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MEDICAL SURGICAL

OVERVIEW OF THE STRUCTURES & FUNCTIONS OF THE NERVOUS SYSTEM


3 PARTS OF THE NERVOUS SYSTEM
1. Central NS
Brain & Spinal cord

2. Peripheral NS
31 Spinal & Cranial

3. Autonomic NS
Sympathetic NS & Parasympathetic NS

Somatic NS

C-8
T - 12
L- 5
S5
C-1

I. Autonomic Nervous System


A. Sympathetic NS (SNS)
1. Fight or Aggression Response
2. Release of Norepinephrine (adrenaline cathecolamine)
= Adrenal Medulla (potent vasoconstrictor)
3. All body activities increased except GIT (GIT decreased motility)
Bodily Effects of SNS
a. Mydriasis = Dilated pupil , to be aware of surroundings
b. Dry mouth
VS = Increase
c. BP & HR
c. RR
d. Constipation
e. Urinary Retention
f. Increased BF to heart, brain, skeletal muscles
4.

Adrenergic or Parasympatholitic Response


Adrenergic Agents

a. Epinephrine (Adrenaline)
S/E : SNS Effects
b. Anti-Psychotics ex. Haldol (Haloperidol) S/E : SNS Effects

B. Parasympathetic NS
1. Flight or Withdrawal Response
2. Release of Acetylcholine (ACTH)
3. All bodily activities decreased except GIT
Bodily Effects of PNS

a. Meiosis = constriction of pupils


b. Increased salivation
c. BP & HR
d. RR =bronchoconstriction
e. Diarrhea =Increased Motility
f. Urinary Frequency

VS:decreased

4.

Cholinergic or Vagal or Sympatholitic Response

a. Beta-Adrenergic Blocking Agents (Beta-Blockers) (all end in lol)


Ex. Propanolol, Metopanolol
Blocks release of norepinephrine, Decrease body activities except GIT (diarrhea)
S/E:
B broncho spasm (bronchoconstriction)
E elicits a decrease in myocardial contraction
T treats HPN
A AV conduction slows down
Given To/As: a. Angina Pectoris
b. MI beta-blockers to rest heart
c. Anti HPN agents: -Beta blockers (-lol)
- Ace inhibitors (-pril) ex ENALAPRIL, CAPTOPRIL
- Calcium antagonist ex. CALCIBLOC or NEFEDIPINE
Created by Nia E. Tubio

b. Cholinergic agents

Created by Nia E. Tubio

d. Anti-arrhythmic agents (arrhythmia= irregular contraction of the heart)


Ex. Mestinon (prostigmine) given to MG to increase ACTH
S/E = PNS
*Antidote anti cholinergic agents Atropine Sulfate S/E SNS

II. CNS (Brain & Spinal Cord)


Part 1 : Parts:
A. Cells neurons = Basic living units
Properties and Characteristics
a. Excitability ability of neuron to be affected by changes in the external environment
b. Conductivity ability of neuron to transmit a wave of excitation from one cell to another
c. Permanent cells once destroyed, can not regenerate (ex. heart, retina, brain, osteocytes)
3 Types of Cells According To Its Regenerative Capacity:
1. Labile once destroyed, can regenerate: Epidermal, GIT, lung cells, GUT cells
2. Stable capable of regeneration BUT limited survival time: salivary gland, pancreas,
liver, kidney cells
3. Permanent cannot regenerate: retina, brain, heart, osteocytes & myocardial cells
B. Neuroglia : can cause brain tumors
Functions & its 4 Types:
1. Astrocyte = maintain integrity of blood brain barrier (semi-permeable/selective)
2. Microglia = stationary cells
3. Ependymal Cells
4. Oligodendrocytes
1. Astrocytes:
# 1 type of brain tumor= Astrocytoma ( 90 95%)
Toxic substance that destroys astrocyte & passes the Blood Brain Barrier
a. Ammonia = a cerebral toxin , product of protein catabolism
Hepatic encephalopathy (liver cirrhosis) = death of liver d/t necrosis
Primary Cause : Malnutrition
Major Cause
: Alcoholism
Early Sign
: Asterixis (Flapping hand tremors)
Late Sign
: Headache, Restlessness, Fetor Hepaticus (ammonia-like breath)
Hepatic Coma -----N.P. Airway
b. Bilirubin
= yellow pigment -------- jaundice (Icteric Sclerae)
others: Bilivedrin = green pigment
Hemosiderin = golden-brown pigment
Hemoglobin = red cell pigment

Hepatitis
* Carotenemia = yellowish discoloration of the skin
*Sign of Tumor in the Pituitary Gland

* Kernicterus (Hyperbilirubinemia)
- Increased bilirubin in the brain, irreversible brain damage

b. Carbon Monoxide :Tx for Carbon monoxide poisoning


= Hyperbaric Oxygenation (100%)
Parkinsons Disease
Early Sign: Pill-Rolling Tremors
d. Lead

Seizure
= Antidote for lead poisoning ------ Calcium EDTA

e. Ketones - acids, CNS depressant


Ketones in Blood
DKA ---- Type 1 DM
d/t increase fat catabolism
free fatty acids
Cholesterol
Leads to: Atherosclerosis
Created by Nia E. Tubio

Ketones ----- DKA : Early Signs = Weakness/ Weight Loss


Late Signs = Acetone Breath & Kussmauls Breathing
3

Leads to Coma
HPN ==MI or Stroke --Death
2. Microglia = Stationary Cells ------- Phagocytosis

Organ
Brain
Blood
Kidney/Liver
Lungs
SC Tissues

Macrophage
---------- Microglia
---------- Monocytes
---------- Kupffer Cells
---------- Alveolar Macrophages
---------- Histiocytes

3. Ependymal Cells = acts as a defense in the CNS along with microglia


secretes a glue ------ Chemoattractants
4. Oligodendrocytes = produces myelin sheath: acts as a cover for neurons
acts as an insulator w/c facilitates rapid nerve impulse transmission
No myelin sheath degenerates neuron
Damage to myelin sheath causes demyelinating disorders

Created by Nia E. Tubio

DEMYELINATING DISEASE
1. ALZHEIMERS DISEASE atrophy of brain tissue due to a deficiency of acetylcholine
- Degenerative disorder
- A type of Dementia
Predisposing Factors: 1. Aging
2. Aluminum Accumulation
S&Sx:
A amnesia loss of memory

*Short-Term -- Anterograde Amnesia


*Long-Term Retrograde Amnesia
A apraxia unable to determine purpose of object thru movement
A agnosia unable to recognize familiar object
A aphasia 2 types:
1. Expressive Broccas aphasia inability to speak ex. (+) nodding
TX: use of picture-boards
- damage to frontal lobe
- Broccas ---- motor speech center in the frontal lobe
2. Receptive Wernickes aphasia unable to understand spoken words ex. (+) illogical thoughts
- damage to Temporal lobe
- Wernickes Area --- general interpretative area
- Common to Alzheimer Receptive Aphasia
- Drug of choice ARICEPT or COGNEX ----- best given : at bedtime
2. MULTIPLE SCLEROSIS (MS) -Chronic intermittent disorder of CNS
Characterized by white patches of demyelenation in brain & spinal cord.
Remission & exacerbation
Common women, 15 35 y/o
Predisposing factor:
1. Idiopathic
2. Slow growing virus
3. Autoimmune (supportive & palliative treatment only) self-killing immunity
Normal Resident Antibodies: 5 types
IgG can pass placenta passive immunity, temporary
IgA body secretions saliva, tears, colostrum
IgM acute inflammation
IgE allergic reactions
IgD chronic inflammation
S & Sx of MS:
1. Visual disturbances :

a. *Blurring of vision = Initial sign


b. Diplopia/ double vision
c. Scotomas (blind spots)
2. Impaired sensation to touch, pain, pressure, heat, cold:
a. Numbness
b. Tingling
c. Paresthesia
3. Mood swings common : EUPHORIA (sense of elation )
4. Impaired motor function:
a. Weakness
b. Spasticity tigas
c. Paralysis
5. Impaired cerebellar function
Triad Sx of MS (INA)
I intentional tremors
N nystagmus
A Ataxia - unsteady gait

CHARCOTS TRIAD (INA)

6. Scanning of Speech
7. Urinary retention or incontinence
8. Constipation
Created by Nia E. Tubio

9. Decrease sexual ability


Dx:
1. CSF analysis thru lumbar puncture : bet. L3 & L4 : Reveals
CHON & IgG
2. MRI reveals site & extent of demyelination
3. Lhermittes Sign : confirmatory Dx of MS
- continuous contraction & pain of the SC following laminectomy ( removal portion of lamina)
Nsg Mgt:
-

Supportive mgt
1.) Administer Meds as ordered
a. ACTH ( adrenocorticotropic hormone) :
Acute exacerbation
to reduce edema at the site of demyelination to prevent paralysis - compression of spinal nerves
b. Baclopen (Lioresol) or Dantrolene Na (Dantrene) : To
c. Interferons to alter immune response
d. Immunosuppressant
e. Diuretics
f. Bethanecol Chloride ( Urecholine)
: N.M.

muscle spasticity

Administer only SC
Monitor S/E : wheezing, bronchospasm
Monitor breath sounds 1 hr. after SC admin.

h. Anti-spasmodic (Prophanthelene Bromide) Pro-banthene & anti-cholinergic


2. Maintain side rails
3. Assist passive ROM exercises promote proper body alignment
4. Prevent complications of immobility (q 2 hr. elderly q 1 hr.)
5. Encourage fluid intake & increase fiber diet to prevent constipation
6. Provide catheterization d/t urinary retention
7. Avoid heat application
8.. Give diuretics
9. Increase fiber & provide acid-ash diet to acidify urine & prevent bacteria multiplication
Ex. Grape, Plums, Cranberry, Orange juice, Prune juice, pineapple juice,Vit C
*3 Causes of UTI In Women

Shorter Urethra F= 1-2.5 inches (3-5 cm.)


Poor Perineal Care
Moist Vaginal Area

M= 5-6-8 inches (16-20 cm)

PART II: Compositions of Cord & Spinal cord


80% - brain mass
10% - CSF
10% - blood
1st: Brain mass
A. CEREBRUM Largest Part Function:

Connects Right & Left cerebral hemisphere


- Corpus collusum
1. Sensory
2. Motor
3. Integrative

Compose of 6 Lobes:
1.) Frontal (garbled speech)
a. Controls motor activity
b. Controls personality development
c. Where primitive reflexes are inhibited
d. Site of development of sense of Humor
Created by Nia E. Tubio

e. Control higher cortical thinking


f. Broccas area speech center
Damage - expressive aphasia
2.) Temporal
a. Hearing
b. Short term memory
c. Wernicke's area gen. interpretative
Damage receptive aphasia
3.) Parietal lobe appreciation & discrimination of sensory impulses
- Pain, touch, pressure, heat & cold
4.) Occipital vision
5.) Insula/island of reil/ Central lobe- controls visceral fx
Function: - activities of internal organ
6.) Rhinencephalon/ Limbic
- Smell, libido, long-term memory

*Anosmia- absence of smell

Basal Ganglia areas of gray matter located deep within a cerebral hemisphere
Extra pyramidal tract
Releases dopamine- a neurotransmitter
Controls gross voluntary unit
Dopamine
:Parkinsons or Huntingtons
Acetylcholine :Myasthenia Gravis & Alzheimers

Dopamine
: Schizophrenia
Acetylcholine : Bipolar Disorder

B. MID BRAIN/ MESENCEPHALON


relay station for sight & hearing
Controls size & reaction of pupil ( Normal: 2 3 mm)
Controls hearing acuity
( Normal Hearing Acuity : 30-40 decibels)
*PERRLA= Pupil dilated round & reactive to light & accommodation :Normal
* Isocoria normal size (equal)
*Anisocoria uneven size damage to mid brain
C. DIENCEPHALON
-------between brain
2 Parts:
1.Thalamus acts as a relay station for sensation
2. Hypothalamus Thermo-regulating center of temp, sleep & wakefulness,
thirst, appetite/ satiety center
Controls some emotional responses like fear, anxiety
Controls pituitary function.
D. BRAIN STEM
a. PONS Pneumotaxic center controls rate & depth of respiration
Cranial 5 8 CNS
b. MEDULLA OBLONGATA- lowest portion of the brain
-controls heart rate, respiratory rate, swallowing, vomiting, hiccups/ singutus
-Vasomotor center
- Site of Spinal Decuissation Termination, CN 9, 10, 11, 12
E. CEREBELLUM smallest part of the brain
- Controls posture, gait, balance, equilibrium
Cerebellar Tests:
a.) R Rombergs test- needs 2 RNs to assist
- Pt. in Normal anatomical position 5 10 min
(+) Rombergs test is (+) ataxia or unsteady gait/drunken movement w/ loss of balance --seen in MS.
b.) Finger to nose test
(+) To FTNT seen in Dymetria inability to stop a movement at a desired point
c.) Alternate pronation & supination
Palm up & down . (+) To alternate pronation & supination or damage to cerebellum
Created by Nia E. Tubio

seen in Dymetria
2nd: CerebroSpinal Fluid (CSF)
10% Blood
10% Compose of lipids
Normal amount produced: 125-250 ml /day
Produced at the Choroid Plexus
Composition: Clear, colorless, odorless: (+) glucose, protein,WBC but not RBC
Fx: cushions the brain
Alters if there is obstruction in the flow of CSF = Increase ICP
Enlargement of the skull posteriorly d/t early closure of the posterior fontanel----Hydrocephalus
3rd: Blood
Stroke: partial/total obstruction in brain blood supply :

2 Commonly Affected artery:


1. ICA or Internal Carotid Artery
2. MCA or Middle Cerebral Artery

*Composition of brain - based on Monroe Kellie Hypothesis


o Skull is a closed container. Any alteration in 1 of 3 intracranial components = increase in ICP
*Normal ICP 0 15 mmHg
Foramen Magnum = the hole in the skull where spinal cord enters
C1 atlas : carrying the entire skull
C2 axis
------------After C1 is the location of the medulla oblongata
Brain Herniation = when the medulla forced thru in the foramen : Observe for signs of ICP
(+) Projectile vomiting , irregular respiration & HR
Observe for 24 hrs. before MRI
DISORDER:

1. INCREASED ICP increase IC bulk is due to increase in 1 of the IC components


A. Predisposing factors:

1.) Head injury


2.) Tumor
3.) Localized abscess
4.) Hemorrhage (stroke)
5.) Cerebral edema
6.) Hydrocephalus
7.) Inflammatory conditions - Meningitis, encephalitis

B. S&Sx
Earliest Sx:
a.) Change or decrease LOC Restlessness to confusion (conscious, lethargy, stupor, coma)
- Disorientation to lethargy
*conscious = awake
- Stupor to coma
Late Sx: a. Change in V/S : always a late sx
1. BP (systolic increase, diastole- same)
Normal adult BP 120/80 : 40 (normal PP)
2. Widening pulse pressure
Ex. Increase ICP = BP 140/80 = 140 80= 60 PP (wide)
3.
RR : Cheyne-Stokes =rapid respiration w/ periods of apnea
4. Temperature increase
DIFFERENCE BET.

SHOCK :
&
INCREASE ICP:
Decrease BP
Increase BP
Increase HR
Decrease HR
CUSHINGS EFFECT
Increase RR
Decrease RR
Decrease Temp
Increase temp
Narrowing PP
Widening PP
b.) Headache
c.) Projectile vomiting
d.) Papilledima (edema of optic disk outer surface of retina)
e.) Abnormal Posturing
1. Decorticate = abnormal flexion of arms
= damage to cortico spinal tract
2. Decerebrate = abnormal extension of arms
= damage to upper brainstem, cerebrum, midbrain & pons
Except: Flaccid = loss of muscle tone, damage to the lower brain, medulla

Created by Nia E. Tubio

f. Uncal herniation unilateral dilation of pupil


g. Possible seizure
Nursing Management:
1.) Maintain patent a/w & adequate ventilation
a. Prevention of hypoxia =decrease tissue oxygenation & hypercarbia =increase in CO2 retention
Hypoxia cerebral edema - increase ICP
Early Sx:

R restlessness
A- agitation
T- tachycardia

Late Sx: B bradycardia


RAT

* Powerful respiratory stimulant : CO2 ---an

E extreme restlessness
D dyspnea
C cyanosis =late

BEDC

CO2 retention/ hypercarbia ---stimulate medulla O.

stimulate lungs to Hyperventilate


2. Before & after suctioning, hyperventilate 100%
- decrease CO2 excrete CO2
Suctioning 10-15 seconds, max 15 seconds
Ambu bag pump upon inspiration
3. Assist in mechanical ventilation
4. Monitor VS & I&O, neuro check
5. Positioning
-- Elevate head of bed 30- 45 degrees angle neck in neutral position
unless C/I to promote venous drainage
4. Limit fluid intake 1,200 1,500 ml/day
(FORCE FLUID means: Increase fluid intake/day 2,000 3,000 ml/day)- not for inc ICP.
5. Prevent complications of immobility
6. Prevent increase ICP by:
a. Maintain quiet & comfy environment
b. Avoid use of restraints lead to fractures
c. Maintain side rails up
d. Instruct patient to avoid activities leading to:Valsalva maneuver or bearing down
-Avoid straining of stool(give laxatives/ stool softener Dulcolax/ Duphalac)
- Excessive cough antitussive (Dextrometorpham)
-Excessive vomiting anti emetic (plasil)
- Avoid Lifting of heavy objects, Bending & stooping
- Avoid clustering of nursing activities
7. Administer meds as ordered:
1.) Osmotic diuretic Mannitol/Osmitrol: promotes cerebral diuresis by
decompressing brain tissue
Nursing considerations: Mannitol
1. Monitor BP S/E: hypotension
2. Monitor I&O every hr. report if < 30cc out put
3. Administer via side drip
4. Regulate fast drip to prevent formation of crystals/precipitate
5. Inform client, will feel flushing sensation as drug is introduced
2.) Loop diuretic - Lasix (Furosemide) in ampule
Nursing Mgt: Lasix
Same as Mannitol except
- Lasix is given via IV push (expect urine after 10-15mins) should be in the
morning. If given at 7am. Pt will urinate at 7:15
Action of Lasix within 15 minutes. Max effect 6 hrs due (7am 1pm)
S/E of LASIX
1. Hypokalemia
(Normal K-3.5 5.5 meg/L)
S&Sx : Compared to Hyperkalemia:
1. Weakness & fatigue
1. Irritability & Agitation
2. Constipation
2. Diarrhea, abdominal cramps
3. (+) U wave in ECG tracing
3. Peaked T-wave
both will lead to arrhythmia
Nursing Mgt:
1. Administer K supplements ex. Kalium Durule, Oral Kcl
Potassium Rich food:
ABCs of K
Vegetables
Fruits
A - asparagus
A apple
B broccoli (highest)
B banana green (highest)
Created by Nia E. Tubio

C carrots

C cantaloupe/ melon
O orange (increase)
Vit A squash, carrots yellow vegetables & fruits, spinach, chesa
Iron raisins,
*Food appropriate for toddler spaghetti! Not milk increase bronchial secretions, no grapes may choke
S/E of Lasix:
2. Hypocalcemia or Tetany: life-threatening (Normal level Ca = 8.5 11mg/100ml)
S&Sx
: Weakness
Paresthesia
(+) Trousseau sign or carpo-pedal spasm pathognomonic
(+) Chvosteks sign
Complications: Arrhythmia
Laryngospasm
N. M. - Administer Ca gluconate IV slowly
Ca gluconate toxicity: Sx : seizure administer Mg SO4
Mg SO4 toxicity administer Ca gluconate : BURP

B BP decrease
U urine output decrease
R RR decrease
P patellar reflexes absent

3. Hyponatremia
S/Sx:

(Normal Na level = 135 145 meg/L)


Hypotension
Signs of Dehydration
Early signs thirst and agitation for adults --------------children: tachycardia, dry mucous m.
Mgt: force fluid 2-3 L/day
Administer isotonic fluid sol
4. Hyperglycemia Increase blood sugar level
P polyuria
P polyphagia
3 Ps of Hyperglycemia
P polydipsia
Nsg Mgt:
a. Monitor FBS (Normal =80 120 mg/dl)
*Lasix can be given to DM but strict FBS monitoring
5. Hyperurecemia increase serum uric acid = by product of purine metabolism
Gouty arthritis

kidney stones- renal colic (pain)


Cool moist skin
Sx joint pain & swelling ----great toe affected ----gouty arthritis
Nsg Mgt of Gouty Arthritis
a.) Cheese (not sardines, anchovies, organ meat)
(Not good if pt taking MAO)
b.) Force fluid
c.) Administer meds Allopurinol/ Zyloprim inhibits synthesis of uric acid drug of choice for gout:
Colchicene acute gout drug of choice ---promotes excretion of uric acid
Kidney stones renal colic (pain). Cool moist skin
Mgt:
1.)
Force fluid
2.)
Meds narcotic analgesic
Morphine SO4
3.) Strain all urine using gauze pads
S/E of Morphine SO4 toxicity
Respiratory depression (check RR 1st)
Antidote for morphine SO4 toxicity Narcan (NALOXONE)
Naloxone toxicity tremors

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Cont. Increase ICP meds


3.) Corticosteroids - Dexamethsone decrease cerebral edema (Decadrone)
*Steroids best given: 2/3 dose am &
1/3 dose pm - to mimic normal diurnal rhythm
4.) Mild analgesic codeine SO
5.) Anti consultants Dilantin (Phenytoin)
Increase ICP what is the immediate nsg action?
Administer Mannitol as ordered
Elevate head 30 75 degrees
Restrict fluid
Avoid use of restraints
*Nsg Priority ABC & safety
Pt. suffering from epiglotitis. What is nsg priority?
a. Administer steroids least priority
b. Assist in ET temp, a/w
c. Assist in tracheotomy permanent (Answer)
d. Apply warm moist pack? Least priority
Rationale: Wont need to pass larynx due to larynx is inflamed. ET cant pass. Need tracheostomy onlyMagic 2s of Drug Monitoring Toxicity Level: DLADA
Drug

