to undergo regeneration:

⚫ Labile- GI, skin, stem cells in BM

⚫ Stable- bone, liver cells

⚫ Permanent or Fixed- cardiac muscle cells, brain cells, photoreceptors in retina

FACTORS WHICH CONTRIBUTE TO THE DEVELOPMENT OF CANCER

1. Oncogenic Viruses + oncogene

2. Carcinogens .

2.1. Chemical – forms electrophiles (highly reactive ion)

2.1.A. Industrial Compound

⚫ Vinyl Chloride-
- plastic manufacture
 - asbestos factories
- construction works

⚫ Polycyclic Aromatic DNA damage.

- vehicle emissions
- oil refineries

2.1.B .Foods and Preservatives

⚫ Nitrates
⚫ Talc
⚫ Food Sweeteners

2.2. Radiation – additive effect (high energy)

1. Ionizing Radiation – cancer induction

2. X-ray- repeated diagnostic x-ray procedures
3. Radioactive Isotopes- radiation therapy used to treat disease
4. Sunlight/ Ultraviolent rays- excessive exposure to UV rays increases risk of
skin cancer
5. Radon- decay of Uranium found in soil and rocks; associated with lung
cancer
6. Electromagnetic Radiation- associated with higher incidence of cancer

3. Immunologic Defects

4. Age

5. Gender

6. Heredity

7. Poverty

8. Stress

9. Lifestyle Practices
a. Smoking
b. Nutrition
c. Obesity
d. Sexual and reproductive factors

Characteristics of Cancer Cells:

1. Anaplasia – used to describe lack of normal cell proliferation and differentiation in
cancerous tissue

General Rule:
The more undifferentiated the tumor
The more frequent the mitosis
The more rapid the rate of growth

2. Cell surface and membrane alteration

3. Metabolic Changes
4. Antigenic Changes

STAGES OF CANCER DEVELOPMENT

1. Initiation- alteration in the structure of cellular DNA.

2. Latency/Promotion- proliferation of abnormal cells due to repeated exposure of

promoting agents ( substances that will promote the growth of an initiated cancer
cell).
3. Progression- exhibit increased malignant behavior, rapid proliferation of cancer
cells, Irreversible.

5. Invasion- process by which malignant cells move through the basement

membrane and gain access to blood vessels and lymphatic channels.

⚫ Regional invasion - cancer cells invade surrounding tissues & organs

⚫ Metastasis - spread to a distant body sites
⚫ Route: Vascular, Lymphatic, Surgical

⚫ Regional Invasion occurs by:

A. Cellular proliferation
B. Loss of contact inhibition
C. Secretion of cystic substance
- HYALURONIDASE- destroys intracellular cementic substances

Mechanism of Metastasis:
1. Invasion of Neoplastic cells to adjacent tissues caused by:

⚫ Increasing tumor size.

⚫ Loss of tumor cohesiveness with increasing motility.
⚫ Destruction of the supporting tissues of an organ.
⚫ Factors in the host response to tumor cell invasion.

2. Spread of tumor cells via:

a. Lymphatic system
b. Blood vessels
c. Direct expansion of tumors in body cavities

Example:
Ovarian CA – seed the entire peritoneal cavity
CNS CA – spread via gravity in the cerebral site

3. Establishment and growth of tumor cells at the secondary site

https://youtu.be/0OAi4sxScXg ( URL- Overview on CA)

https://youtu.be/P4gz6DrZOOI (URL- Physiology of Cell)
https://youtu.be/g7iAVCLZWuM (URL- Cell Cycle)
COMPARISON BETWEEN NORMAL AND MALIGNANT CELL
CHARACTERI NORMAL CELL
STICS
MITOTIC Leads to 2 daughter cells
DIVISION
APPEARANC Homogenous in size, shape and
E growth
Cohesive, forms regular patterns
of expansion
Uniform in size to nucleus
Well differentiated
GROWTH Do not invade adjacent tissue
PATTERN
Proliferation in response to
specific stimuli
Grows in ideal condition
Cell birth is equal to cell death
Stable cell membranes
Constant predictable growth rate
Cannot grow out of specific
environment
FUNCTION Have specific designated
purpose
Contribute to overall well-being
of the host
Function in specific
predetermined manner
OTHERS Chromosomes remain constant
throughout cell division
Cannot invade, erode or spread
MALIGNANT CELL
Leads to multiple
daughter cells
Larger and grows rapidly
than normal,
heterogenous
Not cohesive, irregular
pattern of expansion
Larger, more prominent
nucleus
Lack of pattern in
organization
Invade adjacent tissue
Proliferate in response to
abnormal stimuli
Grows in adverse
condition
Cell birth exceeds cell
death
Loss of control as a
result of cell membrane
change
Erratic growth rate
Able to break off cells
that migrate through
blood stream/ lymphatic
channels
No useful purpose
Parasitic
No normal function,
causes damage instead
Chromosome aberration
occur as cells matures
Invades, erodes, and
spreads, have own blood
supply
Specific Detructive Enzymes:
1. Collagenases
2. Plasminogen Activators
3. Lysosomal Hydrolyses

Classification of Neoplasm: Tissue of Origin

“OMA” – means tumor

- usually attached to a term for a parent tissue of the tumor

Example: “aden” (gland) + oma = Adenoma

- when one or more parent tissue enters into the formation of neoplasm, the
names of a tumor are even more descriptive

Example:
Adenomyoma – benign neoplasm that contains both glandular & myoma cells

3 Most Common Benign Tumors

1. Fibroma
-are tumors of fibrous or connective tissue that can grow in any organ. Fibroids
commonly grow in the uterus.

2. Lipoma
- a slow-growing, fatty lump that is most often situated between the skin and the
underlying muscle layer.

3. Leiomyoma
- smooth muscle in origin
- rarely becomes malignant (1% of case)

JBMAGNO
Malignant Tumors

Carcinoma – epithelial tissue

Sarcoma – mesenchymal origins (bld. Vessels, lymphatics, nerve tissue)

1. Carcinoma in Situ
- neoplasm of epithelial tissue that remains confined to the site of origin

3. Malignant Fibrosarcomas
- may originate from benign fibromas
-bulky, well differentiated tumor
- rarely metastasize

4. Bronchogenic Carcinoma
- 90% of all cases of lung CA
- usually develops in lower trachea and lower bronchi
-when there is metastasis: surgery contraindicated

Adeno – grandular tissue

Angio – blood vessels
Basal cells – epithelium, mainly sun exposed area
Embryonal – gonads
Lympho – lymphoid tissue
Melano – pigmented cells of epithelium
Myo- muscles
Osteo - bone

CLASSIFICATION OF NEOPLASM

Tissue of origin Benign Malignant

Connective tissue

Fibrous tissue Fibroma Fibrosarcoma

Adipose tissue Lipoma Liposarcoma
Bone Osteoma Osteogenic sarcoma

Epithelium

Skin Papilloma Squamous cell

carcinoma

Bone marrow Leukemia

 Multiple myeloma

Muscle tissue

Smooth muscle Leiomyoma Leiomyosarcoma

Nerve tissue

Nerve fibers Neuroma Neurogenic sarcoma

Meninges Meningioma Malignant meningioma

Gonads Dermoid cyst Embryonal carcinoma

Cancer Classification: GRADING & STAGING

I. Grading
-according to histologic or cellular characteristics of tumor

Histopathology:
Gx - grade cannot be assessed
G1 - well differentiated grade
G2 - moderately well differentiated grade
G3 - poorly differentiated
G4 - undifferentiated

II. Staging
- it quantifies the disease or identify the spread of disease

T – stands for the extent of primary tumor

N – involvement of regional lymph nodes
M – extent of metastatic involvement

TNM Classification System:

Tx - tumor cannot be adequately assessed
T0 - no evidence of primary tumor
TIS - Carcinoma in situ
T1T2T3T4- progressive increase in tumor size and/ or involvement

Nx - regional lymph nodes cannot be assessed clinically

No - no evidence of regional node
N1N2N3- increasing involvement of regional lymph nodes

Mx - not assessed
Mo - no distant metastasis
M1M2M3- ascending degree of distant metastasis

eg. BREAST CANCER

TUMOR
Tx- primary tumor cannot be assessed
T0- no evidence of primary tumor
Tis- carcinoma in situ
T1- tumor 2 cm or less
T2- tumor more than 2 cm but not more than 5 cm
T3- tumor more than 5 cm
T4- tumor of any size with direct extension to chest wall or skin

REGIONAL LYMPH NODE

Nx- regional lymph nodes cannot be assessed
N0- no regional lymph node metastasis
N1- metastasis to movable ipsilateral axillary lymph node
N2- metastasis to ipsilateral axillary lymph node fixed to each other or other structures
N3- metastasis to ipsilateral internal mammary lymph node

DISTANT METASTASIS
Mx- presence of distant metastasis cannot be assessed
M0- no distant metastasis
M1- distant metastasis present ( includes metastasis to ipsilateral supraclavicular lymph
nodes

STAGE GROUPINGS
Stage 0- Tis, N0, M0
Stage 1- T1, N0, M0
Stage IIA- T0, N1, M0 ; T1, N1, M0; T2, N0, M0
Stage IIB- T2, N1, M0; T3, N0, M0
Stage IIIA- T0, N2, M0; T1,N2, M0; T2,N2,M0; T3,N1,M0;
T3,N2,M0
Stage IIIB- T4, any N, M0 or any T, N3, M0
Stage IV- any T, any N, M1

COMPARISON BETWEEN BENIGN AND MALIGNANT NEOPLASM

CHARACTERISTICS BENIGN NEOPLASM MALIGNANT

NEOPLASM

Spread of Growth Grows slowly, usually Usually grows rapidly,

continues to grow tends to grow
throughout life unless relentlessly throughout
surgically removed; may life; rarely, neoplasm
have periods of may regress
remission spontaneously

Mode of Growth Grows by enlarging and Grows by infiltrating

expanding; always surrounding tissues;
remains localized; never may remain localized (in
infiltrates surrounding situ) but usually
tissues infiltrates other tissues

Capsule Almost always Never contained within

contained within a
fibrous capsule; capsule
does not prevent
expansion of neoplasm
but does prevent growth
by infiltration; capsule
advantageous because
encapsulated tumor can
be removed surgically
a capsule; absence of
capsule allows
neoplastic cells to
invade surrounding
tissues; surgically
removal of tumor difficult
 Cell Usually well- Usually poorly
Characteristics differentiated; mitotic differentiated;large
figures absent or numbers of normal and
scanty;mature abnormal mitotic figures
cell;anaplastic cells present; cells tend to be
absent anaplastic

Recurrence Recurrence extremely Recurrence common

unusual when surgically following surgery
removed because tumor cells
spread into surrounding
tissues

Metastasis Metastasis never occur Metastasis very

common

Effect of Neoplasm Not harmful to host Always harmful to

unless located in area host, results in death
where it causes unless removed
compression of tissue or surgically or destroyed
obstruction of vital by radiation or
organs; does not chemotherapy; causes
produce cachexia disfigurement, disrupted
organ function,and
nutritional imbalances

Prognosis Very good; tumor Depends on cell type

generally removed and speed of diagnosis;
surgically poor prognosis indicated
if cells are poorly
differentiated and
evidence exists of
metastatic spread; good
prognosis indicated if
cells still resemble
normal and there is no
evidence of metastasis

GENERAL CLINICAL MANIFESTATION OF CANCER:

I. PAIN
Types of cancer pain:

A. Acute pain-usually starts suddenly

B. Chronic pain – usually lasts more than 6 months

Nursing Responsibilities:
⚫ Help patients and families to take an active role in managing pain.
⚫ Provide education and support to correct fears and misconceptions about opioid
use.
II. Bleeding
Nursing Responsibilities:
⚫ Encourage to use a soft, not stiff, toothbrush and an electric not straight edged,
razor to prevent bleeding
⚫ Provide soft foods, increase fluid intake and stool softeners, as ordered
⚫ Handle and move joints and extremities gently to minimize risk for spontaneous
bleeding
⚫ Serum hemoglobin and hematocrit are monitored carefully for changes indicating
blood loss.
⚫ The nurse test all urine, stool, and emesis for occult blood.
⚫ Neurologic assessment.
⚫ Administers fluid and blood products as ordered
⚫ Vasopressor agents are administered as prescribed to maintain blood pressure and
ensure tissue oxygenation

III. Infection- Streptococcus and staphylococcus species

Nursing Responsibilities
⚫ Administer antibiotics promptly.
⚫ Strict asepsis.
⚫ Encourage appropriate hygiene.
⚫ Encourage patient to cough and perform deep breathing exercises.

IV. Anorexia-Cachexia Syndrome

Nursing Responsibilities
⚫ Food should be prepared in ways that make it appealing.
⚫ Unpleasant smells and unappetizing looking foods are avoided.
⚫ Provide small, frequent meals.
⚫ Encourage oral hygiene before mealtime to make meal more pleasant.
⚫ If adequate nutrition cannot be maintained by oral intake, nutritional support via the
enteral route.

DETECTION AND PREVENTION OF CANCER:

I. Primary Prevention Measures- ideal method of preventing cancer.

1. Optimal Dietary Patterns and Lifestyle Changes

-dietary factors are related to 50% of all environmental cancers.
-avoid obesity
- practice moderation in consumption of salt-cured, smoked and
nitrate-cured foods
- fresh vegetables
- increase fiber intake
- increase vit. A
- increase foods rich in Vit.C
JBMAGNO
- increase Vit. E
- reduce alcohol intake
 2. Minimize exposure to Carcinogens
- stop smoking
- avoid exposure to asbestos fiber and constant environmental dust
- avoid exposure to chemicals
-avoid radiation exposure
- avoid overexposure to the sun

3. Obtain adequate rest and exercise to reduce stress

II. Secondary Prevention- Early Detection

A. Health history and PE

B. Screening Methods
1. Mammography, Pap Smear, Prostate exam, digital rectal exam

⚫ Mammography- radiographic technique used to detect breast cyst and

tumor especially those not palpable on physical examinaton.
Responsibilities:
1. No mammogram for a week before monthly period.
2. No deodorant, talcum powder or lotion under arms or breast on the day
of the test.

⚫ Pap smear- or pap test, cervical smear, smear test

⚫ Prostate exam- during examination, patient will stand and feet apart.
- normally prostate is 2-4 cms long, triangular in shape, firm and rubbery.
⚫ Digital rectal exam

2. Self-care practices
2.1. Breast Self Exam- women should be told about the benefits and
limitations of BSE. The importance of prompt reporting of any new breast
symptoms to a health professional should be emphasized.

2.2.Testicular exam- it is best to do a TSE during or right after a hot

shower or bath.

Procedure:
Examine one testicle at a time.
Use both hands to gently roll each testicle (with slight pressure) between your fingers.
Place your thumbs over the top of your testicle, with the index and middle fingers of each
hand behind the testicle, and then roll it between your fingers.
You should be able to feel the epididymis (the sperm-carrying tube), which feels soft,
rope-like, and slightly tender to pressure, and is located at the top of the back part of
each testicle.
⚫ When examining each testicle, feel for any lumps or bumps along the front or sides.
Lumps may be as small as a piece of rice or a pea.

3. Sigmoidoscopy and fecal occult blood test- annual flexible sigmoidoscopy

and FOBT every 5 years, starting at age 50 years

C.Teaching early Warning Signs of Cancer

⚫ Change in bowel or bladder movement

⚫ A sore / wound that does not heal
⚫ Unusual bleeding or discharge
⚫ Thickening of breast/lump
⚫ Indigestion / dyspepsia
⚫ Obvious change in wart or mole
⚫ Nagging/ hoarseness
⚫ Unexplained weight loss
⚫ Prolonged anemia

Diagnosis of Cancer and Related Nursing Consideration:

⚫ Patients with suspected cancer undergo extensive testing to:

⚫ Determine the presence of tumor and its extent.
⚫ Identify possible spread of disease or invasion of other body tissues.
⚫ Evaluate the function of involved and univolved body system and organs.
⚫ Obtain tissue and cell of analysis, including evaluation of tumor stage and grade.

Nursing Responsibilities:

⚫ Help relieve fear and anxiety.

a. Explaining the tests to be performed.
b. The sensations likely to be experienced.
c. Patient’s role in the test procedures.

https://youtu.be/UCNx78zIrwU ( URL- Grading and Staging)

https://youtu.be/2OUkQrYHgSU ( URL- Mammogram)

Diagnostic Tools in Detecting Cancer

1. Laboratory Tests
-can be used to diagnose a specific organ dysfunction or metabolic aberration that may
be caused by malignant condition.

◼ CBC & Differential count

Increase in WBC – Acute Lymphocytic Leukemia (ALL)
Increase in RBC – Aplastic Anemia
Increase in Alkaline Phosphate – Osteogenic CA

◼ Serum Electroyles
 Ca – increase suggestive of bone metastasis
Na – decrease suggestive of Bronchogenic CA
K – decrease suggestive of Liver CA

◼ Examination of body fluids (sputum & Urine)

◼ Tumor Markers or Proteins associated with specific cancer- marker used to monitor
response to antineoplastic treatment and to determine the client’s prognosis in a
variety of cancer.
Example:
1. Serum prostate- specific antigen (PSA)- proteins produced by cells of the
prostate gland. Normal value: less than 4.0 ng/ml ( nanogram/ml)
2. Alpha-fetoprotein (AFP)- increase level in the blood suspects certain cancer of the
liver, testes or ovaries. Normal value: less than 10 ng/ml.
3. Cancinoembryonic Antigen (CEA)- increase level may suggest colon cancer.
Blood sample will be taken. Normal value: less than 2.5 ng/ml.
4. Homovanillic Acid (HAV)- produced by metabolism of dopamine
-elevated result may be associated with tumors of adrenal gland
-normal accumulation in 24 hr urine collection = 0 to 15 mg
5. Vanillylmandilic Acid (VMA)- urinary metabolite of epinephrine and norepinephrine
-24 hr urine collection normal value = 1.5 to 7.5 mg (adult)
83 mg/kg of BW (infants)
-increased in tumors of adrenal gland and nervous system
6. B-Human Chorionic Gonadotropin (B-HCG)- hormone normally found in blood
and urine during pregnancy.
-used to diagnose trophoblastic disease, germ cell tumors of testes and ovaries
7. Adrenocorticotropic Hormone (ACTH)- measures the level of ACTH in blood to
check problems in pituitary and adrenal gland.

◼ Urine
Bence Jones CHON – urine study; test is done to diagnose or monitor presence of
multiple myeloma.

Photograph of Bence-Jones protein crystals from a human cancer patient

◼ Stool
Guaiac Test – occult blood; test to find hidden blood in the stool to determine GI
bleeding.

◼ Radioimmunoassay – technique that measures tumor antigen in the serum using

radiolabeled antigens.

◼ Flow Cytometry – identifies cellular and DNA characteristics of the tissue that may
yield important diagnostic and prognostic information
-developed at Los Alamos
-it is a method of counting thousands of cells per second.
-cells are tagged with a marker that lights up, or fluoresces, when it and its host cell
pass through the brilliant light of a laser beam. The markers are often artificial antibodies
that bind to proteins found only on the cells of interest.
-the tagged cells are suspended in fluid and run through the cytometer, which sends
them single file through the laser beam, where they light up.
- detector sees the fluorescent light and tells the computer, which tallies the number of
tagged cells.
2. Cytologic Examination
◼ Papanicolaou Test (PapSmear)
- screening test that examines cervical scrapings for abnormality.
- It is used to diagnose cancer in an asymptomatic person and to identify
precancerous lesions or noninvasive cancer.
- It is used to detect inflammation, infection, premalignant changes, and malignancy of
the cervix

Procedure:
⚫ Using a vaginal speculum to enhance visibility, the physician or nurse practitioner
collects the patient’s secretions and cells from the cervix and vagina.
⚫ The fluid and tissue scrapings are placed on glass and sprayed with or immersed in
a fixative.

Exfoliative Cytology
- used to analyze pap smear

Bethesda System Classification

Class I Normal
Class II Inflammation
Class III Mild to Moderate Dysplasia
Class IV Probably Malignant
Class V Malignant

3.Oncologic Imaging

◼ Radiographs/ X-ray
⚫ Chest X-ray- makes images of the heart, lungs, airways, blood vessels, bones
of the spine and chest.
⚫ Mammogram- radiographic test used to detect breast cyst and tumor especially
those nor palpable on physical examination.
 ⚫ CT Scan- x-ra technique that produces sequential cross section of body images
at progressive depths.
Reponsibilities:
a. Wear loose fitting clothing or gown.
b. No jewelry, dentures or hairpins.
c. Not to eat or drink several hours before the test if with contrast medium.
Check for allergy.
d. Female patients should not be pregnant.
e. Remind patient to keep still during the procedure.
f. Sedatives may be given as ordered for claustrophobic patients.
g. Patient may hear slight buzzing or clicking during the procedure.

⚫ MRI- identifies abnormalities by creating cross sectional image of the body,

does not require ionizing radiation.
Responsibilities:
a. No jewelry, pins, hairpins, pacemaker, cochlear implants or metal objects.
b. Sedatives may be given as ordered for claustrophobic patients.
c. Procedure may be done with contrast medium, check for allergies.

◼ Positron Emission Tomography (PET)- studies glucose metabolism in body tissues

and is proving useful in differentiating varying rates of tissue metabolism.
- injection of a small dose of radioactive chemical called radiotracer.
Responsibilities:
a. Tell patient to remain still during the procedure.
b. NPO at least 6 hours before the test.
c. Female patients should not be pregnant.

4.Biopsy- the only definitive way to diagnose cancer. It is essential to obtain and
accurately identify an adequate tissue sample before any cancer therapy is
prescribed.

5. Endoscopy- fiberroptic tubes equipped with a light source are commonly

used to illuminate various body cavities, permitting visual inspection of the
interior of the cavity being examined.

JBMAGNO
 CA SOCIETY RECOMMENDATION FOR EARLY DETECTION OF CANCER IN
ASYMPTOMATIC PERSONS
TEST SEX AGE FREQUENCY

MAMMOGRAPHY F 35-40 1 baseline study

PAP SMEAR F 18 up every year
PROSTATE M 50 up every year
DRE M/F 40 up every year
BSE F 18 up every month
SIGMOIDOSCOPY M/F 50 up every 3-5 years
FECAL OCCULT M/F 60 up every year

Management of Patient with Neoplastic Diseases:

Goals:
1. Complete eradication of malignant disease (cure)
2. Prolonged survival and containment of the cancer cell growth (control)
3. Relief of symptoms associated with the disease (palliation)

⚫ SURGERY- is the most frequently used treatment modality in cancer.

* Diagnostic Surgery: 3 Methods

a. Excisional biopsy – most frequently used for easily accessible tumors of the skin,
breast, and upper or lower gastrointestinal and upper respiratory tracts.
b. Incisional biopsy – performed if the tumor mass is too large to be removed.
c. Needle biopsy – used to sample suspicious masses that are easily accessible
such as some growths in the breasts, thyroid, lung, liver, and kidney. Needle
biopsies are most often performed on an outpatient basis.

* Surgery as Primary Treatment

Goal: TO remove the entire tumor or as much as possible and any involved
surrounding tissue, including regional lymph nodes.

2 Common Procedures:

⚫ Local incision
⚫ Wide or Radical Excision

New Approaches: SURGERY AS PRIMARY TX

A. Video – assisted endoscopic surgery- is fast replacing surgeries associated with
long incisions and extended recovery periods.
Procedure:
1. An endoscope with intense lighting and an attached multi-chip mini camera is
inserted through a small incision into the body.
2. The surgical instruments are inserted into the surgical field through one or two
additional small incisions, each about 3cm long.
3. The camera transmits the image of the involved area to a monitor so the surgeon
can manipulate the instruments to perform the necessary procedure.

B. Salvage surgery
- is an additional treatment option that uses an extensive surgical approach to
treat recurrence of the cancer after a less extensive primary approach is used

Ex. Mastectomy

C. Electrosurgery- makes use of electrical current to destroy the tumor cells.

D. Cryosurgery – uses liquid nitrogen to freeze tissue to cause cell destruction.

E. Chemosurgery – this uses combined topical chemotherapy and layer by layer

surgical removal of abnormal tissue.

F. Laser Surgery – makes use of light and energy aimed at an exact tissue location
and depth to vaporize cancer cells.
G. Stereotactic Radiosurgery – is a single and highly precise administration of high
dose radiation therapy used in some types of brain and head and neck cancer.

Other forms of Surgery:

⚫ Prophylactic Surgery
– involves removing non vital tissues or organs that are at increased risk to
develop cancer.

⚫ Palliative Surgery – make the patient as comfortable as possible and to promote

quality of life as defined by the patient and his or her family.

Goal: to make the patient as comfortable as possible and to promote a satisfying

and productive life for as long as possible.

⚫ Reconstructive Surgery
– may follow curative or radical surgery and is carried out in an attempt to
improve function or obtain a more desirable cosmetic effect.

Nursing Management in Cancer Surgery

⚫ Complete a thorough pre-operative assessment for all factors that may affect the
patients who will be undergoing surgery.
⚫ Provide education and emotional support by assessing patient and family needs and
exploring with the patient and family their fears and coping mechanism.
⚫ Communicate frequently with the health team members to be certain that the
information provided is consistent.
⚫ Assess the patient’s responses to the surgery and monitor possible complications.
⚫ Provide comfort.
⚫ Initiate as early as possible plans for discharge, follow-up and home care and
treatment to ensure continuity of care.
⚫ Patients and family are encouraged to use community resources such as the
Philippine Cancer Society.

RADIATION THERAPY

- it is the use of ionizing radiation to interrupt cellular growth.

- may also be used to control malignant disease when a tumor cannot be removed
surgically or when local nodal metastasis is present, or it can be used neoadjuvantly with
or without chemotherapy to reduce the size of a tumor to enable surgical resection.
Radiation therapy may be used prophylactically to prevent the spread of a primary
cancer to a distant area.

Indications:

⚫ To cure cancer.
⚫ To control malignant disease when a tumor cannot be removed surgically or when
local nodal metastasis is present.
⚫ Prophylactic use
⚫ Palliative use.

2 Types of Ionizing Radiation

⚫ Electronic Rays (x-rays and gamma rays)

Gamma rays- to protect self you need a shield at least as thick as concrete wall
-most penetrating type
X-ray- less penetrating than gamma rays
Alpha particles- can be shielded by a sheet of paper or by human skin
Beta particles- cannot be stopped by a sheet of paper or human skin, needs thicker
shield like wood to stop them

⚫ Particles – electrons, beta particles, protons, neutrons and alpha particles.

Effects of Radiation Therapy:

⚫ Alters the DNA molecule within the cells of the tissue and breaks the strands of the
DNA helix, thus causing cell death.
⚫ It ionizes constituents of body fluids, especially water that results in the formation
of free radicals and irreversibly damaging the DNA. Cells may die immediately or it
may initiate cellular suicide (Apoptosis).

Commonly Transported Radioisotopes:

⚫ Americium-241= Diagnose thyroid disorders, smoke detectors.
⚫ Cesium-137= Cancer treatment.
⚫ Iodine-125,131= Diagnosis & treatment liver, kidney,heart, lung and brain.
⚫ Technetium-99m=Bone and brain imaging; thyroid and liver studies; localization of
brain tumors.

Radiation Measurement Terminology:

Exposure rate = amount radiation possible to receive per unit time.

Dose = total amount of radiation received.

2 Types of Radiation Therapy:

A. External Radiation or teletherapy

- is used depending on the size, shape, and location of the tumor. Different energy levels
are generated to produce a carefully shaped beam that will destroy the targeted tumor,
yet spare the surrounding healthy tissue and vital organs in an effort to reduce the
treatment toxicities for the patient.

Kinds of Teletherapy:

1. Kilovoltage therapy device

– delivers the maximal radiation dose to superficial lesions such as lesions of the
skin and breasts.

2. Linear Accelerators and betatron machines – produce high x-rays and deliver their
dosage to deeper structure with less harm to the skin and less scattering of
radiation within the body tissues.

3. Gamma Rays – are produced from spontaneous decay of naturally occurring

radioactive elements such as Cobalt 60; deliver radiation dose beneath the skin
surface, sparing skin tissue from adverse effects.

4. Particle beam radiation therapy (High Linear Energy) – transfer radiation

accelerates sub atomic particles(nuetron, pions, heavy ions) through body
damaged target cells as well as cells in its pathways.

5. Intraoperative radiation therapy (IORT) – involves delivering a single dose of high-

fraction radiation therapy to the exposed tumor bed while the body cavity is open during
surgery.

IMPLEMENTATION

1. Offer psychological support and teaching

What to expect:

⚫ commonly asked questions

⚫ Painful?
⚫ What will I ask to do during my therapy?
⚫ What happens during the actual intervention?
⚫ Will I be left alone during my intervention?
⚫ What if I become sick during my therapy and need help? What should I do?

2. Diet – increase CHON, CHO, increase fluids ( NPO several hours before treatment)

3. Medication
Compazine-nausea

3. Skin care

⚫ Radiodermatitis- inflammation of the skin after exposure to radiation ( dry,

infection is common)
- wash with water, pat dry
-avoid exposure to sun
-do not remove lines or ink marks
-wear loose-fitting clothing
-shave with electric razor
⚫ Wet reaction or desquamation- weeping of the skin due to the loss of upper
layer, develops 2-3 weeks after, heals 4-6 weeks

Implications:
⚫ Promote rest after therapy.
⚫ Cleanse area with water, pat dry.
⚫ Apply antibiotic lotion as ordered.
⚫ Expose site to air.
JBMAGNO
B. Internal Radiation Implantation or Brachytherapy
- it delivers a high dose of radiation to a localized area.The specific radioisotope for
implantation is selected on the basis of its half-life, which is the time it takes for half of its
radioactivity to decay. Internal radiation can be implanted by means of needles, seeds,
beads, or catheters into body cavities or interstitial compartments.

2 Kinds of Implants:

⚫ Sealed
⚫ Unsealed

2 Types of Radioisotopes:

◼ Intracavity Radioisotope - is frequently used to treat gynecologic cancers. In these

malignancies, the radioisotopes are inserted into specially positioned applicators
after their placement is verified by x-ray.
- Uses Cesium137 or Radium226.

Nursing Considerations:

⚫ Remain in place for prescribed period and then are removed, generally 24-72 hours.
⚫ Patients are maintained on bed rest and log rolled.
⚫ An indwelling catheter is inserted.
⚫ Low residue diets and anti-diarrheal agents, such as diphenoxylate (Lomotil)

◼ Interstitial Radioisotopes- used in treating prostate, pancreatic or breast cancer.

- it may be temporary or permanent, depending on the radioisotope used which
usually consists of seeds, needles, ribbons, beads, wires or small catheters
positioned to provide a local radiation source and less frequently dislodged.

Ex. Iridium192, iodine125, Cesium137, Gold198 and Radon222

Principle of Radiation Protection – depends on 3 factors

⚫ The distance between the nurse and the patient.

⚫ The amount of time spent in actual proximity to the patient
⚫ The degree of shielding provided

Precautionary measures:

⚫ Place patient in a private room.

⚫ Place a sign on the patient’s door and on the patient’s chart indicating that the
patient is receiving internal radiation therapy.
⚫ Observe principles of time and distance.
⚫ Check all linens, bedpans and emesis basin routinely to see if the sealed source has
been accidentally lost from the tissue.
⚫ If sealed source is dislodged, but has not fallen out of the patient’s body,
notify the x-ray radiation department at once.
⚫ If fallen out, do not pick it up with bare hands. Use forceps and place it in a lead
container.
⚫ Most patients are placed on bed rest and instructed to remain in certain positions so
that the emanations from the element will reach the correct area.
⚫ Visitors will spend limited time in the room to 30 minutes daily, seeing that visitors
maintain a 6-foot distance from the radiation source.
⚫ Prohibit visits by children or pregnant visitors.

Special precautions – Patient receiving internal radiation therapy from an

unsealed source:
⚫ Observed the principles of time, distance and shielding for radiation protection.
⚫ Wear gloves when handling bedpans, bed linens and patient’s clothes.
⚫ Dispose of urine, feces and vomitus according to policy.
⚫ Handle dressings with forceps and dispose of them according to policy.
⚫ Follow hospital procedure for disposal of patient’s bed linens and clothing.

Common Side Effects of Radiation Therapy

External Radiation

Head and Neck

⚫ irritation of oral mucous membranes with oral pain and risk of infection.
⚫ Loss of taste.
⚫ Irritation of the pharynx and esophagus with nausea and indigestion.
⚫ Increase intracranial pressure.

Chest
- Inflammation of lung tissue with increase susceptibility to infection.

Abdomen
- nausea, vomiting, diarrhea, anorexia

Pelvis
- diarrhea, cystitis, sexual dysfunction, Urethral and rectal stenosis

General Side Effects:

SKIN: change in texture and/or color, moist desquamation(rare); alopecia
BLOOD: bone marrow depression with leucopenia, anemia and thrombocytopenia.
Depressed Immune Function
Fatigue

Internal Radiation
General Effects:
1. Elevated temperature.
2. Cervical implant: Urinary frequency, diarrhea, nausea, vomiting and
anorexia.
3. Head and Neck: mucositis, oral pain and risk for infection, anorexia.

Skin Care Treatment

⚫ Apply the special skin care lotion four times a day, starting immediately.
⚫ Do not wash off treatment markings. Tatoos, if done, are permanent.
⚫ Keep skin clean and dry. Expose the skin to air as much as possible.
⚫ Protect the skin in the treatment area from the sun and cold by using scarves, hats
or other clothing.
⚫ Cornstarch may be used for dry, itchy skin.
⚫ Irritated skin, a different lotion may be needed.
⚫ Bathing – clear water and pat dry. Use mild soap.
⚫ Clothing: wear soft, loose cotton clothing over the treatment area.
⚫ Shampooing – use baby shampoo.
⚫ Shaving – use electric razors.
⚫ Do not rub or scratch the skin in the treatment area.
⚫ Do not use lotions or creams not approved by the doctor.
⚫ Do not use deodorants, perfumes or make-up in the treatment area.
⚫ Do not use ice packs or heating pads
⚫ Do not use tape in the treatment area.

Post Removal of Source

⚫ Betadine douche
⚫ Enema
⚫ Out of bed
⚫ Avoid direct sunlight
⚫ cream
⚫ Resume Sexual intercourse within 7-10 days

Factors affecting the side effect of Radiation Therapy:

⚫ body site irradiated

⚫ radiation dose
⚫ extent of body area treated
⚫ method of radiation therapy

https://youtu.be/E44W54z_Ykw (URL- MRI)

https://youtu.be/-xL4qPBH48U
https://youtu.be/6F3gNFL5IL8
https://youtu.be/7ScVu-ZGfu8
https://youtu.be/rzNzNBqay5k
https://youtu.be/MZRfzLQb92A
(URL- CT SCAN)
( URL- Cryotherapy)
( URL- Stereotactic/ Gamma Knife)
(URL- Teletherapy)
( URL- Brachytherapy)

JBMAGNO
CHEMOTHERAPY
-used primarily to treat systemic disease rather than lesions that are localized
and amenable to surgery or radiation.

Goals:
⚫ To cure
⚫ Control
⚫ Palliation of manifestations

Indication:
⚫ disease is widespread
⚫ the risk of undetectable disease is high
⚫ the tumor cannot be resected and is resistant to radiation therapy

2 Types of Chemotherapy

⚫ Adjuvant chemotherapy
-it is started after initial treatment with either surgery or radiation therapy.

⚫ Neoadjuvant Chemotherapy
-refers to the preoperative use of chemotherapy to reduce the bulk and lower the
stage of a tumor making it amenable to surgery even to possible cure with
subsequent local therapy.

Classes of Antineoplastic Drugs

1. Alkylating Agents

Common adverse effects:

⚫ Acute Myelogenous Leukemia
⚫ Irreversible infertility
⚫ Nephrotoxicity
⚫ Hemorrhagic cystitis

5 Subclasses:

⚫ Nitrogen mustards

Eg: Mechlorethamine
Chlorambucil
Cyclophosphamide
Melphalan
Ifosfamide

⚫ Nitrosoureas (carmustine)

Eg: Streptozocin
Carmustin
Lomustine

⚫ Alkyl sulfonates (busulfan)

Eg: Busulfan

⚫ Triazines (dacarbazine)
 Eg. Dacarbazine
Temozolomide

⚫ Ethylenimines (thiotepa

Eg: Thiotepa
Altretamine

2. Antimetabolites
-Phase-specific, working best in the S phase and having little effect in G0.

Toxic Effects:

⚫ Signs and Symptoms:

⚫ Nausea and vomiting
⚫ Stomatitis
⚫ Diarrhea
⚫ Alopecia
⚫ Leucopenia

Subclasses:

⚫ Folic Acid Analogue

Eg. Methotrexate

⚫ Pyrimidine analogue
Capecitabine
Gemcitabine

⚫ Cystosine arabinoside
Eg. ARA-C
Purine analogues
Fludarabine

3. Cytotoxic/ Antitumor Antibiotics

Action:
⚫ Disrupt DNA replication and RNA transcription.
⚫ Create free radicals which generate breaks in DNA and other forms of
damage.
⚫ Interfere with DNA repair.
⚫ Bind to almost everything they come in contact with and kill cells, probably
by damaging cell membrane.

Examples:
Actinomycin
Bleomycin
Mithramycin
Mitomycin

4. Plant Alkaloids

There are 2 main groups extracted from plant sources:

A. Vinca Alkaloids
Eg.
- Vincristine
- Vinblastin
Action:
Phase-specific acting during mitosis. They bind to a specific protein that
promotes chromosome migration during mitosis and serves as a conduit for
neurotransmitter transport along axons.

Toxicity:

⚫ Depression of deep tendon reflexes

⚫ Paresthesias
⚫ Motor weakness
⚫ Cranial nerve disruptions
⚫ Paralytic ileus

⚫ Etoposide (also called VP-16)

-acts in all phases of the cell cycle, causing breaks in DNA and metaphase arrest.

Toxicity:
⚫ Bone marrow suppression
⚫ Nausea and vomiting
⚫ Hypotension

5. Hormone and Hormone Antagonists

◼ Corticosteroids

-Phase-specific (G1); acts by binding to specific intracellular receptors,

repressing transcription of memory RNA and thereby altering cellular function and
growth.

Ex. Prednisone – main hormone used.

Side Effects:

⚫ Impaired healing
⚫ Hyperglycemia
⚫ Hypertension
⚫ Osteoporosis
⚫ Hirsutism

◼ Hormone antagonists
⚫ Tamoxifen – competes with estradiol receptors in breast tumors.
⚫ Diethylstilbestrol – competes with hormone receptors in endometrial and
prostate tumors
⚫ Anti-androgen (Flutamide) and Luteinizing hormone-releasing hormone- blocks
testosterone synthesis in prostate cancer.

6. Miscellaneous Agents- mechanism of action is unknown or too complex to

categorize.
Eg. Asparaginase, procarbazine
7. Topoisomerase
Types:

◼ Topoisomerase I- interefers with DNA synthesis by inhibiting the enzyme

topoisomerase I, preventing cells from dividing.

Drugs: Irinotecan ( Camptosar)

Topotecan ( Hycamtin)

◼ Topoisomerase II- inhibits type II topoisomerase activity resulting in the

break of DNA.

Drugs:
Etoposide (VePesid)
Doxorubicin ( Adriamycin)
Teniposide (Vumon)

Side effects

⚫ bone marrow supression

⚫ Nausea, vomiting, diarrhea
⚫ Alopecia
⚫ Stomatitis

IMMUNOSTIMULANTS
Types:
⚫ Interferon- has antiviral, anticancer, immunostimulant actions. These are drugs
naturally produced and released by cells after viral infection.

Drugs:
Interferon alfa-2a ( Roferon-A)
Interferon alfa-2b (Intron-A)

⚫ Interleukins- stimulate immune function by increasing the activity of natural killer

cells and platelets.

Drug:
Aldesleukin (Proleukin)

⚫ T-cell and B-cell modulator- stimulates B cells which then stimulate antibody
formation, enhances T-cell activity and increases the activity and proliferation of
monocytes and macrophages.

Drug:
Levamisole (Ergamisol)

Chemotherapeutic administration

1. Oral route
2. IM or SC
3. IV
Risk: Infection & Phlebitis
Management:
⚫ Smallest needle gauge
⚫ Aseptic technique
⚫ Monitor IV site frequently
⚫ Change IV fluid q4hrs

4. Central Venous Catheter Infusion

Risk:
⚫ Infection
⚫ Catheter clot
⚫ Sepsis
⚫ Needle malposition

Management:
⚫ Aseptic technique
⚫ Monitor site daily
⚫ Flush catheter daily/ between use
⚫ Assess for signs of infection

5.Venous Access Device (VADs)

Risk: infection
infiltration from malposition

6.Intra-arterial Route

Risk: infection
bleeding at catheter site
clotting at site

Management:
⚫ dressing change daily and assess infection
⚫ Irrigate/flush catheter
⚫ Avoid kinks in tubing

7.Intraperitoneal - used for ovarian and colon CA, high concentration of agents
delivered to peritoneal cavity via catheter, then, drain
8.Intrathecal

⚫ Ommaya reservoir- is a plastic, dome-shaped device, with a catheter attached to

the underside used to deliver chemotherapeutic agents in patients with brain
tumor.

Chemotherapy Safety Guidelines

⚫ Obtain special training

⚫ Wear: gloves
⚫ disposable, closed, long-sleeved gown
⚫ Label prepared drugs appropriately
⚫ Double bag drugs prepared – transport
⚫ Clean any accidental spill
⚫ Dispose all used materials appropriately
⚫ Dispose all syringes and needles intact

Side Effects and Nursing Management

1. GI System

A. Nausea and Vomiting

Management:
-antiemetics 4-6 hrs before initiated
- Withhold fluids/foods 4-6 hours before
- Support food preferences
- Small frequent feeding/ meals – calories and CHON
-encourage oral hygiene
-may use distraction such as music therapy or relaxation technique
-prevent unpleasant sights, odors and sounds in the environment

B. ＊Diarrhea
Management:
- antidiarrheal
 - everyday perieneal care
- Monitor K, Na, & CL level

＊Constipation
Management:
-increase fiber and fluids
-Have stool softeners

A. Stomatitis

Management:
- perform good oral hygiene
- rinse with lidocaine before meals
- cleanse or rinse with plain water or dilute a water-soluble lubricants after meal
- may use KY jelly for cracked lips
- suck popstick to provide moisture
- avoid spicy and acidic foods
-avoid commercial mouthwash that contains alcohol
-use soft-bristled toothbrush

2. Hematologic System

A. Thrombocytopenia - decrease platelet count ( below 150T –300T)

Responsibilties:
⚫ Avoid bumping/bruising skin
⚫ Protect from physical injury
⚫ Avoid aspirin product
⚫ Avoid IM injection
⚫ Monitor blood count
⚫ Assess/teach bleeding tendencies

B. Leukopenia- WBC below 5T-10T

Responsibilities:
⚫ Careful handwashing technique/aseptic technique
⚫ Reverse isolation
⚫ Assess for respiratory infection
⚫ Avoid crowds or people with infection

C. Anemia
Responsibilities:
⚫ Adequate rest
⚫ Monitor hgb and hct count
⚫ Oxygen PRN
⚫ Adequate protein and caloric intake

3. Intergumentary System

⚫ Alopecia
Responsibilities:
- provide support and encouragement
- scalp tourniquets/ scalp hyperthermia via ice pack can be used
4. Renal System
Responsibilities:
- encourage frequent voiding
- increase oral fluid intake
- Allopurinol (Zyloprim) may be given as ordered to prevent uric acid formation

5. Reproductive System
Responsibility:
- may do banking sperm

6. Neurologic System
Side Effect:
- hearing loss
- paralytic ileus
- loss of tendon reflex

Other Therapeutic Modalities:

A. Immunotherapy
Using Biologic Response Therapy
⚫ It is used to modify the biologic processes that result in malignant cells,
primarily through enhancing the person's own immune responses.

C. Photodynamic Therapy (Phototherapy/ photoradiation/ photochemotherapy)

-this is a new method of treating certain kinds of superficial tumors.

Photofrin – an intravenous dose of photosensitizing compound, which is selectively

retained in higher concentrations of malignant tissue.

C. Bone Marrow Transplant

-primary treatment modality in leukemia
Types:

⚫ Allogenic
⚫ Autologous
⚫ Syngeneic

D. Hormone Therapy
-used as an adjunct to other types of CA therapy
-it can slow tumor growth or prevent re-occurence

PAIN in Cancer

Physiologic causes:
⚫ Bone marrow destruction
⚫ Obstruction of an organ
⚫ Compression of peripheral nerves (sharp-continuous pain)
⚫ Infiltration or distention of tissue (localized dull pain)
⚫ Inflammation, infection and necrosis

Psychological Causes:
depends on the client’s perceived threat.
⚫ Fear or anxiety generated from the effects
⚫ Loss or threat of loss
⚫ Frustration

Assessment:
⚫ Severity and duration (pain scale)
⚫ What, when and where pain occurs
⚫ Understand as client views it.
⚫ Nature of the disease
⚫ Probable life expectancy
⚫ Temperament and psychological state
⚫ Occupational, economic, educational background
⚫ Vital sign
a. Low to moderate pain and superficial in origin (sympathetic)
- Increase BP, PR, RR and muscle tension
b. Severe pain or visceral in origin (parasympathetic)
- decrease BP, PR, N/V, weakness

⚫ Behavior as indicator of pain

-Posture
-Gesture
-Daily activities
Medication Management:
1. Acetaminophen, ASA, NSAIDs (mild pain)
2. Opioids – CODEINE
-added to regimen as pain increases
3. Intraspinal Morphine Administration
- an implantable infusion pump delivers a continual supply of opiate to the
epidural or subarachnoid space

S/E:
Constipation nausea and vomiting sedation
resp.depression Urinary retention

Surgical Management:
⚫ Nerve blocks
-involves interruption of nerve pathways some place along the path of
transmission from periphery to brain.

⚫ Non invasive Modalities

1. Transcutaneous Nerve Stimulation (TENS)
-electrical stimulation of the skin surface over a painful area

JBMAGNO
 BREAST CANCER

Types of breast cancer:

A. Carcinoma in Situ ( Noninvasive carcinoma)

- characterized by the proliferation of malignant cells within the ducts and
lobules, without invasion into the surrounding tissue.

Two types of Carcinoma in Situ:

⚫ Ductal Carcinoma in Situ (DCIS)- characterized by the proliferation of cancer
cells in the milk ducts without invasion to surrounding tissues.
Treatment: simple mastectomy, lumpectomy, tamoxifen x5 years

⚫ Lobular Carcinoma in Situ (LCIS)- characterized by proliferation of cells within

the breast lobules.
Treatment: bilateral total mastectomy, chemoprevention: tamoxifen x5 years

B. Invasive Carcinoma
- arises from the intermediate ducts of the breast and may involve surrounding
breast tissue, lymph, and blood vessels.

Seven types of Invasive Cancer:

1. Infiltrating Ductal Carcinoma

2. Infiltrating Lobular Carcinoma

3. Medullary Carcinoma

4. Mucinous Cancer

5. Tubular Ductal Carcinoma

6. Inflammatory Carcinoma

7. Paget’s Disease of the nipple

Etiology
⚫ Cause is unknown.
⚫ Although genetic, hormonal or biochemical factors are likely to be involved, 70%
of women with breast CA had no known risk factors.

Precipitating factors:
⚫ Reproductive history
⚫ Radiation exposure
⚫ Lifestyle

Predisposing factors:
⚫ Gender
⚫ Race
⚫ Age
⚫ Family history
⚫ Medical history
⚫ Menstrual history

Men – risk factors:

⚫ A 1st degree male or female relative with breast cancer
⚫ Variations in BRCA2 gene
⚫ Klinefelter’s syndrome- XXY syndrome
⚫ Exposure to ionizing radiation

Signs and symptoms:

⚫ Small, hard painless lump in breast, mostly in upper outer quadrant
⚫ Non-tender and fixed lesions
⚫ Lesions are hard with irregular borders rather than encapsulated and smooth
⚫ Nipple discharge
⚫ Change in size and shape of breast
⚫ Dimpling, pulling, or retractions
⚫ Peau d’orange skin
⚫ Persistent skin rash near nipple area
⚫ Flaking or eruption near the nipple

Diagnostic exams
⚫ Breast self-exam- is best performed after menses (day 5 to day 7, counting the
first day of menses as day 1).
⚫ Clinical breast self-exam- is a physical exam of the breasts and the underarm
area by a trained healthcare professional.
⚫ Baseline mammogram- it can detect nonpalpable lesions and assist in
diagnosing palpable masses. Done between age 40-49; annual mammogram
after age 50.
⚫ Imaging Studies:

1. Ultrasonography- is used as a diagnostic adjunct to mammography that will help in

distinguishing fluid-filled cysts from other lesions.
2. CT scan
3. MRI- it is a highly sensitive test that is useful as diagnostic adjunct to mammography.
A magnet is linked to a computer that creates detailed images of the breast without
exposure to radiation.
4. PET scan

⚫ Specimen examinations:
1. Cytologic exam
2. Tissue biopsy

Breast cancer treatment by stage at diagnosis

Stage Tumor Surger Chemo Radiati

s y Tx on
0 CIS TM or Tamoxi For
lumpec fen lumpec
tomy tomy
I Tumors BCT or Consid For
are < 2 MRM ered for BCT
cm in all
diamet invasiv
er & e
confine tumors
d to
breast
II Tumors BCT or Regime For
are < 5 MRM n BCT
cm, or depend
smaller s on
with tumor
mobile size &
 axillary nodal
lymph status
node
involve
ment

TM- BCT-
Total breast
Mastec conser
tomy vation
treatme
nt

Stag Tumors Surger Chemo Radiati

e y Tx on

IIIa Tumors MR Post-op To

are > 5 M & chest
cm, possibl wall &
accompan e pre- possibl
ied by op y axilla
enlarged after
axillary MRM
lymph
nodes
fixed to
one
another or
to
adjacent
tissue
IIIb More MRM Post-op To
advanced & chest
lesions w/ possibl wall &
satelite y pre- possibl
nodules, op y axilla
fixation to after
the skin or MRM
chest wall,
ulceration,
edema
IV All tumors Possibl To To
w/ distant y control control
metastasi lumpec progres progres
s tomy or sion sion
MRM and/or and/or
palliatio palliatio
n n

Treatment:
Medical Management:
1.)Chemotherapy- a combination therapy with other treatments to delay or prevent
recurrence.
⚫ Doxorubicin (Adriamycin)
⚫ Cyclophosphamide (Cytoxan)
⚫ Methotrexate
⚫ 5-fluorouracil

2.) Hormonal therapy- can be used with or without chemotherapeutic drugs indicated
in women who have hormone receptor-positive tumors. The use of hormonal therapy
can be determined by the results of estrogen and progesterone receptor assay.
⚫ Androgens: fluorymesterone (Halotestin)
⚫ Estrogens: diethylstilbestrol ( DES)
⚫ Antihormonal agents: Tamoxifen

3. Radiation therapy- is used to decrease the chance of recurrence.

B. Surgical Management

1. Breast-conserving procedures- usually involves removal of the entire tumor along

with a margin of normal surrounding tissue.
⚫ Lumpectomy
⚫ Wide excision
⚫ Partial mastectomy
⚫ Segmental mastectomy
⚫ Quadrantectomy

2.Axillary lymph node dissection- generally involves the removal of 12-20 nodes.
Sentinel lymph node dissection (SLND) recently has become the standard of care,
axillary lymph node dissection (ALND)reserved for patients with evidence of disease
in the axilla.

COMPARISON OF SENTINEL LYMPH NODE BIOPSY AND AXILLARY LYMPH

NODE DISSECTION
 SENTINEL LYMPH NODE AXILLARY LYMPH NODE
BIOPSY (SLNB) DISSECTION (ALND)
Procedure will take Procedure will be approximately
approximately 15-30 minutes 60-90 minutes
No surgical drain Surgical drain
Done as outpatient surgery General anesthesia will be used
using local anesthesia with IV which requires the patient to be
moderate sedation unless being admitted overnight
performed in conjunction with
total mastectomy
Postoperatively neuropathic Postoperatively there is
sensations may be felt by the presence of neuropathic
patient sensations
Decreased ROM in affected arm Decreased ROM likely
unlikely postoperatively but may postoperatively
occur
Lymphedema incidence Approximately 10-30%
approximately 0-8% lymphedema incidence
Seroma (collection of serous Seroma may occur
fluid in the axilla) may occur postoperatively.
postoperatively

3. Total/ Simple Mastectomy- removal of breast tissue and nipple but not lymph
nodes and muscles.

4. Modified Radical Mastectomy- includes removal of the breast and axillary lymph
nodes but it preserves the pectoralis major muscle.

5. Radical Mastectomy- removal of the breast, nodes, and chest muscles.

6. Breast Reconstruction
⚫ Tissue Expanders- a temporary device is placed on the chest wall deep to the
pectoralis major muscle.

⚫ Transverse Rectus Abdominis Muscle Flap- musculocutaneous flap( muscle,

skin fat, blood supply) is transposed from abdomen to the mastectomy site.

⚫ Latissimus Dorsi Muscle Free Flap- the flap originates from the flat, triangular
muscle running from the upper vertebral column to the arm

⚫ Nipple-Areola Reconstruction- is the making of a nipple/areola shape in a

reconstructed breast. Done as one of the last stages of breast reconstruction.

POTENTIAL COMPLICATIONS AFTER SURGERY:

1. LYMPHEDEMA- results if functioning lymphatic channels are inadequate to ensure
a return flow of lymph fluid to the general circulation. Occurs about 10-30% for
patients who undergo ALND and about 0-8% for patients who had SLNB. To prevent
transient swelling, the patient is advised to perform prescribed exercises, elevating
the arm above the heart and gentle muscle pumping like making a fist and releasing
it.
2. HEMATOMA OR SEROMA FORMATION- may occur after mastectomy or breast
conservation, usually develops 12 hours after surgery. Signs may include swelling,
tightness, pain and bruising of the skin.
3. INFECTION- monitor for redness, warmth around incision, tenderness, foul
smelling drainage, fever and chills.

Nursing management

Diagnostic Phase:
⚫ Minimize uncertainty
⚫ Prevent disease advancement
⚫ Protect emotional well-being
⚫ Establish trusting communication
⚫ Adjuvant Therapy Phase:
⚫ Develop a supportive network
⚫ Minimize adverse physical outcomes
⚫ Manage stress
⚫ Understand family members’ responses

Ongoing Recovery Phase:

⚫ Maintain association with professionals
⚫ Maintain positive outlook
⚫ Redefine self and partner
⚫ Cultivate ongoing support
⚫ Preoperative Nursing Intervention:
⚫ Explain breast CA, correct misconceptions, and treatment options.
⚫ Reduce fear
⚫ Reduce anxiety
⚫ Improve coping ability
⚫ Promote decision-making ability

Postoperative Nursing Intervention:

⚫ Relieve pain and discomfort
⚫ Maintain skin integrity
⚫ Prevent infection, injury
⚫ Promote positive adjustment & coping
⚫ Monitor drainage; monitor bleeding

Nursing Diagnosis:
⚫ Disturbed body image related to loss
⚫ Impaired skin integrity related to surgical Incision
⚫ Risk for infection

JBMAGNO
 PROSTATE CANCER

⚫ a malignant tumor of the prostate gland

⚫ an androgen-dependent adenocarcinoma that is usually slow growing
⚫ the 2nd leading cause of death in males
⚫ 80% of cases diagnosed after age 80
⚫ fertility is not a factor

RISK FACTORS

⚫ Increasing Age
⚫ African
⚫ High Fat Diet : lowest incidence in Japanese; risk of prostate cancer greater in
men whose diet contains excessive amount of red meat and dairy products high
in fats.
⚫ Genetics : 8x more risk if 1st & 2nd degree; familial predisposition in men with
father or brother previously diagnosed with prostate cancer.