Normal Range

Toxicity

Classification

D digoxin
L - lithium
A aminophylline
D Dilantin
A acetaminophen

.5 1.5 meq/L
.6 1.2 meq/L
10 19 mg/100ml
10 -19 mg/100 ml 20
10 30 mg/100ml

2
2
20

D- Digitalis (Digoxin)

increase cardiac contraction = increase CO

200

Cardiac glycosides
Antimanic
Bronchodilator
Anticonvulsant
Narcotic analgesic

Indication
CHF
Bipolar Disorder
COPD
Seizures
Osteoarthritis

Cardiac Glycosides

Nursing Mgt:
1. Check PR, HR (if HR below 60bpm, dont giveDigoxin)
Increase force of cardiac contraction
Digitalis toxicity antidote - Digibind
a. Anorexia
increase cardiac output
b. n/v
GIT
c. Diarrhea
d. Confusion
e. Photophobia
f. Changes in color perception yellow spots-----Xantopsia
L lithium (lithane) decrease levels of norepinephrine, serotonin, and acetylcholine
Anti-manic agent
Lithium toxicity
S/Sx a. Anorexia
*N.M. 1. Force Fluid
b. n/s
2. Increase intake in diet 4-10g/d
c. Diarrhea
d. Dehydration force fluid, maintain Na intake 4 10g daily
e. Hypothyroidism
f. Fine Tremors
CRETINISM the only endocrine disorder that can lead to mental retardation
A aminophyline (Theophylline) ---dilates the bronchial tree
*Seizure= 1st attack
*Febrile seizure= normal 5 y/o
S/Sx : Aminophylline toxicity:
* Epilepsy = succeeding attacks
1. Tachycardia
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11

2. Hyperactivity restlessness, agitation, tremors (CNS excitability)


N.M. ---Avoid giving food with Aminophylline
a.Cheese/butter
food rich in tyramine, avoided only if pt is given MAOI
b. Beer/ wine
c. Hot chocolate & tea caffeine CNS stimulant tachycardia
d. Organ meat/ box cereals anti parkinsonian
MAOI antidepressant
m AR plan
n AR dilcan lead to CVA or hypertension crisis
p AR nate
3 4 weeks - before will take effect
Anti Parkinsonian agents Vit B6 Pyridoxine reverses effect of Levodopa
D dilatin (Phenytoin) anti convulsant/seizure
Nursing Mgt:
1. Mixed with plain NSS or .9 NaCl to prevent formation of crystals or precipitate
o Do sandwich method
o Give NSS then Dilantin, then NSS!
2. Instruct the pt to avoid alcohol bec. alcohol + dilantin can lead to severe CNS depression
Dilantin toxicity: GHAN
*Osteoarthritis: Sign Heberdens nodes
S/Sx:
G gingival hyperplasia swollen gums
i. Oral hygiene soft toothbrush ii. Massage gums
H hairy tongue
A - ataxia
N nystagmus abnormal movement of eyeballs
A acetaminophen/ Tylenol non-opoid analgesic & antipyretic febrile pts
a. Acetaminophen toxicity :
1. Hepato toxicity :
Monitor liver enzyme
SGPT (ALT) Serum Glutamic Pyruvate Transaminase
SGOT- Serum Glutamic Oxaloacetic Transaminase
2. Monitor BUN (10 20)
*Creatinine (.8-1)most reliable, indicative for kidney clearance
b. Acetaminophen toxicity can lead to hypoglycemia:TIRED
T tremors / Tachycardia
I irritability
R restlessness
E extreme fatigue
D depression
Diaphoresis/Nightmares
*Antidote for acetaminophen toxicity Acetylcesteine ---- Prepare suctioning apparatus
Exercise:

The following are symptoms of hypoglycemia except:


a. Nightmares b. Extreme thirst hyperglycemia symptoms

Created by Nia E. Tubio

c. Weakness

d. Diaphoresis

12

PARKINSONS DISEASE (Parkinsonism)

Chronic, progressive disease of CNS characterized by degeneration of dopamine producing cells in


substancia nigra at mid brain & basal ganglia (produces dopamine)

Mngt:
Palliative & Supportive Only
Predisposing Factors:
1. Poisoning (lead & carbon monoxide)
2. Hypoxia
3. Arteriosclerosis
4. Encephalitis
5. Drug Overdose
High doses of the ff:
a. Reserpine (serpasil)-----than only anti-HPN with S/E of depression -----suicidal
----- only HPN known to be link to breast cancer
----- promote safety
b. Methyldopa (aldomet)---Anti-HPN
c. Haloperidol (Haldol) - anti psychotic
d. Phenothiazine
- anti psychotic
S/E of anti-psychotic drugs Extra Pyramidal Symptom
Over medication of anti psychotic drugs
neuroleptic malignant syndrome characterized by tremors (severe)
S/Sx: Parkinsonism:
1. Pill-rolling tremors of extremities 1st Sign
2. Bradykinesia slow movement-----2nd Sign
3. Over fatigue
4. Rigidity (cogwheel type)
------- a. Stooped posture
b. *Shuffling
c.Propulsive gait
5. Mask like facial expression with decrease blinking of the eyelids
6. Monotone speech
7. Difficulty rising from sitting position
8. Mood labilety Depression suicide
Nsg priority: Promote safety
9. Increase salivation drooling type
10. Autonomic signs:
Increase sweating
Increase lacrimation
Seborrhea (increase sebaceous gland)
Constipation
Decrease sexual activity
Nsg. Mgt.
1.) Administer Meds:Anti-parkinsonian agents
Levodopa (L-Dopa)-------short-acting
Carbidopa (Sinemet), Amantadine Hcl (Symmetrel)----long-acting
Mechanism of action: Increase levels of dopa relieving tremors & bradykinesia
S/E of anti-parkinsonian
Anorexia
n/v
Confusion
*Orthostatic hypotension
Hallucination
Arrhythmia, GIT irritation ( administer with meals)
Contraindication:
1. Pt. with glaucoma----because L-dopa intra-ocular pressure (N: 12-21 mmHg)
2. Pt. taking MAOI (Parnate, Marplan, Nardil)
MAOI = Monoamine Oxydase Inhibitor ( anti-depressant)
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13

= Takes effect : 2-6 wks.


=If on MAOI avoid: Tyramine, tryptophan rich foods
ex. aged cheese, liver, beer, alcohol----leads to hypertensive crisisstroke
Nsg. Mgt. when giving anti-parkinsonian
a. Take with meals to decrease GIT irritation
b. Inform pt urine/ stool may be darkened
c. *Instruct pt. not to take food Vit B6 (Pyridoxine) cereals, organ meats, green leafy veg

Because Vit. B6 reverses therapeutic effects of levodopa


Only increase intake of Vit. B6 in taking INH (isoniazid, anti-TB)
Isonicotinic Acid Hydrazide-----effect-----peripheral neuritis

2.) Anti- cholinergic agents relieves tremors


*Artane
mechanism inhibits acetylcholine
*Cogentin
action ---S/E - SNS
3.) Antihistamine Diphenhydramine Hcl (Benadryl) take at bedtime---relieves tremors
S/E: adult drowsiness avoid driving & operating heavy equipment.
Child Hyperactivity (CNS excitability)
4.) Dopamine agonist:
Bromocriptine Hcl (Parlodel)---relieves rigidity, bradykinesia
S/E: CNS depression, Check RR
Nsg. Mgt.
1.)
2.)

3.)

Maintain siderails to prevent falls


Prevent complications of immobility
- Turn pt every 2h
- Turn pt every 1 h elderly
-Turn affected extremity every 30 minutes
Assist in passive ROM exercises to prevent contractures

4.)

Maintain good nutrition: Protein


CHON in am
CHON in pm to induce sleep d/t Tryptopan ex. milk

5.)

Increase fluid in take, high fiber diet to prevent constipation

6.)

Assist in surgery Stereotaxic Thalamotomy


Common complications: a. Subarachnoid hemorrhage
b. Encephalitis
c. Aneurysm
Assist in ambulation

7.)

Created by Nia E. Tubio

14

MYASTHENIA GRAVIS (MG)


A neuromuscular disorder characterized by a disturbance in transmission of impulses from
nerve to muscle cell at neuro muscular junction leading to descending muscle weakness.
Predisposing Factors:
Common in Women, 20 40 y/o, Unknown cause or idiopathic
Autoimmune release of cholenesterase (enzyme that destroys acetylcholine)
Pathophysiology: Cholinesterase destroys ACTH
ACTH

Descending muscle weakness

M.G.

S/ Sx:
1.) Ptosis drooping of upper lid ( initial sign)
Palpebral fissure normal opening of upper & lower lids
2.) Diplopia (double vision)
3.) Mask-like facial expression
4.) Dysphagia
5.) Weakening of laryngeal muscles hoarseness of voice
6.) *Respiratory muscle weakness lead respiratory arrest. Prepare at bedside tracheostomy set
7.) Extreme muscle weakness during activity especially in the morning.
Priority: to watch out for: a. A/W
b. Aspiration
c. Physical immobility
Dx. Test:
1. Tensilon test (Edrophonium Hcl) an anti-cholinesterase/cholinergic agent----short-acting only)
Administer to pt. for temporary relief for 5 10 mins. (+) for M.G.
2. CSF analysis- reveals cholinesterase
Nsg Mgt.
1. Maintain patent a/w & adequate ventilator by:
a.) Assist in mechanical ventilator attach to ventilator
b.) Monitor pulmonary function test using spirometer
2. Monitor VS, I&O neuro check, muscle strength or motor grading scale (4/5, O/S, etc)
3. Siderails up
4. Prevent complications of immobility
5. NGT feeding to prevent complications
6. Administer medication as ordered
a. Cholinergics or anticholinesterase agents
Mestinon (Pyridostinine)
Action: Increases ACTH
Neostignine (prostigmin)
S/E : PNS
b. Steroids, Corticosteroids to suppress immune response
Decadron (dexamethasone)
Monitor for 2 types of Crisis:
Myastinic crisis
Cholinergic crisis
1. Under medication
Cause: Over medication
2. Stress 3. Infection
S/Sx - PNS
S&Sx: 1. Unable to see Ptosis & diplopia
Mgt.
2. Dysphagia
Administer anti-cholinergic
3. Unable to breath
1. Atropine SO4
Mgt.:
Administer cholinergic agents: Mestinon
S/E: SNS dry mouth
7. Assist in surgical procedure Thymectomy (removal of thymus)
8. Assist in plasmapheresis filtering of blood
9. Prevent complication Respiratory arrest----prepare tracheostomy set at bedside
Cause:

Created by Nia E. Tubio

15

GBS GUILLIAN BARRER SYNDROME

A disorder of the CNS characterized by bilateral symmetrical polyneuritis leading to ascending


paralysis
Polyneuritis ----- inflammation of the peripheral nerves
Can leadto slow but complete recovery

Predisposing Factors:
1. Cause unknown, idiopathic
2. Auto immune
3. *R/t antecedent viral infection (from LRTI)
4. Immunizations
S&Sx
1.
2.
3.

4.
5.
6.

Clumsiness -------- Initial sign of GBS


Ascending muscle weakness lead to paralysis
Dysphagia
Decrease or diminished DTR (deep tendon reflexes) -----Paralysis
*Alternate HPN to hypotension complication: Can lead to arrhythmia
Autonomic changes:
a. Increase sweating
b. Increase lacrimation
c. Increase salivation
d. Constipation

Dx:
Most important: CSF analysis thru lumbar puncture reveals increase in : IgG & CHON---same with MS
Nsg Mgt.
1. Maintain patent a/w & adequate vent
a. Assist in mechanical vent
b. Monitor pulmonary function test
2. Monitor vs., I&O neuro check, ECG tracing due to arrhythmia
3. Siderails
4. Prevent complicarions immobility
5. Assist in passive ROM exercises
6. Institute NGT feeding
7. Administer medications as ordered:
1. Anti-cholinergic Atropine SO4
2. Corticosteroids to suppress immune response
3. Anti arrhythmic agents:
a.) Lidocaine /XylocaineS/E: confusion & agitation
b.) Bretyllium------blocks release of norepinephrine
c.) Quinidines/Quinitine anti malarial agent & anti-arrythmic
> Toxic effect Cinchonism
Quinidine toxicity: S/E anorexia, n/v, headache, vertigo, visual disturbances
8.

9.

Created by Nia E. Tubio

*Malaria ---king of tropical disease----antidote----Queen (Quinidine)


Assist in plasmapheresis
Prevent complications a. Arrhythmias b. Respiratory arrest

16

INFLAMMATORY CONDITIONS OF THE BRAIN


Anatomy:
Meninges a 3-fold membrane that covers the brain & spinal cord
Fx:
1. Protection & support
2. Nourishment
3. Blood supply
3 layers:
1. Duramater
(outermost
2. Arachmoid matter (middle)
3. Pia matter
(outermost)

in bet. is sub dural space


sub arachnoid space

where CSF flows L3 & L4

1. MENINGITIS
An inflammation of the meninges of the brain & spinal cord
Etiology:

a.
b.
c.
d.

Meningococcus---most dangerous type


Pneumococcus
Hemophilous influenza common to children
Streptococcus a type of adult meningitis

MOT:

Direct transmission via droplet nuclei (airborne)

S&Sx

Stiff neck or Nuchal Rigidity ------Initial Sign of meningeal irritation


Headache
Projectile vomiting
Photophobia
Fever chills, anorexia
General body malaise
Weight loss
Decorticate/decerebration abnormal posture
Possible seizure
Opisthotonus (arching of the back)-----2nd intital sign

*Pathognomonic Sign:

(+) Kernigs & Brudzinski sign


Leg pain

Neck pain

Dx:
1.

Lumbar Puncture: lumbar/ spinal tap use of hallow spinal needle


Aspiration in the sub arachnoid space between L3 & L4 or L4 & L5.

Nsg Mgt . For Lumbar Puncture------- invasive


1.

2.
3.
Created by Nia E. Tubio

Consent / explain procedure to pt


RN will explain if laboratory exams
MD will explain if operation procedure
Empty bladder, bowel promote comfort
Arch back to clearly visualize L3, L4
17

Nsg Mgt. Post Lumbar:


1.
2.
3.
4.

*Flat on bed 12 24 h to prevent spinal headache & leak of CSF


Force fluid
Check punctured site for drainage, discoloration & leakage to tissue, discomfort
Assess for movement & sensation of extremities

Result:
1. CSF analysis:
Confirms Meningitis

a. Increase CHON & WBC


b. Decrease glucose
c. Increase CSF opening pressure
d. (+) Culture microorganism

(Normal: 50 160 mmHg)

2. Complete blood count CBC reveals increase WBC (Leukocytosis)


Mgt:
1. Adm meds
a.) Broad-spectrum antibiotic: Penicillin
S/E :
1. GIT irritation take with food
2. Hepatotoxicity, nephrotoxcicity
3. Allergic reaction
4.* Super infection alteration in normal bacterial flora

Normal flora: throat streptococcus


Normal flora : intestine E. Coli

Sx: of superinfection of penicillin

Diarrhea

b.) Antipyretic
c.) Mild analgesic for headache
2. Strict respiratory isolation 24 hrs. after start of antibiotic therapy
3. Comfy & dark room due to photophobia & seizure
4. Prevent complications of immobility
5. Maintain F & E balance
6. Monitor VS, I&O , neuro check
7. Provide client health teaching & discharge plan
a. Nutrition Increase CHON & CHO but Small freq feeding
b. *Prevent complication of Hydrocephalus & Nerve Deafness
8. Institute measures to prevent Increase ICP & seizures
9. Rehabilitation for residual deficit ( mental retardation & delayed psychomotor development)
Exercise:

Where to bring 2 y/o post meningitis ?


Audiologist due to damage to post repair myelomeningocele
Urologist -Damage to sacral area controls urination

Created by Nia E. Tubio

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REVIEW:
3 Types of ISOLATION: 1. Strict Isolation
2. Reverse Isolation
3. Enteric
Ex. Pt. with
-Cushings syndrome
reverse isolation
-Aplastic anemia reverse isolation------ bone marrow depletion----pancytopenia
-Cancer any type
reverse isolation
-Post-Liver transplant reverse isolation
-Prolonged use steroids reverse isolation
-Meningitis strict isolation
-Asthma not to be isolated
- Hepatitis A
- Enteric
- Measles Strict
- Mumps Strict
- Pneumonia Strict
- PTB -Strict
REVIEW:
*Thrombosis & Stroke
Initial sign:
Late sign:
* Anemia :

leads to atherosclerosis
Headache
Pruritus ------

Initial sign: Weakness & Fatifue

Blood:
Leukopenia

WBC

Leukocytosis

Anemia

RBC

Polycythemia

Platelets

Thrombocytosis

Thrombocytopenia

Created by Nia E. Tubio

19

CEREBRO VASCULAR ACCIDENT :


Or Stroke, Brain Attack or Cerebral Thrombosis, Apoplexy

A partial or complete disruption in the brains blood supply


2 largest & common artery in stroke :
a. Middle cerebral artery
b. Internal carotid artery
Common to male 2 3x high risk, increases as you grow older

Predisposing factor:
1.
2.

3.

Thrombosis clot (attached)-----------No. 1 cause of Stroke


Hemorrhage
Embolism dislodged clot pulmo embolism---2nd cause
S/Sx: Pulmonary Embolism
1. Sudden sharp chest pain
2. Unexplained dyspnea, SOB
3. Tachycardia, palpitations, diaphoresis & mild restlessness
S/Sx: Cerebral Embolism
1. Headache, disorientation, confusion & decrease in LOC----lead to coma

4. *Compartment Syndrome compression of nerves/ arteries


Test Analysis:
*Femur Fracture
Fx. Complications:> Fat embolism most feared complication w/in 24hrs
>Hemorrhage
*Yellow bone marrow produces fat cells at medullary cavity of long bone
*Red bone marrow provides WBC, platelets, RBC found at epiphysis
Risk factors of CVA:
a.
b.
c.
d.
e.

f.
g.

HPN
DM
MI
Artherosclerosis
Valvular heart disease
Post cardiac surgery-----*Mitral valve replacement
Lifestyle:
1. Smoking nicotine potent vasoconstrictor
2. Sedentary lifestyle
3. Hyperlipidemia genetic-genes that easily binds to cholesterol

h. Obesity ------20% of BW
Overweight -----10% of BW
i. Prolonged use of oral contraceptives
2 types:

- Macro pill has large amount of estrogen


- Mini pill has large amount of progestin
Mini-pill---- Promote lipolysis artherosclerosis HPN stroke
j. Type A personality
Created by Nia E. Tubio

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a. Deadline driven person


b. 2 5 things at the same time
c. Guilty when not dong anything
k. Diet increase saturated fats -----ex. whole milk
l. Emotional & physical stress
S & Sx:
1. Transient Ischemic Attack ( TIA)- 1st sign of Impending stroke attacks
o
o

Headache initial sing of TIA


Dizziness/ vertigo, numbness, tinnitus, visual & speech disturbances, paresis or phlegia (monoplegia 1
extreme) (Paraplegialower extremeties)
Increase ICP, *Temporary memory loss

2. Stroke in evolution progression of S & Sx of stroke


3. Complete stroke resolution of stroke
a.) Headache
b.) *Cheyne-Stokes Resp
c.) Anorexia, n/v
d.) Dysphagia
e.) Increase BP
f.) (+) Kernigs & Brudzinski Sx of Hemorrhage Stroke
g.) Focal & neurological deficit
1. Phlegia
2. Dysarthria inability to vocalize
3. Aphasia
4. Agraphia difficulty in writing
5. Alexia difficulty in reading
6. Homonymous Hemianopsia loss of half of field of vision
Left sided hemianopsia approach Right side of pt the unaffected side
Nsng. Dx. = Unilateral Neglect
Dx.
1.
2.

Computerized Tomography Scan reveals brain lesion


Cerebral Arteriography rveals site & extent of mal-occlusion
Invasive procedure due to inject dye
Allergy test
*All Dx ending in graphy/gram are invasive: injection of a dye, ask if allergic to seafoods
Post-CT Scan
1.) Force fluid to excrete dye because it is nephrotoxic---check BUN & Creatinine
2.) Check peripheral pulse
3.) Check Fluid imbalance----dye is an osmotic diuretic
Nsg. Mgt.
1. Maintain patent a/w & adequate vent
- Assist mechanical ventilation
- Administer O2 inhalation
2. Restrict fluids prevent cerebral edema
3. Instruct client to avoid valsalva maneuver
4. Monitor vs., I&O, neuro check
5. Prevent compl of immobility by:
a. Turn client q2h
Elderly q1h
To prevent decubitus ulcer/ bed sores
To prevent Hypostatic pneumonia type of pneumonia r/t long immobility
b. Egg crate mattress or H2O bed
c. Sand bag or foot board- prevent foot drop
Created by Nia E. Tubio

21

6. NGT feeding if pt cant swallow


7. *Passive ROM exercise q4h to prevent contractures & to promote proper body alignment
8. Alternative means of communication
- Use Non-verbal cues
- Magic slate
- (+) To hemianopsia approach on unaffected side
9. Position pt.: elevate heat 30 degrees angle/ semi-fowlers
10. Maintain siderails
11.Meds
a. Osmotic diuretics Mannitol ( Osmitrol) ---Side-dripfast drip ----S/E: decrease BP
b. Loop diuretics Lasix/ Furosemide-----IV push
3. Corticosteroids Dextamethazone (ends in one)
4. Mild analgesic------codeine Sulfate-------S/E: Respiratory Depression
5. Thrombolytic/ fibrolitic agents tunaw clot
Ex. Streptokinase-----S/E: Allergic Reaction
Urokinase---------S/E: Hypertension
Tissue Plasminogen Activating Factor ( TPAF)----S/E: Chest Pain
*Monitor bleeding time
6. Anti-coagulants Heparin & Coumadin---- sabay
Why : Coumadin will take effect after 3 days---long-acting
Anti-Coagulants
Heparin
(Short-Acting)
Monitor:

PTT (Partial Thromboplastin Time)


If prolonged, indicates bleeding

Antidote:

Protamine Sulfate

Coumadin or Warfarin
(Long-Acting)
PT (Prothrombin Time)
if prolonged, indicates bleeding
Vitamin K (Aquamephyton)

7. Anti-platelet (PASA) aspirin paraanemo aspirin


-the only NSAID that has anti-platelet property
- Do not give to pts. With Dengue, Ulcer & Headache
- Aspirin----- No. 1 ulceronegenic agent
S/E: Tinnitus, Anemia, Heartburn & Dyspepsia
*EPISTAXIS/ nose bleeding--- parameter that indicates effectiveness of thrombolytic therapy
Health Teachings:
1. Avoidance of modifiable lifestyle
- Diet, smoking
2. Dietary modification
- Avoid caffeine, decrease Na & decrease saturated fats
3. Prevent Complications:
*Subarachnoid hemorrhage
4. Rehab for focal neurological deficit
1.
Mental retardation
2.
Delay in psychomotor development

Created by Nia E. Tubio

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CONVULSIVE Disorder (CONVULSIONS)

o A disorder of the CNS characterized by paroxysmal seizures with or w/o loss of consciousness,
abnormal motor activity, alteration in sensation & perception & changes in behavior.
Exercise: Can you outgrow febrile seizure?
Febrile seizure Normal if < 5 y/o
Pathologic if > 5 y/o
Predisposing Factor:
a. Head injury d/t birth trauma------ No .1 cause of convulsions
b. Toxicity of carbon monoxide
c. Brain tumor
d. Genetics
e. Nutritional & metabolic deficit
f. Physical stress
g. Sudden withdrawal to anticonvulsants-----No .1 of status epilepticus
Status epilepticus Drug of Choice: Diazepam & glucos
S & Sx. Of Epilepsy dependent upon stages:
I. Generalized Seizure
1.) Grand mal / tonic clonic seizures-----most common type of seizure
- With or w/o Aura warning symptoms of impending seizure attack
Epigastric pain ---1st sign of aura

This is associated with olfactory, tactile, visual, auditory sensory experience


Epileptic cry fall
*Loss of consciousness 3 5 minutes
Tonic-clonic contractions
Tonic - Direct symmetrical extension of extremities
Clonic - contractions
Post ictal (state of lethargy or drowsiness) sleep- unresponding sleep after tonic clonic

2.) Petit mal seizure (same as daydreaming!)