Signs & Symptoms

⚫ asymptomatic in early stages

⚫ urinary symptoms: frequency, dribbling, retention, obstruction, hematuria,
cystitis, trouble starting your urine stream, weaker than normal urine stream,
⚫ bone metastasis results in hip pain, back ache, weight loss, perineal & rectal
discomfort
Diagnostic studies
⚫ Digital Rectal Exam
⚫ Biopsy
⚫ Transrectal ultrasound
⚫ PSA determination

MANAGEMENT

P-omegranate juice

R-adiation: Brachytherapy

O-rchiectomy/cryoablation

S-urgery: Radical Prostatectomy

T-eletherapy
A-nalgesics
T-he use of chemotherapy
E-hormonal therapy YAN ( Hormone Therapy)

Nursing Problems
⚫ Altered urinary elimination
⚫ Pain
⚫ Sexual dysfunction / Body Image disturbance
⚫ Urinary retention
⚫ Altered role performance

JBMAGNO
 UTERINE CANCER

⚫ CANCER OF THE ENDOMETRIUM

⚫ The most common gynecologic malignancy
⚫ Usually AdenoCA

RISK FACTORS

⚫ Cumulative exposure to estrogen is considered a major risk factor; but OCP in

combination preparation decrease risk by 50%
⚫ Familial tendency
⚫ DM, HPN, gallbladder disease
⚫ Ovarian neoplasms
⚫ Tamoxifen
⚫ Obesity – most important risk factor; Increases estrogen production & bio
availability in muscle & adipose. Overweight by up to 22.7% = 3x more risk;
>22.7% = 9x more risk
Signs and symptoms:

DIAGNOSTIC TEST

⚫ Annual PE/ Gyne Exam

⚫ Biopsy- tissue sample will e examined.
⚫ Pap Smear – 50% of patients with abnormal results
⚫ Schiller’s test (Lugol’s test) – cervical tissue staining
⚫ MRI – evaluates myometrial invasion and lymph node involvement
⚫ CA 125 ( cancer antigen 125)- used to monitor certain cancers during and after
treatment. Normal value is less than 35 units/ml.

Pap smear result:

RESULT PAP smear

CLASS 1 NORMAL
CLASS 2 INFLAMMATION (repeated after
3 months)
CLASS 3 MILD TO MODERATE
DYSPLASIA (repeated within 3
weeks)
CLASS 4 PROBABLY MALIGNANT
(BIOPSY)
CLASS 5 MALIGNANT

STAGES OF ENDOMETRIAL CANCER

0- inner lining of the uterus

I- inner lining to the endometrium
II- uterus and cervix
III- outside of the uterus, vagina, lymph nodes
IV- spread to the bowel, bladder, abdomen or other organs

Management:

Intervention
⚫ Check serum creatinine, BUN, Mg, Ca, K levels before start of therapy
⚫ Use gloves
⚫ Hydrate and monitor I & O
⚫ Do not use ordinary rubber catheter during Chemotherapy- Use TEFLON

JBMAGNO
 LIVER CANCER

⚫ A rare form of cancer with a high mortality rate- fifth most common cancer and
second most common cause of cancer death
⚫ 90% arise from the liver parenchymal cells (hepatoma)
⚫ Some originate from the intrahepatic bile duct (cholangioma)

Lobes of the liver

⚫ The liver is one of the most common sites of metastases; primary cancer usually
is from colon, breast, lung, and urogenital cancer
⚫ Metastatic cancer is 20 times more common than Primary tumor
⚫ MEN ARE AFFECTED 2X MORE than women
⚫ Average age is 50, but may occur at any age

Risk Factors
A-lcoholic beverages
L-iver cirrhosis
C-igarette smoking
O-verexposure to aflatoxin
H-epatitis B,C,D and Schistosomiasis
O-ncogenic foods
L-iver toxins( vinyl chloride, arsenic)
Types of Primary Tumor:
⚫ Hepatocellular CA (HCC or hepatoma)- most common form of primary liver
which starts in hepatocytes.
⚫ Cholangiocellular CA ( cholangioma or bile duct cancer)- cancer begins in
the small tube-like bile ducts within the liver

Signs and Symptoms

⚫ Abdominal mass, RUQ pain, jaundice, anemia
⚫ Cancer signs: weight loss, fatigue, anorexia
⚫ Portal hypertension, ascites, esophageal varices which may rupture and cause
hemorrhage

Diagnostics
⚫ Serum Bilirubin
⚫ Alkaline Phosphatase
⚫ SGOT/ AST
⚫ SGPT/ ALT
⚫ LDH
⚫ Increase WBC, RBC
⚫ Hypoglycemia
⚫ Hypercholesterolemia
⚫ AFP (alpha-feto protein)- tumor marker of 10 liver cases, useful to determine if
metastatic liver Ca & primary liver Ca
⚫ Liver scan, USD, MRI, PET scan
⚫ Needle biopsy
⚫ Increased Serum Ammonia
⚫ Serum Crea, BUN

Management
1. SURGERY- treatment of choice when confined to one lobe; not for patients with
cirrhosis (SUBTOTAL HEPATECTOMY)

TYPES OF SURGERY:
⚫ LOBECTOMY
⚫ CRYOSURGERY

⚫ LIVER TRANSPLANT- has become a practical therapeutic option for patients

with end-stage liver disease or localized HCC. It is not recommended for
widespread malignant disease.

COMPLICATIONS AFTER LIVER TRANSPLANT:

◼ BLEEDING- is common after surgery. Platelets, fresh-frozen plasma, or other
blood products may be administered.
◼ INFECTION- leading cause of death after liver transplant. Susceptibility to
infection is increased by the immunosuppressive therapy to prevent rejection.
◼ REJECTION- is a primary concern after transplant. Immunosuppressive drugs
are used as long term therapy after liver transplant to prevent rejection.

2. Chemotherapy- adjuvant prior to surgery; systemic chemotherapy is not used for

patients with hepatoma. A targeted therapy is used to treat metastatic liver cancer to
inhibit the growth of new blood vessels.

3. Radiation Therapy- for unresectable tumors, palliative so NO significant change in

survival rate.

4. Transcatheter chemoembolization/ TACE ( transarterial chemoembolization)- a

minimally invasive procedure performed to place a catheter in the arteries to the
tumor and an embolic agent is administered mixed with chemotherapeutic agents.

JBMAGNO
 BRAIN TUMOR

⚫ Localized intracranial lesion that occupies space within the skull. The brain is a
frequent site for metastasis from other sites.

Types:
⚫ Primary – originates from cells & structures within the brain
⚫ Secondary – tumors that develop from the outside of the brain

Groups of Tumors:
⚫ Meningioma
⚫ Acoustic Neuroma
⚫ Gliomas
⚫ Metastatic

Incidence
⚫ Cause is Unknown
⚫ Metastatic CA is the most CA in the brain
⚫ 25% of people with CA develop brain metastasis

TUMOR TYPE ORIGIN OF CELLS COMMON

LOCATION S
1. Astrocytoma Astrocytes Cerebellum
2. Brain Stem Astrocytes Brain
Gliomas stem/cerebral
hemispheres
3. Oligodendrocytes Cerebral
Oligodendroglioma hemispheres
4. Ependymomas Ependymal cells Lining of ventricles
(4th ventricle)
5. Undifferentiated Cerebellum
Medulloblastoma cells
6. Germ Cell Embryonal, Pineal
tumor endodermal and hypothalamic
cells similar to regions
those found in
testes & ovaries
7. Lymphomas Lymphocytes Cerebral
hemispheres
8. Papillomas Choroid plexus Within ventricles
9. Meningiomas Arachnoid Lining of dura
granulation
 10. Sarcoma Connective tissue, Dura over cerebral
dura hemispheres
11. Pituitary Pituitary gland Underneath brain
tumors in sella tucica
12. Acoustic Nerve sheath CN 8
neuromas
13. Blood vessels Cerebellum,
Hemagioblastoma medulla
14. Squamous nest Suprasellar region
Craniopharyngioma cells

SIGNS and SYMPTOMS

⚫ Result from enlarging mass which compresses brain structures

⚫ Depend on type of tumor, location, & degree of invasion
⚫ May be localized or systemic

Increased ICP:

A. Classic Signs:
⚫ Headache – is common in morning.

⚫ Vomiting – due to the irritation of vagal center in medulla; vomiting is described

as projectile.
⚫ Papilledema – present in 70% of patients. Decreased visual acuity and double
vision may be experienced by the patient.

A. Cushing’s Triad
TUMOR LOCATION AND ITS MANIFESTATIONS:

FRONTAL LOBE-impaired judgment, impaired sense of smell, memory loss, vision

loss, papilledema
PARIETAL LOBE- impaired speech, inability to write, lack of recognition
OCCIPITAL LOBE- vision disturbances, seizures
TEMPORAL LOBE- seizures, dysphagia
BRAINSTEM- diff swallowing/speaking, drowsiness, hearing loss, uncoordinated gait,
vomiting, headache

Diagnostic Tests

⚫ CT scan-used to identify the location of lesion.

⚫ MRI- allows for detection of small lesions.
⚫ Cerebral Angiography- a procedure that uses a special dye (contrast medium)
and then takes x-ray images of the brain.
⚫ EEG- test to detect problems in the electrical activity of the brain and used to
rule out seizures.
⚫ CSF studies (cytology)- done to detect malignant cells. CNS tumors can shed
cells into CSF.

Management
⚫ Craniotomy – remove tumor whenever possible
⚫ Radiation & Chemotherapy – may follow surgery; also for inaccessible &
metastatic tumors
⚫ Watch for wound breakdown & ICP
⚫ Drug therapy– hyperosmotic agents, steroids, and diuretics to manage increased
ICP

Nursing Management
⚫ VS/NVS monitoring
⚫ Watch for increased ICP
⚫ Administer meds as ordered
⚫ Supportive care for neurological deficits
⚫ Pre – op care/ Chemo Care
⚫ Psychological support
⚫ Document seizure activity
⚫ Watch for pupillary dilatation an loss of light reflex

Chemotherapy Adverse Effects:

⚫ Abdominal cramps
⚫ Diarrhea
⚫ Alopecia
⚫ Bone marrow depression
⚫ Nausea & vomiting
⚫ Stomatitis

Radiation Therapy Adverse Effects:

⚫ Decreased salivation & taste sensation
⚫ Mucositis & pharyngitis
⚫ Desquamation / Epilation
⚫ Erythema
⚫ Headaches
⚫ Myocarditis, Pericarditis & Pneumonitis
⚫ Sweat gland destruction

JBMAGNO
 CERVICAL CANCER

⚫ a disease in which the cells of the cervix become abnormal and start to grow
uncontrollably, forming tumors.

2 TYPES:

⚫ Squamous cell carcinoma- develops from squamous epithelial cells; and

is the most common form of cervical cancer
⚫ Adenocarcinoma- develops from Columnar epithelial cells.

STAGE CHARACTERISTICS
1 Carcinoma confined to Cervix (Cervical Intraepithelial Neoplasia)
CIN1- (mild dysplasia); there is very small amount of cancer, which is
visible only under the microscope; area of invasion is <3 mm deep
and <7 mm wide
CIN2- (moderate dysplasia); area of invasion spread deeper than 5
mm into connective tissue of the cervix and wider than 7mm
CIN3- (severe dysplasia); Considered as Carcinoma in situ
2 Cancer has Extends beyond the cervix but not to pelvic wall; involves
upper two thirds of vagina; cancer does not involve the lower third of
vagina
3 Cancer has spreads to pelvic wall and involves lower 1/3 of vagina
4 Most advanced form of cervical Cancer wherein it spreads to the
other part of the body

ETIOLOGY
-unknown, cervical cancer appears to be related to repeated injuries to the
cervix.

Precipitating Factors:
⚫ Sexual History- Women who had sexual intercourse at an early age (17 y.o)
women
⚫ Multiple sexual partners ,Smoking
⚫ HPV- Humanpapilloma virus
⚫ HIV- Human immunodeficiency virus; damages the body’s immune system
⚫ Diet- Low fruits and vegetables
⚫ Immunosuppressed

Predisposing Factors:
⚫ Age (35-55 y.o)
⚫ Race (Black women: African-american)
⚫ Low socioeconomic status
Signs and Symptoms:
◼ Initial symptoms include:
⚫ Post coital bleeding
⚫ Irregular vaginal bleeding or spotting between periods or after menopause
⚫ Malodorous discharge
◼ Late symptoms include:
⚫ Bleeding becomes more constant and accompanied by pain that radiates to
buttocks and legs
⚫ Weight loss
⚫ Anemia
⚫ Fever

Diagnostic test:
⚫ PAP TEST (Pap smear)- most commonly used for diagnosing cervical cancer.
⚫ Colposcopy- involves the use of a special binocular microscope that is called a
colposcope and similar to a Pap smear
⚫ Pelvic exam- the doctor will examine the abdomen to check for swelling and any
masses.
⚫ Endocervical curettage- scraping the mucus membrane of the endocervical
canal (passageway between cervix and uterus) to obtain a small tissue sample.

MEDICAL-SURGICAL MANAGEMENT
⚫ HPV Vaccine
⚫ Cervical Conization
⚫ Hysterectomy
⚫ Cryosurgery
⚫ Laser Surgery
⚫ Radiotherapy
⚫ Chemotherapy

Nursing Diagnosis:
⚫ Acute Pain related to disease process
⚫ Deficient fluid volume related to excessive bleeding
⚫ Anxiety related to threat of death
⚫ Risk for imbalanced body temperature related to presence of invading pathogens
⚫ Risk for Constipation related to tumor obstruction

NURSING INTERVENTIONS
⚫ Assess vital signs, including temperature, pulse, respiration and blood pressure.
⚫ Obtain client’s assessment of pain to include location, characteristics, onset,
duration, frequency, and intensity; use pain scale for evaluating
⚫ Identify client’s perception of the threat represented by the situation.
⚫ Observe behaviors that can point to client’s level of anxiety.
⚫ Observed for discharges from the vagina and note for its odor, color, and
amount.
⚫ Encourage client to express feelings about the current condition.
⚫ Be available to client for listening.
⚫ Help the patient seek information on stage of cancer, treatment options.
⚫ Provide comfort measures such as quiet environment, and calm activities.
⚫ Administer analgesics as prescribed by the doctor.
⚫ Provide adequate fluid intake including high-fiber foods.
⚫ Encourage client to comply well with treatment regimen.
⚫ Explain the importance of life-long follow up regardless of treatments to
determine the response to treatment and to detect spread of cancer.
⚫ Provide privacy for patient.
 LUNG CANCER

A disease characterized by uncontrolled cell growth in tissues of the lungs; one of the
most common cancers in the world.

Types of Lung Cancer:

⚫ Non-small cell Lung Cancer ( adenocarcinoma)

⚫ Squamous cell carcinoma
⚫ Large cell carcinoma
⚫ Small cell carcinomas

ETIOLOGY
Precipitating Factors:
Carcinogens
◼ Tobacco smoke- 10x more common in cigarette smokers than nonsmokers.
◼ Secondhand(passive) smoke- people who are exposed involuntarily to
smoke in a closed environment like house, automobile or building have
greater risk of developing lung cancer than those people who are unexposed
nonsmokers.
Occupational exposures- chronic exposure to industrial carcinogens such as arsenic,
asbestos, chromates, nickel, oil, and radiation.
Dietary deficits- smokers who eat a diet low in fruits and vegetables have an
increased risk of developing lung cancer
Air Pollution- incidence of lung cancer is higher in urban areas due to build up of
pollutants and motor vehicle emissions.
Ionizing Radiation- exposure to radiation has been associated with the development
of lung cancer.

Predisposing Factors:
⚫ Gender- common in males.
⚫ Genetics-same familial disposition.
⚫ Race- African-american has the highest rate.

Signs and Symptoms:

⚫ Cough or chronic cough
⚫ Dyspnea
⚫ Hemoptysis of blood
⚫ Chest or shoulder pain
⚫ Fever
⚫ Chest pain or tightness
⚫ Weakness
⚫ Anorexia
⚫ Weight loss

Characteristics of Common Lung Cancer

Tumor Growth Metastasis Clinical

type Rate manifestati
ons
Squamous Slow Late Cough,
cell sputum
carcinoma production
Adenocarc Moderat Early Pleural
inoma/non e Effusion
small cell
Large cell Rapid Early Chest wall
carcinoma pain,
hemoptysi
s
Small cell Very Very early Cough,
carcinoma rapid chest pain
Mesothelio Slow Late and Dyspnea,
mas asymptomati pleuritic
c pain

TNM Classification of Lung Cancer

Primary Tumors:
⚫ T0 – no evidence of primary tumor
⚫ TX – tumor cannot be assessed
⚫ Tis - Carcinoma in situ
⚫ T1 - tumor less than 3 cm without invasion
⚫ T2 - tumor more than 3.0 cm in diameter, or a tumor of any size that invades the
visceral pleura
⚫ T3 - tumor of any size with direct extension into an adjacent structure, such as
chest wall

Lymph Node Involvement:

⚫ N0 - no demonstrable metastasis to regional lymph nodes
⚫ N1- metastasis to nodes in the peribronchial and/or ipsilateral hilar region
⚫ N2 – metastasis to nodes ipsilateral hilar to contralateral mediastinal
⚫ N3 - metastasis to contralateral mediastinal or hilar lymph nodes

Metastasis:
⚫ M0 – no metastasis
⚫ M1- distant metastasis, such as to scalene or contralateral hilar lymph nodes,
brain, and lungs
Diagnostic Exams:

◼ Fiberoptic Bronchoscopy- it is used to provide detailed study of the

tracheobronchial tree and allows for brushing, washing, and biopsies.

⚫ Used during treatment of lung condition

⚫ Flexible/rigid; mouth/nose

PREP:
⚫ NPO- 6-12 hours
⚫ Avoid aspirin, blood thinning products

PURPOSE:
⚫ Diagnose lung problems
⚫ Inspect airways
⚫ Take biopsy sample

◼ Low Dose Helical Computed Tomography- Computer controlled x-ray to scan

the entire chest in about 7-15 seconds during a single, breath-hold

◼ Endoscopy with Esophageal Ultrasound- used to obtain a transesophageal

biopsy of enlarged subcarinal lymph nodes not easily accessible by other
means.
◼ Mediastinoscopy ( mediastinotomy)- used to obtain biopsy sample from lymph
nodes in the mediastinum.

◼ Papanicolau test of the sputum- will examine a sample of sputum to determine

whether abnormal cells are present.

Management:
1. Surgery- if patient has localized non-small cell tumor, no metastasis and has
adequate pulmonary function, a surgical resection is the preferred method in treating
patients with lung cancer.
⚫ Lobectomy- removal of a single lobe of the lung
⚫ Pneumonectomy- removal of the entire lung
⚫ Segmentectomy- a segment of the lung is being removed
⚫ Wedge resection- removal of a small, pie-shaped area of the segment
⚫ Chest wall resection with removal of cancerous lung tissue- for cases that
invaded the chest wall
2. Radiation- it is used in controlling neoplasms that cannot be resected surgically. It
can be used to decrease the size of the tumor to make it operable, and to relieve
pressure on vital organs.
3. Chemotherapy- it is used as an adjunct to radiation and chemotherapy and may
provide relief for pain.

Nursing Diagnosis:
⚫ Chronic pain r/t to pressure of tumor on surrounding structures and erosion of
tissues.
⚫ Ineffective airway clearance r/t increase amount of secretions
⚫ Impaired breathing pattern r/t compression of bronchus
⚫ Risk for infection r/t immunosuppression
⚫ Fatigue r/t decreased oxygen supply to the body secondary to anemia.
NURSING INTERVENTIONS:

Diagnostic Phase:
⚫ The nurse should explore the client’s chief complaints such as dyspnea, pain
or recurrent infection
⚫ The nurse should ask about the presence of risks factors including smoking
history, exposure to occupational respiratory carcinogens or family history of the
disease
⚫ Focus on the client education and provide emotional support
⚫ Incorporate aspects assisting the client to cope with anxiety, fear and family
responses.

TREATMENT PHASE
Client undergoing Thoracic Surgery
⚫ Monitor for signs of respiratory failure.
⚫ Monitor for signs and symptoms of tension pneumothorax such as dyspnea,
restlessness, tachycardia and cyanosis.
⚫ Observe for subcutaneous emphysema around incision and in the chest and
neck.
⚫ Assess dressing and incisional area every 4 hours for any signs of bleeding.
⚫ Assess drainage in closed chest drainage system for signs of bleeding.
⚫ Monitor for signs of thrombophlebitis.
⚫ Encourage client perform leg exercises.
⚫ Discourage placing pillows under knees, crossing the legs or prolonged sitting.
⚫ Administer pain medications as ordered.
⚫ Position client as indicated by phase of recovery and surgical procedure.
⚫ Non-operative side-lying position may be used until consciousness is regained.
⚫ Semi-Fowler’s position is recommended once vital signs are stable.
⚫ Avoid positioning client on operative side. If a wedge resection has been
performed.
⚫ Avoid complete lateral positioning after pneumonectomy.
⚫ Gently turn the client every 1 to 2 hours unless contraindicated.
⚫ Avoid traction on chest tubes while changing client position. Check for kinking or
compression of tubing.
⚫ Begin passive ROM exercises of the arm and shoulder on the affected side 4
hours after recovery from anesthesia.
⚫ Encourage client to use arm on affected side in daily activities

JBMAGNO
 LEUKEMIA

⚫ A group of malignant disorders affecting the blood and blood-forming tissues of

the bone marrow, lymph system, and spleen.

⚫ Neoplasm derived from lymphoid or myeloid cells primarily affecting the bone
marrow and peripheral blood.

BM- flexible tissue found in the hallow interior of bones

Types:
⚫ Red marrow- consisting mainly of myeloid tissue (RBC, platelets, most WBC)
⚫ Yellow marrow- fat cells and some WBC develop in YM

NORMAL BLOOD CELLS

1. WBC- involved in protecting the body against both infectious disease and foreign
invaders.
⚫ Granulocytes- neutrophil, eosinophil, basophil
⚫ Agranulocytes- lymphocytes, monocytes, macrophages

2. RBC- carry oxygen to tissues.

3. Platelets- help form blood clots.

CHARACTERISTICS
⚫ Replacement of BM with malignant, immature WBC
⚫ Appearance of abnormal, immature WBCs in peripheral circulation
⚫ General infiltration of cells into liver, spleen & LNs throughout the body

ETIOLOGY

L-eukemia virus: HTLV-1

E-spraying of pesticides
U-se of chloramphenicol
K-apamilya
E-xposure to benzene
M-ay Down Syndrome
I-onizing radiation
A-lkalating agents
Classifications of Leukemia:

1. ACUTE LYMPHOCYTIC LEUKEMIA

⚫ Mostly lymphoblast present in BM
⚫ Age of onset is less than 15 years old

2. ACUTE MYELOGENOUS LEUKEMIA

⚫ Mostly myeloblast
⚫ Age of onset is between 15-39 years old

3. CHRONIC MYELOGENOUS LEUKEMIA

⚫ Arises from the mutation in the myeloid stem cell
⚫ Mostly granulocyte present in BM
⚫ Age of onset is after 50 years old

4. CHRONIC LYMPHOCYTIC LEUKEMIA

⚫ Mostly lymphocytes present in BM
⚫ Age of onset is after 50 years old.

Clinical Manifestations

⚫ Anemia
⚫ Thrombocytopenia
⚫ Leukopenia
⚫ Chloromas
⚫ Gum infiltration
⚫ Hepatosplenomegaly
⚫ Bone pain

Nursing Management
 OVARIAN CANCER

- a cancerous growth arising from the OVARY

Etiology – Unknown

Risk factors:
➢ Older women
➢ Genetics
➢ Infertile women
➢ Endometriosis
➢ Post-menopausal estrogen replacement therapy

Sources/sites:
➢ Surface (epithelium) of the ovary
➢ Fallopian tube
➢ Egg cells (germ cell tumor)

Symptoms are frequently non specific early on and may include:

➢ Bloating,
➢ Pelvic pain,
➢ Difficulty eating and
➢ Urinary frequency

Other symptoms:
➢ Back pain
➢ Constipation
➢ Vaginal bleeding
➢ Weight loss

DIAGNOSIS
➢ Physical examination
➢ CA 125
➢ TVS
➢ Surgery to inspect the abdominal cavity to take biopsies
 Management
➢ Chemotherapy
➢ Surgery
➢ Radiation

COLORECTAL CANCER

• characterized by neoplasia in the colon, rectum or vermiform appendix

Incidence
➢ US- 153,000 newly diagnosed each year
- 56,700 dies at the same period
➢ Phils.- 19,900 men/200,00 population
- 16,000 women/200,000

Etiology - unknown

Precipitating factors:
➢ Diet
➢ Geographic location
➢ Socioeconomic factor
➢ Religion
➢ Inflammatory bowel disease
➢ Tobacco use

Predisposing factors:
➢ Age
➢ Heredity

Clinical Manifestations according to the affected part of the Colon:

Affected Part Clinical Manifestations
Cecum No noticeable alterations in bowel
habits
Ascending Colon Fatigue, Palpitation, Unexplained iron
deficiency anemia, melena
Transverse or Descending Colon Abdominal cramping, diarrhea,
constipation, perforation, “apple core”,
rediograph results
 Rectosigmoid Hematochezia, narrowing of the
caliber of the stool, unexplained
anemia, abdominal distention, feeling
of incomplete evacuation after a
bowel movement, alternating
constipation/diarrhea

DIAGNOSTIC EXAM
➢ Stool occult
➢ DRE
➢ Barium enema
➢ Flexible sigmoidoscopy
➢ Colonoscopy
➢ CEA

MEDICAL MANAGEMENT
➢ IV, blood components
➢ Radiation
➢ Chemotherapy

STAGING OF COLORECTAL CANCER: DUKE’S CLASSIFICATION

A – Tumor is limited to bowel wall

B – Extension of tumor to all layers

C – Metastases of tumor to regional lymph nodes

D – Lymph node metastases, ulcerated carcinoma, distant metastasis

SURGICAL MANAGEMENT:
➢ Segmental resection – removal of the tumor and portions of the bowel on
either side of the growth, as well as the blood vessels and lymphatic nodes.

➢ Abdominoperineal resection with permanent colostomy – removal of the

tumor and a portion of the sigmoid and all of the rectum and anal sphincter.

➢ Temporary colostomy – followed by segmental resection and anastomosis

and subsequent re-anastomosis of the colostomy allowing initial bowel
decompression and bowel prep before resection.

➢ Permanent colostomy – for palliation of unresectable obstructive lesions

 MANAGEMENT
➢ If client submits himself to surgery, prepare him.
➢ Record intake and output.
➢ Monitor increasing abdominal distention and loss of bowel sounds.
➢ Monitor IV fluids and serum electrolytes.
➢ Assess skin turgor, dry mucous membrane and concentrated urine.
➢ Assess drainage and signs of hemorrhage.

NURSING DIAGNOSES
➢ Disturbed body image R/T colostomy
➢ Anxiety R/T impending surgery
➢ Knowledge deficit R/T diagnosis, surgical procedure
➢ Risk for infection

JBMAGNO
 HODGKIN’S LYMPHOMA

➢ A type of lymphoma which is a cancer originating from white blood cells called
lymphocytes.

➢ Characterized by the orderly spread of disease from one lymph node group to
another and by the development of systemic symptoms with advanced
disease.

ETIOLOGY: UNKNOWN

➢ The disease occurrence shows two peaks: the first in young adulthood (age
15–35) and the second in those over 55 years old.

RISK FACTORS:

➢ Sex: Male
➢ Ages: 15–35 and over 55
➢ Family history
➢ History of infectious mononucleosis or infection with Epstein-Barr virus, a
causative agent of mononucleosis
➢ Weakened immune system, including infection with HIV or the presence of
AIDS
➢ Prolonged use of human growth hormone
➢ Exposure to exotoxins, such as Agent Orange

Manifestations:
➢ Fatigue
➢ Fever and chills that come and go
➢ Itching all over the body that cannot be
explained
➢ Loss of appetite
➢ Soaking night sweats/ excessive sweating
➢ Painless swelling of the lymph nodes in the
neck, armpits, or groin (swollen gland)
➢ Weight loss that cannot be explained

Other symptoms that may occur with this disease:

➢ Coughing, chest pains, or breathing problems if there are swollen lymph
nodes in the chest
➢ Pain or feeling of fullness below the ribs due to swollen spleen or liver
➢ Pain in lymph nodes after drinking alcohol
➢ Skin blushing or flushing
DIAGNOSIS:
➢ Blood chem/ CBC- check WBC
➢ Lymph node biopsy
➢ BM biopsy
➢ Chest X-ray
➢ CT scan
➢ PET scan

A staging evaluation is necessary to determine the treatment plan.

➢ Stage I – indicates one lymph node region is involved (for example, the right
neck).
➢ Stage II – indicates involvement of two lymph node areas on the same side of
the diaphragm (for example, both sides of the neck).
➢ Stage III – indicates lymph node involvement on both sides of the diaphragm
(for example, groin and armpit).
➢ Stage IV – involves the spread of cancer outside the lymph nodes (for
example, to bone marrow, lungs, or liver).

TREATMENT:
➢ Stages I and II (limited disease) – can be treated with local radiation therapy,
chemotherapy, or a combination of both.
➢ Stages III – is treated with chemotherapy alone or a combination of radiation
therapy and chemotherapy.
➢ Stage IV (extensive disease) – is most often treated with chemotherapy
alone.

✓ People with Hodgkin’s lymphoma that returns after treatment or does not
respond to treatment may receive high-dose chemotherapy followed by an
autologous bone marrow transplant (using stem cells from yourself).

✓ Additional treatments depend on other symptoms.

They may include:
✓ Transfusion of blood products, such as platelets or red blood cells, to fight
low platelet counts and anemia
✓ Antibiotics to fight infection, especially if a fever occurs
 BONE TUMOR

➢ a neoplastic growth of tissue in bone. Abnormal growths found in the bone

can be either benign (noncancerous) or malignant (cancerous).

Classification:
➢ Primary Tumors
a. Benign neoplastic,developmental, traumatic, infectious, or inflammatory in
etiology
✓ Eg. Osteoma, osteoblastoma

b. Malignant
✓ Eg.osteosarcomaa, chondrosarcoma, Ewing’s sarcoma

➢ Secondary tumors
• include metastatic tumors which have spread from other organs, such as
carcinomas of the breast, lungs, and prostate.

Manifestations:
➢ Pain
➢ Pathologic fracture

TREATMENT:
➢ Chemotherapy
➢ Radiation therapy

MEDICATIONS:
➢ Biophosphonates
➢ Metastron

SURGICAL TREATMENT:
➢ AMPUTATION

❖ Prognosis
➢ depends on the type of tumor, size and location.

JBMAGNO
TOPIC 1 FOUNDATIONAL CONCEPTS AND ASSESSMENTS

A) KEY ELEMENTS UNDERLYING FLUID AND ELECTROLYTE IMBALANCE

1) THE CELL MEMBRANE

CELL
 smallest autonomous functional unit of the body
 in its fetal form it is undifferentiated , but as growth continues the cell differentiates into specific tissue types,
forming organs and systems.
CELL WALL
 a semipermeable membrane that separates the intracellular from the extracellular components, allowing for an
exchange in an effort for the cell to obtain energy, synthesize complex molecules, participate in electrical
events, and replicate.

COMPOSITION

a) PHOSPHOLIPIDS
 arranged in one end hydrophilic and the other end hydrophobic

Hydrophylic head (loving water)

 faces the outside of the membrane, retaining water and adhering to the neighboring cell

Hydrophobic tail (hating water)

 associates with other fatty groups to exclude the hydrophilic groups

b) PROTEINS
 second major component of the cell membrane where most of the functions of the cellular membrane occur
 They transport lipid-insoluble particles acting as carriers to pass these compounds directly through the
membrane. Some proteins form ion channels for the exchange of electrolytes. The type of protein involved
depends on the cell’s function.

c) CELL COAT BUBBLE NA BLUE

 long chains of complex carbohydrates make up glycoproteins, glycolipids and lectins that form the outside
surface of the cell. This intricate coat helps in cell-to-cell recognition and adhesion.

Figure 1-1 The cell membrane

B) BODY FLUID COMPOSITION
Body fluid is composed of water and various dissolved substances (solutes)

1) WATER
Water is the primary component of body fluids and functions in several ways to maintain normal cellular function. Water
provides a medium for the transport and exchange of nutrients and other substances such as oxygen, carbon dioxide,
and metabolic wastes to and from cells; provides a medium for metabolic reactions within cells; and assists in regulating
body temperature through the evaporation of perspiration.

Total body water constitutes about 60% of the total body weight, but this amount varies with age, gender, and the
amount of body fat. Total body water decreases from 45% to 50% of total body weight with obesity and with aging
(Porth & Matfin, 2009). Fat cells contain comparatively little water. In the person who is obese, the proportion of water
to total body weight is less than in the person of average weight; in a person who is very thin, the proportion of water to
total body weight is greater than in the person of average weight. Adult females have a greater ratio of fat to lean tissue
mass than adult males; therefore, they have a lower percentage of total body water.

Functions:
1. Temperature regulation
2. Transport of materials to/from the cells
3. Aqueous medium for cellular metabolism (provides a medium for metabolic reaction)
4. Assist in food digestion (hydrolysis)
5. Acts as solvent in which solute are available for cell function
6. Maintain blood volume
7. Medium of waste excretion
8. Cushion body parts from injury

Factors affecting body water:

1) AGE
Infant 70-80%
Adult 50-60%
Elderly 45-50%

2) SEX
Male 60%
Female 50%

3) BODY FATS
 Fat cells contains little H2O

*To maintain normal fluid balance, body water intake and output should be approximately equal. The average fluid
intake and output is about 2500ml over a 24-hour period.

INSENSIBLE WATER LOSS

 occurs through the skin, lungs and feces
 can increase significantly during
A. Exercise;
B. High environmental temperatures;
C. During illnesses that respiratory rate, perspiration or GI losses
 Table 1-1 Approximate Values Of 24hour Fluid Gain And Loss Of An Adult
Intake (Gain) vs Output (Loss)
H2O (orally) 1,000 Urine 1500
Water in Food 1,300 Feces 200
Oxidation 200 Perspiration 500
Total 2,500 ml Respiration 300
Total 2,500 ml

2) ELECTROLYTES
Body fluids contain both water molecules and chemical compounds. These chemical compounds can either remain
intact in solution or dissociate into discrete particles. Electrolytes are substances that dissociate in solution to form
charged particle called ions. Cations are positively charged electrolytes; anions are negatively charged electrolytes
 electrically charged particles and is expressed in terms of milliequivalent per liter (mEq/L)

*IONS – dissociated electrolyte particles which carry either (+) (-) charge
(+) charge = cations
(-) charge = anions

4 MAJOR FUNCTIONS OF ELECTROLYTES:

1) Assisting with regulation of water balance
2) Regulating and maintaining acid-base balance
3) Contributing to enzyme reactions
4) Essential for neuromuscular activity

Table1- 2 Major Electrolyte Per Body Compartment

EXTRACELLULAR FLUID

ANIONS CATIONS
Chloride (Cl-) (most abundant) Sodium (Na+) (most abundant)
Bicarbonate (HCO3 - ) Calcium (Ca++)
Magnesium (Mg++)

INTRACELLULAR FLUID

ANIONS CATIONS
Phosphorus/Phosphate ( HPO4-2 ) (most abundant) Potassium (K+) (most abundant)
Sulfates (SO4-2) Magnesium (Mg++)
Proteins (Prot-)
 Table 1-3 Electrolyte Distribution
Cations Plasma Interstitial ICF
Sodium (Na+) 142 146 15
Potassium (k+) 5 5 150
Calcium (Ca++) 5 3 2
Magnesium (Mg++) 2 1 27
154 mg/L

Anions Plasma Interstitial ICF

Chloride (Cl) 102 14 1
Bicarb (HCO3) 27 30 10
Phosphate (HPO4-2) 2 2 100
Sulfate (SO4-2) 1 1 20
Organic Acid 5 8 0
Proteinate (Prot-) 16 1 73
154 mg/L
Table 1-4 Common Electrolytes
ELECTROLYTE DISTRIBUTION IN BODY BASIC FUNCTIONS DIETARY
ION FLUID SOURCES
ECF(mEq/L) ICF (mEq/L)
Sodium (Na+) 135-154 15-20 -regulates fluid volume -table salt
within ECF compartment -cheese, milk,
-regulates vascular processed
osmotic pressure meat, poulty,
-controls water distributioj shellfish, fish,
between ECF and ICF eggs and foods
compartments preserved with
-participates in conduction salt (eg ham
of nerve impulses and bacon)
-maintains neuromuscular
excitability
Potassium 3.5-5 150-155 -regulates osmolality of -Fruits,
ICF especially
-participates in bananas,
transmission of nerve oranges, and
impulses dried fruits
-promotes contraction of -vegetables
skeletal and smooth -meats
muscles -nuts
-regulates acid-base
balance by cellular
exchange of hydrogen ions
Calcium 4.5-5.5 1-2 -provides strength and -dairy products
durability to bones and (milk, cheese,
teeth and yogurt
-establishes thickness and -sardines,
strength of cell whole grains
membranes and green leafy
-promotes transmission of vegetables
nerve impulses
-maintains neuromuscular
excitability
-essential for blood
coagulation
-activates enzyme
reactions and hormone
secretions
Magnesium 4.5-5.5 27-29 -activates enzyme -green leafy
systems, mainly those vegetables,
associated with vit. B whole grains,
metabolism and the use of fish and nuts
potassium calcium and
protein.
-promotes regulation of
serum calcium,
phosphorus and
potassium levels
-promotes neuromuscular
activity
Table 1-5 Serum Component
SERUM COMPONENT VALUES
CONVENTIONAL SI
Sodium 135-145 mEq/L 135-145 mmol/L
Chloride 98-106 mEq/L 98-106 mmol/L
Bicarbonate 22-26 mEq/L 22-26 mmol/L
Calcium 8.5- 10.0 mEq/L 2.1-2.6 mmol/L
Potassium 3.5-5.0 mEq/L 3.5-5.0 mmol/L
Phosphate/inorganic 1.7-2.6 mEq/L (2.5-4.5 mg/dl) 0.8-1.5 mmol/L
phosphorus
Magnesium 1.6-2.6 mg/dl (1.3-2.1 mEq/L) 0.8-1.3 mmol/L
Serum osmolality 275-295 mOsm/kg 275-295 mmol/kg

B) BODY FLUID COMPARTMENT (DISTRIBUTION)

Body Fluid is classified by its location inside or outside the cells. Capillary and cell membranes separate total body fluids
into two main compartments: the intracellular and extracellular.

*TOTAL BODY WATER*

Total body water is the equivalent of the fluids that exist in all the fluid compartments. This approximately 60% of the
body weight of an average adult. Expressed in kilograms, 1L of fluid is equivalent of 2.2 lb (1kg).

Figure 1-2 Total Body Fluid

1) INTRACELLULAR FLUID (ICF) (40%)

Intracellular fluid (ICF) is found within cells. ICF is essential for normal cell function, providing a medium for metabolic
processes.
 Make’s up 2/3 of the body’s water or 40% of Body weight
 Larger of the two compartments
 Rich in electrolytes, potassium, magnesium, inorganic and organic phosphates and proteins
2) EXTRACELLULAR FLUID (ECF) (20%)
Extracellular fluid (ECF) is located outside of cells
 contains all the fluid outside the cells
 accounts for 20% of Body weight
 rich in electrolytes: sodium, chloride and bicarbonate

ECF is further classified by location:

a) INSTERSTITIAL FLUID (15%)

 located in the spaces between most cells of the body
 accounts for approximately 15% of Body weight
b) INTRAVASCULAR FLUID (5%)
 blood vessel compartments
 called “plasma”, is contained within the arteries, veins, and capillaries
c) TRANSCELLULAR FLUID (1%)
 includes urine; digestive secretions; perspiration; and cerebrospinal, pleural, synovial, intraocular,gonadal, and
pericardial fluids
the transcellular space contributes approximately 1% of the body fluid, and significant gains and losses do not occur on a
daily basis

Figure 1- 3 Fluid Compartments of the Body

 TOPIC 2: FLUID VOLUME IMPAIRMENT

There are primarily two types of fluid imbalances (a) Fluid volume deficit and (b) fluid volume excess. Both type of
imbalances can be life-threatening and are often seen in acute care settings. Patients with many underlying pathologies
develop one of these fluid imbalances and without careful management, serious and critical conditions may develop

A) FLUID VOLUME DEFICIT

Fluid volume deficit (FVD) is a decrease in intravascular, interstitial, and/or intracellular fluid in the body. Fluid
volume deficits may be the result of excessive fluid losses, insufficient fluid intake, or failure of regulatory mechanisms
and fluid shifts within the body. FVD is a relatively common problem that may exist alone or in combination with other
electrolyte or acid–base imbalances. (Lemone,2017)
ISO-OSMOLAR FLUID VOLUME DEFICIT
 Occurs when sodium and water are lost in equal amounts.

HYPEROSMOLAR FLUID VOLUME DEFICIT

 Occurs when more fluid is lost than sodium, resulting in higher serum osmolality than normal ( > 295 mOsm/kg)

HYPOOSMOLAR FLUID VOLUME DEFICIT

 Occurs when electrolyte loss is greater than fluid (rare).

ETIOLOGY

The most common cause of fluid volume deficit is excessive loss of GI fluids from vomiting, diarrhea, GI
suctioning, intestinal fistulas, and intestinal drainage. Other causes of fluid losses include diuretics, renal disorders,
endocrine disorders, excessive exercise, hot environment, hemorrhage, and chronic abuse of laxatives and/or enemas.
Other factors involved in inadequate fluid intake include inability to access fluids, inability to request or to swallow
fluids, oral trauma, or altered thirst mechanisms. Older adults are at particular risk for fluid volume deficit.

PATHOPHYSIOLOGY

Fluid volume deficit can develop slowly or rapidly, depending on the type of fluid loss. Loss of extracellular fluid
volume can lead to hypovolemia, decreased circulating blood volume. Electrolytes often are lost along with fluid,
resulting in an isotonic fluid volume deficit. When both water and electrolytes are lost, the serum sodium level remains
normal, although levels of other electrolytes such as potassium may fall. Fluid is drawn into the vascular compartment
from the interstitial spaces as the body attempts to maintain tissue perfusion. This eventually depletes fluid in the
intracellular compartment as well. Hypovolemia stimulates regulatory mechanisms to maintain circulation. The
sympathetic nervous system is stimulated, as is the thirst mechanism. ADH and aldosterone are released, prompting
sodium and water retention by the kidneys. Severe fluid loss, as in hemorrhage, can lead to shock and cardiovascular
collapse. (Lemone,2017))
PATHOPHYSIOLOGY

Table 2-1 Pathophysiology, ECF Fluid Loss

ECF FLUID LOSS

Fluids Shift from Interstitial to Intravascular to Restore Vascular Volume & Hypernatremic state

Fluids are
reabsorbed
from the
colon

* If fluid loss is continues and regulatory mechanism fails = DHN

MANIFESTATIONS
With a rapid fluid loss (such as hemorrhage or uncontrolled vomiting), manifestations of hypovolemia develop
rapidly. When the loss of fluid occurs more gradually, the patient’s fluid volume may be very low before manifestations
develop. Rapid weight loss is a good indicator of fluid volume deficit. Each liter of body fluid weighs about 1 kg (2.2 lb).
The severity of the fluid volume deficit can be estimated by the percentage of rapid weight loss: A loss of 2% of body
weight represents a mild FVD; 5%, moderate FVD; and 8% or greater, severe FVD (Metheny, 2000). Loss of interstitial
fluid causes skin turgor to diminish. When pinched, the skin of a patient with FVD remains elevated. Postural or
orthostatic hypotension is a sign of hypovolemia. A drop of more than 15 mmHg in systolic blood pressure when
changing from a lying to standing position often indicates loss of intravascular volume. Venous pressure falls as well,
causing flat neck veins, even when the patient is recumbent. Compensatory mechanisms to conserve water and sodium
and maintain circulation account for many of the manifestations of fluid volume deficit, such as tachycardia; pale, cool
skin (vasoconstriction); and decreased urine output. The specific gravity of urine increases as water is reabsorbed in the
tubules.

MULTISYSTEM EFFECTS OF FLUID VOLUME DEFICIT

 Mucous Membranes
 Dry; may be sticky
 Decrease tongue size, longitudinal furrows increase
Urinary
 Decrease urine output
 Oliguria (severe FVD)
 Increase in urine specific gravity
 Neurologic
 Altered mental status
 Anxiety, restlessness
 Diminished alertness/condition
 Possible coma (severe FVD)

Integumentary
 Diminished skin turgor
 Dry skin
 Pale, cool extremities

Cardiovascular
 Tachycardia
 Orthostatic hypotension (moderate FVD)
 Falling systolic/diastolic pressure (severe FVD)
 Flat neck veins
 Decrease venous filling
 Decrease pulse volume
 Decrease capillary refill
 Increase hematocrit

Potential Complication
 Hypovolemic shock

Musculoskeletal
 Fatigue

Metabolic Processes
 Decrease body temperature (isotonic FVD)
 Increase body temperature (dehydration)
 Thirst
 Weight loss
2-5% mild FVD
6-9% moderate FVD
>10% severe FVD

DIAGNOSTICS
Laboratory and diagnostic tests may be ordered when fluid volume deficit is suspected. Such tests measure the
following:

1) Serum electrolytes.
In an isotonic fluid deficit, sodium levels are within normal limits; when the loss is water only, sodium levels are high.
Decreases in potassium are common.

2) Serum osmolality.
Measurement of serum osmolality helps to differentiate isotonic fluid loss from water loss. With water loss,
osmolality is high; it may be within normal limits with an isotonic fluid loss.

3) Hemoglobin and hematocrit.

The hematocrit often is elevated due to loss of intravascular volume and hemoconcentration.
 4) Urine specific gravity and osmolality.
As the kidneys conserve water, both the specific gravity and osmolality of urine increase.

5) Central venous pressure (CVP).

The CVP measures the mean pressure in the superior vena cava or right atrium, providing an accurate assessment of
fluid volume status.

Central venous pressure (CVP)

Is the blood pressure in the venae cavae, near the right atrium of the heart. CVP reflects the amount of blood
returning to the heart and the ability of the heart to pump the blood back into the arterial system.
It is acquired by threading a central venous catheter (subclavian double lumen central line shown) into any of
several large veins. It is threaded so that the tip of the catheter rests in the lower third of the superior vena cava. The
pressure monitoring assembly is attached to the distal port of a multilumen central vein catheter.

Figure 2-1 Central Venous Pressure Line

The CVP catheter is an important tool used to assess right ventricular function and systemic fluid status.
 Normal CVP is 2-6 mm Hg.
 CVP is elevated by :
 overhydration which increases venous return
 heart failure or PA stenosis which limit venous outflow and lead to venous congestion
 positive pressure breathing, straining,
 CVP decreases with:
 hypovolemic shock from hemorrhage, fluid shift, dehydration
 negative pressure breathing which occurs when the patient demonstrates retractions or mechanical negative
pressure which is sometimes used for high spinal cord injuries.

MEDICAL MANAGEMENT
Correction of fluid loss depends on the acuteness and severity of the fluid deficit. Goals are to replace F/E (Na
primarily) that have been loss.

1) Fluid Restoration
a) Oral rehydration
The safest and most effective treatment for fluid volume deficit in alert patients who are able to take oral fluids.
Adults require a minimum of 1500 mL of fluid per day or approximately 30 mL per kg of body weight (ideal body weight
is used to calculate fluid requirements for obese patients) for maintenance. Fluids are replaced gradually, particularly in
older adults, to prevent rapid rehydration of the cells.
  For mild fluid deficits in which a loss of electrolytes has been minimal (e.g., moderate exercise in warm
weather), water alone may be used for fluid replacement.

 When the fluid deficit is more severe and when electrolytes have also been lost (e.g.,FVD due to vomiting and/or
diarrhea, strenuous exercise for longer than an hour or two), a carbohydrate/electrolyte solution such as a
sports drink, ginger ale, or a rehydrating solution (e.g., Pedialyte or Rehydralyte) is more appropriate. These
solutions provide sodium, potassium, chloride, and calories to help meet metabolic needs.

b) IV Rehydration
When the fluid deficit is severe or the patient is unable to ingest fluids, the IV route is used to administer replacement
fluids. (please refer to table of IV FLUIDS)
Generally Isotonic ECFVD is treated with Isotonic Solutions
Hypertonic ECFVD is treated with Hypotonic Solutions
Hypotonic ECFVD is treated with Hypertonic Solutions

2) Monitor for complications of fluid restoration

 client with severe ECFVD accompanied by severe heart, liver and kidney disease can’t tolerate large volumes of
fluid or sodium without the risk of development of heart failure
 Unstable clients needs to be monitored to detect ↑ pressure from fluids
Monitor 1) Fluid volume status by CVP insertion
2) Lab values (Na, K, BUN, Osmolarity)
3) Body Weight
4) Urine output

3) Correction of Underlying Problem

Medication
 Antiemetic
 Antidiarrheal
 Antibiotics
 antidiuretics to reduce body temp

NURSING MANAGEMENT
Nurses are responsible for (a) identifying patients at risk for fluid volume deficit, (b) initiating and carrying out
interventions to prevent and treat fluid volume deficit, and (c) monitoring the effects of therapy.
1. VS every 2-4 hours, report changes from baseline VS; Assess CVP every 4hrs (if patient has CVP access)
® Hypotension, tachycardia, low CVP, and weak, easily obliterated peripheral pulses indicate hypovolemia.

2. I & O every 8 hours or hourly (Record all output accurately)

Renal client / relatives to report urine output ‹ than 30 m/L x 2 consecutive hours or ‹ 240 ml x 8 hour period
® Urine output should normally be 30 to 60 mL per hour. Urine output of less than 30 mL per hour in adults indicates
inadequate renal perfusion and an increased risk for acute renal failure and inadequate tissue perfusion

3. Administer IV fluids as prescribed using an infusion pump. Monitor for indicators of fluid overload if rapid fluid
replacement is ordered: dyspnea, tachypnea, tachycardia, increased CVP, jugular vein distention, and edema.
® Rapid fluid replacement may lead to hypervolemia, resulting in pulmonary edema and cardiac failure, particularly in
patients with compromised cardiac and renal function.

4. Weight patient daily and record

®In most instances (except third spacing), changes in weight accurately reflect fluid balance.
 5. Monitor laboratory values: electrolytes, serum osmolality, blood urea nitrogen (BUN), and hematocrit.
® Rehydration may lead to changes in serum electrolytes, osmolality, BUN, and hematocrit. In some cases, electrolyte
replacement may be necessary during rehydration.

6. Monitor for changes in level of consciousness and mental status.

®Restlessness, anxiety, confusion, and agitation may indicate inadequate cerebral blood flow and circulatory collapse.
A fluid volume deficit can lead to decreased perfusion of renal, cerebral, and peripheral tissues. Decreased cerebral
perfusion leads to changes in mental status and cognitive function, causing restlessness, anxiety, agitation, excitability,
confusion, vertigo, fainting, and weakness.

7. Institute safety precautions, including keeping the bed in a low position, using side rails as needed, and slowly
raising the patient from supine to sitting or sitting to standing position.
® Using safety precautions and allowing time for the blood pressure to adjust to position changes
reduce the risk of injury.
The patient with fluid volume deficit is at risk for injury because of dizziness and loss of balance
resulting from decreased cerebral perfusion secondary to hypovolemia.

8. Teach patient and family members how to reduce orthostatic hypotension

® Teaching measures to reduce orthostatic hypotension reduces the patient’s risk for injury. Prolonged
bed rest increases skeletal muscle weakness and decreases venous tone, contributing to postural
hypotension. Prolonged standing allows blood to pool in the legs, reducing venous return and cardiac
output.

NURSING DIAGNOSIS
1) Fluid Volume Deficit
Patients with a fluid volume deficit due to abnormal losses, inadequate intake, or impaired fluid regulation require close
monitoring as well as immediate and ongoing fluid replacement.

2) Ineffective Tissue Perfusion

A fluid volume deficit can lead to decreased perfusion of renal, cerebral, and peripheral tissues. Inadequate renal
perfusion can lead to acute renal failure. Decreased cerebral perfusion leads changes in mental status and cognitive
function, causing restlessness, anxiety, agitation, excitability, confusion, vertigo, fainting, and weakness.

3) Risk for Injury

The patient with fluid volume deficit is at risk for injury because of dizziness and loss of balance resulting from decreased
cerebral perfusion secondary to hypovolemia.

IV THERAPY
Intravenous (IV) therapy is the administration of fluids or medication via a needle or catheter (sometimes called a
cannula) directly into the bloodstream.

INDICATIONS FOR INTRAVENOUS THERAPY

Patients receive a variety of substances via IV therapy, including fluids, electrolytes, nutrients, blood products, and
medications.

1. Patients can receive life-sustaining fluids, electrolytes, and nutrition when they are unable to eat or drink adequate
amounts.
2. The IV route also allows rapid delivery of medication in an emergency. Many medications are faster acting and more
effective when given via the IV route. Other medications can be administered continuously via IV to maintain a
therapeutic blood level.
3. Patients with anemia or blood loss can receive lifesaving IV transfusions.
4. Patients who are unable to eat for an extended period can have their nutritional needs met with total parenteral
nutrition (TPN).

TYPES OF INFUSIONS
1) Continuous Infusion
In a continuous infusion, the physician orders the infusion in milliliters (mL) to be delivered over a specific
amount of time; for example, 100 mL per hour. The infusion is
kept running constantly until discontinued by the physician. An IV controller or roller clamp allows the solution to infuse
at a constant rate.

2) Intermittent Infusion
Intermittent IV lines are “capped off” with an injection port and used only periodically. Thus intermittent IV
therapy is administered at prescribed intervals. You must ensure that an intermittent catheter is patent (not occluded
with a clot) before injecting a drug or solution. Draw back with a syringe to check for backflow of blood before injection.

3) Bolus
A bolus drug (sometimes called an IV push or IVP drug) is injected slowly via a syringe into the IV site or tubing
port. It provides a rapid effect because it is delivered directly into the patient’s bloodstream. Bolus drugs can be
dangerous if they are given incorrectly, and a drug reference should always be checked to determine the safe amount of
time over which the drug can be injected.

4) Piggy Back/Secondary Infusion

Some IV medications, such as antibiotics, need to be infused over a short period of time. For example, an
antibiotic may be mixed with 50 mL of dextrose solution and infused over 30 minutes. If the patient already has a
primary continuous IV infusing, the antibiotic (secondary) infusion can be “piggybacked” into the primary IV line. In
order for the piggyback medication to infuse, it must hang higher than the primary infusion. Piggyback medications can
be infused using either gravity or a controller. The medication in the piggyback must be compatible with any other
solution that is in the primary IV tubing.

METHODS OF INFUSION
1)Gravity Drip
Gravity can be used to drip a solution into a vein. The solution is positioned about 3 feet above the infusion site. If it is
positioned too high above the patient, the infusion may run too fast. Positioned too low, it may run too slowly. Flow is
controlled with a roller, screw, or slide clamp. A mechanical flow device can be added to achieve accurate delivery of
fluid with minimal deviation.

Factors Affecting Flow Rates

a) Change in catheter position.
A change in the catheter’s position may push the bevel either against the wall of the vein, which will decrease the flow
rate, or away from the wall of the vein, which may increase the flow rate.
Careful taping and avoidance of joint flexion above the site minimizes this problem. Patients may need to be reminded
to keep flexion to a minimum when an IV is placed near a joint.

b)Height of the solution.

Because infusions flow by gravity, a change in the height of the infusion bag or bottle or a change in the level of the bed
can increase or decrease the flow rate. The flow rate increases as the distance between the solution and the patient
increases. A patient may alter the flow rate greatly simply by standing up. The ideal height for a solution is 3 feet above
the level of the heart.

c) Patency of the catheter.