- Blank stare
- Decrease blinking eye
- Twitching of mouth
- *Loss of consciousness 5 10 seconds (quick & short)
- *Common to children
II. Localized/partial seizure
1. Jacksonian seizure or Focal seizure
tingling/jerky movement of index finger/thumb &
spreads to shoulder &
1 side of the body with janksonian march
2. Psychomotor/ Focal-motorseizure
-*Automatism stereotype repetitive & non-purposive behavior
- Clouding of consciousness not in contact with environment
- Mild hallucinatory sensory experience
Created by Nia E. Tubio

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3 Types of HALLUCINATION:
1.
2.
3.

Auditory
schitzophrenia
paranoid type
Visual Korsakoffs psychosis chronic alcoholism
Tactile addict
substance abuse

III. Status Epilecticus


Continuous, uninterrupted seizure activity leading to hyperpyrexia coma death
Drug of Choice : Diazepam & Glucose
Pathophysiology:

Status Epilepticus
Increase electrical firing in the brain: if left untreated
Increase Heat production -------hyperpyrexia
Increase metabolism using glucose & O2 ------need for glucose therapy
Coma------Death

Dx: For All Types:


1.
2.
3.

CT scan revealsbrain lesion


EEG electroencephalography --revealsHyperactivity brain waves
ECT therapy

Nsg. Mgt.
Priority Airway & Safety
1.

*If with seizure: S/E is PNS

Maintain patent a/w & promote safety Before seizure:


1. Remove blunt/sharp objects
2. Loosen clothing of pt.
3. Avoid restraints----can lead to fracture
4. Maintain siderails
5. Turn head to side to prevent aspiration
6. Tongue guard or mouth piece to prevent biting of tongue (emergencyclean piece of cloth)
7. Avoid precipitating stimulus bright glaring lights & noises, drafts
8. Administer meds
a. Dilantin (Phenytoin) ( toxicity level 20 )
S/E:
Gingival hyperplasia
H-hairy tongue
A-ataxia
N-nystagmus
b. Acetaminophen- febrile pt
Mix only with NSS, sandwich method
- Dont give alcohol lead to CNS depression
c. (Tegretol) Carbamazepine
d. Phenobarbital (Luminal) -------common S/E: hallucination & mild arrythmia
e. Diazepam

2. Institute seizure & safety precaution


By Post seizure: Administer O2 inhalation. Suction apparatus ready at bedside
3. Monitor onset & duration of
- Type of seizure
Created by Nia E. Tubio

24

- Duration of post ictal sleep----the longer the duration, the danger of status epilepticus
4. Assist in surgical procedure
- Cortical resection
Exercise: 1 y/o grand mal immediate nursing action = a/w & safety
a. Mouthpiece 1 yr old little teeth only
b. Adm o2 inhalation post!
c. Give pillow safety
d. Prepare suction
Neurological Assessment:
4 Objectives of Neurological Assessment:
1. To know the exact neurological deficit
2. To localized lesion
3. For rehabilitation
4. Guidance in nursing care
2 Types of N.A.

1. Glasgow Coma Scale (GCS) objective measurement of LOC or quick neuro check
3 components of ECS (MVE)
M motor
6
V verbal response
5
E eye opening 4
15---- highest score
Scaling:
15 14 Conscious
13 11 Lethargy
10 8 Stupor
7 Coma
3 Deep coma lowest score ( no 0 score on any response, lowest is only 1)
2.

Comprehensive Neuro Exam


A. Survey of Mental status & speech (Comprehensice Neuro Exam)
1.) LOC & Test of memory
2.) Levels of orientation
3.) Cranial Nerve assessment
4.) Motor assessment
5.) Sensory assessment
6.) Cerebral test Romhberg, finger to nose
7.) DTR
8.) Autonomics
1. a. Levels of consciousness (LOC)
1. Conscious (conscious) awake levels of wakefulness
2. Lethargy (lethargic)
drowsy, sleepy, obtunded
3. Stupor (stuporous)
awakened by vigorous stimulation
Pt. has general body weakness, decrease bodily reflex
4. Coma (Comatose)
Light (+) all forms of painful stimulations
Deep (-) to painful stimulation
*Watch out for the rise & fall of the chest
b. Different types of pain stimulation
o Dont prick
1. Deep sternal pressure/stimulation: 3x fist knuckle
With response
light coma
Without response deep coma
2. Pressure on great toe 3x
3. Orbital pressure pressure on orbits only below eye
4. Corneal reflex/ blinking reflex
*Wisp of cotton used to illicit blinking reflex among conscious patients
*Instill 1-drop saline solution unconscious pt if (-) response pt is in deep coma

Created by Nia E. Tubio

25

c. Test of memory consider educational background


a. Short term memory
What did you eat for breakfast?
Damage to temporal lobe (+) antero grade amnesia
b. Long term memory
(+) Retrograde amnesia damage to limbic system (rhinencephalon)
2. Levels of orientation:
1st: Time
2nd:: Person
3rd: Place
Exercise:

Describe a conscious pt ?
a. Alert not all pt are alert & oriented to time & place
b. Coherent
c. Awake
d. Aware
3. Cranial Nerve Assessment: 12 pairs of cranial nerves

I
II
III
IV
V
VI
VII
VIII
IX
X
XI
XII

Olfactory
Optic
Oculomotor
Trocheal
Trigeminal
Abducens
Facial
Acoustic/auditory (V)
Glossopharyngeal
Vagus
Spinal accessory
Hypoglossal

Old
Opie
Occasionaly
Tries
Trigonometry
And
Feels
Very
Gloomy
Vague
And
Hypoactive

s
s
m
m
b
m
b
s
b
b
m
m

smallest CN
largest CN

longest CN

Some
Say
Marry
Money
But
My
Brother
Says
Bad
Business
Marry
Money

I. Olfactory dont use ammonia, alcohol, cologne irritating to mucosa use coffee granules, vinegar
* Hyposmia decrease sensitivity to smell
*Diposmia distorted sense of smell
*Anosmia absence of sense of smell
*Either of 3 might indicate head injury damage to cribriform plate of ethmoid bone where olfactory cells are
located or indicate inflammation condition sinusitis
II Optic (Sensory or Vision)
1. Test of visual acuity or central or distance vision (test of near vision)
Use Snellens Chart:
a. Snellens Alphabet -----used for literate client
b. Snellens E chart --------used for illiterate
c. Animal Chart -----used for children
Normal: 20/20 vision
20 numerator is constant: 20 ft (6-7 m) distance from the chart
20 denomenator ---vision distance the person can see the letters
OD Rt eye
20/20 =20/200 blindness cant read E biggest
OS left eye
20/20
OU both eye
20/20
2. Test of Peripheral Vision/ visual field: facing the client
a. Superiorily
b. Bitemporally
Created by Nia E. Tubio

26

c. Inferiorly
d. Nasally
Common Disorders
1. Glaucoma (Normal 12 21 mmHg intra-ocular pressure)
- Increase IOP - Loss of peripheral vision tunnel vision
2. Cataract opacity of lens - Loss of central vision, Blurring or hazy vision
3. Retinal detachment curtain veil like vision & floaters
4. Macular degeneration black spots
III Oculomotor, IV (Throclear), VI (Abducens)
Tested simultaneously because it controls or innervates the movement of extrinsic ocular muscle
*6 Cardinal Gaze Extrinsic Ocular Movement
Rt eye
IO

SO

LR

MR

N
O
S
E

left eye

SR
Throclear controls superior oblique (1)
Abducens - lateral rectus (1)
9. Oculomotor- controls the size & response of pupil (Pupil size 2 -3 cm or 1.5 2 mm)
- controls opening of the eyelids
- controls the 4 gaze
V Trigeminal
Largest nerve consists of - ophthalmic, maxillary & mandibular branch
1. Sensory controls sensation of the face, mucus membrane; teeth & corneal reflex
Unconscious instill drop of saline solution
2. Motor controls muscles of chewing/ muscles of mastication
*Trigeminal neuralgia difficulty in chewing & swallowing
- damage to the trigeminal nerve
- Drug of Choice: Tegritol
-Extreme food temperatire is not recommended
-Avoid hot or cold preparation
Exercise:

Trigeminal neuralgia, RN should give


a. Hot milk, butter, raisins
b. Cereals
c. Gelatin, toast, potato all correct but
d. Potato, salad, gelatin salad easier to chew

VI Facial:
a. Sensory controls taste anterior 2/3 of tongue: Test cotton applicator with sugar.
-Put applicator with sugar to tip to tongue.
-Start of taste insensitivity: Age group 40 yrs old
b. Motor- controls muscles of facial expression, smile frown, raise eyebrow
if Damage causes --------Bells palsy or facial paralysis
Cause of Bells palsy in children---No 1 cause : R/T forcep delivery
Temporary only, resolve w/in 4-6 months
*Most evident clinical sign of facial symmetry: Nasolabial folds
VIII Acoustic/ Vestibulocochlear
a. Cochlear ----controls hearing
Created by Nia E. Tubio

27

b. Vestibule-----controls balance (kinesthesia /position sense)


-----Movement & orientation of body in space
------located in the inner earif it movesthe head moves too--kinesthesia

*Menieres Disease----only disease of the inner ear----loss of balance---Nsg. Priority: Safety


Parts of Ears:
Outer tympanic membrane, pinna, oricle (impacted cerumen), cerumen
Middle hammer, anvil, stirrup or melleus, incus, staples. Mid otitis media
Eustachean ear
Inner ear- meniere ear, sensory hearing loss
Remove vestibule menieres dse disease inner ear
*Archimedes law --Bouyancy
*Daltons law Partial pressure of gases (Diffusion)
*Inertia law of motion (dizziness, vertigo)
Exercise:
1.) Pt. with multiple stab wound in the chest
- Movement of air in & out of lungs is carried by what principle?
- Diffusion Daltons law
2.) Pregnant check up ultrasound reveals fetus is carried by amniotic fluid
- Archimedes
3.) Severe vertigo d/t Inertia
Test for acoustic nerve: ---------Repeat words uttered
IX Glossopharyngeal
X Vagus

controls taste the posterior portion 1/3 of the tongue


controls gag reflex

Test 9 10
Pt say ah check uvula (in the middle tonsils) should be midline
If there is deviation from L to R ----Damage to cerebral hemisphere
Gag reflex place tongue depression post part of tongue
Dont touch uvula
Gag reflex----vagal stimulation -----PNS Effect
XI Spinal Accessory

- controls sternocleidomastoid (neck) & trapezius


Shrug shoulders, put pressure. Pt should resist pressure. Paresis or phlegia

XII Hypoglossal - movement of tongue say ah


If L or R deviation-----damage to the cerebral hemisphere
- Push tongue against cheek. Normal= tongue in midline,
if (-) disorder called ------- Short frenulum lingue or tongue tied bulol

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EYES
A. External Parts:
1. Orbital cavity
made up of connective tissue, protects eye from trauma.
2. EOM (Extrinsic Ocular Muscles ) involuntary muscles of eye, needed for gazing movement.
3. Eyelashes/ eyebrows
aesthetic purposes
4. Eyelids palpebral fissure
opening upper & lower lid. Protects eye from direct sunlight

5.
6.

Meibomean gland secrets a lubricating fluid inside eyelid


a.) Stye/ sty or Hordeolum- inflamed Meibomean gland
Conjunctiva
Lacrimal apparatus tears

B. Intrinsic Coat
I. Sclerotic coat outer most
a.) Sclera white. Occupies posterior of eye. Refracts light rays
b.) Canal of sclera site of aqueous humor drainage
c.) Cornea transparent structure of eye
II. Uveal Tract provides nutritive care
Uveitis inflammation of the uveal tract
Consist of:
a.) Iris colored muscular ring of the eye
2 Muscles of Iris:
1. Circular smooth muscle fiber
2.radial smooth muscle fiber

- Constricts the pupil


- Dilates the pupil

2 Chambers of the Eye:


1. Anterior
a.) Vitereous Humor maintains spherical shape of the eye
b.) Aqueous Humor maintains intrinsic ocular pressure
(Normal IOP= 12-21 mmHg)
II. Retina (innermost layer)
a. Optic discs or blind spot nerve fibers only
No auto receptors
Cones (daylight/ colored vision)
Phototopic vision

Rods night, twilight vision


Scotopic vision = Vit. A deficiency rods insufficient

b. Maculla lutea yellow spot center of retina


c. Fovea centralis area with highest visual acuity oracute vision
Physiology of Vision:
4 Physiological Processes for Vision to occur:
1. Refraction of light rays bending of light rays
2. Accommodation of lens
3. Constriction & dilation of pupils
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4. Convergence of eyes
*Unit of measurements of refraction Diopters
*Normal eye refraction
Emmetropia
*PERRLA ---Normal Reaction
ERROR of Refraction:
1.
2.
3.
4.

Myopia - near sightedness


Tx: biconcave lens
Hyperopia
- farsightedness Tx: biconvex lens
Astigmatisim
-distorted vision Tx: cylindrical
Presbyopia
- old slight inelasticity of lens d/t aging Tx: bifocal lens or double vista

*Accommodation of lenses based on Thelmholtz Theory of accommodation


Near vision:
-Ciliary muscle contracts
-Lens bulges

Far vision:
- Ciliary muscle dilates / relaxes
-Lens is flat

Convergence of the Eye:


Error:
1.

2.
3.
4.

Exotropia 1 eye normal


Esophoria
Strabismus- squint eye
Amblyopia prolong squinting

corrected by corrective eye surgery

1. GLAUCOMA
An increase Intra Ocular Pressure if untreated, atrophy of optic nerve disc blindness
- Preventable but not curable
Predisposing Factors:
1.
2.
3.
4.
5.
Type:
1.
2.
3.

High risk group 40 y/o & above


HPN
Hereditary
Obesity
Recent eye surgery, trauma, inflammation

Chronic -------- (open angle G.) *most common type


Obstruct in flow of aqueous humor at trabecular meshwork of canal of schlema
Acute --------- (close angle G.) *Most dangerous type
Forward displacement of iris to cornea leading to blindness.
Chronic--------- (closed angle) - Precipitated by acute attack

S/Sx:
1. *Loss of Peripheral Vision a Tunnel-like vision
2. *Halos/Rainbows around lights
3. Headache & Dizziness
4. n/v
5. Steamy cornea
6. Eye discomfort
7. *Ocular Pain
7. If untreated gradual loss of central vision blindness
Diagnosis:
1. *Tonometry reveals increase IOP >12- 21 mmHg
2. Perimetry reveals decrease peripheral visual field
3. *Gonioscopy reveals abstruction in anterior chamber
Nursing mgt:
1. Enforce CBR
2. Maintain siderails
3. Administer meds
a.) *Miotics lifetime ------ contracts ciliary muscles & constricts pupil.
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Ex. Pilocarpine Na (Carbachol)


b.) Epinephrine eye drops ------decrease formation & production of aqaueous humor
c.) Carbonic anhydrase inhibitors. ----- Promotes increase out flow of aquaeous humor(drainage)
Ex. Acetazolamide (Diamox)
2.

d.) Timoptics (Timolol maleate)- Increase outflow of aquaous humor (drainage)


Surgery:
Invasive:
a.) Trabeculectomy --- eye-trephining
removal of trabelar meshwork of canal or schlera to drain aqueous humor
b.) *Peripheral Iridectomy portion of iris is excised to drain aqueous humor
Non-invasive:
a. Trabeculotomy (eye laser surgery)

Nursing Mgt.: Pre operative for all types of surgery:


1. Apply eye patch on unaffected eye to force weaker eye to become stronger.
Nursing Mgt. Post-operative all types of surgery
1. Position unaffected/ unoperated side - to prevent tension on suture line.
2. Avoid valsalva maneuver
3. Monitor symptoms of IOP
a.) Headache
b.) n/v
c.) Eye discomfort
d.) Tachycardia
2. Eye patch for both eyes post-operatively

2. CATARACT
A partial/ complete opacity of lens, can lead to blindness
Predisposing Factor:
1.
2.
3.
4.

Aging : 90-95% (degenerative/ senile cataract)---60 y/o & above


Congenital (very rare)
Prolonged exposure to UV rays
DM

S/Sx:

1. *Loss of Central Vision - Hazy or blurring of vision


2.
3.

4.

Painless
Milky white appearance at center of pupil
*Decrease perception of colors
*Elderly can only see Red & Green

Dx:
1. Opthalmoscopic exam reveals (+) opacity of lens
Nsg Mgt:
1. Reorient pt. to environment due opacity
2. Siderails
3. Medications
a.) *Mydriatics dilate pupil not lifetime Ex. Mydriacyl
b. ) Cycloplegics
paralyzes ciliary muscle. Ex. Cyclogyl
c.) Atrophine
4. Surgery
a.

b.

E extra
C - capsular
C cataract
L - lens
E extraction

Partial removal of lens

I - intra
C - capsular
C cataract
L - lens
E extraction

Total removal of lens & surrounding capsules

Complications of Lens Extraction: Hemorrhage


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Retinal Detachment
Endopthalmitis
Nursing Mgt:
1.Position unaffected/ unoperated side - to prevent tension on suture line.
2.Avoid valsalva maneuver
3.Monitor symptoms of IOP
a.) Headache
b.) n/v
c.) Eye discomfort
d.) Tachycardia
4.Eye patch both eyes - post op

3. RETINAL DETACHMENT
- The separation of 2 layers of retina, can lead to blindness
Predisposing factors:
1.
2.
3.
4.
5.

*Severe myopia near sightedness


Diabetic Retinopathy
Trauma
*Following lens extraction
HPN

S/Sx:
1.
2.
3.
4.

*Curtain veil like vision


Flashes of lights
*Floaters d/t seepage of blood (Photopsia)
Gradual decrease in central vision

Dx: Opthaloscopic exam


Drug of Choice: Cycloplegics
Nursing Mgt:
1.
2.

Siderails (all visual disease)


Surgery:
a.) Cryosurgery (cold application)
b.) *Scleral buckling
c.) Diathermy ------heat application

4. MACULAR DEGENERATION
-----the appearance of black spots in the eyes

Created by Nia E. Tubio

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Created by Nia E. Tubio

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Addisons Disease

PATHOGNOMONIC SIGNS
Bronze-Like Skin

Angina Pectoris

Levines Sign

Appendicitis

Rebound Tenderness

Asthma

Wheezing On Expiration

Bulimia Nervosa

Chipmunk Face

Cataract (loss of central vision)

Hazy Vision

Cholecyctitis

(+) Murphys Sign

Cholera

Rice-Watery Stool

Cushings Disease

Moon Face Appearance

Dengue

Petechiae

Diptheria

Pseudomembrane

Down Syndrome

Protrusion Of Tongue

Down Syndrome

Simean Creases on Palms

Emphysema

Barrel Chest

Glaucoma (peripheral vision)

Tunnel-like Vision

Graves Disease (Hyperthyroidism)

Exopthalmus

Hepatitis

Jaundice

Hyperpituitarism ( Acromegaly)

Carotenemia ( yellowish skin)

Kawasaki Disease

Strawberry Tongue

Leprosy

Leioning Face

Liver Cirrhosis

Spider Angioma

Malaria

Chills

Measles

Kopliks spot

Meningitis

(+) Kernigs & Brudzinskis Sign

Myasthenia Gravis

Ptosis

Pancreatitis( Ectopic Pregnancy)


Parkinsons Disease
Patent ductus Arteriosus

(+) Cullens Sign (ecchymosis of umbilicus)


(+) Grey-Turners (ecchymosis of flank)
Pill-Rolling Tremors
Machine-like Murmur

Pernicious Anemia

Beefy Red Tongue

Pneumonia
PTB
Pyloric Stenosis

Rusty Sputum
Low-Grade Fever
Olive Shape Mass

Retinal Detachment
Systemic Lupus Erythematosus
Tetanus
Tetany
Tetralogy Of Fallot
Thombophlebitis

Curtain Veil-Like Vision


Butterfly rash
Risus Sardonicus
(+) Trousseau & (+) Chvostek Sign
Clubbing of Fingers
(+) Homans Sign

Typhoid Fever

Rose Spots in Abdomen

Created by Nia E. Tubio

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RELATED DISORDERS:
1. COPD = # 1 cause: Smoking ----- 4 Types: ---- all needs bronchodilators
BRONCHITIS
Blue bloaters
Dyspnea on Exertion
Lead to cor pulmonale

Created by Nia E. Tubio

ASTHMA
Wheezing on Expiration
Cause by allergens
Hereditary
Reversible

BRONCHOIECTASIS
Hemoptysis
Undergo Pneumonectomy
Bronchoscopy

EMPHYSEMA
Barrel Chest
Pink Puffers
Dyspnea at Rest
Lead to Cor Pulmonale
Cause by Allergens
Hereditary
CO2 narcosis
Purse Lip Breathing
Irreversible
Terminal Stage

35

To Prevent STD Local practice monogamous relationship


CGFNS/NCLEX condom

ENDOCRINE SYSTEM
The endocrine system integrates body functions by the synthesis & release of hormones.
Hypothalamus: link between the nervous system & the endocrine system.

ENDOCRINE GLANDS:
Secrete their products directly into the bloodstream
Different from exocrine glands
Exocrine glands: secrete through ducts unto epithelial surfaces or into the GIT
Parts:
Pituitary Gland
Adrenal Glands
Pancreas
Thyroid Glands
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Parathyroid Glands
Gonads

HORMONES:
- Are chemical substances that are secreted by the endocrine glands.
- Can travel moderate to long distances or very short distances.
- Acts only on cells or tissues that have receptors for the specific hormone.
- Target Organ: The cell or tissue that responds to a particular hormone
- Regulation of Hormones: Negative Feedback Mechanism
When the hormone concentration rises, further production of that hormone is inhibited.
When the hormone concentration falls, the rate of production of that hormone increases.