A small clot or fibrin sheath may occlude the catheter lumen and decrease or stop the flow rate. Clot formation
can result from irritation, increased venous pressure, or backup of blood into the line.
Avoid use of a blood pressure cuff on the affected extremity because of the resulting transient increase in venous
pressure. A regular flush schedule helps maintain patency.
NEVER exert pressure with a saline or heparin flush in an attempt to restore patency; doing so may dislodge a clot into
the vascular system or rupture the catheter

2) Electronic Control Devices

Electronic pumps and controllers regulate the rate of infusion. Controllers measure the amount of solution
delivered and depend on gravity to deliver the infusion.
Pumps use positive pressure to deliver the solution. Pumps are often used for central lines to help overcome the high
pressure of the central circulation.
Pumps and controllers are used for the infusion of precise volumes of solution. Institution policy often dictates
use of controllers for infusion of potent medications, such as heparin, concentrated morphine, and chemotherapy
solutions, and for very fast or slow rates. Some electronic infusion devices are portable and are designed to be worn on
the body. These are called ambulatory infusion devices. It is important to know the type of pump being used and its
manufacturer’s guidelines.

TYPES OF IVF SOLUTIONS

There are two types of IVFs, crystalloid and colloid solutions.

1) Colloids
Fluids that expand the circulatory volume due to particles that cannot cross a semipermeable membrane. They pull fluid
from the interstitial space into the intravascular space, increasing fluid volume. This can be a great advantage in cases of
large losses of fluid, such as severe trauma and haemorrhage. The main disadvantage are cost and the risk of volume
overload, including pulmonary edema.
Types of colloids are dextrans and hetastarches

2) Crystalloids
Work much like colloids but do not stay in the intravascular circulation as well as colloids do, so more of them need to
be used. They are cheaper and are more convenient to use.
 primary fluid for IV therapy containing electrolytes but lacks large protein molecules
 They provide hydration and calories to patients and include dextrose, normal saline, and Ringer’s and lactated
Ringer’s solution.

2 IVF CLASSIFICATION
According to tonicity and according to purpose

TONICITY
Tonicity of IV Solutions
 Intravenous fluids may be classified as isotonic, hypotonic, or hypertonic.
Isotonic fluids have the same concentration of solutes to water as body fluids. Hypertonic solutions have more solutes
(i.e., are more concentrated) than body fluids. Hypotonic solutions have fewer solutes (i.e., are less concentrated) than
body fluids. Water moves from areas of lesser concentration to areas of greater concentration.
Therefore, hypotonic solutions send water into areas of greater concentration (cells), and hypertonic solutions pull
water from the more highly concentrated cells.

1) Isotonic Solutions
 Normal saline (0.9% sodium chloride) solution is an isotonic solution that has the same tonicity as body fluid.
When administered to a patient requiring water, it neither enters cells nor pulls water from cells; it therefore
expands the extracellular fluid volume.
 A solution of 5% dextrose in water (D5W) is also isotonic when infused, but the dextrose is quickly metabolized,
making the solution hypotonic.
2 ) Hypotonic Solutions
 Hypotonic fluids are used when fluid is needed to enter the cells, as in the patient with cellular dehydration.
They are also used as fluid maintenance therapy.
An example of a hypotonic solution is 0.45% sodium chloride solution.

3) Hypertonic Solutions
 Examples of hypertonic solutions include 5% dextrose in 0.9% sodium chloride and 5% dextrose in lactated
Ringer’s solution.
o Hypertonic solutions are used to expand the plasma volume, as in the hypovolemic patient. They are
also used to replace electrolytes.

Table 2-2 Commonly Administered Iv Fluids With Nursing Implications

1) ISOTONIC SOLUTIONS  Monitor for fluid overload;
0.9% Saline discontinue fluids and notify the
Lactated Ringer’s solution healthcare provider
 Do not administer lactated ringer’s
solution to patients with severe liver
disease as the liver may be unable to
convert the lactate to bicarbonate
and the patient may become
acidotic. Do not administer if the
patient has a blood pH of >7.50
 If administering lactated ringer’s
solution, monitor potassium levels
and cardiac rhythm; if abnormals are
present, notify the health care
provider
2) HYPOTONIC SOLUTIONS  Monitor for inflammation and
0.45% Saline or 0.25% Saline infiltration at IV insertion site as
D5W hypotonic solutions may cause cells
to swell and burst, including those at
the insertions site; this narrows the
lumen of the vein
 Monitor blood sodium levels
 Do not administer to patients at risk
for increased intracranial pressure
(e.g head trauma, stroke,
neurosurgery)
 Do not administer to patients at risk
for third-space shifts (burns, trauma,
liver disease, malnutrition)
3) HYPERTONIC SOLUTIONS  Monitor for inflammation and
Hypertonic fluids have a tonicity >350 mEq/L infiltration at IV insertion site as
and include the ff: hypertonic solutions cause cells to
 Fluids containing shrink, exposing the basement
medications membrane of the vein
 D5W sodium chloride  Monitor blood sodium levels
 D5W in lactated ringer’s  Monitor for circulatory overload
solution  Do not administer to patients with
 Total parenteral diabetic ketoacidosis or impaired
solutions cardiac or kidney function.
ACCORDING TO PURPOSE
1) Hydrating
 Replace water loss
 Dilute meds
 Keep veins open

2) Nutritional
 Promotes faster recuperation

3) Maintenance
 Replace electrolyte loss at ECF level
 Maintenance in patients with no oral intake
 Replace fluid loss
 Treatment for dehydration

4) Volume expander
 Increase osmotic pressure thus maintain circulatory volume

INTRAVENOUS ACCESS
Intravenous therapy can be administered into the systemic circulation via the (1) peripheral or (2) central veins.

1) Peripheral veins lie beneath the epidermis, dermis, and subcutaneous tissue of the skin. They usually provide easy
access to the venous system.
2) Central veins are located close to the heart. Special catheters that end in a large vessel near the heart are called
central lines.

ADMINISTERING PERIPHERAL INTRAVENOUS THERAPY

Precatheterization (Preparation)

1) Check Physician’s Order

 A physician’s order is necessary to initiate IV therapy. The order should include solution, volume, rate, and
route. If medication is ordered, the order should also include the medication, dosage, and frequency.
2) Wash Hands
 Before beginning the procedure, wash your hands for 15 to 20 seconds. Wear gloves when inserting the catheter
and any time you have a risk of exposure to body fluid.
3) Gather Equipment
 Obtain the following equipment and inspect it for integrity.

4) Assess and Prepare Patient

 Several factors should be considered before venipuncture. The type of solution, condition of vein, duration of
therapy, catheter size needed, patient age, patient
activity, presence of disease or previous surgery, presence of a dialysis shunt or graft, medications being taken by the
patient (such as anticoagulants), and allergies must be assessed before a venipuncture. Provide privacy for the
procedure, explain the procedure to the patient, and evaluate the patient’s knowledge of the procedure by talking with
the patient before assessing the upper arms for suitable venipuncture sites.

5) Select Site and Dilate Vein

 Proper vein selection is important to accommodate the prescribed therapy and to minimize potential
complications.
 Considerations for Vein Selection
 Age of patient
 Availability of sites
 Size of catheter to be used
 Purpose of infusion therapy
 Osmolarity of solution to be infused
 Volume, rate, and length of infusion
 Degree of mobility desired

General Considerations When Initiating Intravenous Therapy

 When multiple sticks are anticipated, make the first venipuncture distally and work proximal with subsequent
punctures.
 If therapy will be prescribed for longer than 3 weeks, a long-term access device should be considered.
 Avoid using venipunctures in affected arms of patients with radical mastectomies or a dialysis access site.
 If possible, avoid taking a blood pressure on the arm receiving an infusion because the cuff interferes with
blood flow and forces blood back into the catheter. This may cause a clot or cause the vein or catheter to
rupture.
 No more than two attempts should be made at venipuncture before getting help.
 Immobilizers should not be placed on or above an infusion site.

 Hand veins are used first if long-term intravenous therapy is expected. This allows each successive
venipuncture to be made proximal to the site of the previous one, which eliminates the passage of irritating
fluids through a previously injured vein and discourages leakage through old puncture sites.

 Hand veins can be used successfully for most hydrating solutions, but they are best avoided when irritating
solutions of potassium or antibiotics are anticipated.

 Vein size must also be considered. Small veins do not tolerate large volumes of fluid, high infusion rates, or
irritating solutions. Large veins should be used for these purposes.

Figure 2-2 Peripheral veins used for IV Therapy

6) Select the needle (catheter)
 Needles have been largely replaced with flexible plastic catheters that are inserted over a needle. The needle (or
stylet) is removed after the catheter is in place.
 These are available in a variety of sizes (gauges) and lengths. For patient comfort, choose the smallest gauge
catheter that will work for the intended purpose. Use smaller gauge catheters (20 to 24 gauge) for fluids and
slow infusion rates. Use larger catheters (18 gauge) for rapid fluid administration and viscous solutions such as
blood. Also consider vein size when choosing a catheter gauge.

Figure 2-3 Gauge of Needle and its Recommended Use

7) Put on gloves
 Follow standard precautions whenever exposure to blood or body fluids is likely. Wearing latex or vinyl gloves
provides basic protection from blood and body fluids.

8) Prepare the site

 Apply the solution in a circular motion, starting at the intended site and working outward to clean an area 2 to 3
inches in diameter. If alcohol is used, it should be applied with friction for at least 30 seconds or until the final
applicator is visually clean.
9) Insert the catheter
 Hold the catheter with the bevel (slanted opening) of the needle facing up.

10) Stabilize the Catheter and Dress the Site

 A common problem in IV therapy is dislodgement of the catheter. Secure taping keeps the catheter in place and
stable, thus preventing complications caused by damage to the intima of the vein.

11) Label the Site

 The IV setup should be labeled in three areas: the insertion site, the tubing, and the solution container. Once the
venipuncture procedure is completed, label the setup with the date, time, catheter type and size, and your
initials.

12) Dispose of Equipment

 All needles, catheters, and blood-contaminated equipment should be disposed of according to institution policy
in a tamper-proof, nonpermeable container.

13) Educate the Patient

 Patients have the right to receive information on all aspects of their care in a manner they can understand. They
also have the right to accept or refuse treatment. Explain the rationale for the IV therapy that has been ordered.

14) Calculate Drip Rate

 All IV infusions should be monitored frequently for accurate flow rates and complications associated with
infusion therapy.

15) Document
 Document your actions and the patient’s response in the medical record according to institution policy. All IV
solutions are also documented on the medication administration record.
 Table 2-3 Complications Of Peripheral Iv Therapy
Local Complications of IV Signs and Symptoms Nursing Interventions
Therapy
Hematoma Ecchymoses Remove catheter
Swelling Apply pressure with 2x2
Inability to advance catheter Elevate extremity
Resistance during flushing
Thrombosis Slowed or stopped infusion Discontinue catheter
Fever/malaise Apply cold compress to site
Inability to flush catheter Assess for circulatory
impairment
Phlebitis Redness at site Discontinue catheter
Site warm to touch Apply cold compress initially;
Local swelling then warm
Pain Consult physician if severe
Palpable cord
Sluggish infusion rate
Infiltration Coolness of skin at site Discontinue catheter
(Extravasation) Taut skin Apply cool compress
Dependent edema Elevate extremity slightly
Backflow of blood absent Follow extravasation
Infusion rate slowing guidelines
Have antidote available
Local Infection Redness and swelling at site Discontinue catheter and
Possible exudate culture
Increase WBC count site and catheter
Elevated T lymphocytes Apply sterile dressing
over site
Administer antibiotics if
ordered
Venous Spasm Sharp pain at site Apply warm compress to site
Slowing of infusion Restart infusion in new site if
spasm continues
Table 2-4 Systemic Complication of Peripheral IV Therapy
Complication Signs and Symptoms Nursing Interventions
Septicemia Fluctuating temperature Restart new IV system
Profuse sweating Obtain cultures
Nausea/vomiting Notify physician
Diarrhea Initiate antimicrobial therapy
Abdominal pain as
Tachycardia ordered
Hypotension Monitor patient closely
Altered mental status
Fluid Overload Weight gain Decrease IV flow rate
Puffy eyelids Place patient in high Fowler’s
Edema position
Hypertension Keep patient warm
Changes in input and output Monitor vital signs
(I&O) Administer oxygen
Rise in central venous Use microdrip set or
pressure (CVP) controller
Shortness of breath
Crackles in lungs
Distended neck veins
Air Embolism Lightheadedness Call for help!
Dyspnea, cyanosis, Place patient in
tachypnea, expiratory Trendelenburg’s
wheezes, cough position
chest pain,hypotension Administer oxygen
Changes in mental status Monitor vital signs
Coma Notify physician

ALTERNATIVE ACCESS ROUTES

Central Venous Catheters

Central venous catheters terminate in the superior vena cava near the heart. They are used when peripheral
sites are inadequate or when large amounts of fluid or irritating medication must be given. Central catheter devices
include a percutaneous catheter, peripherally inserted central catheter (PICC), tunneled catheter, and implanted port.
These devices can have one, two, or three lumens in the catheter or one or more port chambers. Each lumen
exits the site in a separate line, called a tail. Multilumen catheters allow for the administration of incompatible solutions
at the same time. Be careful not to confuse a central catheter with a dialysis catheter. Dialysis catheters should be used
only for dialysis and not for IV therapy, and should be accessed only by physicians or specially trained dialysis nurses.
1) Percutaneous Central Catheter
A percutaneous central catheter is inserted by a physician into the jugular or subclavian vein. After insertion,
correct placement is determined by x-ray before the catheter is used.
These short-term central venous catheters may remain in place up to several weeks, but usual placement time is
7 days. These catheters are inserted at the bedside and are cost effective for short-term central venous access in the
acute care setting.
 2) Peripherally Inserted Central Catheter (PICC)
A PICC line is a long catheter that is inserted in the arm and terminates in the central circulation. This device is
used when therapy will last more than 2 weeks or the medication is too caustic for peripheral administration.

3) Tunneled Catheters
Central venous tunneled catheters (CVTCs) are intended for use for months to years to provide long-term
venous access. CVTCs are composed of polymeric silicone with a Dacron polyester cuff that anchors the catheter in place
subcutaneously. The catheter tip is placed in the superior vena cava.

4) Ports
A port is a reservoir that is surgically implanted into a pocket created under the skin, usually in the upper chest.
An attached catheter is tunneled under the skin into a central vein. An advantage of a port is that, when not in use, it
can be flushed and left unused for long periods.
Ports can be used to administer chemotherapeutic agents and antibiotics that are toxic to tissues and are suitable for
long-term therapy. Ports should be accessed only by specially trained RNs. Most ports require the use of special
noncoring needles that are specifically designed for this purpose.

A) FLUID VOLUME EXCESS

Fluid volume excess results when both water and sodium are retained in the body. Fluid volume excess may be caused
by fluid overload (excess water and sodium intake) or by impairment of the mechanisms that maintain homeostasis. The
excess fluid can lead to excess (1) intravascular fluid (hypervolemia) and (2) excess interstitial fluid (edema).

ETIOLOGY
Fluid volume excess usually results from conditions that cause retention of both sodium and water. These
conditions include heart failure, cirrhosis of the liver, renal failure, adrenal gland disorders, corticosteroid
administration, and stress conditions causing the release of ADH and aldosterone. Other causes include an excessive
intake of sodium-containing foods, drugs that cause sodium retention, and the administration of excess amounts of
sodium-containing IV fluids (such as 0.9% NaCl or Ringer’s solution). This iatrogenic (induced by the effects of treatment)
cause of fluid volume excess primarily affects patients with impaired regulatory mechanisms.

PATHOPHYSIOLOGY
In fluid volume excess, the extracellular compartment is expanded. This increase in volume increases the
pressure in the vasculature. Baroreceptors sense the increase in pressure and increase in their firing to the central
nervous system (CNS). In response, the SNS is inhibited, and RAAS functions declines. The resulting vasodilation
promotes pooling of blood and lowering of blood pressure. Reabsorption of sodium in the renal tubules is reduced, and
more urine is excreted.
MANIFESTATIONS
Excess extracellular fluid leads to hypervolemia and circulatory overload. Excess fluid in the interstitial space
causes peripheral or generalized edema. The manifestations of fluid volume excess relate to both the excess fluid and its
effects on circulation.
 Peripheral edema, or if severe, anasarca (severe generalized edema)
 Full bounding pulse, distended neck and peripheral veins, increased central venous pressure, cough, dyspnea
(labored or difficulty breathing), orthopnea (difficult breathing when supine)
 Dyspnea at rest
 Tachycardia and hypertension
 Reduced oxygen saturation
 Moist crackles on auscultation of the lungs, pulmonary edema
 Increased urine output (polyuria)
 Ascites (excess fluid in the peritoneal cavity)
 Decreased hematocrit and BUN
  Altered mental status and anxiety
 Pulmonary edema
Fluid overload can occur in either the extracellular or intracellular compartments of the body.

1) EXTRACELLULAR FLUID OVERLOAD

 Occurs in either the intravascular compartment or in the interstitial area

EDEMA- most common term associated with fluid overload found in the interstitial or lung tissue
HYPERVOLEMIA- when an overabundance of fluid occurs in the intravascular compartment
ISOTONIC FLUID VOLUME EXCESS- type of fluid overload wherein sodium and water remain in equal
proportions with each other. Also results from a decreased elimination of sodium and water.
ANASARCA- generalized edema

CAUSES OF EXTRACELLULAR FLUID OVERLOAD

 Excessive sodium intake through diet
 administration of hypertonic fluids
 D545 normal saline solution
 D5.9 normal saline solution
 10% Dextrose
 3% normal saline solution
 Diabetes insipidus
 Congestive heart failure
 Cirrhosis

 Renal failure
 Cushing’s syndrome
 Hyperaldosteronism

MANIFESTATIONS OF EXTRACELLULAR FLUID OVERLOAD

 Pitting peripheral edema
 Periorbital edema
 Shortness of breath
 Shift of interstitial fluid to plasma
 Bounding pulse and jugular venous distention
 Anasarca
 Rapid weight gain
 Moist crackles
 Tachycardia
 Hypertension
2) INTRACELLULAR FLUID OVERLOAD
 also known as water intoxication
 Hypotonic fluid from the intravascular space moves by osmosis to an area of higher solute
concentration inside the cell. Cells run the risk of rupturing if they become too overloaded with fluid.

CAUSES OF INTRACELLULAR FLUID OVERLOAD

 Hypotonic intravenous administration
 0.45% normal saline solution
 5% dextrose in water
 Excessive nasogastric tube irrigation with free water
 Excessive administration of free water via enteral tube feedings
 Syndrome of inappropriate antidiuretic hormone
 Psychogenic polydipsia
 MANIFESTATIONS OF INTRACELLULAR FLUID OVERLOAD
 Neurological
 Cerebral edema
 Headache
 Irritability
 Confusion
 Anxiety
 Muscle weakness
 Twitching
 Respiratory
 Dyspnea on exertion
 Increased respirations
 Gastrointestinal
 Nausea and vomiting
 Increased thirst
 Cardiac
 Elevated blood pressure
 Decreased pulse

DIAGNOSTICS
1) Serum electrolytes and serum osmolality are measured, but usually remain within normal limits.
2) Serum hematocrit and hemoglobin often are decreased due to plasma dilution from excess extracellular
fluid.
3) Additional tests of renal and liver function (such as serum creatinine, BUN, and liver enzymes) may be
ordered to help determine the cause of fluid volume excess.
4) Chest radiograph- to check for presence of pulmonary congestion
5) ABG- fluid in the alveoli impairs gas exchange resulting in hypoxia as evidenced by a low PO2

MEDICAL MANAGEMENT
Managing fluid volume excess focuses on prevention in patients at risk, treating its manifestations, and
correcting the underlying cause.
1) DIURETICS
 Commonly used to treat fluid volume excess. They inhibit sodium and water reabsorption, increasing
urine output.
 The three major classes of diuretics, each of which acts on a different part of the kidney tubule, are as
follows:
a) Loop diuretics
 Inhibit sodium and chloride reabsorption in the ascending loop of Henle
 Furosemide
 Ethacrynic acid
 Bumetanide
 torsemide
b) Thiazide-type diuretics
 Promote the excretion of sodium, chloride, potassium and water by decreasing absorption in the distal
tubule
 Bendroflumethiazide
 Chlorothiazide
  Hydrochlorothiazide
 Metolazone
 Polythiazide
 Chlorthalidone
 Trichlormethiazide
 Indamide
 Xipamid

c) Potassium-sparing diuretics
 Promote excretion of sodium and water by inhibiting sodium-potassium exchange in the distal tubule
 Spironolactone
 Amioride
 Triamterene

2) FLUID MANAGEMENT
 Fluid intake may be restricted in patients who have fluid volume excess. The amount of fluid allowed
per day is prescribed by the primary care provider. All fluid intake must be calculated, including meals
and that used to administer medications orally or IV.

3) DIETARY MANAGEMENT
 Because sodium retention is a primary cause of fluid volume excess, a sodium-restricted diet often is
prescribed. The primary dietary sources of sodium are the salt shaker, processed foods, and foods
themselves.

NURSING MANAGEMENT
Nursing care focuses on preventing fluid volume excess in patients at risk and on managing problems
resulting from its effects.

1. Closely monitor for the vital signs including heart sounds every 2-4hours or as frequent as necessary.
® Hypervolemia can cause hypertension, bounding peripheral pulses, and a third heart sound (S3) due
to the volume of blood flow through the hearts.

2. Auscultate lungs for presence or worsening of crackles and wheezes; auscultate heart for extra heart
sounds.
® Crackles and wheezes indicate pulmonary congestion and edema. A gallop rhythm (S3) may indicate
diastolic overloading of the ventricles secondary to fluid volume excess.

3. Place in Fowler’s position if dyspnea or orthopnea is present.

® Fowler’s position improves lung expansion by decreasing the pressure of abdominal contents on the
diaphragm.

4. Monitor oxygen saturation levels and arterial blood gases (ABGs) for evidence of impaired gas
exchange (SaO2 < 92% to 95%; PaO2 < 80 mmHg). Administer oxygen as indicated.
® Edema of interstitial lung tissues can interfere with gas exchange and delivery to body tissues.
Supplemental oxygen promotes gas exchange across the alveolar-capillary membrane, improving
tissue oxygenation.

5. Assess for the presence and extent of edema, particularly in the lower extremities and the back, sacral,
and periorbital areas.
® Initially, edema affects the dependent portions of the body—the lower extremities of ambulatory
patients and the sacrum in bedridden patients. Periorbital edema indicates more generalized edema.

6. Obtain daily weights at the same time of day, using approximately the same clothing and a balanced
scale.
® Daily weights are one of the most important gauges of fluid balance. Acute weight gain or loss
represents fluid gain or loss. Weight gain of 2.2 lbs is equivalent to 1 L of fluid gain.
 7. Administer oral fluids cautiously, adhering to any prescribed fluid restriction. Discuss the restriction with
the patient and significant others, including the total volume allowed, the rationale, and the importance
of reporting all fluid taken.
® All sources of fluid intake, including ice chips, are recorded to avoid excess fluid intake

8. Provide oral hygiene at least every 2 hours. Oral hygiene contributes to patient comfort and keeps
mucous membranes intact; it also helps relieve thirst if fluids are restricted.
® Oral hygiene contributes to patient comfort and keeps mucous membranes intact; it also helps relieve
thirst if fluids are restricted.

9. Teach patient and significant others about the sodium-restricted diet.

® Excess sodium promotes water retention; a sodium-restricted diet is ordered to reduce water gain.
Reducing sodium intake will help the body excrete excess sodium and water.

10. Administer prescribed diuretics as ordered, monitoring the patient’s response to therapy.
® Loop or high-ceiling diuretics such as furosemide can lead to rapid fluid loss and manifestations of
hypovolemia and electrolyte imbalance.

NURSING DIAGNOSIS
1) Fluid Volume Excess
Nursing care for the patient with excess fluid volume includes collaborative interventions such as
administering diuretics and maintaining a fluid restriction, as well as monitoring the status and effects of the
excess fluid volume.

2) Risk for Impaired Skin Integrity

Tissue edema decreases oxygen and nutrient delivery to the skin and subcutaneous tissues, increasing
the risk of injury.

3) Impaired Gas Exchange

With fluid volume excess, gas exchange may be impaired by edema of pulmonary interstitial tissues.
Acute pulmonary edema is a serious and potentially life-threatening complication of pulmonary congestion.

LEARNING ACTIVITIES:

1.) Watch a video on:

Capillary exchange and Edema Video (you.tube) URL:
https://www.youtube.com/watch?v=6ecmOuCIoNc

2) Watch a video on:

Fluid Volume Deficit and Excess Video (you.tube) URL:
https://www.youtube.com/watch?v=Ft2YuF8AOBQ

3) Watch a video on:

Isotonic, Hypotonic, Hypertonic IV Solutions Video (you.tube) URL:
https://www.youtube.com/watch?v=51FkahHUBwc&feature=youtu.be
Fluid and Electrolyte

A B
cell wall surrounds the plant cell - gives it shape and
protection
Semipermeable membrane- facilitate
molecules intra to extra cellular
sensitization of molecules
cell membrane a protective outer covering - regulates
interaction between the cell and its
environment
cytoplasm a gel-like material inside the cell where most
of the cell's life processes take place

- Shape
- Activities of the cell
nuclear membrane allows certain substances to pass between
the nucleus and the rest of the cell
- Permit passage of chon
- In out of cell
nucleus the control center of the cell
-imoratant part of the cell
-DNS
chromosomes contains the code that controls the cell -
transmits hereditary characteristics
nucleolus the area of the nucleus where ribosomes are
made

- Larges portion
- Self response to stress
mitochondria releases energy from digested foods
- ATP
chloroplasts manufactures food in the plant cell through
photosynthesis
Golgi bodies packages and transmits cellular material
throughout the cell
- Secretion and intra cellular transport
vacuole storage space for water, wastes, & other
cellular material
endoplasmic reticulum place where materials are processed and
moved around inside the cell

Chon and lipid Synthesis

ribosomes produces proteins within the cell
-RNA protein synthesis
lysosomes contains digestive chemicals that help break
down food molecules
cytoskeleton helps the animal cell maintain its shape and
move
 - folds inward to form the channel allowing
the dissolve substances to flow inside
- -micro villi
- Receptor mediated- clotting endo cytosis
- Cell absorbs the metabolize, hormone, chon
and viruses,
- Inward budding then close,

Eg. Cholesterol (LDL receptor)

Exo
- secreted outside the cell. From inside the
HYDROPHOBIC HEAD cell to the intracellular membrane.
- -Mag retain ng water in and out of the cell
- In- edema
Out- hypovolemia
HYDROPHOBIC TAIL
- expels water and separate the contants
outside the ce;;

-no need for any energy/ medium

-continuous process to maintain balance

Constantly move throughout the body

Needs energy to move to another area- Needs ATP
SODIUM POTASSIUM PUMP
-ACTIVE KASI NEED NG MEDIUM

Osmosis-
- water that moves
- Stops: when enough water achieve to
achieve homeostasis
- Low to high

3 Na in order to enter si ATP sa ICF

2 K to get out sa ICF

Endo-
- paloob, engulf

WBC- engulf the bacteria

Pino cytosis
-ability of extra cellular water to move
 - = amino acid
HYPOTONIC - Glucose
- higher solute in the cell compare to the - Medium is the protein
plasma
- h20 is transported into the cell
- Swell
- 0.45 saline solution
- Dehydrated Pt

HYPERTONIC
- lower solute concentration in the cell
- mag shrink kay mag labas sa cell ang water
- 5% dextrose
- 0.9% NaCl
- Edema

ISOTONIC
- Same concentration
- No change in cell volume
- Same distribution
- 0.9%NSS
- Plain LR (lactated ringers’ solution)
These will in tell the need of the cell
This is how to describe the IVF
FILTRATION
- IT HAPPENS WHEN particles in the
capillaries transfer to the tse
-
HYDROSTATIC PRESSURE (high to low)
- Created by pumping acion of the heart ad
gravity against the capillary wall
GFR

DIFFUSION
- Solutue that moves
- Osmosis- water
- High concentration to low

SIMPLE DIFFUSION
- Random movement of the particle to a
particular solution
- High to low
- Wla mag facilitate
- O2 , co2

FACILITATED DIFFUSION
- Carrier mediated diff
- May carrier protein in the membrane
- Large molecule
F&E Topic 2 

   
Plasma‐ fluid part of the blood  Osmolar 
CVP‐ measure the pressure in main vena cava 
‐ Low body fluid volume 
‐ To assess the status 
 

 
ADH‐ 

 
Usually may gna attach na catheter gna insert sa vena 
cava 
2‐6 mmhg 
Katong baall dapat ang leve naka kwan diri para normal 
Stenosis 
Congestion 
 
Hindi na strain or ubo para maka kuha ng tama na result 
  Decrease – hypovolemic shock 
Ortho static hypotension  ‐fluid shifting 
‐ Sudden drop of blood BP‐ changing of position  Bleeding 
Tachycardia   
‐ Compensatory blood circulation  Spinal Cord injury‐ demonstrate retraction 
Hypovolemia  ‐lalum na sternum 
‐ Blood pressure‐ dependent to to bld volume  ‐good indicator nag dec ang cvp 
‐ Confusion   
‐ Hypotension 
 Thirst 
Dry skin 
Wt loss 
Sticky mucos 
  
 
Total Parenteral Nutrition (TPN) 
  ‐ Bag na murag nay milk 
 
Adult‐ Isotonic 
‐ PLR 
Pedia‐ Hypo 
 
Oral‐ Orisol 
Pedia‐ pedia light 
 
Respiratory distress‐ complication of fluid restoration 
 

 
‐ For maintenance 

 
 
Head ache‐ +ICP 
 
Steps para mag bangon to prevent hypovolemic shock 
 1st side lying position 
2nd  semi fowler 
3rd fowler 
4th sit on bed 
 

 
 
Patent iv line 
‐  Iv flow 
‐ Flush NSS 
 
  
Very slow infusion 
 

 
 
 
Main line/ primary infusion= side drip 
 
Infuse thru gravity drip 
 

 
 

   
 
D5water, dextrose/ glucose= makes the solution hypo 
 
Burn=PLR 
Liver probm= 
 

 
Plasma expander 
 
Lactated‐ cannot be metabolize‐ can lead to acidosis  Warm 
Local swelling 
Tenderness 
Pain 
Palpable cord‐subayon ug ugat , nag inflame, very 
prominent an vein. 
 