2 BASIC PATHOPHYSIOLOGICAL DISORDER OF THE ENDOCRINE

A. Hyposecretion/ Hypoactivity

B. Hypersecretion / Hyperactivity

D/T
1. Congenital absence of glands
Ex. No pancreas

D/T
1. Tumor w/n or outside the gland
Ex. Tumor in adrenal gland

2. Surgical removal of glands


Ex. Total Thyroidectomy
Primary Disease Problem in target gland; autonomous

Secondary disease problem outside the target gland;


Most often d/t a problem in pituitary gland

Parts:
I. PINEAL GLAND
Function:

Secretes Melatonin
Inhibits leutenizing hormone (LH) secretion
Regulates body clock, sleeping pattern or circadian rhythm

II. PITUITARY GLAND (Hypophysis Cerebri)


The main gland located at base of the brain at Sella Turcica
Fx: Master gland of body/ Master clock of body---it controls all the metabolic activity of the body
2 Divisions:
Anterior Pituitary Gland Adenohypophysis

Posterior Pituitary Gland Neurohypophysis

A. ANTERIOR PITUITARY GLAND


Function:
1. Responsible for Growth Hormone (GH) (Somatotropic Hormone)
Function: For elongation of long bones
*Puberty age: 9 y/o 21 y/o & the Epiphysial plate closes at 21 y/o
DISORDER:

Hypopituitarism
*Dwarfism -- Children

1. Frohlicks Syndrome
Created by Nia E. Tubio

GH

hH

Hyperpituitarism
Acromegaly -- Adult
1. Gigantism
37

-Dwarf w/ obesity
- Mentally retarded
- Loss of reproductive ability d/t genital atrophy
2. Simmonds Disorder/ Pituitary Cachexia
- Appearance of a wizened old man
- Premature senility, Skin dry & wrinkled
- Mental retardation
- Male: Absence of spermatogenesis
- Female: Amenorrhea

- If s/s appear before closure of epiphyseal plate


- rapid growth of long bones
2. Acromegaly
- If s/s appear after closure of epiphyseal plate
- Hyperthrophy of soft tissue & bone thickness
- Disproportional growth
Enlargement of cartilage ( nose & ears)
Enlargement of larynx (deep voice)
Progmatism: Protrusion of jaw
Square face & jaw
Macroglossia Obstructive Sleep Apnea

Dx:
- X-ray, MRI or CT scan: pituitary tumor
- Plasma hormone levels: decreased
Tx:

Drug of Choice in acromegaly:


Octreotide (Sandostatin) --S/E: Seizure & GIT irritation
Somatostatin Hormone - antagonizes the release of GH
2. Melanocytes Stimulating Hormone (MSH)
Function: For skin pigmentation
DISORDER:
*Albinism ---hyposecretion of MSH
----prone to develop skin cancer & blindness

*Vitiligo -----hypersecretion of MSH

3. Prolactin/ Lactogenic Hormone


Initiates milk let-down reflex with help of oxytocin
Promotes development of mammary gland/breast tissue
Disorder: Prolactin Deficiency : Failure to lactate
4. Adrenocorticotropic Hormone ACTH
Development & maturation of adrenal cortex
S & Sx in Deficiency:
- Results in diminished cortisol secretion.
- Weakness, fatigue, weight loss, and hypotension.
5. LH -----Progesterone
6. FSH----Estrogen
B. POSTERIOR PITUITARY GLAND: secretes---1.) Oxytocin
a. Promotes uterine contractions-----preventing bleeding/ hemorrhage.
- Best time to administer Oxytocin: after placental delivery to prevent uterine atony.
b. Initiates the Milk let-down reflex with help of prolactin.
2.) Anti-Diuretic Hormones (ADH) /ADH-replacement ---Vasopressin or Pitressin
Function: Prevents urination conserve H2O
Regulates water metabolism
Released during stress or in response to an increase in plasma osmolality to stimulate
reabsorption of water & decreased urine output
DISORDERS OF THE POSTERIOR PITUARY GLAND
1. DIABETIS INSIPIDUS (DI)
The hyposecretion of ADH
Disorder w/ massive polyuria d/t either lack of ADH or kidneys insensitivity to it
Cause:
Idiopathic/ unknown
Predisposing factor: PITT
1. Pituitary surgery
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2. Inflammation
3. Trauma
4. Tumor
Pathophysiology :

Diabetes Insipidus
Disorder of

H20 metabolism

ADH

* Alcohol inhibits release of ADH

Prevents renal tubules from reabsorbing H20


POLYURIA

S &Sx:

Polydipsia
Dehydration

F & E imbalance

(excessive urine output 5-29 L/24 hrs.)

Diluted Urine

Urine Specific gravity

Other S & Sx:


2. Sx of Dehydration:
Excessive thirst, Agitation, Poor skin turgor, Dry mucus membrane
3. Weakness & Fatigue
4. Hypotension if left untreated
5. Hypovolemic shock *Anuria Late sign hypovolemic shock
6. Weight loss
Dx:

1.Decrease urine specific gravity- concentrated urine


2.Serum Na = Increase d/t compensation to attract more H2o

(N = 1.015 1.035)
(N =135 -145 meq/L)

Mgt:
1. Force fluid 2,000 3,000ml/day
2.Administer IV fluid replacement as ordered ( Isotonic fluid solution)
3. Monitor VS, I&O
4.Administer meds as ordered (Commercially-Prepared ADH)
a. Pitressin Tannate
Oily preparation: Give deep I.M.
b. Vasopressin Tannate
May cause lipodystrophy , rotate site of administration
Will cause vasoconstriction--Monitor BP before & after
c. Desmopressin Acetate
Given by Nasal Spray
d. Lypressin
5. Prevent complications:
Most feared complication Hypovolemic shock
2. SYNDROME OF INAPPROPRIATE ANTI-DIURETIC HORMONE (SIADH)
- An increase production of ADH or Hypersecretion of ADH
- Idiopathic/ unknown
Predisposing Factor:
1.

2.

Head injury
R/T Bronchogenic cancer or lung cancerEarly Sign of Lung Ca : Cough productive, non productive

3. Hyperplasia of Pituitary gland


4. Increase size of organ d/t increase # of cells
S&Sx
1.
2.
3.
4.

5.
Created by Nia E. Tubio

Fluid Retention
Increase BP HPN
Edema
Wt gain
Danger of Water Intoxication

(The only Endocrine Gland with Water Intoxication)


39

Cerebral Edema

Increase ICP
Complications of SIADH
Seizure Activity

Dx :
1. Urine specific gravity increase: Reveals a diluted urine
2. Serum Na ----Decrease
3. Low serum osmolality
4. High urine osmolality (urine osmolality >100 mosmol/kg)
5. Normal renal function (low BUN <10 mg/dL), absence of hypothyroidism & glucocorticoid deficiency &
recent diuretic therapy.
Nsg Mgt:

1.Restrict fluid. (<1,000 ml/day)


Takes 3-10 days to work
2. Administer meds as ordered
If the patient has evidence of fluid overloading, a history of CHF, or is resistant to treatment, loop diuretics
(Furosemide) may be added as well.
a. Diuretics-----both ----Osmotic (Mannitol)---for the Increase ICP (side-drip)
----Loop (Lasix)---------for edema----IV push
b. Chronic treatment: lithium or demeclocycline which inhibit ADH action.
3. Monitor strictly V/S, I&O, neuro check increase ICP
4. Weigh daily
5. Assess for presence edema
6. Provide meticulous skin care
7.Prevent complications : Increase ICP & Seizure
8. Maintain sodium balance
Increase sodium intake
If the serum sodium is below 120 or if the patient is seizing, emergency treatment: 3% NaCl.
May be followed by Furosemide.
Excessively rapid correction of hyponatremia may cause central pontine myelinolysis.
Patients with a plasma sodium concentration greater than 125 mmol/l rarely need specific therapy for
hyponatremia.
III. ADRENAL GLAND

Located at the top of the kidney


2 Parts:

A. Adrenal Cortex (Outermost layer)


1.

Zona Fasiculata secrets glucocorticoids


Ex. Cortisol, Corticosterone
--Controls glucose metabolism (SUGAR)
Increase blood glucose levels by increasing rate of gluconeogenesis
Increase protein catabolism
Increase mobilization of fatty acids
Promote sodium and water retention
Anti-inflammatory effect
Aid the body in coping with stress

2.

Zona Reticularis secrets traces of glucocorticoids & androgenic hormones


M Testosterone
F Estrogen & progesterone

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Fx: Promotes development of secondary sexual characteristics


3. Zona Glomerulosa - secretes mineralocortisone/mineralocorticoids
Ex. Aldosterone, corticosterone, Deoxycorticosterone
Fx: Promotes Na & H2O reabsorption & excretion of potassium (SALT)
Regulate fluid and electrolyte balance
Stimulate reabsorption of sodium, chloride and water
Stimulate potassium excretion
Under the control of the Renin-Angiotensin-Aldosterone system
Summary: Adrenal Cortex Hormones
Sugar
Salt
Sex
B. Adrenal Medulla

(Innermost layer)

Secrets cathecolamines
a. Epinephrine
b. Norephinephrine (Potent vasoconstrictor)
Released during fight or flight situations SYMPATHETIC effect

DISORDERS OF THE ADRENAL CORTEX:

CODE: 3 Ss
Addisons Disease

Hypoglycemia
Hyponatermia
Loss of pubic

ugar
alt
ex

Cushings Syndrome

Glucocorticoid
Mineralcoritcoid
Androgen

Hyperglycemia
Hypernatremia
Hirsutism

CONNS DISEASE
1. ADDISONS DISEASE
- Hyposecretion of adrenocortical hormones leading to:
a. Metabolic Disturbances (sugar)
b. F&E Imbalances- Na, H2O, K
c. Deficiency of neuromuscular function (salt & sex)
Predisposing Factors:
1. Atrophy of adrenal gland
2. Fungal infections
Sx of
3. Tubercular infections
Hypoglycemia
T tremors, tachycardia
I irritability
R - restlessness
E extreme fatigue
D diaphoresis &

Pathophysiology :

S
Created by Nia E. Tubio

- Hypoglycemia
- Decreased Plasma cortisol

Tolerance To Stress ---- Addisonians Crisis

Sugar
-

Melanocyte secreting hormone

Hyperpigmentation (discoloration of skin & m. m.)


Tan

- Decreased Volume
Salt

= BRONZE-SKINNED

Hypovolemia --- Hypotension

- Hyponatremia ---- Dehydration (Extreme thirst & agitation)----Weight Loss


41

- Hyperkalemia
influence cardiac polarization
Arrythmia ---Cardiac Arrest
Sex

Sx of
Hyperkalemia
I irritability
D diarrhea

- Decrease sexual hormone ---- libido & sexual urge


Loss of axillary & pubic hair
Breast atrophy

S & Sx:
1. Hypoglycemia
2. Hyponatremia
Hypovolemia
a. Hypotension
b. Dehydration
c. Weight loss
3. Hyperkalemia
4. Decrease libido & loss pf pubic hair/axilla
* Pathognomonic Sign = Bronze-like skin pigmentation d/t decrease cortisol w/c will stimulate pituitary gland to release MSH
Dx :
1.
2.
3.
4.

FBS decrease FBS (N 80 120 mg/dL)


Plasma cortisol decreased
Serum Na decreased
Serum K increased

Normal
Na = 135 -145
meq/L
K = 3.5 5.5

Nsg Mgt:
1. Monitor VS, I&O to determine presence of Addisonian crisis
2. Administer isotonic fluid as ordered
3. Diet increase calorie or CHO
Increase Na, Increase CHON, Decrease K
4. Force fluid d/t hyponatremia & dehydration
5. Meticulous skin care d/t bronze-like skin
6. Maintain patent IV line
7. Administer meds as ordered
a.) Steroids supplementation

Corticosteroids - (Decadron) or Dexamethazone


Hydrocortisone (cortisone)- Prednisone
Betamedasone

Nsg. Mgt. with Steroids

1. Administer 2/3 dose in AM & 1/3 dose in PM in order to mimic the normal diurnal rhythm.
2.
3.
4.
5.
6.
7.
8.
9.

Give on full stomach, after meal or w/ milk or w/ antacid ( gastric irritants)


Monitor blood sugar level ( will cause hyperglycemia)
Limit fluid intake ( will cause retention of water)
Monitor body weight at least once a day
Give calcium preparation ( can cause osteoporosis)
Avoid any form of skin trauma/injury
( Steroids increases capillary fragility-----ecchymosis)
Not given to children---can cause growth retardation
Monitor S/E (Cushings syndrome S/Sx)
a. HPN
b. Hirsutism
c. Edema
d. Moon face & buffalo hump

10. Taper the dose (withdraw gradually from drug) to prevent complication of Addisons Crisis

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Sudden withdrawal--------- Acute exacerbation of Addisons Crisis characterized by :


Sudden hypoglycemia, severe
Hypotension
Hypovolemia, severe
Hypocalcemia
Weight loss
Sudden severe Hypokalemia------ Arrhythmia
Cardiac arrest
Leads to progressive stupor & coma
Nsg Mgt: Addisonian Crisis (Coma)
1. Assist in mechanical ventilation
2. Administer steroids
3. Force fluids
11. Can suppress immune response-------prone to infection
Avoid sources of infection
Avoid crowded areas, people with RTI
Place on reverse isolation
b.) Mineralocorticoids.
8.

Ex. Flurocortisone

HT & Discharge planning


a. Avoid precipitating factors leading to Addisonian crisis
1.
2.
3.

Sudden withdrawal crisis


Stress
Infection

b. Prevent complications
1. Addisonian crisis
2. Hypovolemic shock
9. Hormonal Replacement Therapy lifetime
10. Important follow up care
2. CUSHINGS SYNDROME
Hypersecretion/ increase secretion of adrenocortical hormone
Predisposing Factors:
1.

Hyperplasia of adrenal gland

2. Tubercular infection: spread of infection to adjacent organs Milliary TB (TB of the Adrenal Gland)
Hyperglycemia
(3 Ps)

Pathophysiology:

Created by Nia E. Tubio

- Hyperglycemia
Sugar

Lead to DM

Buffalo Hump & Moon Face d/t abnormal fat distribution


-

Salt

polyuria
polydipsia
polyphagia

Increase steroids w/c

- Hypokalemia

WBC

Increase susceptibility to infection (reverse isolation)


Sx of
Hypokalemia
W eakness &
Fatigue

43

Arrythmia ---Cardiac Arrest


- Hypernatremia--- fluid retention

Hypervolemia (Increase intravascular volume)

Edema

HPN

Anasarca
Obese Trunk w/ thin extremities
Sex

- Virility, Hirsutism, Muscularity of female


Striae & Acne, Enlarged clitoris

S & Sx:
1.
2.

3.
4.

Hyperglycemia ( Difference From DM: 3 Ps + Glycosuria + Weight Loss)---Complication of Cushings: DM


Hypernatremia
a. HPN
b. Edema
c. Wt gain
d. Moon face (oily w/ acne)
Buffalo hump
Obese trunk
Classic Signs
Pendulous abdomen
Thin extremities
Hypokalemia
Easy Bruising

Dx:
1.
2.
3.

4.
Nsg Mgt:
1.
2.
3.
4.

5.

FBS increase
Plasma cortisol increase
Na increase
K - decrease
Monitor VS, I&O
Weigh patient daily & assess presence of edema
Reverse isolation
Restrict Na
Administer meds as ordered
a. K- Sparing Diuretics (Aldactone) spironolactone
- Promotes excretion of NA while conserving potassium
- Not lasix due to S/E hypoK & Hyperglycemia!

6. Provide Dietary intake Low in CHO, low in Na & fats


High in CHON & K

7. Skin care d/t acne & striae


8.

Prevent complication
- Most feared arrhythmia & DM
- Endocrine disorder lead to MI Hypothyroidism & DM

9. Hormonal Replacement Therapy : Lifetime


Receive Cortisol Inhibitor
Ex. Aminogluthetemide
Metotane
Trilostane
*Metyrapone

10. Surgery:
a. Surgical Removal: Bilateral Adrenolectomy
b.
Created by Nia E. Tubio

Destruction:

Cobalt Therapy
44

3. CONNS DISEASE/ PRIMARY ALDOSTERONISM


- Results from adenoma ( benign tumor of the adrenal cortex)
Increase aldosterone
HPN, Increase ADH, General Edema
DISORDER OF THE ADRENAL MEDULLA:
4. PHEOCHROMOCYTOMA
- Benign tumor of the adrenal medulla
Hyperactive

Increase catecholamines

Epi/Nore

SNS response

All lead to 5 Hs

Hypertension
Headache
Hyperglycemia
Hypermetabolism
Hyperhidrosis & Other S/Sx

Goal:
1. Cobalt Therapy
2. Adrenalectomy
Dx :
VMA ( Vanillylmandellic Acid)
Done to evaluate the level of catecholamines in the blood & urine
Normal: Blood 0.2 0.9 mg %
Urine 0.2 7 mg % for 24 hrs. urine sample
IV. THYROID GLAND
Abnormal Physical Findings:
a. With tenderness
b. No nodular consistency
c. Marked asymmetry
d. Palpable upon swallowing

Normal:
Not tender
- With nodular consistency
- Only 1
- Never palpable unless with goiter

Anatomy:
Thyroid Glands secretes 3 hormones:
T3
Tri-indotyronine

T4
-Tetraiodothyronine/ Tyroxine

3 molecules of iodine
Function:
Effects:

Thyrocalcitonin
Function: Inhibits effects of parathormone
Promotes Calcium reabsorption

4 molecules of iodine

Metabolic or Calorigenic hormone


CNS:
GIT:

Increase metabolism brain


Motility

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Physiology:
Essential Elements In The Production Of Thyroid Hormones
Plasma Iodide
+
Tyrosine
Thyroglobulin

(iodine iodized in plasma by active transport)


(derived from CHON in diet + amino acid)
(in storage form)
Released in blood circulation in the form of

T3 & T4
Through the Feedback mechanism
Ex. APG ------secretes Trophic Hormones ( any hormone that stimulate a target organ)
TSH ------target organ-----Thyroid gland------- T3 & T4
ACTH---------------target organ-----Adrenal cortex------ Steroids
(Adrenocothropic hormone)

Normal:
T3 = 70 -170 % mg
T4 = 4.7 11 ug%

THYROID DISORDERS
1. SIMPLE GOITER
Enlargement of the thyroid gland d/t iodine deficiency
- No increase in T3 T4, below or Normal
Toxic Goiter : If there is an increase in T3 T4
Predisposing Factors:

1. Goiter Belt area ------ Endemic Goiter ---cause by goiter belt area

*A non-toxic goiter can lead to


Toxic goiter anytime if:
> Prolonged exposure to cold
weather
> Stress
> Infection
All can cause an increase in

a. Place far from sea no iodine seafoods rich in iodine

2. Mountainous area results to an increase intake of goitrogenic foods Ex. Baguio/Cordilllera


Ex. Turnips (singkamas) radish, peas, strawberries, sweet potato, beans, kamote, cassava (root crops), nuts, broccoli

3. Goitrogenic Drugs that contains progoitrin--- an anti-thyroid agent that has no iodine
Ex.

Anti thyroid agents


(PTU) prephyl thiupil
Lithium carbonate, Aspirin PASA, Cobalt, Phenyl butasone
Sporadic Goiter if caused by goitrogenic drugs or from an increase intake of goitrogenic foods
S & Sx :
1. Enlarged TG
2. Mild restlessness
3. Mild dysphagia
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Dx.

1. Thyroid Scanning Reveals enlarged TG


2.
3.

Done to evaluate the amount of Iodine 131 accumulated by the thyroid gland
*Serum Thyroid Stimulating Hormone (TSH)
Result: Increase (Confirmatory Dx of Goiter)
T3, T4 Determination
More reliable test, more potent & rapid effect on metabolism
Result : Serum T3, T4 will Normal or below N

Nsg Mgt:
1. Administer meds as ordered:
a. Iodine solution Logols solution or Saturated Solution of K iodide (SSKI)
- Violet/Purple Color
Nsg Mgt For Lugols Solution

1. Use straw to prevent staining of teeth


2. Prophylaxis 2 -3 drops , Treatment 5 to 6 drops
b. Thyroid Hormone / Agents
1. Levothyroxine (Synthroid)
2. Liothyronine (cytomel)
3. Thyroid extract

Drugs Given Using Straw To


Prevent Staining
1. Tetracycline
2. Iron preparation
3. Nitrofurantoin
(Macrodantin)

Nsg Mgt for Thyroid Hormones/agents

1. Monitor VS HR d/t tachycardia & palpation


2. Take it early AM S/E : Insomnia
3. Monitor S/E:
Tachycardia, palpations
Insomnia
Restlessness agitation
Heat intolerance
HPN

Signs of Hyperthyroidism

4.

Encourage increase intake iodine


1. Seaweeds highest source 99%
2. Seafood: Highest iodine content: 1st: Oysters 2nd: Crabs 3rd: Lobster
3. Iodized salt easily destroyed by heat, take it raw not cooked
5. Assist surgery: Sub-Total Thyroidectomy
2. HYPOTHROIDISM

Least iodine: Shrimps

The Hyposecretion of T3, T4 leading to MI, Atherosclerosis, HPN & stroke.