Intervene‐ DC the IV 
‐Apply cld compress initially then apply warm 
‐alternate warm and cold compress. 
 
.225 % NaCl‐ maintenance para sa pedia 
 

 
 
72hrs lng ang IV site‐ patent or not kay transfer ng site 
to avoid local transmission 

 
 
KVO= prevent clotting 

 
Most common but neglected  
Apply warm to relax the veins 
 
SYSTEMIC COMPLICATION 
 

 
 
Hematoma‐ redish to bluish discoloration sa iv site 
Thrombosis‐ Apply cold compress 
 

 
 
Poor sterility 
More than 3 days ang canula.  
 
Culture to know the type of bacteria. 

 
  
   
  Alternative routes 
Edema‐ +fluid volume deficit   
Assessment‐ auscultation of breath sound kay needed. 
Crackles kung may fluidly overload 
 

 
Presence of air that travels in the system.   
1st step‐ Pwd I off ang line 
 
Trendelenburg para duon magtravel ang air. 
 
IV routes sa module 
Needle‐ different colors  
 
Guage‐ The high the gaude number mas maliit ang 
needle 
The lower the guage the bigger the the needle.   
  3. take years para gamitin, chemo 
BT‐ g19  Costic medication 
Neonate‐ purple / yellow   
Adult‐ pink  4. pocket inserted underneath the skin 
  ‐   
IV solution‐ label   
 
NaCl‐ yellow 
LR Pink‐  
Water 
Brown‐ Mannitol “tonicity”‐hypertonic solution=+ICP, 
cerebral edema 
Green – PNSS 
Violet‐ d5IMB 
   
   
  
 
Pull ang blood kay naga decline ang pressure 

 
 
Bipedal‐ 2 foot na maga 
Kung 1 kay pitting edema 
 

 
 
 
 
 
Water intoxication‐ too much h2o 
‐ Pwd din sa infants 
‐  
 
Coffee ground‐ bleeding, reaction mix with gastric acid 
 
  Irrigate using NGT if nag inom zonrox 
 
 
 
 
Pano malaman isotonic‐ Generalize edema. 
 
Extracellular‐ Periheral 
Isotonic‐ Mapti tyan, generalize 
‐ Na laki ang tyan 

 
 
ELECTROLYTR IMBALANCE 
 
 

   
 
D10 water‐ kiddie meal, iv for neonates 
  
   
Osmolality‐ malapot or malabnaw ang blood 
 
 
 
 
 
 

 
 
‐ THE MOST ABUNDANT SOLUTE IN ECF(sa labas 
sya) 
‐ Idealy a balnce between sodium and water 
Hypernatremia 
Hyponatremia 
 

 
HYPONATREMIA 

 
 
Decrease of sodium in the body 
PATHOPHYSIOLOGY 
‐Unable to compensate 
‐decrease serum sodium, fluid shifts (more 
concentrated 
“Where the water/Fluid flow there the electrolytes go” 

 
‐ +na ang nawawala kay yun ang ag appear. 
 

 
Sodium fnx‐ Nerve and muscle contraction 
‐affected and nerve impulses 
Heart= compensatory mechanism 

 
Kung maraming electrolyte ang nawawala kay mas 
severe ang effect. 

 
Stay focus on the late signs  LOW AND SLOW(all manifestations) 
Paralytic ileus‐ absence of bowel movement 

 
  Createnine‐ +24hrs urine level
K FNX 

‐Heart and Muscle Contraction 
 

 
5‐30 bowel sound 

 
  
+6months ang stored bld na wala nagamit kay mag +K 
level. 
‐can predispose the pt to hyperkalemia 

 
TIGHT AND CONTRACTED 
 
Contracy kay paspas pero di effective kay di maka push 
ng bld kaya bumababa ang bld pressure. 
 
Profound muscle weakness‐ pagod na muscle 

 
  
 

 
 

 
  
Predispose to blding 
 

 
 Really Large Fluid Loss 
Antibiotics (Aminoglycoside) 
Young Mothers

 
 
CRAY 
Consumption of alcohl in excess 
  
 

 
CALM ANG QUIET 

 
Pa‐ arterial 

 
  

 
 
 TOPIC 4 ACID- BASE IMBALANCE

The body constantly works to maintain a balance

(homeostasis) between acids and bases. Without that balance,
cells can’t function properly. As cells use nutrients to produce
energy they need to function, two-by products are formed—carbon
dioxide (CO2) and hydrogen. Acid-base balance depends on the
regulation of free hydrogen ions (H+) in body fluids determines the
extent of acidity and alkalinity, both of which are measured in pH.
Remember, pH levels are inversely proportionate to H+
concentration, which means H+ concentration increases, pH
decreases (acidosis). Conversely, when H+ concentration
decreases, pH increases (alkalosis).

Key Elements:
a. Acids – are hydrogen ion donors
b. Bases – are hydrogen ion acceptors
c. pH – expression of hydrogen concentration in a solution
d. pCO2 – Partial pressure of Carbon Dioxide the measure of carbon dioxide within arterial or venous blood.
e. HCO3 -- Bicarbonate is a byproduct of the body's metabolism.

2 Categories of Metabolic Processes:

a. Volatile -- can be eliminated from the body as a gas, e.g. Carbonic acid ((H2CO3) is the only volatile acid
produced in the body.
b. Nonvolatile -- that must be metabolized or excreted from the body in fluid
e.g. Lactic acid, hydrochloric acid, phosphoric acid, and sulfuric acid

Regulatory Mechanisms:
Regulatory Mechanisms:
A. Chemical buffers
 are substances that prevent major changes in pH by removing present in body fluid, buffers bind with
hydrogen ions to minimize the change in pH. If body fluids become too basic or alkaline,buffers release
hydrogen ions, restoring the pH.
1. Carbonic-Bicarbonate System, Bicarbonate (HCO3–)
 a weak base; when an acid is added to the system, the hydrogen ion in the acid combines with
bicarbonate, and the pH changes only slightly. Carbonic acid (H2CO3) is a weak acid produced when
carbon dioxide dissolves in water. If a base is added to the system, it combines with carbonic acid, and
the pH remains within the normal range. Although the amounts of bicarbonate and carbonic acid in the
body vary to a certain extent, as long as a ratio of 20 parts bicarbonate (HCO3–) to 1 part carbonic
acid (H2CO3) is maintained, the pH remains within the 7.35 to 7.45 range.
 Acts in few seconds
2. Phosphates
 important intracellular buffers, helping to maintain a stable pH within the cells.
3.Protein Buffer
 contribute to buffering of extracellular fluids. Proteins in intracellular fluid provide extensive buffering for
organic acids produced by cellular metabolism

B. Respiratory System
 Regulates carbonic acid in the body by eliminating or retaining
carbon dioxide. Carbon dioxide is a potential acid; when combined with water, it forms carbonic acid , a volatile
acid. Acute increases in either carbon dioxide or hydrogen ions in the blood stimulate the respiratory center in
the brain. As a result, both the rate and depth of respiration increase. The increased rate and depth of lung
ventilation eliminate
carbon dioxide from the body, and carbonic acid levels fall, bringing the pH to a more normal range. Although
this compensation for increased hydrogen ion concentration occurs. within minutes, it becomes less effective
over time. Patients with chronic lung disease may have consistently high carbon dioxide levels in their blood.
Alkalosis, by contrast, depresses the respiratory center. Both the rate and depth of respiration decrease, and
carbon dioxide is retained. The retained carbon dioxide then combines with water to restore carbonic acid
levels and bring the pH back within the normal range.
 Starts within minutes good response by 2 hours, complete by 12- 24 hours

C.Renal System
 Responsible for the long-term regulation of acid–base balance in the body. Excess nonvolatile acids
produced during metabolism normally are eliminated by the kidneys, The kidneys also regulate
bicarbonate levels in extracellular fluid by regenerating bicarbonate ions as well as reabsorbing them in
the renal tubules. Although the kidneys respond more slowly to changes in pH (over hours to days),
they can generate bicarbonate and selectively excrete or retain hydrogen ions as needed. In acidosis,
when excess hydrogen ion is present and the pH falls, the kidneys excrete hydrogen ions and retain
bicarbonate. In alkalosis, the kidneys retain hydrogen ions and excrete bicarbonate to restore acid–
base balance.
 Starts after few hours, complete by 5 to 7 days

Four (4) Types of Acid – Base Imbalance:

1. Respiratory Acidosis
2. Respiratory Alkalosis
3. Metabolic Acidosis
4. Metabolic Alkalosi

Note: Not a clinical diagnosis or disease, rather they are clinical syndromes associated with a wide variety of
diseases.

Acidosis  any pathologic process that cause a relative excess of acid (volatile or fixed in the body)
Alkalosis  indicates a primary condition resulting in excess in base
 Table 4-1 Normal Gas Values

NORMAL GAS VALUES

pH 7.35 – 7.45

PO2 80 – 100%

PaCO2 35 – 45 mmHg

HCO3 22 – 26 mEq/L

CAUSES OF ACIDOSIS

RESPIRATORY ACIDOSIS
(Carbonic Acid Excess)
Why patient hypoventilates, carbon dioxide builds up in the bloodstream and pH drops below normal –
respiratory acidosis. The kidneys try to compensate for a drop in pH by conserving bicarbonate (base) ions, or
generating them in the kidneys, which in turn raises the pH.

>> pH 7.35; PaCO2 >42 mmHg ; HCO3 normal

Causes:
a.Acute respiratory conditions (pulmonary edema, pneumonia, COPD)
 less surface area decreases the amount of gas exchange that can occur, thus impending carbon
dioxide exchange.
b. Depression of respiratory center(Drugs eg narcotics; head injuries)
 all metabolic acid are nonvolatile excreted to the kidneys, except carbonic acid which is excreted as
gas
c. Iatrogenic cause: inadequate mechanical ventilation
 excessive oxygen administration to client with COPD which hypoventilation occurs

Manifestations
a. Hypercapnia, due to rapid rise of PaCO2 level
b. Headache, CO2 dilates cerebral blood vessels
c. Warm and flushed skin, related to the peripheral vasodilation as well as to impaired gas exchange
d. Fine flapping tremors
e. Decreased reflexes
f. Rapid, shallow respirations; elevated pulse rate ; tachycardia
g. Decreasing level of consciousness
 Figure 4-1 Signs and Symptoms of Respiratory Acidosis

Medical Management
a. ABG analysis
b. Chest Xrays, can help pinpoint some cause, eg COPD, pneumonia
c. Serum electrolytes level, in acidosis potassium leaves the cell, so expect serum level to be elevated
d. Bronchodilators, to open constricted airways
e. Supplemental oxygen
f. Drug therapy to treat hyperkalemia

Nursing Diagnoses
 Ineffective breathing Pattern related to hypoventilation
 Impaired gas exchange related to alveolar hypoventilation
 Anxiety related to breathlessness
 Risk for injury related to decreased level of consciousness

Nursing Management
1. Maintain patent airway
® For easy access in case cardiac arrest may happen.
2. Monitor vital signs
® Respiratory acidosis can cause tachycardia, alterations in cardiac rate, respiratory rate and hypotrension.
3. Monitor neurologic status and report significant changes
® As it may progress to shock and cardiac arrest.
4. Administer oxygen as ordered
® To be given at lower doses most especially to COPD patients as it stimulates patients to breathe.
5. Accurate intake and output records
® To evaluate renal function.
6. Report any variations in ABG level.
METABOLIC ACIDOSIS
(Base Bicarb Deficit)
The underlying mechanisms in metabolic acidosis are a loss of bicarbonate from extracellular fluid, an
accumulation of metabolic acids, or a combination of the two.

>> pH 7.35; pCO2 normal ; HCO3 <26 mEq/L

Causes:
a. Diabetic ketoacidosis  decrease insulin prevents glucose uptake , thus, stored fats are oxidized (
acetoacetic acid) and is metabolize for energy
b. Renal insufficiency decreased ability of the kidney to excrete acids
c. Prolonged vomiting, severe diarrhea due to ,loss of alkaline substances

Manifestations
Metabolic acidosis typically produces respiratory, neurologic, and cardiac sign and symptoms. As acid
builds up in the bloodstream, the lungs compensate by blowing off carbon dioxide.
a. Weakness, fatigue, general malaise
b. Anorexia, nausea, vomiting, abdominal pain
c. Decrease level of consciousness
d. Rapid, deep, labored breathing (Kussmaul’s respirations) the first clue to metabolic acidosis
e. Decrease cardiac output and blood pressure
f. Skin is warm and dry, as a result of peripheral vasodilation
g. Diminished muscle tone and reflexes
Compensation:
- Increase respiratory rate/ depth to blow off carbon dioxide

Figure 4-2 Signs and Symptoms of Metabolic Acidosis

Medical Management
a. ABG analysis
b. Serum potassium levels usually elevated as hydrogen ions move into the cells and potassium moves out
to maintain electroneutrality
c. Rapid acting insulin to reverse diabetic ketoacidosis and drive potassium back into the cell.
d. Intravenous Sodium bicarbonate to neutralize blood acidity in patients with bicarbonate loss
e. Fluid replacement

Nursing Diagnoses
• Decreased cardiac output secondary to dysrhythmias and / or fluid volume deficits
• Risk for sensory/ perceptual alterations related to changes in neurological functioning secondary to acidosis
• Risk for fluid volume deficit related to excessive loss from the kidneys or gastrointestinal system

Nursing Management
Nursing care includes immediate emergency interventions and long-term treatment of the condition and
its underlying causes. Observe the following guidelines:
a. Monitor vital signs
b. Monitor neurologic status.
® Changes can occur rapidly that prompt doctor’s referral.
c. Maintain patent IV line.
® For emergency situations and antibiotic administration.
d. Careful administration of sodium bicarbonate
® The chemical can inactivate many drugs or cause them to precipitate.
e. Proper positioning.
® To promote chest expansion and facilitate breathing.
f. Record intake and output
® To evaluate renal Function

RESPIRATORY ALKALOSIS
(Carbonic Acid Deficit)
In metabolic alkalosis, the underlying mechanisms include a loss of hydrogen ions ( acid) , a gain in
bicarbonate or booth. Above normal PaCO2 indicates that the lungs are compensating for alkalosis. Renal
compensations more effective, but slower as well.

>> pH 7.45; PaCO2 <35 mmHg; HCO3 normal

Causes
a. Vomiting loss of hydrochloric acid from the stomach
b. Diuretic therapy (thiazides, loop diuretics) can lead to a loss of hydrogen, potassium from the kidneys
c. Cushing’s disease causes retention of sodium and chloride and urinary loss of potassium and hydrogen
d. Hyperventilation most common cause of acute respiratory alkalosis
e. Severe anemia, acute hypoxia 20 high altitude overstimulation of the respiratory system causes to
breathe faster and deeper

Manifestations
a. Slow, shallow respirations
b. Nausea, vomiting
c. polyuria
d. Twitching , weakness and tetany
e. Hyperactive reflexes
f. Numbness and tingling sensation
g. Confusion or syncope lack of carbon dioxide in the blood may lead to hyperventilation
h. Dysrhythmia : related to hypokalemia and hypocalcemia

Buffering Response:: shifting of acid from intracellular fluid to blood

Movement of bicarbonate into cell in exchange of chloride
Renal compensation :: increase bicarbonate excretion; decrease hydrogen ion secretion

Figure 4-3 Signs and Symptoms of Respiratory Alkalosis

Medical Management
a. Identify and eliminate causative factor if possible
b. Sedative or Anxiolytics agents may be given to relieve anxiety and restore a normal breathing pattern.
c. Respiratory support, e.g. oxygen therapy to prevent hypoxemia ; breathe into a paper bag  this forces the
patient to breathe exhaled carbon dioxide, thereby raising the carbon dioxide
d. ABG analysis key diagnostic test in identifying respiratory alkalosis
e. ECG  may indicate arrhythmias or the changes associated with hypokalemia or hypocalcemia

Nursing Diagnosis
• Ineffective breathing pattern related to hyperventilation
• Altered thought processes related to altered cerebral functioning

Nursing Management
1. Allay anxiety whenever possible
® To prevent hyperventilation.
2. Monitor vital signs, and report changes
3. Report variations in ABG and ECG
® Changes can help evaluate patients condition.
4. Maintain a calm, quiet environment
®Stress and fatigue can lead the patient to hyperventilate
METABOLIC ALKALOSIS
(Carbonic Acid Excess)
A condition in which there is an increased pH and increased HCO3

 pH > 7.45 ; HCO3 above 26 mEq/L ; PCo2 normal

Causes
1. diuretic therapy  cause loss of H+, A-, k+ but precipitates ↑HCO3 level
2. ingestion of NaHCO3 or excessive NaHCO3 to correct acidosis
3. aldosterone excess  ↑ Na retention, ↑ H+ and bicarbonate regeneration
4. prolonged steroid therapy  same with aldosterone effects
5. prolonged gastric suctioning or vomiting  loss or H+ ions; sengstaken, Blakemore tube ( a thick catheter
with triple lumen with 2 balloons; inflated at the orifice of the stomach and esophagus to apply pressure thus
prevent bleeding, the 3rd lumen is for suctioning gastric contents)
6. Massive blood transfusion (whole blood)  ( citrate anticoagulant which is use for storing blood is
metabolize to bicarbonate)

Manifestations
 Increased myocardial activity, palpitations
 Increased heart rate
 Rapid , shallow breathing
 Dizziness, lightheadedness
 Hyperactive reflexes
 Nausea, vomiting

Figure 4-4 Signs and Symptoms of Metabolic Alkalosis

Laboratory Findings
 ABG analysis
 Serum electrolyte levels low potassium, calcium and chloride, HCO3 elevated
 ECG changes, low T wave

Medical Management
 Replacement of electrolytes
 Antiemetics may be administered to treat underlying nausea and vomiting
 Acetazolamide (Diamox)  to increase renal excretion

Nursing Diagnoses
 Ineffective breathing pattern related to hypoventilation
 Impaired gas exchange related to alveolar hypoventilation
 Anxiety related to breathlessness

Nursing Management
1. Monitor vital signs
2. Assess patient’s level of consciousness
® Apathy and confusion may be evident in a patient’s conversation.
3. Administer oxygen
® Treat hypoxemia
4. Monitor Intake and output
® To evaluate renal function.

ACID BLOOD GAS (ABG) ANALYSIS

 is an essential part of diagnosing, and managing a patient’s oxygenation status and acid-base balance
 the usefulness of this diagnostic tool is dependent on being able to correctly interpret results.

Table 4-2 Evaluation Of Abnormal Blood Gas Values

NORMAL GAS VALUES
pH 7.35 – 7.45
PaO2 80 – 100%
PaCO2 35 – 45 mmHg
HCO3 22 to 26 mEq/L

Identifying The Primary Process

pH

Low Normal High

Acidemia No abnormality or Alkalemia

Mixed acid disorder

High Low Low High

PCO2 HCO3 PCO2 HCO3

Respiratory Metabolic Respiratory Metabolic

Acidosis Acidosis Alkalosis Alkalosis
Figure 4-5 Acid Base Mnemonic
Table 4-3 Steps to ABG Analysis
STEPS TO ABG ANALYSIS
1 Look at the pH
a. if  ACID-BASE BALANCE
b. Fully or completely compensated acid- base disorder
c. Mixed acid – base disorder
If  pH acidosis pH alkalosis
2 Look at the PCO2, if….
Alkalosis Acidosis
Evaluate the pH – PCO2 relationship for possible RESPIRATORY
3 PROBLEM
pH Respiratory
PCO2 Alkalosis
pH Respiratory
PCO2 Acidosis
4 Look at the HCO3, Normal? , if…..
Acidosis Alkalosis
Evaluate the pH, HCO3, and base excess for METABOLIC PROBLEM
5 pH
HCO3 Metabolic Acidosis
Base -2
pH
HCO3 Metabolic Alkalosis
Base +2
Look for Compensation
NOTE: Renal (HCO3) compensates for respiratory problem
Respiratory (PCO2) compensates for renal problem
6
2 Degrees of Compensation
a. Partial - compensatory component is appropriately abnormal but pH
is not yet in normal range, either acidotic or alkalotic
ex. pH PCO2 HCO3
METABOLIC ALKALOSIS PARTIALLY COMPENSATED
b. Full - Compensatory component alters enough to return pH to normal
Ex. pH 7.45 PCO2 HCO3
METABOLIC ALKALOSIS VS RESPIRATORY ACIDOSIS FULLY
COMPENSATED

pH SHOWS THE PRIMARY PROBLEM

7.40 is absolutely normal

(7.35 – 39 = slightly acidic 7.41-45 = slightly alkaline)

Evaluate oxygenation
7 PO2 < 80 mmHg – hypoxemia; hypoventilation
60-79 Mild Hypoxemia
40-59 Moderate hypoxemia
< 40 Severe Hypoxemia
PO2 > 100 mmHg – hyperventilation
Learning Activities
1. Video on ABG interpretation (https://youtu.be/EML9vE1nOgk)
2. How to perform Allen’s Test ( https://youtu.be/D1tJO0RW9UM )
3. Example Case Analysis:
A 69-year-old with chronic obstructive pulmonary disease (COPD) is admitted with an acute respiratory
infection. You are the nurse assigned to care of this client.
a.) What would this client’s ABGs look like?
b.) What will you do to help improve the client’s respiratory status?
c.) Why is a client with COPD given oxygen at a low flow rate?
d.) Why is this client’s PaCO2 different than a client who does not have COPD?
e.) What teaching does this client require in order to prevent development of metabolic alkalosis?
4. Different exercises to enhance skills in ABG interpretations
a. pH 7.26
CO2 53
HCO3 24
PO2 50
b. pH 7.52
CO2 29
HCO3 23
PO2 100
c. pH 7.18
CO2 44
HCO3 20
PO2 92
 TOPIC 5
BURNS

Figure 5-1 Burn Injury

A burn is an injury from exposure to heat, chemicals, radiation or electric current leading to sequence of
physiologic events . For severe burn cases if untreated it can lead to irreversible tissue damage. Injuries
result from direct contact with or exposure to any of heat source and the heat energy from the source is
transferred to the tissues of the body
Many burn can be prevented, and most major burns occur in the home during cooking, improper use of
electrical appliances and work related handling chemical, hot objects. Infants and adults have greater risks to
morbidity and mortality when they sustain burn injuries due to several contributing factors.

4 Major goals relating to burns

 Prevention
 Institution Of Life-Saving Measures For The Severely Burned Person
 Prevention Of Disability And Disfigurement Through Early Specialized Individual Treatment
 Rehabilitation Through Constructive Surgery And Rehabilitative Programs
Review of The Skin Anatomy and Physiology

The skin is the largest organ of the body, having . a surface area of 15 -20 square feet. It provides covering for
the body thereby protecting the body’s organ and tissues from the external environment.

Figure 5-2 The Skin Structure

The skin has two layers . the epidermis and the dermal layer. The epidermis is the outer of the skin
and it in thin but tough . protecting the internal structures from bacteria, viruses, fungi and trauma. It is
compose of keratinocyte and melanocyte cells. The dermis is the inner layer of the skin and is considered as
“True Skin” , compose of thick layer of fibrous and elastic tissue. It is of composed collagen fibers consisting
mast cells responsible for phagocytosis and release histamine in burn injury. The dermal layer also serve as
supporting and nutritional bed because most of the blood vessels, nerves, sweat and sebaceous glands, hair
follicles are located.

Table 5-1 The Function of The Skin

Function Of The Skin Mechanism
Protection of the internal structures against It covers the internal structures of the body
infection and trauma from the external environment
Sensation Receptor endings of nerves senses
temperature, pain, light touch, pressure

Fluid Balance Prevents H20 loss and extra H20 release

through perspiration ; serves as water
repellant
Temperature Regulation Body continuously produces heat as result of
food metabolism and this heat is primarily
dissipated in the skin
Vitamin D Production Skin expose to UV light can convert
cholesterol molecules to vit. D
Immune Response Function Several dermal cells are important
components of the immune system e.g.
langerhaus cells, interleukin 1
Physiologic Response to Burn Injury
Burns are cause by a transfer of energy from a heat source to the body through conduction and
electromagnetic radiation leading to skin disruption causing increase fluid loss, massive infection,
hypothermia, scarring, compromised immunity ,change in body function ,appearance and body image . In
severe cases, fluid and electrolyte imbalance ensue. If a person inhales products of combustion , respiratory
function is compromised. Cardiac dysrhythmia and circulatory failure , profound catabolic state increasing
caloric expenditure and nutritional deficiencies are also manifestations in serious burn injury. Gastrointestinal
motility if altered , leads to ulcer and paralytic ileus. If dehydration is severe , it slows down the glomerular
filtration rate, renal clearance of toxic wastes may lead to tubular necrosis and acute renal failure.