Classified According To Onset of S & Sx:
1. CRETINISM appear during childhood / only endocrine d/o that leads to mental retardation
2. MYXEDEMA appear in adulthood (both pitting & non-pitting edema)
Classified According To Cause:
1. PRIMARY
failure of thyroid to secrete T3 T4
2. SECONDARY failure of APG to secrete TSH
3. TERTIARY
- failure of Hypothalamus to secrete TRH (Thyroid Releasing Hormone)
Predisposing Factors:

1. Iatrogenic causes disease caused by medical intervention or surgery


2.Atrophy of TG d/t:
a.
b.

c.
Created by Nia E. Tubio

Irradiation
Trauma
Tumor & Inflammation
47

3.Iodine deficiency
4.Autoimmune Hashimoto disease
Pathophysiology:
Hypothalamus

APG secretes-----TSH---stimulate----Thyroid Gland---secrete--- T3 T4


Any disorder of T.G. will decrease T3 T4
Leading to Tertiary causes or Hypothyroidism
Altered Metabolism
Hypometabolic
Hypoactive

Memory Impairment
Decrease O2 in metabolism
Weight Gain
Decrease VS
Unable to tolerate Cold weather

S&Sx:
Everything decreased except weight gain & menstruation w/c are both increase
Early Sx :

Weakness & Fatigue


Loss of appetite
Weight gain
Cold Intolerance Myxedema - Coma
Constipation
Dry skin

Late Sx :

Brittle hair/ nails


Non pitting edema d/t increase accumulation of mucopolysacharide in SQ tissue
Hoarseness of voice only endocrine d/o that can be Dx thru telephone conversation
Decrease libido
Decrease VS Hypotension, Bradycardia, Bradypnea & Hypothermia
Lethargy
Memory Impairment leading to Psychosis
Menorrhagia (high)

Dx:

1. T3 T4 Determination: Serum T3 T4 Decrease


2. Serum Cholesterol: Increase can lead to MI
3. Radio Iodine Uptake (RAIU): Decrease
- Use to evaluate the amount of radiation RAI 131 accumulated by the T.G. & excreted by the kidneys
- Most reliable Diagnostic Test
Normal Uptake : 15 - 40 %
Urine : 40 80%

of the administered dose


Result: Directly proportional to Uptake, inversely proportional to urine

Nsg Mgt In RAIU:


1. No iodine in diet prior to test
2. Taken P.O. RAI 131 cocktail (liquid)

2 Endocrine D/O that leads to Cardiac


Complications
1. DM
2. Hypothyroidism

Nsg Mgt:

1. Monitor strictly V/S. I&O to determine presence of Myxedema Coma


A severe form of hypothyroidism
Characterized by:
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48

Hypotension
Hypoventilation
Bradycardia
Bradypnea, Hyponatremia & Hypoglycemia
That can lead to progressive stupor & coma
Important Mgt For Myxedema Coma:

1. Assist in mechanical ventilator


2. Administer thyroid hormone
3. Administer IVF replacement
2.

Monitor VS, I&O

3. Provide dietary intake : Low in calories d/t weight gain


4. Skin care d/t dry skin
5. Comfortable & warm environment d/ to cold intolerance that can lead to Coma
6.
7.

8.

Administer IVF replacements


Force fluid
Administer meds as ordered Take AM
Supplement Thyroid Hormones/Extract
Synthetic:

Levothyroxine S/E: Constipation

Thyroid Extracts: Proloid ( Thyroglobulin)


Cytomel
Synthroid
Euthroid
Thyrolar
Eltroxime
9.

Health teaching & discharge plan


a. Avoidance precipitating factors leading to myxedema coma:
1. Exposure to cold environment
2. Stress
3. Infection
4. Use of sedative, narcotics, anesthetics not allowed CNS depressants V/S already down

b. Prevent Complications: Hypovolemic shock, Myxedema coma, HPN, LHF, MI, Stroke
c. Hormonal replacement therapy - lifetime
d. Importance of follow up care
3. HYPERTHYROIDISM GRAVES DISEASE or THYROTOXICOSIS
TOXIC GOITER/ BASEDOU/ PARRYS DISEASE
-

The hypersecretion of T3 & T4

Predisposing Factors:

1. Autoimmune Disease Release of LATS


2.

3.

Exopthalmos
Enopthalmos severe dehydration depressed eye
Excessive iodine intake
Hyperplasia of TG d/t increase # of cells

Pathophysiology:

1. Theory Of LATS: (Long Acting Thyroid Stimulator)


In blood, there is gamma globulin

that causes

Iodine Accumulation
Thyroid Hyperplasia

W/c will manifest the TRIAD SYMPTOMS:


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49

1. GOITER d/t iodine accumulation


2. EXOPTHALMOS (eye signs seen in EPS)
3. HYPERTHYROIDISM (seen in EPS)
2. EPS ( Exopthalmus Producing Substance)
APG -----releases EPS----responsible for the Triad S & Sx
Proptosis (downward displacement of eyeball)
Lid lag (sleepy eyes)
Infrequent blinking
Fixed stare
DALYRIMPLE SIGN
Peri-orbital Edema
Von Graefe ------------ failure of eyelids to follow movement of eyes when looking down
3. Hyperthyroidism ---------- Hyperactive, Voracious but losing weight, hypermetabolic
T3 T4 ------the cause is over-excitability of SNS
Tremors

Hallucinations

Diaphoresis

Palpitation

Nervousness

Irritability

Insomnia

S & Sx:

1. Increase appetite : Hyperphagia but weight loss d/t increase metabolism


2.
3.
4.

5.
6.
7.
8.
9.

Skin is moist
Heat intolerance
Diarrhea most common gastric complications of Graves Disease
All VS increase = HPN, Tachycardia, Tachypnea, Hyperthermia
CNS changes
Goiter
Exopthalmos
Constipation common in advanced
Amenorrhea
graves disease
d/t constant increase in T3

Dx:

1. Serum T3 & T4 - Increased


2. RAIU : Increase
3. Thyroid Scanning: Reveals an enlarged TG
Nsg Mgt:
1. Monitor VS & I & O To determine presence of thyroid storm or most feared complication: Thyrotoxicosis
2. Administer meds as ordered

a. Antithyroid Agents
1. Prophylthiouracil (PTU)
2.
3.

Methimazole (Tapazole)
Neomercazole ( Carbimazole)
Most Toxic S/E for prolonged Used: Agranulocytosis
Common S/S: Complications R/T infections
- Fever, Sore throat, Mild Leukocytosis
Dx Test To Check For Toxicity: Differential Platelet Count
If not available, Monitor CBC
Throat Swab & Culture
Most feared complication : Thrombosis ----Stroke CVS

b. Adrenergic Blocking
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To control the symptoms brought about by the over-excitability of SNS


- Propanolol, Inderal, Betaloc, Neobloc, Metoprolol, Nadol, Visken, Aptin, Sotalex, Corgard
3. Diet Increase caloric intake to correct weight loss
4. Skin care
5. Comfy & cool environment
6. Maintain siderails d/t restlessness
7. Provide bilateral eye patch (dry material) to prevent drying of eyes
8. Hormonal Replacement Therapy
10. Importance of follow-up care
11. Assist in surgery Subtotal Thyroidectomy
Tx:
1. RAI 131
To reduce size of T.G.
Isotope: Risk of genetic abnormalities or genetic mutation
2. Surgery :

Subtotal Thyroidectomy
Nsg Mgt: Peri-Operative
1. Administer Lugols solution (SSKI) K iodide
Function: To decrease vascularity of TG
To prevent bleeding & hemorrhage during & after surgery
To increase firmness
Promote T3 T4 storage
2. Diet :
a. High in calories
Increase CHO
Increase CHON
Increase in polyunsaturated fats
To satisfy increase in appetite & restore loss of glycogen reserve
b. Avoid stimulant in diet (No colas, caffeine)
c. Increase fluid intake
d. Monitor body weight
e. Provide physical & mental rest to reduce metabolism
f. Provide quiet & calm environment to decrease irritability
3. If (+) for exopthalmus -----dryness of the cornea ----corneal ulceration---blindness

Nsg Mgt:
1. Cover eyes w/ bilateral eye patch
2. Instill saline to moisten eyes ( Drug: Methylcellulose OD)
3. Elevate head on pillow to promote drainage & reduce peri-orbital edema
4. Give psychological preparation by telling pt. that eye signs will remain
even after surgery
Nsg Mgt: Post-Operative Thyroidectomy
Complication:

1. Watch out for signs of Thyroid Storm or Thyrotoxicosis


- If no emotional preparation pre-operative: Stress
- Post-opt wound infection
Pathphysiology: Pre-opt (euthyroid state----post-opt----thyroid compensates for T3 T4 production
(Hyperthyroid d/t stress, infection)
Increase PR, Increase BP
Triad Signs of Thyroid Storm: HAT
a. Hyperthermia
b. Agitation
c. Tachycardia ----------Early Sign: Fever w/ Tachycardia
Nsg Mgt Thyroid Storm:
1.

Created by Nia E. Tubio

Monitor VS & neuro check


51

Agitated might decrease LOC


2. Antipyretic fever/ TSB
Tachycardia - blockers (-lol)
3. Siderails agitated
Complication

2. Watch for inadvertent (accidental) removal of parathyroid gland


Secretes Parathormone (Calcium Reabsorption)
TETANY : Hypocalcemia
If 1 removed
If 2 removed
If 3 or more removed

No sign of tetany
Mild signs of tetany
- Classic Sx of Tetany:
(+) Trousseau sign & (+) Chvostecks sign
(Twitching of fingers)
(Facial paralysis)

Nsg Mgt:
1. Administer calcium gluconate
Slowly to prevent arrhythmia
Ca gluconate toxicity antidote MsSO4
Complication

3. Watch out for accidental Laryngeal nerve damage


Sx:

Hoarseness of Voice
Aphonia (no voice)

2 recurrent laryngeal nerves that control vocal cords (bilateral laryngeal)


Responsible for voice production

If 1 removed whispery, hoarseness


If Trauma only Whispery, Hoarseness
Edema on glottis Whispery, Hoarseness
If 2 removed Aphonia -----start speech therapy
Nsg Mgt:
1. Encourage pt to talk or speak postoperatively
2. Notify physician immediately
4. Watch out for Signs of Laryngeal Spasm--------- Inflammation of Larynx
Sx: DOB
SOB

Narrow opening ---- O2 cannot enter

Laryngeal Spasm
Nsg Mgt:
1. Prepare at bedside tracheostomy
5. Watch Out for Signs of bleeding Post-Subtotal Thyroidectomy
D/T : Failure to administer Loguls Solution (SSKI) pre-opt
Failure to tie/ ligate blood vessels --------bring back to OR for emergency operation
Sx:
Feeling of fullness at incision site
Feeling of Choking sensation
BP -------- Rapid, feeble, thready pulse
Rapid but shallow respiration
Cold, Clammy diaphoretic skin
Nsg Mgt:
1. Check soiled dressing at nape area (Slip hand under neck to check for dampness)
2. Evaluate VS
3. Notify Physician immediately
Bleeding can lead to-------------- 1. Respiratory Obstruction
D/T blood occlusion & Hematoma
Accumulation of Tracheobronchial secretions
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Can also lead to Laryngospsam/Laryngoedema


Prepare for Emergency Tracheostomy
OTH ER DIAGNOSTIC TEST FOR THYROID DISORDERS:
1. Protein Bound Iodine (PBI)
- Done to evaluate amount of iodine attached to protein molecule of the blood
Normal: 4-8 ug %
Nsg. Care:
1. 2-3 days prior to test, no taking of foods & drugs containing iodine
Ex. Seafoods, iodized salt,
No cough syrup, ASA
Estrogenic Preparations: Pills, Dyes, X-ray
2. Basal Metabolic Rate (BMR)
- Done to evaluate O2 consumption when client is at rest
Nsg Mgt:
1. At night, NPO for 12 hrs.
2. Ensure client had a good night sleep to decrease anxiety level
Procedure:
1. When client no activity yet, no food yet
2. Clamp nose, breathe through tube connected to a tank w/ machine evaluating O2 consumption
3. TBMR (Theoretical)
- Compute pulse pressure + PR/ minute 111
- Not conclusive, but if s/s submit to other test

( Normal: 20-30)

Summary:
HYPOTHYROIDISM
Lethargy
Memory Impairment
Diarrhea
Decrease VS
ALL DECREASE
Except:
Wt: Weight Gain
Menstruation: Menorrhagia

T3
T4

HYPERTHYROIDISM
Agitation & Restlessness
Hallucination
Constipation
Increase VS
ALL INCREASE
Except:
Weight Loss
Amenorrhea

V. PARATHYROID GLAND

Anatomy:

A pair of small nodules located behind the Thyroid Gland


There are 4 Parathyroid glands
PTH------secretes---- PARATHORMONE
Function: Essential to the absorption of Calcium & secretion of Phosphorus by renal tubules
Promotes reabsorption of Calcium
Regulates cardiac rythmicity
Essential for blood coagulation
*Thyrocalcitonin Antagonizes secretion of parathyroid hormone

CODE: CALCIUM
DISORDERS OF THE PARATHYROID GLAND

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1. HYPOPARATHYROIDISM
Hypoactive PTH or a decreased secretion of parathormones
HYPOCALCEMIA
(TETANY)

HYPERPHOSPHOTEMIA
[If Ca decreases, phosphate increases]

Uncontrolled spasm/Hyperactivity
Predisposing Factors:
1. Following subtotal thyroidectomy d/t accidental removal of PTH
2. Atrophy of parathyroid gland due to
a. Inflammation
b. Tumor
S&Sx:

1. Acute Tetany
a.
b.
c.
d.
e.
f.
g.

Tingling sensation
Paresthesia
Dysphagia
Laryngospasm
Bronchospasm
Seizure
Most feared complications
Arrhythmia

Pathognomonic Sign of Tetany:

a. (+) Chvostecks Sign : Tap facial nerve, if facial spasm of facial muscle (+)
b. (+) Trousseaus /Carpopedial spasm: Occlude blood flow to vascular extremity (legs)
Use tourniquet Test for 1-2 min. & observe for carpopedial spasm
2.

Chronic tetany
a. Loss of tooth enamel
b. Photophobia & cataract formation
c. GIT changes : Anorexia, N/V & generalized body malaise
d. CNS changes : Memory impairment, Irritability

Dx:

1.
2.
3.
4.
Nsg Mgt:
1.

Serum Calcium
Serum Phosphate
X - ray of long bone
CT Scan

Decrease
(N 8.5 11 mg/100ml or 4.5 -5.5 mEq/L)
Increase
(N 2.5 4.5 mg/100ml)
Increase bone density
Reveals degeneration of basal ganglia

Administration of meds:
a. Acute Tetany:
Administer Ca gluconate IV, slowly to prevent cardiac arrest
b.

Chronic tetany
1. Give Oral Ca supplements
Ex.

Ca gluconate
- Calci-aid
Ca carbonate
- Calsan
Ca lactate
Ca chloride 10% - Caltrate

2. Give Vit. D for calcium to be readily absorb


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Vitamin D (Cholecalceferol)
Drug

Diet

Cholecalceferol

Sunlight

Calcidiol

Calcitriol

7am 9am

Commercially-Prepared: *Calciferol
Hytakerol
Calcidiol
*Rocatriol
Dihydrotachysterol
3. Give Phosphate binder for excretion of phosphate
Ex. Aluminum OH gel (ampho gel) S/E: Constipation
Antacid
AAC
Aluminum Containing Acids

MAD
Magnesium Containing Antacids

Aluminum OH gel

Milk or Magnesia

Constipation

Diarrhea

*Maalox: Magnesium & Aluminum With Lesser S/E


2. Avoid precipitating stimulus such as bright lights & noise to prevent seizure
3. Diet : Increase Ca & decrease phosphorus
- Dont give milk due to increase phosphorus
Diet : Also For Osteoporosis
a. Baked Salmon
b. Dilis/Anchovies
c. Green Turnips (Singkamas)
4. Bedside: Tracheostomy set d/t laryngospasm
5. Encourage to breath with paper bag in order to produce mild respiratory acidosis
To promote increase ionized Ca levels
6. Most feared complication : Seizure & arrhythmia
7. Hormonal Replacement Therapy: Lifetime
8. Institute Seizure & safety precautions
9. Important follow up care
2. HYPERPARATHYROIDISM / Von Reclinghausen
- Increase secretion of parathormones
- HYPERCALCEMIA -------w/c can lead to Hypophosphotemia
Pathophysiology:
PTH

Increase bone resorption


Normal: Ca 99% bones
1% blood

Hypercalcemia
Hypophospotemia

Calcium loss from bones


Reverse effect: Ca in bone goes to blood

Bone Demineralization
bones are brittle
Leads to bone fracture

Created by Nia E. Tubio

Hypercalciuria
Formation of Calcium crystals in Urine
Nidus/ Nucleus
55

Forms Kidney Stones


Predisposing Factors:
1. Hyperplasia of the parathyroid gland
2. Over compensation of PTG d/t Vit D deficiency
Children Rickets
Adults Osteomalacia
Vitamin D deficiency
*Sippys diet Vit D diet not good for pt with ulcer: 2 -4 cups of milk & butter
*Karrels diet Vit D diet not good for pt with ulcer: 6 cups of milk & whole cream
*Food rich in CHON eggnog combination of egg & milk
S/Sx:
1. Bone fracture
a. Bone pain (especially at back)
2. Kidney Stones
a. Renal colic
b. Cool moist skin & body malaise
3. GIT changes: Anorexia, N/V, Ulcerations ----- only endocrine D/O that causes ulceration
4. CNS involvement: Irritability, Memory impairment
Dx :

1. Serum Ca: Increase


2. Serum phosphorus: Decreases
3. X-ray of long bones : Reveals bone demineralization
Tx:

Hypo : Replacement w/
commercial preparation
Hyper: Removal or Destruction of

1. Removal of the gland - Parathyroidectomy


2. Destruction of the gland Cobalt Therapy
3. Drug of Choice: Calcitonin ---- inhibits resorption

ACID-ASH DIET

Nsg Mgt: Kidney Stone

3 Cs

1. Force fluids : 2,000 3,000/day or 2-3L/day


2.
3.
4.

Isotonic solution
Warm sitz bath for comfort
Strain all urine with gauze pad
5. Acid Ash diet to acidify urine
6. Adm meds as ordered
a. Narcotic analgesic Morphine SO4, Demerol
S/E Respiratory Depression
Antidote - Narcan/ Naloxone
Naloxone toxicity Tremors
7. Siderails
8. Assist in ambulation
9. Diet low in Ca, increase phosphorus lean meat
10. Prevent complication of Parathyroidectomy : Most Feared Renal Failure
11. Hormonal Replacement Therapy: Lifetime
12. Importance of follow up care
VI. PANCREAS

1G

Cranberry
Calamansi
Vit. C
Grapefruit

- Located behind the stomach , a mixed gland


Pancreas: Consists of

Acinar Cells (Exocrine gland)

Islets of Langerhans (Endocrine Gland: Ductless)

Secrete Pancreatic juices

Secretes 3 Types of Cells

Flows in the pancreatic duct


Cells
Created by Nia E. Tubio

Cells

Delta Cells
56

Aids in digestion (in stomach)

Secretes Glucagon
Fx: Hyperglycemia

Secretes Insulin
Fx: Hypoglycemia

Secretes Somatostatin
Fx: Antagonizes Growth Hormones

DISORDER OF THE PANCREAS


1. PANCREATITIS
Acute inflammation of the pancreas leading to Pancreatic Edema, Hemorrhage & Necrosis d/t

Autodigestion
(Self-digestion )

Cause: Unknown/idiopathic
Alcoholism
Obstruction in the pancreatic duct ---- backflow of pancreatic juice to the pancreas
Will cause autodigestion
Pathognomonic Sign: (+) Cullens Sign
(+) Grey Turners Spots

- Ecchymosis of umbilicus (bluish color)


- Ecchymosis of flank area

Both Signs Means Hemorrhage

2. CHRONIC HEMORRHAGIC PANCREATITIS Bangugot


Predisposing Factors: Unknown
Risk factor:
1.
2.

History of hepatobiliary disorder


Alcohol
3. Drugs:
Thiazide diuretics
Oral contraceptives
Aspirin
Penthan
4. Obesity
5. Hyperlipidemia
6. Hyperthyroidism
7. High intake of fatty food Saturated fats
3. DIABETES MELLITUS
- A metabolic disorder characterized by non-utilization of CHO, CHON,& fat metabolism
d/t
1. Absolute Insulin Deficiency
- Cause is unknown but the islets of langerhans do not produce insulin
- Congenital
- Beta-Cell damage by VIRUS ----- Human Leukoantigin----Human Leuko Antibodies
(Chicken Pox)
Autoimmune: Destroys B-cells
2. Relative Insulin Deficiency
- Capable of producing insulin but not used efficiently d/t
Blocked by chemical antagonist at site of production
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Epinephrine

Thyroxin

Glucogen

Glucagon

All causes Glucogenolysis

Physiology:
Pancreas glucose ATP (Main fuel of cell) (reserve glucose glycogen)
Glucogenesis ( synthesis of glucagons)
Glycogenolysis ( breakdown of glucagons)
Liver will undergo
Gluconeogenesis (formation of glucose from CHO sources CHON & fats)

Pathphysiology:
DIABETES MELLITUS
Little or No Supply of Insulin

CHO Metabolism

CHON metabolism

CHO utilization of glucose

breakdown of stored glucose

Cell Starvation

Cell weakness
d/t
cellular starvation

Hyperglycemia

Lipolysis

Cell to Tissue Starvation

Oxidation of fatty acid

Stimulate Satiety Center


(Hypothalamus)

Glucose go to blood

Hyperlipidemia

Ketone Production

POLYPHAGIA
(excessive hunger)

Weight loss

DKA (Diabetic

Blood Osmolarity
Ketoacidosis)

(result from increase breakdown of fats)


kidney
Kidneys tubular secretion
Coma

POLYURIA

Death

Diabetic

Stimulate thirst center

(needs O2)
Glucose in blood
Act as osmotic diuretic (Increase)

ECF dehydration
POLYDIPSIA
(excessive thirst)

Renal tubules fail to reabsorb glucose


HONKC
GLYCOSURIA
Irritate perineal area
Fungi in the area
(-) Nitrogen Balance
Pruritus
A. CLASSIFICATION:
1.

TYPE 1
IDDM
Brittle Disease
Juvenile Onset
Common among children
Non- obese
Weight loss
Symptomatic
Absolute Deficiency
Created by Nia E. Tubio

DKA
Early Sx:
Weight loss
Weakness
Late Sx:
Acetone-breath
odor
Kausmauls
Respiration

Tissue Wasting (Cachexia)


2.

TYPE II
NIDDM

Adult/ Maturity onset


40 y/o & Above
Obese
Weight gain
Asymptomatic
Relative Deficiency
58

Tx: Insulin Administration


Diet
Exercise

Tx: OHA (Oral Hypoglycemic


Agents)
Diet Regimen
Exercise
Complication:
H hyper
O osmolar
N non
K ketotic
C coma

Complications:
Diabetic Ketoacidosis (DKA)
Metabolic Acidosis
Tx: Sodium Bicarbonate
Incidence Rate:

Incidence Rate:

- 10% of population with DM have Type I

- 90% of population w/ DM have Type II


Mid 1980s increase in type II d/t
fast food chains

Predisposing Factor:

Predisposing Factors:

1. 90% hereditary total destruction of pancreatic dells


2. Virus
3. Toxicity to carbon tetrachloride (CC14)
4. Drugs Steroids
Lasix - Loop diuretics
DIABETES
S/Sx:
MELLITUS
1. 3 PS + G
2. Weight loss
3. Anorexia
4. N/V
5. Blurring of Vision
6. Increase susceptibility to infection
7. Delayed/ poor wound healing

ia

1. Obesity lack insulin receptors binding site


- # 1 cause of Type 2 DM
2. Hereditary

Polyuria
Polydips

S/Sx:
1. 3 Ps + G
2. Asymptomatic

Polyphagia

3. GESTATIONAL DM
Occurs during pregnancy & terminates upon delivery of child
Predisposing Factors:
1. Unknown/ idiopathic
2. Influence of maternal hormones
S/Sx :
Same as type II
1. Asymptomatic
2. 3 Ps & 1G
Mgt:
1. Type of delivery: CS d/t macrosomia (large baby)
Sx of Hypoglycemia on Newborn:
1. High pitched shrill cry
2. Poor sucking reflex
B. COMPLICATIONS OF DIABETES MELLITUS
1. HYPERLIPIDEMIA
Formation of atheromatous plaques (atherosclerosis) in the arteries
Narrowed arterial lumen

blood flow) -----result to thickening of BV--- inelastic blood vessels

Formation of vascular lesion ( micro/macro-angiopathy)


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Vascular Degeneration
Cerebral blood flow
vessels

Coronary arteries

Brain

Heart

CVA

Myocardial Ischemia

Retinal Blood Vessels

Eyes

In 30 minutes

Renal blood vessels

Kidney

Lower extremities

Retinopathy
Nephropathy
(Kimmiel-Stiel Wilson Syndrome)
Cataract

Irreversible M.I.

Tissue Ischemia
Peripheral Neuritis

RENAL FAILURE
Retinal Hemorrhage
Exudation

Aggregation of CHON
In Retinal Molecules
Opacified
3 Pathies of
DM
Nephropathy
Retinopathy

Peripheral blood

Diabetic Cataract

Tissue Necrosis

Diabetic Gangrene
Hardening of renal tubules
Ischemia
KSW
Sx:
Proteinuria
Edema
Puffiness of
eyelids

1st d/t Ischemia


PERIPHERAL NEURITIS
Sx:
Numbness of
exremity
Coldness of extremity
Tingling sensation of

Sx of Nephropathy is a progressive destruction of glomeruli --RF


2. DIABETIC KETOACIDOSIS (DKA)
- Acute complication of Type I DM due to severe hyperglycemia leading to CNS depression & Diabetic Coma.
Predisposing Factors:
1. Stress ------ # 1 cause of DKA
Nsg Mgt:
2. Hyperglycemia
3. Infection
1. Can lead to coma: assist in mechanical ventilation
4. Missed dose/Omitting dose of insulin
2. Administer .9NaCl isotonic solution
Sx:
3 Ps & 1 G
Followed by .45 NaCl hypotonic solution
Early Sx:
To counteract dehydration.
Weight loss
3. Monitor VS, I&O, blood sugar levels
Weakness
4. Administer meds as ordered:
Late Sx:
a. Insulin therapy IV push
Anorexia, N/V, Dim Vision
Regular Acting Insulin : Clear
Acetone-breath odor
(2-4hrs, peak action)
Kausmauls Respiration
b. To counteract acidosis Na HCO3
(rapid, shallow breathing)
CNS depression, Coma
5. Antibiotic to prevent infection
Cherry Red Lips
Dx :
1. FBS: Increase
2. Hct: Increase (compensate d/t dehydration)
C. DIAGNOSTIC PROCEDURES FOR DIABETES MELLITUS:

1. FBS/ FPG (Fasting Plasma Glucose)


-

NPO 6-8 hrs. or NPO 12 hrs. with sips of water

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2. RBS (Random Blood Sugar)


-

No NPO, anytime

3. PPBS ( Post Prandial Blood Sugar) Determination


-

Test 1-5 Use to Diagnosed Glycemia

NPO 2 hrs. after diet of 100 gm CHO

4. Hgt (Hemaglukotest)
-

Finger prick or Capillary Blood Glucose Determination (CBg)

5. OGTT ( Oral Glucose Tolerance Test)


- NPO 6-8 hrs. then collect fasting specimen (am)
Administer p.o. 100 gms: Urine
Glucose + fruit juice

Blood

After 1 hr. -----extract venous blood ---- Rise glucose Increase BS (Normal)
2 hrs. --- next extraction
---- start to normalized Decreased BS
Final 3 hrs. --- next extraction
---- w/in normal BS
(+) Diabetic if: Rise glucose till the 3rd extraction still not normal & there is sugar in urine

6. BT, CT (Benedicts Test) (Clini Test)

Test For Glycosuria

- Double voided or 2nd voided specimen = accurately test presence of glucose in urine
- Discard 1st void, offer 1-2 glass of H20 after 1 hr. or 30 minutes collect urine
7. Acetest

To test for presence of ketone bodies in urine (Ketonuria) (Result from incomplete breakdown of fats)
How? Get acutest tablet (creamy/white/ off-white in color) ---drop in urine
If there is no change (-), if color changes to purple (+) for ketonuria

8. Glycosylated HgB

(HgBAC)

- To evaluate the amount of glucose attached to the hemoglobin of the blood for the previous 120 days---lifespan of HgB

D. MANAGEMENT OF DIABETES MELLITUS: Supportive & Palliative


1. TYPE 1 DM
INSULIN THERAPY
A. Sources:

1. Animal source beef/ pork : rarely given because it causes allergic reaction
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2.
3.

Human has less antigenetic property


Ex. Humulin most commonly used
If kid is allergic to chicken dont give measles vaccine, it comes from chicken embryo.
Artificially compound

B. Types of Insulin
Types of Insulin

1. Rapid Acting Insulin


- Regular Acting
- Humulin R
- Semi-Lente
- Crystallized Zinc
- Velosulin
- Novolin R
- MC Actrapid

Onset

Peak

Given

Color &
Consistenc
y

Durati
on

30 minutes
after
administrati
on

2-4 hrs.

3x/day

Clear

6-8 hrs.

1-2 hrs

8-16
hrs.

OD

Cloudy

24 hrs.

3-4 hrs.

16-24
hrs.

Cloudy,
Mixed

36 hrs.

2. Intermediate Insulin
- NPH (Non-protamine
Hagedorn 1)
- Humulin N
- Monotard
- Lente
- Globin
- Novolin L
3. Long Acting Insulin
- Ultra Lente
- PZI (Protamine Zinc
Insulin)
- Humulin U

5 Rs Of Insulin Administration
1. Right Patient: Give insulin only if there are signs of glycosuria & hypergylcemia
2. Right Drug : Administer right type of Insulin
3. Right Route: Not given P.O., insulin destroyed in the GIT by proteinase
Given: SQ, IM, I.V.
Humulin R
Crystalline Zinc
Regular Insulin
4.

Incorporated w/ water, given by drip (IVF)

Right Time:
Best time given 60-90 minutes before meal or an hour before meal
Physiologic effect of insulin will parallel the absorption of glucose

5.

Right Dose: Know stock dose of insulin


10 ml vial
40 units/ml or 80 units/ml or 100 units/ml
Nsg Mgt For Insulin Therapy:
1.

Administer insulin at room temperature. Do not expose to sunlight


Refrigerate insulin once opened only
Before administration, gently roll vial between palms. Avoid shaking to prevent formation of
bubbles

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2. Use gauge 25 26 needle : Tuberculin syringe


3. Administer insulin at either 45 or 90 depending on the client tissue deposit.
5. Dont aspirate after injection
Rotate injection site to prevent lipodystrophy (atrophy/ hypertrophy of SQ tissue)
Deltoid
Rectus Femoris R & L
Vastus Lateralis
Gluteus Maximus

IM

Upper Arm R & L


Below breast
Lower Central Abdominal Wall
Lateral thigh R & L
Below scapula R & L
Buttocks R & L

SQ

6. Most accessible site abdomen


7. When mixing 2 types of insulin, aspirate
1st regular/ clear before cloudy to prevent contaminating clear insulin & to promote accurate calibration.
8. In giving insulin:
Before meals but if pt. eating already: Give insulin
If pt. already eaten 2 hrs. : Do not give, repeat CBC> MD will adjust the dose
9. 1ml or cc of tuberculin = 100 units of insulin
- - 1 cc = 10 units = 100 units
- - .5cc = 5 units = 50 units
- - .1 cc = 1 unit = 10 units
6 units RA
10. Monitor for signs of complications:
a. Allergic reactions
b. Lipodystrophy
c. Somogyis Phenomenon
Rebound Effect of Insulin characterized by hypoglycemia followed by periods of hyperglycemia
(Insulin Shock, Hyperinsulinism, Insulin Overdose, Hyperglycemia)
d/t

Sx:

Occurs w/ insulin overdose


Prolonged NPO, vomiting
Long interval of insulin from the serving of food
* If allowed to eat, give anything to eat an hour after administration of insulin

Hunger Pangs
Double Vision
Pallor, cold clammy skin
Tremors

Mgt:
1. Give 20-30 gm of carbo
2. Drugs

4-8 ounces of softdrinks


4-8 ounces of fruitjuice
1 tbs. of sugar ---best alternative, put
in oral cavity
5 ml of honey
5 ml of karo syrup
2-4 pcs. Of candies
2 slices of graham crackers

Epinephrine 1.1000 SQ
Glucagon
1-2 mg IM
*IV glucose H20 ---- D50% by IV push
---- D5W by venoclysis
2. TYPE 2 DIABETES MELLITUS
Most Feared Complication of Type II DM
Hyper
Osmolar
Created by Nia E. Tubio

osmolarity = severe dehydration


63

Non
Ketotic
Coma

- absence of lipolysis
- no ketosis
S/Sx: headache, restlessness, seizure, decrease LOC

Dx :

1. FBS: N 80 120 mg/dl


2.
3.
4.

Increase , 3 consecutive times


3 Ps & 1G = confirmed DM
Oral Glucose Tolerance (OGTT)
Most sensitive test
Random Blood Sugar : Increased
Alpha Glucosylated Hgb : Elevated
(Normal: <9 %)

Normal:
BUN = 10-20
mg/100ml
Creatinine = .8 1
mg/100ml
Hgb:

Hct:

Female = 12-14 gm %
Male = 14-16 gm%
Average = 42 %
Female = 36-42 %

Nsg Mgt:
- Same as DKA except dont give NaHCO3!
1. Can lead to coma assist mechanical ventilation
2. Administer .9NaCl isotonic solution, followed by .45NaCl hypotonic solution to counteract dehydration.
3.Monitor VS, I&O, blood sugar levels
4.Administer meds
a.) Insulin therapy IV
Regular Acting Insulin clear
b.) Antibiotic to prevent infection
Tx:
1. Give OHA
O ral
H ypoglycemic
A gents

Fx: Stimulates pancreas to secrete insulin

Classifications of OHA:

1.

1st Generation Sulfonylureas


Fx: Given to stimulate B-cell to secrete endogenous insulin
a. Chlorpropamide (Diabenase)
b. *Tolbutamide (Orinase)
c. Tolazamide (Tolinase)
d. *Acetonexamide (Dymelor)
e. Glibenclamide (Euglucon)
f. Gliclazide (Diamicron)
g. Glipizide (Minidiab)

2.

2nd Generation Sulfonylureas


a.
Diabeta (Micronase)
b.
Glipside (Glucotrol)

Monitor For:
GI upset
Headache
Paresthesia
Weakness
Tinnitus

C/I:
Pregnant Women
Surgery
Allergy
Infection
Stress
Kidney/liver damage
*Presence of any of
these even if pt. is
NIDDM insulin is
required

3. Biquanides
- Increase uptake of glucose by the cell but prolonged use may cause lactic acidosis
Ex. Metformin
Glucophage
Nsg Mgt or OHA:
1.
Administer with meals to lessen GIT irritation & prevent hypoglycemia
2.
Avoid alcohol (alcohol + OHA = severe hypoglycemic reaction) ---leads to antabuse (Disulfiram)
toxicity
Nsg Mgt For DM:
1. Monitor for PEAK action of OHA & insulin
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64

3.
4.

5.

Monitor VS, I&O, neurocheck, blood sugar levels.


Administer insulin & OHA therapy as ordered.
Monitor signs of hyperglycemia & hypoglycemia.
-Pt DM hinimatay
- You dont know if hypo or hyperglycemia - Give simple sugar
(Brain can tolerate high sugar, but brain cant tolerate low sugar!)
*Cold, clammy skin Hypoglycemia Orange Juice or simple sugar
*Warm to touch, dry Hyperglycemia Administer insulin

DIABETIC
DIET

6. Provide nutritional intake of Diabetic Diet:


7.

8.

-Or offer alternative food products or beverage.


CHO
=
-Lots of orange juice.
50%
Exercise after meals to promote increase glucose utilization
CHON =
- After strenuous exercise, glucose is already consumed even w/o insulin
Pre-breakfast insulin: For pt. who exercised alreadydecrease dose of insulin
Athletes: Take snacks in between exercise
Monitor complications of DM
a. Atherosclerosis HPN, MI, CVA
b. Can affect the small minute capillaries of eyes & kidney leading to : Microangiopathies (thickening)
c. Eyes Diabetic retinopathy , Premature cataract & blindness
d. Kidneys Recurrent pyelonephritis & Renal Failure
2 Major Cause of
e. Gangrene formation
Renal Failure
f. Peripheral Neuropathy
- Diarrhea/ Constipation
1. DM
- Sexual impotence (Complication of HPN & DM)
g. Shock

9. Foot Care Mgt d/t delayed wound healing especially of extremities


a.
b.
c.
d.
e.
f.
g.

Avoid waking barefooted


Cut toe nails straight
Apply lanolin lotion prevent skin breakdown
Avoid wearing constrictive garments
No Crossing of legs
Avoid local cold application in extremities
Never elevate legs on pillow to prevent tissue ischemia unless there are sx of leg edema

10. Encourage annual eye & kidney exam


11. Avoid smoking d/t vasoconstriction
12. Monitor urinalysis for presence of ketones or Blood or serum more accurate
13. Assist in surgical wound debridement
14. Monitor signs of DKA & HONKC
15. Assist surgical procedure: BKA or above knee amputation
D. DM ASSOCIATED WITH OTHER DISORDER
a.) Pancreatic tumor
b.) Cancer
c.) Cushings syndrome

3 Main Food Groups

Increase Fat Catabolism


Free Fatty Acids
Cholesterol

Ketones

Atherosclerosis
HPN
MI

DKA

Anabolism
Catabolism
1. CHON
Glucose
Glycogen
2. CHON Amino Acids
Nitrogen
3. FATS
Fatty Acid
Free
Fatty Acid
(Choles
terol & Ketones)

Coma
Death

Stroke

HEMATOLOGICAL SYSTEMS
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Overview:
I . BLOOD-FORMING ORGANS
1.Thymus removed myasthenia gravis
2. Liver largest gland (occupies most of the right hypochondriac region)
3. Lymph nodes
4. Lymphoid organs Payers Patches (located between the small intestine- site of salmonella thypi)
5. Bone marrow
6. Spleen
Ex.
Varicosities
Deep Vein Thromboplehbities

II. BLOOD VESSELS

1. Veins SVC, IVC, Jugular vein, superficial blood towards the heart
2. Artery deep seated, carries blood away from the

Ex.
Aneurysm
Buergers Disease
Raynauds Disease

- 2 largest artery : Aorta, carotid


3.

Capillaries

III. BLOOD
Blood
Formed Elements

45 %

55% Plasma & Serum

Cellular Components:

Plasma CHONs (Liver)

1. RBC (Erythrocytes)
- largest
(Normal: 4 6 M/mm3)

1. Albumin - largest, most abundant plasma

- Anucleated (no nucleus)


- Biconcave discs
- Has molecules of Hgb (red cell
pigment)
- Transports & carries O2
Hgb:
%
gms %

F = 12-14 gms
M = 14-16

Fx: Maintains osmotic pressure preventing


edema,
If decrease albumin- Ascites
Promotes skin integrity
2. Globulins
a. Alpha Transports steroids,
hormones & bilirubin
b.
- Transports iron & copper
c. Gamma Transport immunoglobulins
or antibodies
3. Prothrombin (CF2) Fibrinogen (CF1)

Hct : 3x Hgb
F = 36-42 %
M = 42-48 %

CLOTTING FACTOR 1-13


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CF 1 = Fibrinogen

From

CF 2 = Prothombin

Pakistan

CF 3 = Thrombin

To

CF 4 = Ca #

China

CF 5/6 = Proaccelerin - Labile factor

People

CF 7 = Procenvertion - Stable Factor

Power

CF 8 = Anti- HFA

Against

CF 9 = Christmas Factor/ Anti-hemophilia

Communism

CF 10 = Stuart-Prower

Start

CF 11 = Plasma Thromboplastin

Peace

CF 12 = Hageman

Hate

CF 13 = Fibrin Stabilizing Factor

Fire

COAGULATION PATHWAY/CASCADE
Intrinsic Factor

Extrinsic Factor

Stage 1

EF TF
CF 12

TF (CF3)
CF 9

CF 11
CF 9--------------------------------------------------CF 10 ------------------------------------------ CFS
Creates------Prothrombinase----------------- CF 2
Product of Stage 1

Stage 2

Thrombin
Stage 3
CF 1
Fibrin
Clot -------- --Clot dissolved
Tissue Plasminogen Activator
Plasminogen
Plasmin

Stage 4

I. DISORDERS OF THE BLOOD


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Pathophysiology:
BLOOD DYSCRASIA

Production of blood cells


(PANCYTOPENIA)

Production of both normal


& defective cells

Spleen Disorder

Defect in Coagulation
Mechanism

Life span of
RBC
8-120 days
1. ANEMIA
- A condition in which the hemoglobin concentration is lower than normal
- Results from :
1.
2.
3.
4.

Pathophysiology:

Decreased Erythropoiesis (Formation-maturation process of RBC)


Increased Hemolysis
Bone Marrow Depression
Blood loss
1st Sign of
ANEMIA:

Hgb Count
Reduction in the O2 carrying capacity of the blood
TISSUE HYPOXIA

Brain Restlessness
Headache, Irritability
Syncope, Vertigo

Heart
Anginal Pain
PR

Respiratory
RR
Dyspnea

Fatigability
Palpitation

D/T compensation
of the body

Hallmark & Basis of


Anemia
All symptoms cause

GIT
Anorexia
Angular Cheilosis

Skin
Mucus Membrane

Lesions at the
corner of the
mouth

D/T decreased
Hgb that gives
color to skin
KOILONYCHIA
d/t atrophy of
epidermal cells
D/T decreased
RBC

Pallor
Brittle nails & hair
(Spoon-shaped nails)

Intolerance to Cold

Normal shape of nails = Biconcave & 180


Substances Needed For Maturation Of RBC:
CAUSES:
Created by Nia E. Tubio

1. CHON
formation of all
tructure/membrane
2. Iron/Fe
- formation of
pigment hemoglobin
3. Vit. B 12
- responsible for synthesis of
nucleic acid
4. Folic Acid - matures the cell

68

I. DECREASED ERYTHROPOIESIS
Production maturation of RBC
Absence of any one of the factors
For RBC maturation will cause
Type I:
A. IRON DEFECIENCY ANEMIA

- Cells are microcytic (small) & hypochronic d/t inadequate absorption of iron leading to hypoxemic injury
HYPOCHROMIC ANEMIA HYPOPROLIFERATIVE ANEMIA
Pathophysiology: The body stores of iron decrease, leading to depletion of hemoglobin synthesis
Incidence Rate:
1. Common in developed country d/t high cereal intake & accidents
2. Common in tropical countries blood sucking insects
3. Women 15 45 y/o of reproductive yrs
4. Common among the poor d/t poor nutritional intake
Predisposing Factors:

1. Chronic blood loss- most common cause


a. Trauma
b. Menstruation
c. GIT bleeding
2.

Inadequate intake of food rich in iron

3.

Inadequate absorption or iron d/t :


a. Chronic diarrhea (Metabolic Acidosis)
b. Malabsorption syndrome (Celiac Disease)
c. High cereal intake with low animal CHON ingestion
d. Subtotal gastrectomy
4. Improper cooking of food/ Alcoholism

Common:
Suicide - common in teenager
Poisoning common in children
(aspirin)
Aspiration common in infant
Accidents common in adults
Choking common in toddler
SIDS common in infant in US
Bleeding:
Hematemesis vomiting of
blood
Melena
passage of
dark stool
- Bleeding in
Upper GIT
- Doudenal
Cancer
Decreased
O2
Atrophy of
cells

S/Sx:
1.

Asymptomatic

2. General body malaise


3. All Sx of Anemia + PICA
+

Cerebral
Hypoxia
abnormal appetite or craving for non-edible food Ex. Chalk

PLUMMER VINSONS SYNDROME

Atropic Glossitis inflammation of tongue


Stomatitis mouth sores
Dysphagia

Dx :
1.
2.
3.
4.
5.
6.
7.

RBC
Hgb
Reticulocyte
Hct
Iron
Ferritin
Bone Marrow Aspiration = Most Definitive

Nsg Dx:
Activity
Intolerance

Tx:
1. Blood Transfusion = Packed RBC
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Nsg Mgt:
IRON-RICH
FOOD:
1ST: organ meat,
liver
2nd: eggyolk
3rd: raisins, legumes
dried fruits
nuts

1. Monitor signs of bleeding of all hematologic test including urine, stool & GIT
2.
3.

4.
5.

Complete bed rest dont overtire pt


Encourage iron rich food
Instruct the pt to avoid taking tea (Tannates - impairs iron absorption)
Administer meds: Hematinic Agents or drugs that will increase blood heme
a.) Oral iron preparation
Ferrous SO4
Fe gluconate
300 mg OD
Fe Fumarate
Fortifier
Fergon, Feorol, Iberet
*Liquid Preparations: W/ brassy taste, disguise by chilling

Nsg Mgt Of Oral Iron Medication:

1. Administer w/ meals to lessen GIT irritation/or 0ne hours before meals


2. If diluting in iron liquid prep administer w/ straw
3.
4.

Give Orange juice for absorption


Monitor & inform pts S/E

5. If pt cant tolerate oral iron preparation

IRON Side-Effects:
Anorexia
N/V
Abdominal Pain
Diarrhea/ Constipation
Melena

Administer parenteral iron preparation


1. Iron dextran (IV, IM)
2. Sorbitex (IM only)
3. Inferon, Jectofer
Nsg Mgt Parenteral Iron Preparation:

1. Administer using Z tract method to prevent discomfort, discoloration leakage to tissues.


2.
3.

Dont massage injection site. Ambulate to facilitate absorption.