Categories of Burn Injury

MILD
 Partial thickness < 15% adult
 Full thickness burns < 2% adult
OTHER CRITERIA
 Does not involve eyes ,ears, nose, hands, face , feet , perineum
 No electrical burns / inhalation injuries
 Adult younger than 60 yrs. Old
 No pre existing disease and other injury with the burn
MODERATE
 Partial thickness burn 15 to 25 % adult TBSA
 Full thickness 2% to 10 % adult TBSA
 Plus minor category criteria
SEVERE
 Partial thickness > 25% adult TBSA
 Full thickness burns are > 10% adult TBSA
 Burns are accompanied by other injuries
 Presence of other criteria in the previous categories

Factors s Determining Burn Severity

1. Burning Agent/ Cause
2. Location/Body parts involve
3. Age
4. Depth of the burn
5. Size of the burn
6. History of cardiac, pulmonary, renal, hepatic disease
7. Injuries sustained during burn injury

Burning Agent and Location

The higher the temperature of the burning agent and longer duration of contact can cause more severe injury.
Burns sustained in the head, neck and chest is associated with higher mortality rate because of
bronchoconstriction secondary to histamine release causing edema , carbon monoxide poisoning secondary
to smoke inhalation, chest constriction secondary to circumferential burns. Burns sustained in the perineum
area requires special care, these said areas are prone to infection because of stool and urine contamination.
Table 5-2. Types of Burn Injury
Cause /Type Causative Agent Priority Treatment
Thermal open flame Extinguish flame (stop, drop,
steam and roll)
hot liquids (water, grease, tar, Flush with cool water
metal) Consult fire department
Chemical -Acids Neutralize or dilute chemical
Strong alkalis Remove clothing
Organic compounds Consult poison control center
Electrical Direct current Disconnect source of current
Alternating current Initiate CPR if necessary
Lightning Move to area of safety
Consult electrical experts
Radiation Solar Shield the skin appropriately
X-rays Limit time of exposure
Radioactive agents Move the patient away from
the radiation source
Consult a radiation expert

Age, Depth and Size of The burn

Individuals below 2 years old and above 60 yeas old are of higher risk to morbidity and mortality rates when
sustaining burn injury secondary to immature and poor immune system, fluid and electrolyte status , and
existence of co-morbidities.
Another factor affecting burn severity is the depth and size of the burn, the deeper and bigger the burn injury
involved , result to more serious injuries and damage and longer healing time .For third degree burns , skin
grafting is required for a definitive wound closure. Burn size more than 20% in adult and more than 10% of the
body surface area requires fluid resuscitation.

Table 5-3 Burn Depth

History of cardiac, pulmonary, renal, hepatic disease and Injuries sustained during burn injury
Pre-existing disease conditions would reduce normal compensatory responses to minor hypovolemia Optimum
systemic functioning is very vital for the burned client to respond to the burn management such as fluid
resuscitation, nutritional correction and infection prevention. Injuries sustained during burn injury like fractures
requires prolong hospitalization and additional management.

Stages of Interdisciplinary Care

The clinical course of treatment for the burn patient are divided into three stages. These stages are useful to
determine the clinical needs of the patient. The assessment and management of the burned patient involves
different group of physicians,nurses and other health are specialists collaborating with each other to manage
the patient’ s recovery.

Table 5- 4. Stages Of Burn Care

Phase Duration Priorities

Emergent / immediate onset of injury to 1st aid, prevention of shock
Resuscitative completion of fluid Prevention of respiratory
resuscitation 48 -72 HRS distress
post injury Detection and treatment of
injury
Wound assessment/initial
care
Acute Beginning of diuresis to Wound care and closure
need completion of prevention or treatment, of
wound closure complication nutritional
support
Rehabilitative From major wound Prevention of scars and
closure to return of contractures
individual’s optimal level Physical, occupational,
of physical and vocational rehabibi;itation
psychosocial adjustment Functional cosmetic
reconstruction , psychosocial
counseling

I. Emergent / Resuscitative Phase

Starts with the onset of injury to completion of fluid resuscitation 48 -72 HRS post injury The goal in this phase
is to preserve vital functions and prevent hypovolemic shock.
Pre -Hospital Care
 Remove person from source of burn
 Assess ABC and trauma
 Cover burn with sterile or clean cloth
 Remove constricting clothes and jewelry
 Transport immediately

Emergency Care for Minor Burn

 Administer pain medication
 Administer Tetanus prophylaxis
 Wound care
 Apply topical antibiotics

Emergency Care for Major Burns

 Evaluate degree and extent of burn
 Established patent airway and administer oxygen for burn victims in enclosed area
 Venoclysis and assess for hypovolemia
 Maintain NPO and insert NGT
  Insert foley catheter
 Tetanus prophylaxis and give pain medication

Fluid management is one approach to treat burn patients. Within minutes of burn injury , a massive amount
of fliud shifts from the intracellular and intravascular compartments into the interstitium (thirdspacing). This kind
of shift is called burn shock and it continues until capillary integrity is restored within 24-36 hours of the injury.
Fluid resuscitation is indicated for burns greater than 20% TBSA in adults, greater than 10% BSA in children,
patients older than 65 or younger than 2 years of age and patient with preexisting disease that would reduce
normal compensatory responses to minor hypovolemia (Cardiac, pulmonary, renal, hepatic , diabetes).

Computation of Body Surface Area Burn

The extent of the burn injury size is expressed as percentage of the total body surface area (TBSA). Several
methods are use to determine the extent of the injury. The “Rule of Nines” is a rapid method of estimation of
the burn size. This method divides the body into 5 surface areas- head, trunk, arms, legs and perineum and
percentage that equal or total to the sum of nines are assigned except the perineum which is only one percent.

Figure 5-5 Rule of Nines

Common Formula for Fluid Resuscitation

Fluid resuscitation is the administration of the intravenous fluids to restore the circulating blood volume during
the acute period of capillary permeability in order to prevent burn shock . Crystalloids are administered during
the first 24 hours after burn injury.Two commonly used formulas are the Parkland and modified Brooke
formula. These formulas specify to infuse the 50% volume of fluid during the first 8 hours and the remaining
50% to be infused over the next 16 hours.
In Parkland formula , lactated Ringer solution is administered 4 ml X kg X % TSBA burn. Modified Brooke
lactated Ringer solution is administered 2ml X kg X % TSBA burn. Hourly urine output is measured to
determine if fluid resuscitation is effective. Cardiac and respiratory status are also monitored.

Other interventions during Resuscitative Phase

 Elevate the head of the bed to 30 degrees for facial and head burns
 Elevate circumferential burns of the extremities with a pillow above the level of the heart
 Assess for infection, tracheal or laryngeal edema
 Protective isolation techniques Shave hair around wound margins
 Monitor gastric output and Ph for stress ulcer (Curling’s Ulcer )
 Administer anti- ulcer drugs
 Avoid IM and SQ administration
 NPO until with bowel sound
 Monitor daily weights
 2. Acute Phase
Begins with hemodynamic stability, capillary permeability restored and diuresis begun Restorative therapy
to wound closure and infection control are the primary concern. Aseptic technique and adequate
debridement of wound , tetanus immunization, IV antibiotics , topical anti-bacteria therapy wound care are
the basic management.

Escharotomy is one approach in wound care wherein dead tissues and eschar are remove by making
an incision . Management post escharotomy include assessment of pulses, color, movement, and
sensation of affected extremity ,if bleeding is present control it with pressure and pack incision gently with
fine mesh gauze for 24 hours after. Fasciotomy is another approach in wound care where the fascia is cut
to relieve pressure so as to to reduce tissue death. Hydrotherapy can also be utilize, through shower, bed
bath and total immersion. If total immersion is use, the tank is lined with plastic liners and decontamination
every after use is done to prevent cross infection, the temperature of the water to be use is 37 degrees
Celsius and the immersion process should not exceed more than 30 minutes to prevent chilling.
For wound dressing , it may open or close dressing depending on the burn area involve in order to
maintain circulation, and allows motion. For Joints , light dressing is required to allow movement, face
dressings should be open type of dressing, and for finger and toes, it should be wrapped individually.
Wound closure as a part of wound care is important. Biological, synthetic and biosynthetic dressings is
applied or skin grafting is performed . For graft care, elevate and immobilized graft site, keep site free
from pressure, monitor for infection and protect area from sunlight.

Table 5-5 Common Antimicrobial Agent

Antimicrobial Agent Advantage Side Effects

Silver Sulfadiazine cream Effective against most gram- May cause hypersensitivity
positive and gram-negative reaction in 5%-7% of all
organism patients;

Soothing on application Associated with an initial

decrease in WBC’s
Softens the eschar and
increases joint mobility

Absorbed slowly reducing the

Mafenide acetate cream
chance of nephrotoxicity
Effective against most gram-
positive and gram-negative
organism
Rapidly diffuses through
eschar (improved
effectiveness in established
infections)
Painful on application;
May cause hypersensitivity
reaction in 5%-7% of all
patients;
Associated with acid-base
derangements

Permits open treatment of

Silver nitrate solution
wounds; thus, increasing
mobility
Effective against most gram- Hyponatremia, hypokalemia,
positive and gram-negative and hypochoridemia
organism
Decreased penetration of
eschar

Requires large bulky

dressings
3. Rehabilitative Phase
Starts from acute care to hospital discharge, the goals are directed for the burned patient to gain independence
and achieve maximal use of the affected part, promote wound healing, minimize deformities, increase strength
and function and provide emotional support.

Nursing Management
1. Remove person from source of burn
®To remove the patient from the heat source and prevent further injury
2. Assess ABC and trauma
®To assess the extent of the injury so as to initiate and prioritize appropriate interventions
3. Cover burn with sterile or clean cloth
®Keeps air off the area, reduces pain and protects blistered skin.
4. Remove constricting clothes and jewelry
® Burn areas swells quickly , constrictive clothing can compromise circulation
5. Transport immediately
® for prompt medical intervention for severely burn patients,
Emergency Care for Minor Burn
1. Administer pain medication
® to ease pain and promote comfort
2. Administer Tetanus prophylaxis
®Tetanus is a possible complication of any burn because the damaged tissue is easily infected. The person
needs tetanus or booster shot, depending on date of last injection. Tetanus booster should be given every 10
years.
3. Wound care
® Promotes speedy healing and prevent infection
4. Apply topical antibiotics
® Promotes speedy healing and prevent infection
Emergency Care for Major Burns
1. Evaluate degree and extent of burn
®To determine the appropriate fluid replacement and prevent shock
2. Established patent airway and administer oxygen for burn victims in enclosed area
®Systemic oxygenation is impaired by toxic gases released in most fires Inhaled smoke contains carbon
monoxide and cyanide and can travel to the alveoli and trigger inflammatory reactions that lead to
bronchospasm and impaired gas exchange .
3. Venoclysis and assess for hypovolemia
® To maintain the tissue perfusion . Burn injuries greater than 10% TBSA and including the dermis result in
circulatory compromise secondary to fluid loss via damaged tissue, widespread vasodilation as well as
increase capillary permeability and fluid shifts (third spacing). This can result in hypovolemia leading to burns
shock.
4. Maintain NPO and insert NGT
®Gastric stasis or ileus can result from potassium shifting secondary to massive burn, Insertion of a
nasogastric tube and commencement of enteral feeds should be considered for those who sustain significant
burn injuries and/or facial burns and are unable to tolerate adequate oral intake.
5. Insert foley catheter
® Insert a Foley catheter so that urine output can be monitored as a guide for volume status. Insert a Foley
catheter in patients with burns >15% TBSA. Adequate urine output is 0.5 mL/kg/h in adults and 1.5 mL/kg/h in
children.
6. Tetanus prophylaxis and give pain medication
®Tetanus is a possible complication of any burn because the damaged tissue is easily infected and pain
relievers promote comfort.

Other interventions during Resuscitative Phase

1. Elevate the head of the bed to 30 degrees for facial and head burns
®To minimize facial edema
2. Elevate circumferential burns of the extremities with a pillow above the level of the heart
®To prevent or reduce swelling and pain
3. Assess for infection, tracheal or laryngeal edema
®For prompt medical intervention
4. Protective isolation techniques Shave hair around wound margins
®Hair and hair follicles harbor bacteria that increase the bacterial load, delaying wound healing and increasing
the risk of infection.
5. Monitor gastric output and Ph for stress ulcer
®To early detect development of Curling’s ulcer
6. Administer anti- ulcer drugs
®to prevent or correct Curling’s ulcer
7. Avoid IM and SQ administration
®Poor absorption of medications following burn injury due to fluid shifts
8. NPO until with bowel sound
®To prevent abdominal distention secondary to paralytic ileus , a complication of burns
9. Monitor daily weights
®For proper nutritional management . Severe burn is associated with significant changes in body weight due to
resuscitation volumes, fluid shifts, a hypermetabolic state, prolonged bed rest, and caloric intake.

Nursing Diagnoses and Management

1. Impaired gas exchange related to carbon monoxide poisoning, smoke inhalation upper airway loss
 Maintain adequate perfusion
® To ensure adequate oxygenation and maintain vital organs function
2. Ineffective airway clearance related to edema and effects of smoke inhalation
 Maintain patent airway.
® To prevent respiratory distress
3. FVD related to ↑ capillary permeability and evaporative losses from burn wound
 Restore optimal fluid balance and perfusion of vital organs
® to promote healing and prevent further complications related to burn injury
4. Pain related to tissue/nerve/emotional impact injury
 Assess level of discomfort
® To determine the appropriate pain intervention
 Administer pain relievers and antibiotics
® Pain relievers promote comfort and damaged tissue is easily infected
 Provide emotional support to allay fear and anxiety
® To allay fear and anxiety
 Learning Activities

1. Assignment on the layers of epidermis Epidemis layers

https://www.youtube.com/watch?v=0X46aImj6nw
2. Compare Lund and Browder , Berkow’s Formula for computing fluid resuscitation
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC449823/
https://books.google.com.ph/books?id=6DHMDwAAQBAJ&pg=PA8&lpg=PA8&dq=lund+and+browder+
vs+berkow+formula&source=bl&ots=igUYn-
TNil&sig=ACfU3U2J4uw3hvcgPlaSJDYSmes9vg5jEg&hl=en&sa=X&ved=2ahUKEwih9bCGx7LqAhWQ
A4gKHTMbB_EQ6AEwF3oECAkQAQ#v=onepage&q=lund%20and%20browder%20vs%20berkow%20
formula&f=false
3. Using the Rule of Nines , assign the percentage distribution to the given body areas involved, if the
TBSA is 28 %
Head
Chest and abdomen
Perineum
4. Work example for fluid resuscitation
(1) A 25 year old man weighing 70 kg with a 30% flame burn was admitted at 4 pm. Computation for his Total
fluid requirement for first 24 hours using Parkland Formula 4 ml × (30% total burn surface area) × (70 kg) =
8400 ml in 24 hours
2) Half to be given in first 8 hours, half over the next 16 hours
Will receive 4200 ml during 0-8 hours and 4200 ml during the next 16 hours
TOPIC 6 – URINARY ELIMINATION DISORDERS

Review of Anatomy and Physiology of the Renal System

Figure 6-1 Urinary System

The renal system is responsible for maintaining homeostasis in the body by carefully regulating fluid and
electrolytes, acid – base balance, removing wastes, and providing hormones responsible for red blood cell
production, hypertension and bone metabolism. The renal system is composed of the upper and lower urinary
tract.

Lower Urinary System A.

Bladder
The bladder is an extra peritoneal organ that lies behind the symphysis pubis . Its main function is for
storage of urine. As volume of urine increases, starting from 300-500 ml, awareness of the need to void
develops. Voluntary voiding is accomplished by stimulation of the parasympathetic nerve fibers causing
coordinated contraction of the detrusor muscle and the bladder body.

B. Urethra
The urethra drains urine from the bladder to an exterior opening of the body, the external urethral
orifice. In females, the urethra is about 3 to 4 cm. (1.5 in.). In males, the urethra is about 15 to 20 cm (6 to 8
in.) Micturition, or urination, is the process of releasing urine from the bladder into the urethra.

Upper Urinary System

Figure 6-2 Structure of the Kidneys

Kidneys
The two kidneys lie on the posterior wall of the abdomen outside the peritoneal cavity (dorsal body wall). Each
kidney of the adult human that weighs about 150g is about the size of an indented region called the hilum
through which passes the renal artery and vein, lymphatic, nerve supply. The outer part is the cortex and inner
region called medulla. The medulla is divided into multiple cone shaped masses called renal pyramids. The
base of each pyramid terminates in the papilla, which projects into the space of renal pelvis, a funnel shaped
continuation of the upper end of the ureter. The outer border of the pelvic is divided into minor calyces, the
walls up the calyces, pelvis that contain contractile elements that propel the urine toward the bladder, where
urine is stored until it is emptied by micturition.
The functional unit of the kidney is the nephron. Millions of nephrons are present in each human kidney
which aid in the urine production and process of removing metabolic waste products from the blood. These
significant structures extend between the cortex and the medulla. At one end of the nephron is closed,
expanded and folded into a double-walled cuplike structure called the Bowman’s capsule. This capsule
encloses glomerulus, the nephron’s primary structure in filtering function.

Functions of Kidney

Kidney performs different functions in order to maintain homeostasis in the body by excreting metabolic
waste products and reabsorbing necessary elements for the body. The following are the functions of the
kidney:
1. Formation of urine
 The formation of urine happens in three phases which are filtration, reabsorption and secretion. Each
of these processes happens in the body in order to create homeostasis by removing those metabolic
waste products and reabsorbing helpful substances.

a. Filtration
 The filtration process is nonselective, passive process which forms essential blood plasma without
blood protein but both of it is normally too large to pass through the filtration membrane. If any of the
two appeared in the urine, it would mean that there is a problem in the glomerular filters. The water
and solute are smaller than proteins that are forced through the capillary walls and pores of
Bowman’s capsule into the renal tubule.
b. Reabsorption
 Tubular reabsorption is achieved by active and passive transfer mechanism

ACTIVELY REABSORBED
 Sodium,
 potassium,
 calcium,
 phosphate,
  uric acid.
PASSIVELY REABSORBED
 Urea, water,
 chloride,
 some bicarbonates
 some phosphate .

Most reabsorption occurs in the proximal tubule which conserves needed substances but does not reabsorb
metabolic waste products.

c. Secretion
 Some of substances such as hydrogen and potassium ion, creatinine, and ammonia, move from
the peritubular capillary blood and secreted by the tubule cells into the filtration. Excreting
nitrogenous waste products , unnecessary and excess substances .

2. Body’s Water Volume Regulator

Regulation of water in the body contained in the blood is greatly influenced by antidiuretic hormone (ADH), also
called vasopressin. Vasopressin is produced in the hypothalamus and stored in nearby pituitary gland.
Receptors in the brain monitor the blood’s water concentration causing the release of ADH in the bloodstream
if the amount of salt and other substances is too high. ADH in the bloodstream causes more water to be
reabsorbed into the bloodstream. In the absence of ADH, the collecting ducts become impermeable to solute
and water, making it less concentrated than plasma and the urine is diluted.

3. Excretion of Metabolic Waste Products

 The kidney functions as the body’s main excretory organ, eliminating the body’s metabolic waste
products and serves as the primary mechanism for excreting drug metabolites. 25g to 30g of
urea is produced as the end product of protein breakdown and excreted daily making it the
major waste product of protein metabolism. Other waste products are creatinine, phosphates
and sulfates. Uric acid, formed as a waste product of purine metabolism, is also eliminated in
the urine.

4. Blood Pressure Regulator

 Regulating blood pressure is linked to the kidneys' ability to excrete enough sodium chloride
(salt) to preserve normal sodium balance, extracellular fluid volume and blood volume.

5. Regulation of Acid-Base Balance

 The kidney also adjusts the body’s acid-base balance to prevent such blood disorders as
acidosis and alkalosis. It helps maintain normal pH by retaining or excreting hydrogen ions and
regenerating lost buffer. The kidneys excrete acids that the lungs cannot excrete and they can
excrete hydrogen ions or reabsorb bicarbonate to correct acidosis. They can reverse this
process to correct alkalosis. Only renal mechanisms can remove metabolic acids and excess
bases from the body.
6. Regulation of Red Blood Cell Production
 Decreasing amount of oxygen in the renal blood flow activates the release of erythropoietin.
Erythropoietin stimulates the bone marrow to produce red blood cells, thereby increasing the
amount of hemoglobin available to carry oxygen.
7. Vitamin D Synthesis
 The kidneys are also responsible for the final conversion of inactive vitamin D to its active form,
1,25-dihydroxychole-calciferol. Vitamin D is necessary for maintaining normal calcium balance
in the body.
8. Secretion of Prostaglandins
 The kidneys also produce prostaglandin E and prostacyclin, which have a vasodilatory effect and
are important in maintaining renal blood flow.

Renal Excretory Study

 URINALYSIS - assessed the nature of the urine produce and evaluates the color, ph and specific
gravity, determines the presence of glucose (glycosuria, protein, blood(hematuria), ketones (
ketonuria) and analyzes sediment for cells (WBC, called pyuria, casts bacteria, crystals)

Nursing Responsibilities:
• Cleanse perineal area,
• spread labia and cleanse meatus from front to back using antiseptic sponge,
• for males, retract foreskin for uncircumcised penis and cleanse glans antiseptic sponge,
• must be analyze 1 hour after of collection,
• For 24 Hour urine collection ( creatinine clearance) discard the first voided urine,
• collect all subsequent urine in a sterile container for 24 hours.

• Kidney, ureter ,bladder X-ray (KUB ) - plain film abdominal flat plate x-ray identifying the number and
size of kidneys with tumors, malformations and calculi ; no special preparations needed

• IVP – fluoroscopic visualization of the urinary tract after injection with a radiopaque dye

Nursing Responsibilities - Test for iodine sensitivity, enema before the procedure, 8 hours, NPO, push fluids
after.
• ULTRASOUND – non- invasive visualization of the kidney, ureter, bladder through the use of sound
waves

Nursing Responsibilities-
• Supine position,
• NPO not required,
• cleanse conducting gel from skin after the procedure

• CYSTOSCOPY – use of lighted scope to inspect the bladder (CYSTOSCOPE); maybe use to remove
tumors, stones, or other foreign materials or use to implant radium, place catheters in the ureters.

Nursing Responsibilities Before the Procedure

Explain the procedure will be done under local or general anesthesia, secure consent, administer sedative as
ordered, NPO for general anesthesia, or NPO after light breakfast for local anesthesia, enema as ordered ,let
client assume a lithotomy position

Post Procedure
Mild analgesic or warm sitz bath to relieve pain, I &O and temperature monitoring, explain that hematuria
expected post 24-48 hours, assess for clots, burning sensation upon urination maybe felt, and force
fluids.

• RENAL BIOPSY – removal of kidney tissue for microscopic study

Open method promotes better visualization but high risk for infection, close method none by aspiration with a
fine needle and has less risk for infection
Nursing Responsibilities before and during the procedure
 Secure consent,NPO after midnight,assess hemoglobin and coagulation studies ,assist client to
assume
 Prone position with a pillow below the abdomen, apply pressure for 20 minutes on the aspirated
area after the procedure
Post Procedure
Flat bedrest for 24 hours, monitor for hemorrhage, hypotension, dizziness, tachycardia ,pallor , back, flank and
shoulder pain, avoid strenuous activities, coughing, sneezing and straining, encourage fluid to avoid urinary
retention and clots, monitor hemoglobin, assess for hematuria and if present should cease 24 hours after the
procedure. Administer analgesics

BLOOD CHEMISTRY AND HEMOGLOBIN TESTS - these tests or panels are groups of tests that
measure many chemical substances in the blood that are released from body tissues or are produced
.For kidney function, creatinine and blood urea nitrogen .

Nursing Responsibilities
 NPO is not required for BUN , hemoglobin and creatinine , instruct the client not to eat red meat a day
prior to creatinine test ,intake of red meat can affect the result.

A. Infectious Disorders

Figure 6-3

URINARY TRACT INFECTION

An infection (UTI) cause by bacteria, virus, fungus, that occurs in the urinary tract.

Risk for UTI

 increases when a patient has indwelling catheter, (retained catheter)
 urinary retention
 urinary and fecal incontinence
 poor perineal hygiene practices.
 renal scarring from previous infection,
 decrease ureteral peristalsis,
 presence of urinary tract obstruction,
 being a female,
 sexual activity.

COMMON CAUSATIVE MICROORGANISMS

 escherichia coli ,
 staphylococcus, streptococcus,
 enterobacter, klebsiella
 aerobacter, pseudoaeriginosa.
Pathophysiology

The epithelium of the kidneys, ureter and bladder are sterile in healthy individuals, infection begins
when bacteria enters , usually starting at the opening of the urethra travelling up to the bladder. If the flushing
or urinating cannot stop the bacteria it can move up further to the ureters and kidney. Lower pyelonephritis
tract infection( UTI) rarely cause complications but upper UTI if untreated can spread into the blood stream
potential for chronic illness and death .

1. URETHRITIS – is inflammation of the urethra.

Causes
 Microorganisms
o (Escherichia coli,
o Chlamydia Trichomonas,
o Neisseria gonorrhoeae,
o herpes simplex virus type 2
 trauma
 hyper-sensitivity to chemicals in products such as vaginal deodorants
 spermicidal jellies
 bubble bath detergents.

Signs and Symptoms

 dysuria
 frequency
 urgency
 bladder spasms.
 A urethral discharge may be noticed.

Medical Diagnosis
Based on patient signs and symptoms, urinalysis, and urethral smear
Medical Treatment
Antimicrobials when it is caused by microorganisms. If the patient is sexually active, the patient and the
sexual partner may be treated with antimicrobials to prevent reinfection.

Nursing Intervention
1. Sitz baths are
soothing ® Reduce the
pain .
2. Instruct female patients to wipe from front to back after toileting
® To deter transmission of microorganism from anus to the
urethra
3. Discourage bubble baths and vaginal deodorant sprays.
® It has chemicals that can alter natural pH, leaving you more vulnerable to vaginal and urinary tract infection.
4. Instruct uncircumcised male patients to clean the penis under the foreskin regularly.
® The foreskin is the sheath of skin that covers the head (glans) of the penis.Without regular cleaning, a
buildup of a whitish-yellow substance known as ‘smegma’ can occur which may cause infection.
5. Advise patients to void after swimming.
® To flush bacteria present in pool or sea water

3. CYSTITIS - is inflammation of the urinary bladder. Thick colored dark tea

colored, (clowdy)

COMMON CAUSES
Bacterial contamination, prolonged immobility, renal calculi, urinary diversion, indwelling catheters , radiation
therapy, and treatment with some types of chemotherapy.

Signs and Symptoms

urgency, frequency, dysuria, hematuria, nocturia, bladder spasms, incontinence, and low-grade fever.
Urine may be dark, tea colored, or cloudy. Fever, fatigue, and pelvic or abdominal discomfort and
bladder spasms experienced as pain behind the symphysis pubis.

Medical Diagnosis
Urinalysis, culture, and sensitivity. The presence of bacteria does not mean that the patient has an
infection unless the patient also has white blood cells (WBCs) in the urine.
Medical Treatment
Antibiotic, mild analgesic such as acetaminophen is useful for relieving discomfort. Phenazopyridine
(pyridium) and Oxybutynin chloride (Ditropan may be ordered for 2 to 3 days to decrease discomfort and
bladder spasms.

Nursing care
1. Advise patient to complete the entire course of antibiotics and take analgesics as ordered.
® To stop the infection from returning, as well as reduce the risk of the bacteria becoming resistant to the
antibiotics. Analgesics promote comfort and alleviate pain.
2. If phenozopyradine is given, advise patient that the drug causes red-orange urine. ® . Change
in color of the urine may cause the patient to be alarm 3. Warm sitz bath.
® To promote comfort
4. Oral fluid intake.30m/kg of fluid per day.
® To increase urine formation and flush the urinary tract
5. To reduce risk of future infection, teach patient to, wear cotton undergraments, avoid tight-fitting clothing in
the perineal area.
® Wearing looser, cotton clothing will allow air to keep the area around the urethra dry. Tight-fitting jeans can
trap moisture and help bacteria grow.
6. Take shower instead of tub bath, avoid caffeine drinks, apple, grapefruit, orange these irritates the bladder,
maintain high fluid intake and void often, Wiping from front to back after voiding for female and drink a glass
of water after swimming ,before and after intercourse to flush the bacteria.
® Soaking in the bathtub makes the bacteria and harsh chemicals from your bubble bath to get inside and
irritate the urethra
7. Avoid caffeine drinks, apple, grapefruit, orange ® Acidic food sources irritates the bladder,
maintain high fluid intake and void often R. To increase urine formation and flush the urinary tract 8.
Wiping from front to back after voiding for female
® To deter transmission of microorganism from anus to the urethra 9.
Drink a glass of water after swimming ,before and after intercourse. ®
To flush the bacteria.

3. PYELONEPHRITIS – inflammation of the renal pelvis. It may affect one or both kidneys. (ascending
infection)

Cause
Acute pyelonephritis is most often caused by an ascending bacterial infection, but it may be bloodborne.
Chronic pyelonephritis most often is the result of reflux of urine from inadequate closure of the ureterovesical
junction during voiding. It is also usually caused by long standing UTIs with relapses and reinfections, may
even lead to chronic renal failure.