Monitor S/E:
a.) Pain at injury site
b.) Localized abscess (nana)
c.) Lymphadenopathy
d.) Fever/ chills
e.) Urticaria itchiness
f.) If (+) to Hypotension ------------Anaphylactic shock
Give epinephrine (SNS Effect)

B. FOLATE DEFICIENCY ANEMIA


- Cell is macrocytic, hypochromic anemia
- A form of MEGALOBLASTIC ANEMIA
- Anemias characterized by abnormal large RBC 2nd to impaired DNA synthesis d/t deficiency of Folic acid
Pathophysiology:
Folic acid impaired DNA synthesis in the bone marrow impaired RBC development, impaired nuclear
maturation but cytoplasmic maturation continues large size
Causative Factors:
1. Alcoholism
2. Mal-absorption
3. Diet deficient in uncooked vegetables
Sx: All symptoms of Anemia
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C. PERNICIOUS ANEMIA
- A megaloblastic chronic anemia characterized by deficiency of intrinsic factor secreted by the parietal cells
leading to Hypochlorhydria---------decrease Hcl acid secretion
- A Vit. B12 deficiency
Predisposing Factors:
1. Subtotal Gastrectomy partial removal of the stomach
2. Atrophy of gastric mucosa (elderly) ------ # 1 cause
3. Hereditary
4. Inflammatory disorder of ileum
5. Autoimmune
6. Strict vegetarian diet
7. Gastrointestinal malabsorption----Crohns Disease/ Cancer of stomach

Pathophysiology:

Largest part of GIT = Large


Intestine
Widest part of GIT = Stomach

STOMACH (composed of different cells)


Parietal or ergentaffen Oxyntic cells

Function: Produce Intrinsic Factor

Function: Secrets Hcl acid

INTRINSIC FACTOR
Binds w/ Vit. B12 to promote absorption
For maturation of RBC

HYDROCHLORIC ACID
Aids in digestion
Decreased Digestion ----- Dyspepsia & Weight Loss

Disorder in the Process


Diet: High caloric Intake to correct Wt loss
Immature RBC
Killed by Spleen
Heme----Globin
Ferroes------------Ferretin = Bilirubin ----- Jaundice
S/Sx:
1.
2.

3.

All Sx of Anemia +
GIT changes
a. RED BEEFY TONGUE = PATHOGNOMONIC SIGN
b. Dyspepsia indigestion
c. Wt loss, mild diarrhea
d. Jaundice
CNS Most dangerous anemia d/t neurologic involvement d/t deficiency in Vit. B 12
a. Tingling sensation
b. Paresthesia (numbness) in extremities
c. (+) Rombergs test = Ataxia
d. Psychosis

Dx:

Tx:

1. Peripheral Blood Smear = shows giant RBCs, WBCs w/ giant hypersegmented nuclei
2. Very High MCV
3. Shillings Test = reveals inadequate absorption of Vit. B 12
4. Intrinsic Factor Antibody Test
Common Route: Dorsogluteal
1. Vit. Supplementation : Folic Acid 1 mg daily
Ventro2. Diet Supplementation

3. Lifetime monthly injection of IM Vit. B 12 as ordered -----not oral---pt. may developed drug toleranceNo S/E
Nsg Mgt :
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1.

Enforce CBR

2. Diet high calorie or CHO----Increase CHON, iron & Vit C


3. Avoid irritating mouthwashes. Use of soft bristled toothbrush is encourage
4.

Avoid applying electric heating pads can lead to burns


II. INCREASE HEMOLYSIS/ HEMOLYTIC ANEMIA
- Destruction of RBC greater than the rate of formation
----all + Hyperbilirubinemia-----JAUNDICE + TEA-COLORED URINE
Causes:
1.
2.
3.

Post-viral injection
Exposure to ionizing radiation
Prolong use of toxic drugs & medications (penicillin, chloramphenicol)

Type II:
A. SICKLE CELL ANEMIA
- A severe chronic incurable hemolytic anemia that results from heritance of the sickle hemoglobin gene.
Causative Factor:
1. Genetic inheritance of the sickle gene- HbS gene
Pathophysiology:
Decreased O2, Cold, Vasoconstriction can precipitate sickling process
Factors cause defective Hgb to acquire a rigid, crystal-like C-shaped configuration
Sickled RBCs adhere to endothelium pile up & plug the vessels ischemia results pain, swelling & fever
Sx:
1. Jaundice
2. Enlarged skull & facial bones
3. Tachycardia, murmurs & cardiomegaly
Primary sites of thrombotic occlusion: spleen, lungs & CNS
4. Chest pain, dyspnea
Complications:
1. Sickle Cell Crises = Results from tissue hypoxia & necrosis
2. Acute Chest Syndrome = Manifested by a rapidly falling Hgb level, tachycardia, fever & chest infiltrates in the CXR
Tx:
1. Bone marrow transplant
2. Hydroxyurea = Increases the Hgb
3. Long term RBC transfusion = Packed RBC
Surgery For Hemolytic anemia = Spleenectomy
Nsg Mngt:
3 Nursing Priority:
1. Manage the pain
Support & elevate acutely inflamed joint
1. A/W Avoid deoxygenating
Relaxation techniques
activities
Analgesics
2. Prevent and manage infection
- High altitude is bad
Monitor status of patient
2. Fluid Deficit Promote
Initiate prompt antibiotic therapy
hydration
3. Promote coping skills
3. Pain & Comfort
Provide accurate information
Allow patient to verbalize her concerns about medication, prognosis & future pregnancy
4. Monitor and prevent potential complications
Provide always adequate hydration
Avoid cold, temperature that may cause vasoconstriction
5. Monitor and prevent potential complications
Leg ulcer
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Aseptic technique
Priapism = Sudden painful erection
Instruct patient to empty bladder, then take a warm bath
B. POLYCYTHEMIA
- Refers to an INCREASE volume of RBCs -----reverse of sickle cell anemia
- The hematocrit is ELEVATED to more than 55%

Classified as Primary or Secondary

1. POLYCYTHEMIA VERA
- Primary Polycythemia
- A proliferative disorder in which the myeloid stem cells become uncontrolled

Causative Factor: Unknown

Pathophysiology:
The stem cells grow uncontrollably
The bone marrow becomes HYPERcellular & all the blood cells are increased in number
The spleen resumes its function of hematopoiesis and enlarges
Blood becomes thick & viscous causing sluggish circulation
Overtime, the bone marrow becomes fibrotic
Sx:
1. Skin is ruddy
2. Splenomegaly
3. Dizziness, blurred vision, HA
5. Angina, dyspnea & thrombophlebitis
Dx:
1. CBC- shows elevated RBC mass
2. Normal oxygen saturation
3 Elevated WBC & Platelets

POLYCYTHEMIA
Earliest Sign : Headache
Late Sign: Pruritus
Complication: Stroke,
Thrombosis

Complications:
1. Increased risk for thrombophlebitis, CVA MI
2. Bleeding d/t dysfunctional blood cells
Tx:
1. To reduce the high blood cell mass- PHLEBOTOMY
2. Allopurinol
3. Dipyridamole
4. Chemotherapy to suppress bone marrow
Nsg Mngt:
1. Primary role of the nurse is EDUCATOR
2. Regularly assess for the development of complications
3. Assist in weekly phlebotomy
4. Advise to avoid alcohol & aspirin
5. Advise tepid sponge bath or cool water to manage pruritus
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III. BONE MARROW DEPRESSION/ HYPOPLASTIC ANEMIA


- Inadequate abnormal cells-------Hypoplastic anemia/Aplastic Anemia
- All Sx + decreased WBC --------------Leukopenia ----------risk for infection
+ decreased PLATELETS--- Thrombocytopenia----- bleeding

when all 3 are present ----- PANCYTOPENIA

WBC
(Leucocytes 5,000 10,000/mm3)
GRANULOCYTES
3 Types:
1. Polymorphonuclearneutrophils (PMNs)
- Most abundant 60-70% WBC
- Lifespan of 24-48 hrs.
Function: Short-term Phagocytosis
For acute inflammation
2. Polymorphous Basophils (PMBa)
-Involved in Parasitic infection
- Release of chemical mediator for inflammation
(Serotonin, Histamine, Prostaglandin, Bradykinins)
-Absorbs large fat particles after ingestion of high fat meal

NON-GRANULOCYTES
A. Monocytes (Macrophage)
-Largest WBC
- Involved in long term phagocytosis
- For chronic inflammation
- Other name macrophage
Macrophage in CNS- Microglia
Macrophage in skin Histiocytes
Macrophage in lungs Alveolar macrophage
Macrophage in Kidneys Kupffer cells
B. Lymphocytes
3 Types:

3. Polymorphous Eosinophils (PMEo)


- Involved in Allergic reactions
HIV
Window Period:
6 months
Incubation:
6 months to 5
yrs.
Sx:
Kaposi Sarcoma
Dx Test:
Western
Blot Test
Drug of Choice:
Zidovudine ( AZT or
SIGNS OF PLATELET
DYFUNCTION
1. Petecchiae
2. Ecchymosis/bruises

1. B Cell L
Bone marrow or bursa dependent
- Arises from bone marrow
2. T Cell
Devt of immunity
- From thymus
- Target cell of HIV
3. NK Cell
Natural killer cell
-Have both antiviral & anti-tumor properties
C. Platelets (Thrombocytes)
(Normal: 150,000 450, 000/ mm3)
- Promotes homeostasis prevention of blood loss by
activating clotting
- Consists of immature or baby platelets known as
Megakaryocytes Target of Dengue Virus
-

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Normal lifespan 9 12 days

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A. APLASTIC ANEMIA
A condition characterized by decreased number of RBC as well as WBC & platelets
- Common among clients undergoing chemotherapy, Cobalt therapy, Radiation therapy
- Stem cell disorder d/t bone marrow depression leading to pancytopenia all RBC are decreased
Decrease RBC
Anemia

Decrease WBC
Leucopenia

Decrease platelets
Thrombocytopenia

Susceptibility to infection
Fever

Petechia
(Purpura)

No clotting
Bleeding

Ecchymosis

Bruising

Predisposing Factors :

1.

Environmental Toxins & Chemicals Pesticides, Benzene & its derivatives


2.
radiation
3.
Immunologic injury
4. Certain drugs causes bone marrow depression
a. Chemotherapeutic agents, = Methotrexate, Nitrogen Mustard (anti-metabolite), Vincristine
b. Broad Spectrum antibiotic =Chlorampenicol, Sulfonamides bactrim
(Pt severe isolation)
c. Phenybutazones
5. Heavy Metals
Pathophysiology:
Toxins cause a direct bone marrow depression acellular bone marrow decreased production of blood elements
Sx:
1. All Sx of Anemia +
2. Leucopenia increase susceptibility to infection
3. Thrombocytopenia
4. Splenomegaly
5. Retinal hemorrhages
Dx:
1. CBC- decreased blood cell numbers
2. Bone marrow aspiration at posterior iliac crest: Confirms the anemia- hypoplastic or acellular marrow replaced by fats
Fatty streaks in bone marrow
Tx:
Bone Marrow Transplantation
1. Bone Marrow Transplantation
1.
Syngeneic
BMT
2. Immunosuppressant drugs

donor
from twins
3. Rarely, steroids
2. Allogenic BMT
4. Blood transfusion = Fresh Whole blood
Related or unrelated as
Nsg Mgt:
long
1. Removal of underlying cause
as compatible (Human
2. Blood transfusion as ordered
leukocyte antigen)
3. CBR
3. Autologous BMT
4. O2 inhalation
Own self
5. Reverse isolation d/t leukopenia
- harvest marrow during
6. Monitor signs of infection
7. Avoid SQ, IM or any venipuncture site
8. Use electric razor when shaving to prevent bleeding
9. Administer meds:
Immunosuppressant
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Anti lymphocyte globulin (Alg) given via central venous catheter, 6 days 3 weeks to achieve max therapeutic effect of
drug.
IV. BLOOD LOSS
- Cells are normocytic (normal size), normochronic (normal content) but d/t surgery, menstruation------anemia
- All Sx + Hypovolemia
- Blood Transfusion = Fresh Whole blood
OTHER BLOOD RELATED PROBLEMS
1. DISSEMINATED INTRAVASCULAR COAGULATION (DIC)
- Acute hemorrhagic syndrome characterized by wide spread bleeding & thrombosis d/t a deficiency of clotting
factors (Prothrombin & Fibrinogen).
Predisposing Factor:

1. Rapid BT d/t hemolysis


2.
3.
4.

5.
6.
7.
8.

Massive trauma
Massive burns
Septicemia
R/T Hemolytic reaction & Anaphylaxis
Neoplasia new growth of new tissue (tumor)
Pregnancy
Septicemia

S/Sx:
1.
2.
3.
4.
5.

6.

Petechiae widespread & systemic (lungs, lower & upper trunk)


Ecchymosis widespread
Oozing of blood from venipunctured site
Hemoptysis cough blood
Hemorrhage
Oliguria---------------LATE SIGN

Dx :
1.
2.
3.
4.

CBC reveals decrease platelets


Stool for occult blood (+)
Specimen stool
Opthalmoscopic exam sub retinal hemorrhage
ABG analysis metabolic acidosis

Nsg Mgt:

1. Monitor signs of bleeding All hematologic test + urine, stool, GIT


2.
3.

4.

Administer isotonic fluid solution


Administer O2 inhalation
Administer meds:

a.

Vit K aquamephyton

b. Pitressin or vasopressin -----t o conserve H20 & has vasoconstriction effect----Most Common S/E: Chest Pain
5.

NGT lavage
- Use iced saline lavage 1st to induce vasoconstriction inside the stomach

6. Monitor NGT output


7. Provide heplock
8. Prevent complication: Hypovolemic shock----Early Sign: Restlessness & Cool moist Skin
Late Sign of hypovolemic shock : Anuria
9. Give Heparin-----short-acting
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DIAGNOSTIC TEST FOR BLOOD DYSCRASIAS


1. CBC, Hgb, Hct
2. BT, CT, PT
3. ERYTHROCYTE INDEX
MCV = Mean Corpuscolar Volume -----to evaluate size of RBC
MCH = Mean corpuscular Hgb -----------to evaluate the Hgb content of RBC
MCHC = Mean corpuscular Hgb Concentrationto evaluate Hgb content of Pack RBC (in grams /100ml)
(Normal: 30-36 grams/100ml)

4. COOMBS TEST

RBC
Normal Size: 80-94 cu micron
< 80 ---- Microcytic Cell
ANISOCYTOSIS
> 94 ----- Macrocytic Cell
(abnormal size)

- To evaluate the presence of immune bodies that adheres to


RBC causing hemolysis/agglutinization of RBC
(Rh Incompatibility, ABO Incompatibility)

Normal Hgb content of RBC: 22-28


micromicrogram
< 22
5. SCHILLING TEST
- To evaluate rate of absorption of Vit. B12 (Cyanocobalamine)
- Use to diagnosed Pernicious Anemia
Procedure: Administer P.O. radioactive Vit. B12 ------24 hr. urine
Check (+) (-) of Vit. B12 ------ if (-) Pernicious Anemia (do not give P.O. give parenterally)
------ if (+) in urine ---normal
Common in Pts. Who undergone gastrectomy/ cancer----they do not have intrinsic factor

6. BONE MARROW ASPIRATION/PUNCTURE/TAP


POIKILOCYTOSIS = abnormality in shape
of RBC
METARUBRICYTE = abnormal RBC w/

- To evaluate size, shape, character of RBC cells


- Invasive (consent)
- Local anesthesia (lidocaine 1-2%)
- Sites: Sternum
------ Position: Supine
A & P Iliac Crest ------ Position: Supine (A) & Prone/Lateral (P)
- Pediatric pts. --- use the long bones (femur, humerus)-----as we grow older the # of marrows in long bones decreases
- Apply pressure dressing over site to prevent bleeding

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7. LYMPH NODE BIOPSY


- Site : Cervical LN, Axilla LN, Inguinal LN

IV. BLOOD TRANSFUSION:


Objectives:
1.
2.
3.
4.

To replace circulating blood volume


To increase O2 carrying capacity of blood
To combat infection if theres decrease WBC
To prevent bleeding if theres platelet deficiency

Packed RBC = 250


ml
Refrigerated = 3-5
days

Nsg Mgt & Principles in Blood Transfusion


1.

2.

3.

Proper refrigeration
Proper typing & cross matching
Type O universal donor
AB universal recipient
85% of people are RH (+)
Aseptically assemble all materials needed:
a.) Filter set
b.) Isotonic or PNSS or .9NaClfor flushing to prevent Hemolysis
Hypotonic solution Cell swells or burst
Hypertonic solution Cell will shrink or crenate
c.) Needle gauge 18 - 19 or large bore needle to prevent hemolysis.
d.) Instruct another RN to recheck the following .
Pts name, blood typing & cross typing expiration date, serial number Most important
e.) Check blood unit for bubbles, cloudiness, dark in color & sediments indicates bacterial contamination.
Return to blood bank, do not dispose
f.) Never warm blood products may destroy vital factors in blood.
- Warming is done if with warming device only in EMERGENCY!
- Within 30 mins room temp only!
g.) Blood transfusion should be completed < 4hrs because blood that is exposed at room temp for > 2h causes blood
deterioration------can lead to bacterial contamination
h.) Avoid mixing or administering drug at BT line leads to hemolysis
i.) Regulate BT 10 12 gtts/min KVO or 100cc/hr to prevent circulatory overload
j.) Monitor VS before, during & after BT especially q15 mins for 1st hour
- Majority of BT reaction occurs within 1h.

BLOOD TRANSFUSION REACTIONS:


BT REACTIONS:
1. HEMOLYTIC REACTION
Sx:
Headache
Dizziness
Dyspnea
Palpitation
Lumbar/Sternal flank pain
Hypotension, Flushed Skin---red port wine urine

H
A
P
C
A
T
C
H
expired

Hemolytic Reaction
Allergic Reaction
Pyrogenic Reaction
Circulatory Reaction
Air Embolism
Thrombocytopenia
Citrate Intoxication
Hyperkalemia d/t
blood

Nsg Mgt:
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1. Stop BT
2. Notify Doc
3. Flush with plain NSS
4. Administer isotonic fluid sol to prevent acute tubular necrosis & counteract shock
5. Send blood unit to blood bank for reexamination
6. Obtain urine & blood samples of pt & send to lab for reexamination
7. Monitor VS & Allergic Rxn
2. ALLERGIC REACTION
S/Sx:
1.
2.
3.
4.
5.

Fever/ chills
Urticaria/ pruritus
Dyspnea
Laryngospasm/ bronchospasm
Bronchial wheezing

Nsg Mgt:
1.
2.
3.
4.

Stop BT
Notify Doc
Flush with PNSS
Administer antihistamine diphenhydramine Hcl (Benadryl)
If (+) Hypotension anaphylactic shock administer epinephrine
5. Send blood unit to blood bank
6. Obtain urine & blood samples send to lab
7. Monitor VS & IO
8. Adm. Antihistamine as ordered for Allergic Rxn, if (+) to hypotension indicates anaphylactic shock
Shock -----administer epinephrine
9. Administer antipyretic & antibiotic for pyrogenic Rxn & TSB

3. PYROGENIC REACTION:
S/Sx:

a.) Fever/ chills


b.) Headache
c.) Dyspnea

d.) Tachycardia
e.) Palpitations
f.) Diaphoresis
(Pyrogens -----fever-producing agents)

Nsg Mgt:
1.
2.
3.
4.
5.
6.
7.
8.

Stop BT
Notify Doc
Flush with PNSS
Administer antipyretics, antibiotics
Send blood unit to blood bank
Obtain urine & blood samples send to lab
Monitor VS & IO
Tepid sponge bath offer hypothermic blanket

4. CIRCULATORY OVERLOAD
Sx:
-

Dyspnea

Created by Nia E. Tubio

PRIORITY CASES
Hemolytic Reaction = 1st
d/t Hypotension---attend to
destruction of Hgb
------ O2----- Brain Damage
Circulatory Reaction = 2nd
Allergic Reaction
= 3rd
Pyrogenic Reaction = 4th
But:
Anaphylactic
= 1st priority
Hemolytic
= 2nd

79

Orthopnea
Rales or crackles
Exertional discomfort

Nsg Mgt:
1.
2.
3.

Stop BT
Notify Doc
Administer diuretics

ONCOLOGIC NURSING
Oncology study of neoplasia new growth
Benign (tumor)

Malignancy (cancer)

Well differentiated
Encapulation (+)
Metastasis (-)
Prognosis good
Surgery

Poorly or undifferentiated
(-)
(+)
Poor prognosis
1. Chemotherapy Many S/E
2. Radiation
3. Surgery
most preferred treatment
4. Bone marrow transplant - Leukemia only

Predisposing Factors: (Carcinogenesis)


G genetic factors
I immunologic factors
V viral factors
a. Human Papiloma Virus causing warts
b. Epstein Barr Virus
E environmental Factors 90%
a. Physical irradiation, UV rays, nuclear explosion, chronic irritation, direct trauma
b. Chemical factors
- Food additives (nitrates
- Hydrocarbon vesicants, alkalies
Warning / Danger Sx of CANCER
- Drugs (stillbestrol)
- Urethane
C change in bowel /bladder habits
- Hormones
A a sore that doesnt heal
- Smoking
U unusual bleeding/ Discharge
Male:
st
T thickening of lump breast or
1 Lung Cancer Bronchogenic d/t smoking
nd
elsewhere
2 Liver Cancer Hepatic d/t alcohol
rd
I indigestion/Dysphagia
3 Prostate cancer 40 y/o & above (middle age & above)
th
O obvious change in wart/ mole
4 Testicular Cancer 30 y/o
N nagging cough/ hoarseness
BPH 50 & above
U unexplained anemia
A - anemia
Female:
S sudden wt loss
1st Breast Cancer 40 yrs old & up
Mammography 15 20 mins (SBE 7 days after mens)
2nd Cervical Cancer 90% Multi-sexual partners
5% Early Pregnancy
3 LS
TRIAD
3rd Ovarian Cancer common to squamous cell type
Sx
4th Uterine Cancer

CLASSES OF CANCER:

Large
Lump
Loaded

Tissue Typing:
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1.

Carcinoma arises from surface epithelium & glandular tissues

2.

Sarcoma- from connective tissue or bones

3.