Signs and Symptoms

High fever, chills, nausea, vomiting, and dysuria. Severe pain or a constant dull ache in the flank area. The
patient with chronic pyelonephritis experience fatigue, hypertension, increase BUN and creatinine and a slight
aching over one or both kidneys.

Medical Diagnosis
Urinalysis, urine culture and sensitivity, CBC, IVP, cystoscopy

Medical Treatment
Antibiotics, urinary tract anti-septics, analgesics, and antispasmodics. Additional medications may be needed
to treat hypertension. Adults are advised to dink at least eight 8-oz glasses of fluids daily. Intravenous fluids
may be ordered if the patient has nausea and vomiting. Dietary salt and protein restriction may be imposed on
the patient with chronic disease. follow-up cultures to determine whether the infection has been resolved.

Nursing Interventions
1. Record the presence of signs and symptoms.
® To assess the presence and severity of the
UTI
2. Record history of previous urinary disorders.
® To determine if the UTI is recurring or a
reinfection
3. Fluid intake at least 8 oz of glasses a day.
® To promote urine formation and to flush the bacteria.
4. Advise patient to complete the entire course of antibiotics and take analgesics as ordered.
® To stop the infection from returning, as well as reduce the risk of the bacteria becoming resistant to the
antibiotics. Analgesics promote comfort and alleviate pain.
5. Limit physical activity and exercise ® To conserve energy
6. Protein and salt dietary restrictions if advised by the physician.
® Protein increases metabolic waste product build up and salt cause water retention of which the failing
kidneys might not able to filter and excrete those.
 TOPIC 5
BURNS

Figure 5-1 Burn Injury

A burn is an injury from exposure to heat, chemicals, radiation or electric current leading to sequence of
physiologic events . For severe burn cases if untreated it can lead to irreversible tissue damage. Injuries
result from direct contact with or exposure to any of heat source and the heat energy from the source is
transferred to the tissues of the body
Many burn can be prevented, and most major burns occur in the home during cooking, improper use of
electrical appliances and work related handling chemical, hot objects. Infants and adults have greater risks to
morbidity and mortality when they sustain burn injuries due to several contributing factors.

4 Major goals relating to burns

 Prevention
 Institution Of Life-Saving Measures For The Severely Burned Person
 Prevention Of Disability And Disfigurement Through Early Specialized Individual Treatment
 Rehabilitation Through Constructive Surgery And Rehabilitative Programs
Review of The Skin Anatomy and Physiology

The skin is the largest organ of the body, having . a surface area of 15 -20 square feet. It provides covering for
the body thereby protecting the body’s organ and tissues from the external environment.

Figure 5-2 The Skin Structure

The skin has two layers . the epidermis and the dermal layer. The epidermis is the outer of the skin and
it in thin but tough . protecting the internal structures from bacteria, viruses, fungi and trauma. It is compose of
keratinocyte and melanocyte cells. The dermis is the inner layer of the skin and is considered as “True Skin” ,
compose of thick layer of fibrous and elastic tissue. It is of composed collagen fibers consisting mast cells
responsible for phagocytosis and release histamine in burn injury. The dermal layer also serve as supporting
and nutritional bed because most of the blood vessels, nerves, sweat and sebaceous glands, hair follicles are
located.

Table 5-1 The Function of The Skin

Function Of The Skin Mechanism
Protection of the internal structures against It covers the internal structures of the body
infection and trauma from the external environment
Sensation Receptor endings of nerves senses
temperature, pain, light touch, pressure

Fluid Balance Prevents H20 loss and extra H20 release

through perspiration ; serves as water
repellant
Temperature Regulation Body continuously produces heat as result of
food metabolism and this heat is primarily
dissipated in the skin
Vitamin D Production Skin expose to UV light can convert
cholesterol molecules to vit. D
Immune Response Function Several dermal cells are important
components of the immune system e.g.
langerhaus cells, interleukin 1
Physiologic Response to Burn Injury
Burns are cause by a transfer of energy from a heat source to the body through conduction and
electromagnetic radiation leading to skin disruption causing increase fluid loss, massive infection,
hypothermia, scarring, compromised immunity ,change in body function ,appearance and body image . In
severe cases, fluid and electrolyte imbalance ensue. If a person inhales products of combustion , respiratory
function is compromised. Cardiac dysrhythmia and circulatory failure , profound catabolic state increasing
caloric expenditure and nutritional deficiencies are also manifestations in serious burn injury. Gastrointestinal
motility if altered , leads to ulcer and paralytic ileus. If dehydration is severe , it slows down the glomerular
filtration rate, renal clearance of toxic wastes may lead to tubular necrosis and acute renal failure.

Categories of Burn Injury MILD

 Partial thickness < 15% adult
 Full thickness burns < 2% adult
OTHER CRITERIA
 Does not involve eyes ,ears, nose, hands, face , feet , perineum
 No electrical burns / inhalation injuries
 Adult younger than 60 yrs. Old
 No pre existing disease and other injury with the burn
MODERATE
 Partial thickness burn 15 to 25 % adult TBSA
 Full thickness 2% to 10 % adult TBSA
 Plus minor category criteria
SEVERE
 Partial thickness > 25% adult TBSA
 Full thickness burns are > 10% adult TBSA
 Burns are accompanied by other injuries
 Presence of other criteria in the previous categories

Factors s Determining Burn Severity

1. Burning Agent/ Cause
2. Location/Body parts involve
3. Age
4. Depth of the burn
5. Size of the burn
6. History of cardiac, pulmonary, renal, hepatic disease
7. Injuries sustained during burn injury

Burning Agent and Location

The higher the temperature of the burning agent and longer duration of contact can cause more severe injury.
Burns sustained in the head, neck and chest is associated with higher mortality rate because of
bronchoconstriction secondary to histamine release causing edema , carbon monoxide poisoning secondary
to smoke inhalation, chest constriction secondary to circumferential burns. Burns sustained in the perineum
area requires special care, these said areas are prone to infection because of stool and urine contamination.
Table 5-2. Types of Burn Injury
Cause /Type Causative Agent Priority Treatment
Thermal open flame Extinguish flame (stop, drop,
steam and roll)
hot liquids (water, grease, tar, Flush with cool water
metal) Consult fire department
Chemical -Acids Neutralize or dilute chemical
Strong alkalis Remove clothing
Organic compounds Consult poison control center
Electrical Direct current Disconnect source of current
Alternating current Initiate CPR if necessary
Lightning Move to area of safety
Consult electrical experts
Radiation Solar Shield the skin appropriately
X-rays Limit time of exposure
Radioactive agents Move the patient away from
the radiation source
Consult a radiation expert

Age, Depth and Size of The burn

Individuals below 2 years old and above 60 yeas old are of higher risk to morbidity and mortality rates when
sustaining burn injury secondary to immature and poor immune system, fluid and electrolyte status , and
existence of co-morbidities.
Another factor affecting burn severity is the depth and size of the burn, the deeper and bigger the burn injury
involved , result to more serious injuries and damage and longer healing time .For third degree burns , skin
grafting is required for a definitive wound closure. Burn size more than 20% in adult and more than 10% of the
body surface area requires fluid resuscitation.

Table 5-3 Burn Depth

History of cardiac, pulmonary, renal, hepatic disease and Injuries sustained during burn injury
Pre-existing disease conditions would reduce normal compensatory responses to minor hypovolemia Optimum
systemic functioning is very vital for the burned client to respond to the burn management such as fluid
resuscitation, nutritional correction and infection prevention. Injuries sustained during burn injury like fractures
requires prolong hospitalization and additional management.

Stages of Interdisciplinary Care

The clinical course of treatment for the burn patient are divided into three stages. These stages are useful to
determine the clinical needs of the patient. The assessment and management of the burned patient involves
different group of physicians,nurses and other health are specialists collaborating with each other to manage
the patient’ s recovery.

Table 5- 4. Stages Of Burn Care

Phase Duration Priorities

Emergent / immediate onset of injury to 1st aid, prevention of shock
Resuscitative completion of fluid Prevention of respiratory
resuscitation 48 -72 HRS distress
post injury Detection and treatment of
injury
Wound assessment/initial
care
Acute Beginning of diuresis to Wound care and closure
need completion of prevention or treatment, of
wound closure complication nutritional
support
 Rehabilitative From major wound Prevention of scars and
closure to return of contractures
individual’s optimal level Physical, occupational,
of physical and vocational rehabibi;itation
psychosocial adjustment Functional cosmetic
reconstruction , psychosocial
counseling

I. Emergent / Resuscitative Phase

Starts with the onset of injury to completion of fluid resuscitation 48 -72 HRS post injury The goal in this phase
is to preserve vital functions and prevent hypovolemic shock.
Pre -Hospital Care
 Remove person from source of burn
 Assess ABC and trauma
 Cover burn with sterile or clean cloth
 Remove constricting clothes and jewelry
 Transport immediately

Emergency Care for Minor Burn

 Administer pain medication
 Administer Tetanus prophylaxis
 Wound care
 Apply topical antibiotics

Emergency Care for Major Burns

 Evaluate degree and extent of burn
 Established patent airway and administer oxygen for burn victims in enclosed area
 Venoclysis and assess for hypovolemia
 Maintain NPO and insert NGT
 Insert foley catheter
 Tetanus prophylaxis and give pain medication

Fluid management is one approach to treat burn patients. Within minutes of burn injury , a massive amount
of fliud shifts from the intracellular and intravascular compartments into the interstitium (thirdspacing). This kind
of shift is called burn shock and it continues until capillary integrity is restored within 24-36 hours of the injury.
Fluid resuscitation is indicated for burns greater than 20% TBSA in adults, greater than 10% BSA in children,
patients older than 65 or younger than 2 years of age and patient with preexisting disease that would reduce
normal compensatory responses to minor hypovolemia (Cardiac, pulmonary, renal, hepatic , diabetes).

Computation of Body Surface Area Burn

The extent of the burn injury size is expressed as percentage of the total body surface area (TBSA). Several
methods are use to determine the extent of the injury. The “Rule of Nines” is a rapid method of estimation of
the burn size. This method divides the body into 5 surface areas- head, trunk, arms, legs and perineum and
percentage that equal or total to the sum of nines are assigned except the perineum which is only one percent.
Figure 5-5 Rule of Nines

Common Formula for Fluid Resuscitation

Fluid resuscitation is the administration of the intravenous fluids to restore the circulating blood volume during
the acute period of capillary permeability in order to prevent burn shock . Crystalloids are administered during
the first 24 hours after burn injury.Two commonly used formulas are the Parkland and modified Brooke
formula. These formulas specify to infuse the 50% volume of fluid during the first 8 hours and the remaining
50% to be infused over the next 16 hours.
In Parkland formula , lactated Ringer solution is administered 4 ml X kg X % TSBA burn. Modified Brooke
lactated Ringer solution is administered 2ml X kg X % TSBA burn. Hourly urine output is measured to
determine if fluid resuscitation is effective. Cardiac and respiratory status are also monitored.

Other interventions during Resuscitative Phase

 Elevate the head of the bed to 30 degrees for facial and head burns
 Elevate circumferential burns of the extremities with a pillow above the level of the heart
 Assess for infection, tracheal or laryngeal edema
 Protective isolation techniques Shave hair around wound margins
 Monitor gastric output and Ph for stress ulcer (Curling’s Ulcer )
 Administer anti- ulcer drugs
 Avoid IM and SQ administration
 NPO until with bowel sound
 Monitor daily weights

Acute Phase
Begins with hemodynamic stability, capillary permeability restored and diuresis are the

PRIMARY CONCERN
Restorative therapy to wound closure and infection control

MANAGEMENT
 Aseptic technique
 adequate debridement of wound,
 tetanus immunization,
 IV antibiotics,
 topical anti-bacteria therapy wound care

Escharotomy - dead tissues and eschar are remove by making an incision .

Management
 assessment of pulses, color, movement, and sensation of affected extremity ,
  if bleeding is present control it with pressure and pack incision gently with fine mesh gauze for
24 hours after.

Fasciotomy - fascia is cut to relieve pressure so as to reduce tissue death. (open lng ang part to
relieve the pressure)

MNGT:
Hydrotherapy - shower, bed bath and total immersion.

If total immersion
-the tank is lined with plastic liners and decontamination every after use is done to prevent cross
infection, the temperature of the water to be use is 37 degrees Celsius and the immersion process
should not exceed more than 30 minutes to prevent chilling.

WOUND DRESSING , it may open or close dressing depending on the burn area involve in order
to maintain circulation, and allows motion.

Joints- light dressing is required to allow movement

Face dressings - open type of dressing
Finger and toes- wrapped individually

Wound closure as a part of wound care is important.

Biological, synthetic and biosynthetic dressings is applied or skin grafting is performed.

GRAFT CARE,
 elevate and immobilized graft site,
 keep site free from pressure,
 monitor for infection
 protect area from sunlight.(maka dry sa graft site)

SIGNS OF INFECTION
 inflammation
 pus
 fever
 redness
 pain
 swelling/ loss of fnx

Table 5-5 Common Antimicrobial Agent

Antimicrobial Advantage Side Effects

Agent
Silver Effective against most gram-positive and gram- May cause hypersensitivity
Sulfadiazine negative reaction in 5%-7% of all
cream organism patients;

Soothing on application Associated with an initial

decrease in WBC’s
Softens the eschar and
increases joint mobility
 Absorbed slowly reducing the chance of
nephrotoxicity

Mafenide Effective against most grampositive and gram- Painful on application;

acetate negative
cream organism May cause hypersensitivity
reaction in 5%-7% of all
Rapidly diffuses through eschar (improved patients;
effectiveness in established
infections) Associated with acid-base
derangements
Permits open treatment of wounds; thus,
increasing mobility

Silver nitrate Effective against most gram positive and gram- Hyponatremia, hypokalemia,
solution negative and hypochloridemia
organism
Decreased penetration of
eschar

Requires large bulky

dressings

Rehabilitative Phase

Starts from acute care to hospital discharge,

GOALS
 to gain independence
 achieve maximal use of the affected part,
 promote wound healing,
 minimize deformities,
 increase strength and function
 provide emotional support.

Nursing Management
1. Remove person from source of burn
®To remove the patient from the heat source and prevent further injury 2.
Assess ABC and trauma
®To assess the extent of the injury so as to initiate and prioritize appropriate interventions
3. Cover burn with sterile or clean cloth
®Keeps air off the area, reduces pain and protects blistered skin.
4. Remove constricting clothes and jewelry
® Burn areas swells quickly , constrictive clothing can compromise circulation 5.
Transport immediately
® for prompt medical intervention for severely burn patients,

Emergency Care for Minor Burn

1. Administer pain medication
® to ease pain and promote comfort
2. Administer Tetanus prophylaxis
®Tetanus is a possible complication of any burn because the damaged tissue is easily infected. The person
needs tetanus or booster shot, depending on date of last injection. Tetanus booster should be given every 10
years.
3. Wound care
® Promotes speedy healing and prevent infection
4. Apply topical antibiotics
® Promotes speedy healing and prevent infection

Emergency Care for Major Burns

1. Evaluate degree and extent of burn
®To determine the appropriate fluid replacement and prevent shock
2. Established patent airway and administer oxygen for burn victims in enclosed area
®Systemic oxygenation is impaired by toxic gases released in most fires Inhaled smoke contains carbon
monoxide and cyanide and can travel to the alveoli and trigger inflammatory reactions that lead to
bronchospasm and impaired gas exchange .
3. Venoclysis and assess for hypovolemia
® To maintain the tissue perfusion . Burn injuries greater than 10% TBSA and including the dermis result in
circulatory compromise secondary to fluid loss via damaged tissue, widespread vasodilation as well as
increase capillary permeability and fluid shifts (third spacing). This can result in hypovolemia leading to burns
shock.
4. Maintain NPO and insert NGT
®Gastric stasis or ileus can result from potassium shifting secondary to massive burn, Insertion of a
nasogastric tube and commencement of enteral feeds should be considered for those who sustain significant
burn injuries and/or facial burns and are unable to tolerate adequate oral intake.
5. Insert foley catheter
® Insert a Foley catheter so that urine output can be monitored as a guide for volume status. Insert a Foley
catheter in patients with burns >15% TBSA. Adequate urine output is 0.5 mL/kg/h in adults and 1.5 mL/kg/h in
children.
6. Tetanus prophylaxis and give pain medication
®Tetanus is a possible complication of any burn because the damaged tissue is easily infected and pain
relievers promote comfort.

Other interventions during Resuscitative Phase

1. Elevate the head of the bed to 30 degrees for facial and head burns
®To minimize facial edema
2. Elevate circumferential burns(whole surface area of circumference anterior and posterior) of the extremities
with a pillow above the level of the heart
®To prevent or reduce swelling and pain
3. Assess for infection, tracheal or laryngeal edema
®For prompt medical intervention
4. Protective isolation techniques Shave hair around wound margins
®Hair and hair follicles harbor bacteria that increase the bacterial load, delaying wound healing and increasing
the risk of infection.
5. Monitor gastric output and Ph for stress ulcer
®To early detect development of Curling’s ulcer(occur to burn injury/ stress ulcer , too long bed ridden)
6. Administer anti- ulcer drugs
®to prevent or correct Curling’s ulcer
7. Avoid IM and SQ administration
®Poor absorption of medications following burn injury due to fluid shifts
(ivtt)
8. NPO until with bowel sound
®To prevent abdominal distention secondary to paralytic ileus, a complication of burns
9. Monitor daily weights
®For proper nutritional management. Severe burn is associated with significant changes in body weight due to
resuscitation volumes, fluid shifts, a hypermetabolic state, prolonged bed rest, and caloric intake.

Nursing Diagnoses and Management

1. Impaired gas exchange related to carbon monoxide poisoning, smoke inhalation upper airway loss
 Maintain adequate perfusion
® To ensure adequate oxygenation and maintain vital organs function
2. Ineffective airway clearance related to edema and effects of smoke inhalation  Maintain patent
airway.
® To prevent respiratory distress
3. FVD related to ↑ capillary permeability and evaporative losses from burn wound
 Restore optimal fluid balance and perfusion of vital organs
® to promote healing and prevent further complications related to burn injury
4. Pain related to tissue/nerve/emotional impact injury
 Assess level of discomfort
® To determine the appropriate pain intervention
 Administer pain relievers and antibiotics
® Pain relievers promote comfort and damaged tissue is easily infected
 Provide emotional support to allay fear and anxiety
® To allay fear and anxiety

Learning Activities

1. Assignment on the layers of epidermis Epidemis layers

https://www.youtube.com/watch?v=0X46aImj6nw
 2. Compare Lund and Browder , Berkow’s Formula for computing fluid resuscitation
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC449823/
https://books.google.com.ph/books?id=6DHMDwAAQBAJ&pg=PA8&lpg=PA8&dq=lund+and+browder+
vs+berkow+formula&source=bl&ots=igUYn-
TNil&sig=ACfU3U2J4uw3hvcgPlaSJDYSmes9vg5jEg&hl=en&sa=X&ved=2ahUKEwih9bCGx7LqAhWQ
A4gKHTMbB_EQ6AEwF3oECAkQAQ#v=onepage&q=lund%20and%20browder%20vs%20berkow%20
formula&f=false
3. Using the Rule of Nines , assign the percentage distribution to the given body areas involved, if the
TBSA is 28 %
Head
Chest and abdomen
Perineum
4. Work example for fluid resuscitation
(1) A 25 year old man weighing 70 kg with a 30% flame burn was admitted at 4 pm. Computation for his Total
fluid requirement for first 24 hours using Parkland Formula 4 ml × (30% total burn surface area) × (70 kg) =
8400 ml in 24 hours
2) Half to be given in first 8 hours, half over the next 16 hours
Will receive 4200 ml during 0-8 hours and 4200 ml during the next 16 hours
B. Obstructive Disorders

Figure 6- 4 Renal Calculi ( Urolithiasis )

Renal calculi is the formation of stones in the urinary tract . These are crystalline structures that form from the
components of urine.

Pathophysiology
Most calculi are precipitations of calcium salts (phosphate and oxalate),uric acid, magnesium ammonium
phosphate (struvite) or cystine. These substances are normally found in the urine.

Oxalate- staghorn

Factors Fostering Calculi Formation

 Concentrated urine (create precipitation)
 Excessive intake of vitamin D, animal protein (uric acid stone), oxalates, sodium, sucrose, vitamin C,
calcium based antacids
 Familial history
 Immobility, urine stasis, sedentary lifestyle
 Altered urine pH
 Lack of kidney substance that inhibits calculi formation
Signs and Symptoms
 Pain depends on the location of the stone.
 Nausea,
 vomiting
 hematuria
 signs and symptoms of UTI

Medical Diagnosis
 Urinalysis,
 urine culture sensitivity
 IVP,
 ultrasound
 Computed tomography (CT) scan (Mas ok, more clear visualization)

Medical, Surgical and Pharmacologic Management

Phases of Stone Management

1. Acute phase
 narcotics, antispasmodic, anti -emetic, warm bath to relieve flank pain (vasodilation)

2. Elimination of stone
 Waiting to be passed out
 Mechanical intervention
 Surgical intervention

3. Long term prevention of recurrence

 OFI (3-4l/day), diet, medication

1.POTASSIUM CITRATE THERAPY - It attaches to calcium in the urine, preventing the formation of mineral
crystals ; prevents the urine from becoming too acidic .

2.THIAZIDES – increases urinary Ca excretion

3. ALLOPURINOL – prevents formation of uric acid nidus

FOR SMALL STONES

4. Alpha blockers or α-adrenergic-antagonist - It relax muscle tension in the ureter and facilitate passage E.g.
tamsulosin
5. Sodium bicarbonate
6. Pain relievers

Surgical and Non-surgical Management of Stone

Often calculi pass spontaneously, if it does not pass and symptoms continues , other options may be used to
destroy or remove the calculus.
Surgical management are indicated if there is progressive renal damage, obstruction of urine flow , presence
of infection and severe pain. The surgical procedures are

Nephrolithotomy (removal of kidney stones)

ureterolithotomy (removal of stones in the ureters) .
For non-surgical approach, options include ureteral stent placement, lithotripsy, cystoscopy stone removal,
and percutaneous nephrolithotomy.

Ureteral Stent- are small tubes inserted into the ureter to treat or prevent a blockage that prevents the flow of
urine from the kidney to the bladder.

Lithotripsy is a process of eliminating a calculus in the renal pelvis, ureter, bladder by crushing the stone. It
can be accomplished by Extracorporeal shock wave lithotripsy (ESWL) which utilizing sound, laser, or
shockwave energy with a use of a lithotripter. It is guided by an ultrasound probe; the energy is directed to the
stone through a water-filled cushion.

Table 6-1 Complications of ESWL

Relate d to Shock Fragments Related to Shock waves

colic Bruising /hematoma
Incomplete fragment urosepsis
Blocking of ureters by the multiple stone
fragments

Cystoscopy/Ureteroscopy - use of lighted scope or a tube inserted into the urethra into the bladder and
ureters to remove stone and uses a laser fiber to crush the stone in the case of ureteroscopy.

Percutaneous nephrolithotomy – The surgeon creates a tunnel directly through the skin into the kidney and
uses ultrasound or electrohydrolysis to break the stone into pieces. this approach is usually used when stones
are large and cannot be broken with lithotripsy.

Dietary Management
Prevention of stone recurrence is important .Apart from high fluid intake to keep urine diluted dietary
restrictions are also important and the dietary restrictions depend on the type of stone.
 Table 6- 2 Recommended Diet for Stone Management

Acid Ash Diet ( To acidify the urine)
Calcium Stones
 cranberry, prune juice,meat, egg,
poultry,fish,grapes, whole grains
 limit milk and other dairy products
Alkaline Ash Diet ( To alkalinize the urine)
Oxalate Stones
 milk, vegetables, fruits except prunes,
cranberry, plums
 Avoid tea, chocolate, rhubarb,
spinach

Uric Acid Stones -

 Reduce foods high in purine like liver,
brain, kidneys, venison, shellfish,
meat soup, gravies, legumes

Nursing Management
1. administer prescribed analgesics
2. reassure client that most stones smaller than 4mm can pass out spontaneously
3. provide education to prevent future and recurrence of stone
4. encourage OFI
5. instruct client to avoid foods that contribute to the diagnosed type of stone

Nursing Diagnoses
 Acute pain related to renal calculi
 Ineffective coping related to anxiety , low activity level and inability to perform ADL  Impaired urinary
elimination related to renal calculi
 Risk for infection
 Nutrition imbalance, less than body requirements related to nausea

C.Glomerular Disorder Nephrotic

Syndrome
 is an alteration of kidney function caused by increased glomerular basement membrane permeability to
plasma protein (albumin).

Altered glomerular permeability result in

CHARACTERISTIC SYMPTOMS
 gross proteinuria, generalized edema (anasarca), (mataba ang bata)
 hypoalbuminemia,
 oliguria,
 increased serum lipid level (hyperlipidemia)(mataas ang cholesterol na present sa bld).

It maybe primary, wherein the pathology is the kidney itself or secondary of which nephrotic syndrome is
the renal manifestation of a systemic disease. Nephrotic syndrome , usually occurs in children between
ages 2-6 but may affect adults , both sexes and any race.
Pathophysiology
Normally large protein cannot pass through the glomerulus. Proteinuria occurs because of changes to capillary
endothelial cells of the glomerulus. The mechanism of damage to these structures is unknown in primary and
secondary glomerular diseases, but evidence suggests that T cells may upregulate a circulating permeability
factor or downregulate an inhibitor of permeability factor in response to unidentified immunogens and
cytokines. Other possible factors include hereditary defects in proteins that are integral to the slit diaphragms
of the glomeruli, activation of complement leading to damage of the glomerular epithelial cells and loss of the
negatively charged groups attached to proteins of the Glomerular Basement Membrane.

Figure 6-5 Pathophysiology of Nephrotic Syndrome

Signs and Symptoms

 Massive proteinuria,
 hypoalbuminemia,
 generalized edema,
 hyperlipidemia
 Lipiduria ,
 hypercoagulability
 hypertension.

Medical Diagnosis
 Urinalysis,
 serum albumin,
 renal ultrasound (glomerular fnx)
 biopsy.
 Serologic studies for infection and immune abnormalities e.g. antinuclear antibody.

Medical/Pharmacologic Management
 Blood-pressure medications, ACE inhibitors and ARBs, which curb the pressure in the glomeruli and
lower the amount of protein in the urine
 Diuretics to reduce swelling
 Cholesterol-lowering drugs
  Blood thinners, or anticoagulants
 Corticosteroids
 Limit salt to reduce swelling and low in saturated fats and cholesterol diet.  Dialysis if conservative
management is not effective .

Nursing Management
1. Limit oral fluid intake, low sodium, protein and saturated food sources diet
® Too much water and sodium can contribute to high blood pressure and edema.Moderate to low protein will
reduce the amount of protein lost in the urine and preserve kidney function. patients with nephrotic syndrome
have high levels of
cholesterol and triglycerides, saturated fat food sources like butter ,lard , full fat dairy, sour cream, pastry and
biscuits, coconut milk , chicken skin and visible fat on meat increase the risk of heart disease.

2. Intake and Output

® Accurate measurement of intake and output determines fluid balance

3. Skin care
® Skin irritation and breakdown is likely related to edema
4. R Protection against infection
® Reverse isolation, vitamin C rich diet
5. Monitor lymphocytes & WBC
® To determine immune-compression and presence of infection
6. Monitor complications (pulmonary edema, hypertension, CHF, renal failure, stroke, )
® For prompt medical intervention and prevent further complications
7. Report fever, malaise & adverse effects of medications.
® For prompt medical interventions

Nursing Diagnoses
a. Fluid Volume
b. Imbalanced Nutrition: Less Than Body Requirements
c. Fatigue
d. Deficient Knowledge
e. Risk For Infection
- Malfunction due to neurological dysfunction
- Interderence of the bladder normal
echanism cause by the disruption of the

- Problem c neurons and impulses

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TOPIC 9 RENAL FAILURE