Multiple myeloma from bone marrow


Pathological fracture of ribs & back pain

4. Lymphoma from lymph glands


5. Leukemia from blood
1. LEUKEMIA
-

Cancer of the WBC

Pathology:

Uncontrolled abnormal proliferation ---------------immature WBC known as Blast Cells


activity of cell
Proliferation of BLAST CELLS

cellular metabolism
prone to infection

Invade/Infiltrate vital organs


Spleen
Spleenomegaly

Liver
Hepatomegaly

Temperature

Crowd/ Congest/Accumulate

Kidney

Brain

RF

ICP

Joint Pain, Swell


Hinder/Prevent Production of Cells
RBC

Platelets

CLASSIFICATION:

1. ACUTE LEUKEMIA

ONSET

DURATION

CELLS

Sudden

Short < 6 months

Immature blast cells

2. CHRONIC LEUKEMIA
Gradual
long duration
- Characterized by periods of remission (absence) & exacerbation (recurrence)

Mature WBC

PREDOMINANT CELLS PRESENT IN BLOOD:


1. Acute/Chronic Lymphocytic Leukemia =
2. Acute/ Chronic Myelocytic Leukemia =

Lymphocytes &

monocytes ---- ALL (common to children)

myeloblasts ----- CML (common to Adult)

Cells Derived
1. Bone Marrow
Granulocyte
Created by Nia E. Tubio

Agranulocyte

2. Lymphoid Tissue
Agranulocyte
81

Immature

immature

immature

Myeloblast

Monoblast

mature

Myelocyctes

Monocyte

Lymphocyte

2. BREAST CANCER
Predisposing Factors:
1. Family Hx (mother/sister)
2. Obesity
3. Unmarried at age 40 y/o
4. Married w/o children
5. Married w/ children but did not breastfeed
6. Women w/ prolonged menstruation
7. Early menarche at 11 y/o
8. Late menopause at 52 y/o
9. 1st pregnancy at age 35 y/o
Prevention:

SBE

Early Sign of Breast Ca:


Non-tender
Non-mobile
Painless breast
mass/lump

= 7-10 days after menstruation


= after menopause----- 1x/month
Late Sign of Breast Ca:

Sx:
1. Dimpling of skin
2. Orange skin
3. Asymmetry of breast
4. Discharges of nipple
Dx:
1. Mammography
2. Breast Biopsy = Best confirmatory Dx
Tx:

MASTOIDYNA = breast
pain

Common Site Of Breast Ca


UPPER OUTER QUADRANT
LEFT

1. Surgery:
Lumpectomy
Modified Mastectomy mass, tissue, pectoralis major or minor at axillary
Radical Mastectomy - leave either pectoralis major or minor muscle

3. ONCOLOGIC EMERGENCIES
Obstructive or Compressive Disorders
Superior vena cava syndrome
Pericardial effusion/cardiac tamponade
Leukostasis
Spinal Cord Compression
Metabolic Disorders
Hypercalcemia
Symptoms of SIADH
Tumor lysis syndrome

PROGNOSIS
Lung = 6 yrs
Breast = 2-6 yrs.
Colon = 2-6 yrs.
Pancreatic = 3-6 months
Liver = 3 mnths

3. Disruptions of hematologic/im-munologic function


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DIC
Septic shock

3. BRAIN TUMOR
Location:
1. Supratentorial Cerebrum, anterior 2/3 of the brain
2. Infratentorial Cerebellum, brainstem, posterior 1/3 of the brain
*Both will manifest Increased ICP

Early Sign of Brain Tumor:


PAPILLEDEMA
(tumor compress on optic
chiasm)

Both will undergo Brain Surgery:


a. CRANIOTOMY/CRANIECTOMY
- Use general endotracheal anesthesia (For all brain surgery)
If surgery lasts for more than 2 hrs, assured of patent airway
- Type of incision: Coronal or Butterfly
- Skin Preparation: Shaving of head done at stage 3 of anesthesia
Nursing Management:
DONTS POST-OPERATIVE:
1. Do not put client on Trendelenberg position---- it will increase ICP & abdominal content will compress stomach
2. If pt. in shock: Supine w/ pillow, head turned to one side
3. If pt. not in shock: Supratentorial---- elevate head 45 degrees (SF) ---- to promote venous return to heart
Infratentorial ---- elevate head 10-15 degrees ------ to prevent compression of brain stem
--- turn head to one side, unoperated side especially if bone flap not returned
--- allowed on affected side but not more than 20 minutes to prevent ischemia
4. Do not give narcotic agent/analgesic
No Demerol------ respiratory depressant
5. No suctioning---- mere suction will trigger coughing----- Increased ICP
--- If needed: Oropharyngeal suctioning only
--- Nasal suctioning will damaged nasal mucosa---leakage of CSF
6. Do not restrain client
-- Makes client agitated --- Increased ICP
7. No rectal tube, rectal movement or manual extraction of feces.
-- Vagal stimulation------Bradycardia
Treatment Modality:
1. Radiotherapy

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Therapeutic Modality:
1. CHEMOTHERAPY
Use various chemotherapeutic agents that kills cancer cells & kills normal rapidly producing cells GIT, bone
marrow, and hair follicle.
Classification of Cytotoxic Agents:
Cell-Cycle Non-specific
1. Alkylating Agents

Classification of Cytotoxic Agents:


Cell-Cycle Specific
1. Antimetabolite
(S phase)

Action:
Binds w/ DNA & prevents cell replication
Nitrogen Mustard
Cyclophosphamide (Cytoxan)
Chlorambucil (Leukeran)
Nitrosureas
Carmustine
Lomustine
Alkylating-like agents
Busulfan (Myeleran)
Carboplatin
Cisplatin (Platinol)* common
Thiotepa
Ifex (Ifosfamide)
2. Antitumor/Anti-Neoplastics Antibiotics
Action: Inhibits cell division by interfering
w/ synthesis of nucleic acid
Bleomycin
Doxorubicin
Dactinomycin
Mitomycin
Idarubicin
Adriamycine (Doxorubicin)
Mithramycin
Plimcamycin
Actinomycin

Action: Foster cell death by


interfering w/ the cellular metabolic
process
Cytarabine (Cytosar/Ara C)
5-fluorouracil (5-FU)
Hydroxyurea
6-mercaptopurine
(Purinethol)
Methotrexate (Mexate)

2. Vinca/Plant Alkaloids
(M phase)
Action: Mitotic Inhibitors
Docetaxel
Etoposide (Toposar)
Vinblastine (Velban,Velbie)
Vincristine (Oncovin)

Classification of Cytotoxic Agents


1. Hormones & Steroids
Action:
Reduces cellular metabolism by
providing a non-favorable
environment for growth of Ca cells
Estrogens
DES (Post-menopausal)
(Diethylstibestrol)
Ethinyl estridiol
Antiestrogens
Tamoxifen
Raloxifene
Others
Aminogluthetimide
Asparaginase
Leuprolide
Mitotane
Androgens (Pre-menopausal)
Fluoxymesterone
Testosterone Propionate
Halotestin
Antiandrogens
Bicalutamide
Flutamide
Progestins
Medroxyprogesterone
Megestrol acetate

Side-Effects:

PROTOCOL IN THERAPY

1. GIT - -Nausea & Vomiting

6 cycle of Chemotherapy
Interval of 28 days

Nsg Mgt:
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1.

Administer anti-emetic (Plasil) 4 6h before start of chemotherapy


Ex.
Ondansetrone Zofran
Alprazolan - Zanax
2. Withhold food/ fluid before start of chemo
3. Provide bland diet post chemotherapy: Avoid spic foods---irritants
Ex. Non irritating / non spicy
4. Avoid bulky course diet
5. Advise Neutropenic Diet : Avoid raw foods, raw vegetable
- Diarrhea
1. Administer anti diarrhea 4 6h before start of chemo
2. Monitor urine, I&O qh
- Stomatitis/ Mouth Sores

Doxorubicin
-Toxic to myocardium
- Do not give if client is not
hooked up to a cardiac
monitor

1. Oral care offer ice chips/ popsickles


Use alkalanizer for mouth sores
2. Inform patient that 10-15 days after chemotherapy there will be hair loss Temporary Alopecia
- Loss from other hair of the body
- Hair will grow back after 4 6 months post chemo.
-Bone Marrow Depression --------Leukopenia/Anemia
1. Enforce CBR
2. O2 inhalation
3. Reverse isolation
4. Monitor signs of bleeding
5. Inform pt. it will last only for 21 days
2. Reproductive Organ Sterility
1.

Do sperm banking before start of chemo

3. Renal System Increase uric acid


1.

Administer allopurinol/ xyloprin (gout)


Fx: Inhibits uric acid
Acute gout colchicines
Increase secretion of uric acid

3. Neurological Changes peristalsis paralytic ileus


Most feared complication following any abdominal surgery
Vincristine plant alkaloid causes peripheral neuropathy
Mngt:
1. Cancer drugs can be very potent------- it can destroy normal cells
2. Protect yourself from Ca drugs that can destroy the skin: cover everything
3. Increase fluid intake post-chemo d/t drugs are hepato-toxic
4. Avoid exposure of Ca drugs to light----reduces the potency of the drug---cover w/ carbon paper, dim lights
REVERSE ISOLATION TECHNIQUE
1. Private room, laminar air flow (positive pressure room)
2. Sterile linen, sterile hygiene equipment
3. Dedicated equipment
4. Put on shoe covers, mask & cap, sterile gown & gloves.
5. Low bacteria diet: no fresh fruits & vegetables; avoid drinking water allowed to stand for more than 15 min.
6. No fresh flowers or potted plants
7. Institute prophylactic oral hygiene regimen before, within 30 minutes after each meal & q2Hq4H during waking hours
8. May use tsp salt, pinch of baking soda & 8 oz. of H2O or saline
9. Avoid alcohol- or glycerine-based mouthwash
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10. Use softbristled toothbrush


11. Use foam stick moistened with mouthwash to remove debris from mucosa
12. May apply topical anesthetic, as prescribed
13. Encourage fluid intake of 2000 ml/day
14. Encourage bland diet high in CHON to promote healing.
Avoid hard or spicy food
Avoid citrus juices
15. If patient has difficulty in eating & maintaining fluid intake, parenteral nutrition may be necessary
16. Assess the need for use of antifungal or antibacterial agents
2. RADIATION THERAPY
Involves use of ionizing radiation that kills cancer cells & inhibit their growth & kill rapidly producing cells.
Types of Energy Emitted:

1. Alpha rays
2. Beta rays
3. Gamma ray

rarely used doesnt penetrate skin tissues


internal radiation more penetration
external radiation penetrates deeper underlying tissues

2 Methods of Delivery:

1. External Radiation

- Involves electro magnetic waves


Ex. Cobalt Therapy, Teletherapy, External Beam Radiation

Nursing Responsibility:
a.

Explain that it is a painless procedure

b. During procedure: Pencil Markings on skin indicating area to be radiated


c.
d.
e.
f.
g.
h.

Tell pt. not to erase markings & cleanse area only w/ H2O. No soap. Pat dry.
Avoid sunlight over site
Avoid pressure over the site
Avoid hot/cold application over site
Avoid use of oil cream solution/lotion to prevent skin reaction
Observed for S/S of RADIATION SICKNESS

Locally Manifested
- Erythema
- Dryness of skin
- Loss of skin hair
- Blister formation
- Skin desquamation

2. Internal Radiation

Systematically
- Leukopeniabone marrow
- Sterility---- Gonadsboth sensitive to radiation

Injection/ implantation of radioisotopes proximal to CA site for a specific period of time.


- Form of wire, seed, needle
- Isotope inside clients body

Administering ISOTOPE:
a. Implant or Intracavitary Implantation
- Insert isotope into body cavity
- Radium seed/Radom seed (sealed)
b. Brachytherapy
- Intralesion/ intratumor
- Cesium 135 (sealed)
c. P.O.
- RAI 135, RAI 131 (unsealed liquid)
d. Intra-arterial Perfusion
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- RA Gold 198 (liver cancer)


- RA Phosphorus (bone cancer)
2 Types:
a. Sealed Implant

Radioisotope with a container & doesnt contaminate body fluid.


Ex. Radium Seed, Radom Seed, Cesium 135

b. Unsealed Implant

Radioisotope without a container & contaminates body fluid.


- Liquid given either P.O. or Intra-arterial
Ex. Phosphorus 32, RAI, RA

Nursing Responsibility:
1. Isolate patient.
2. Offer diversional therapy
3. Post at door radiation sign
4. Separate set of utensils
5. articles not needed in room should be removed
6. In Unsealed: All excreta, vomitus are considered contaminated. Throw directly to toilet bowl
7. Observe for Time:
Longer exposure means more radiation
Not more than 5 minutes/exposure, 30 minutes/shift
Distance: 3-8 ft. from site
Shielding: Stay at the farthest part/ use lead apron
8. Prevent accidental dislodgement of the radium:
Place on CBR
NO bed pan, insert indwelling catheter
Give diet constipation: Decreased fiber & roughage
Once dislodge, pick-up w/ long forcep, put in lead container
9. Use scanner, Geiger counter to detect remaining traces of radiation
10. Tell partner to resume sex, once edema has subsided
11. Tell pt. if dysuria & burning in urination: SUSPECT URETHRAL ATHROPHY
Meatus, Urinary bladder---- CYSTITIS, HEMATURIA
3 Factors Affecting Exposure:
a. Half life
b. Distance
c. Time
d. Shielding

Time period required for half of radioisotopes to decay.


- At end of half life less exposure
The farther the distance lesser exposure
The shorter the time, the lesser exposure
Rays can be shielded or blocked by using rubber gloves & gamma use thick lead on concrete.

S/E & Mgt:


a.) Skin errythema, redness, sloughing

1. Assist in bathing pt
2.
3.
4.

Force fluid 2,000 3,000 ml/day


Avoid lotion or talcum powder skin irritation
Apply cornstarch or olive oil

b.) GIT Nausea / Vomiting /

Stomatitis

1. Administer antiemetic 4 6h before start of chemo - Plasil


2 Withhold food/ fluid before start of chemo
3. Provide bland diet post chemo
Non irritating / non spicy
Dysglusia decrease taste sensitivity
-When atrophy papilla (taste buds) 40 y/o
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c.) Bone Marrow Depression


1.
2.
3.
4.

Enforce CBR
O2 inhalation
Reverse isolation
Monitor signs of bleeding

CARDIOVASCULAR SYSTEM
OVERVIEW:
HEART:
-

Muscular, pumping organ of the body


Occupies most of the Left mediastinum
Weigh 300 400 grams
Microscopic
Resembles a closed fist
Covered by a serous membrane Pericardium
2 Parts

Parietal layer

Pericardial Space
Fluid prevent Friction rub

Cardio Physiology:
The main functions of this
system are:
To transport oxygen,
hormones & nutrients to
the tissues
To transport waste
products
to the

Visceral layer

CONSISTS OF 3 LAYERS:

1. Epicardium
2. Myocardium
3. Endocardium

Outermost - ( Essential, coronary arteries arelocated here) --------- M.I. & AP


Inner Responsible for pumping action/ Most dangerous layer -- Cardiogenic shock & RHD
Innermost layer Connected to Tunica Intica ------------------------ Endocarditis

2 CHAMBERS:

1. Upper Collecting/ Receiving chamber - Atria


2. Lower Pumping/ Contracting chamber Ventricles

VALVES & HEART SOUNDS:

1. Atrioventricular Valves - Tricuspid & Mitral Valve


Closure of AV valves gives rise to 1st heart sound or S1 or lub

2. Semi-lunar Valve Pulmonic & Aortic


Closure of semilunar valve gives rise to 2nd heart sound or

S2 or dub

Extra heart Sound:

S3 d/t Increased Ventricular Filling -Ventricular Gallop

Left CHF, Left ventricular hypertrophy

S4 d/t Forceful Atrial Contraction - Atrial Gallop

MI, HPN, Pulmonic Stenosis, Aging

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CORONARY ARTERIES:
The Blood supply of the heart comes from the Coronary arteries
a. Right coronary artery
b. Left coronary artery
Both supply the myocardium with blood
1.Arises from the base of the aorta : RMCA & LMCA
CONDUCTION SYSTEM OF THE HEART:
1.

Sino atrial node (SA node) (or Keith-Flock node)


Location: Junction of SVC & Right Atrium
Function: Primary pace maker of heart
Initiates electric impulse of 60 100 bpm

2. Atrioventicular Node (AV node or Tawara node)


Location: Inter atrial septum
Delay of electric impulse to allow ventricular filling of 0.8 milliseconds
Slowest conduction
3.

Bundle of His
Location: Interventricular septum
Branches out into: Rt main Bundle Branch & Lt main Bundle Branch

4.

Purkenjie Fiber
Location: Walls of ventricles-- Ventricular contractions
Fastest conduction

Physiology
The intrinsic conduction system causes the heart muscle to depolarize in one direction
The rate of depolarization is around 75 beats per minute (60-100/min)
The SA node sets the pace of the conduction
This electrical activity is recorded by the Electrocardiogram (ECG)
Sympathetic system INCREASES HR
Parasympathetic system (Vagus) DECREASES HR
ANATOMY OF THE HEART

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SA node

AV

Septum
Purkenjie Fibers

Bundle of His

BLOOD SUPPLY:
Amount of blood the heart pumps out in each beat
Stroke Vol.

X HR/min

Cardiac Output

(Normal C.O: 4-6 L/min)

Total Peripheral Resistance

= Blood Pressure

Factors in Cardiac Output:


1. Systole
2. Diastole

- Contraction
- Relaxation

The PRELOAD refers to the amount of blood contained in the ventricle at the end of a diastole.
Degree of stretching of the heart muscle when it is filled-up with blood
(reduced with hypovolemia)
The AFTERLOAD force that LV has to exert in order to pump blood to the aorta.
The resistance to which the heart must pump to eject the blood
(increased with HPN)
Control is neural (central & peripheral) & hormonal
Baroreceptors in the carotid & aorta
Hormones- ADH, Adrenergic hormones, Aldosterone & ANF
ADH increases water retention
Aldosterone increases sodium retention & water retention secondarily
Epinephrine & NE increase HR & BP
ANF= causes sodium excretion
The vascular system consists of the arteries, veins & capillaries
The arteries are vessels that carry blood away from the heart to the periphery
The veins are the vessels that carry blood to the heart
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The capillaries are lined with squamos cells, they connect the veins & arteries
The lymphatic system also is part of the vascular system & the function of this system is to collect the extravagated fluid from the
tissues & returns it to the blood
IRREGULARITIES:
1. Complete Heart Block Insertion of pacemaker at Bundle Branch
Metal Pace Maker change q3 5 y/o
2. ECG Tracings
Prolonged PR
ST segment Depression
ST elevated
T wave inversion
Widening QRS

Atrial Fibrillation
Angina Pectoris
MI
MI
Arrhythmia

3. Coronary Artery Disease


Atherosclerosis
Angina Pectoris
MI

Myocardial Injury
Myocardial Ischemia
- Myocardial Necrosis

DISORDERS OF THE HEART


I. CORONARY ARTERY DISEASE/ ISCHEMIC HEART DISEASE
Results from the focal narrowing of the large & medium-sized coronary arteries d/t deposition of atheromatous plaque in the
vessel wall
If 50% of the left coronary arterial lumen is reduced or 75% of the other coronary artery, becomes significant
Pathophysiology:
Fatty streak formation in the vascular intima
T-cells & monocytes ingest lipids in the area of deposition
Potential
For:
Thrombosis
Embolism

Atherosclerosis
Narrowed arterial lumen
Reduced coronary blood flow

With Coronary occlusion

Without Coronary Occlusion

Myocardial Ischemia ( 8-10 seconds : Anginal Pain)


Chest Pain

Myocardial Necrosis
Akinesia/Dyskinesia of the myocardium

SAVERS

*DECREASED CARDIAC OUTPUT

S sudden onset
(myocardial &
anginal)

CARDIOGENIC SHOCK

A anterior or
substernal

Renal Damage
(Acute Renal Failure)

V vague
Created
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discomfort

E exercise

PULMONARY EDEMA
Right Ventricular
Hypertrophy
91

Electrical Failure

Right Ventricular
Hypertrophy

Rales
Cough
Hemoptysis
Orthopnea
Excertional
dyspnea
Easy
fatigability

Dysrrythmia
Ventricular Fibrillation
Sudden Heart Arrest

Sx of Right
CHF

Pitting Edema

Weight Gain

Ascites

Hepatomegaly

(+) Hepato-Jugular Reflux

Dyskinesia
- difficult
contraction of
the
myocardium
Akinesia
-temporary

1. ATHEROSCLEROSIS
ATHEROSCLEROSIS
- Narrowing of artery d/t fat/ lipid deposits
at tunica intima.

Sx of Left CHF

ARTEROSCLEROSIS
- Hardening of artery d/t calcium & CHON
deposits at tunica media.

Predisposing Factor:
1. Sex male
2. Black race
3. Hyperlipidemia - Genetic
4. Smoking
5. HPN
6. DM
7. Oral contraceptive/Steroids - prolonged use
8. Sedentary lifestyle
9. Obesity >20 % of Body weight
10. Hypothyroidism

LAYERS OF THE ARTERY


TUNICA ADVENTITIA outer
TUNICA INTIMA
innermost
TUNICA MEDIA
- middle

Sx:
1.
2.
3.
4.
5.

Chest pain
Dyspnea
Tachycardia
Palpitations
Diaphoresis

Tx:
1. PTCA
2. CABG
(Refer to MI for management)

2. ANGINA PECTORIS
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A clinical syndrome characterized by paroxysmal chest pain d/t temporary myocardial ischemia usually relieved by
REST or NGT nitroglycerin
Reversible, no dead cells yet
Chest pain resulting from coronary atherosclerosis or myocardial ischemia (tissue ischemia)

3 COMMON TYPES OF ANGINA


1. Stable Angina
- The typical angina that occurs during exertion
- Relieved by rest and drugs & the severity does not change
- < 15 minutes
2. Unstable Angina

Variant Angina
smoking
Angina Decubitus
when lying-down

From
pain

-Occurs unpredictably during exertion & emotion


- Severity increases with time & pain may not be relieved by rest & drug
- Mimics M.I.
3. Variant angina
- Prinzmetal angina, results from coronary artery VASOSPASMS
- May occur at rest
Pathophysiology:
STERLING LAW = the greater the myocardium fiber stretch
= the greater the pressure on contraction
For Myocardium to survive: Supply = Demand
If < then it will suffer ISCHEMIA
If blood supply decreased or 8-10 seconds (partially occluded)
Suffer Ischemia
CHEST PAIN (Anginal Pain)
If more than 30 minutes, the heart cannot withstand
Myocardial Infarction/Necrosis
CHEST PAIN
Angina Pectoris:
Predisposing Factor:

1.
2.
3.
4.
5.
6.

7.
8.
9.
10.

Sex male
Black raise
Hyperlipidemia
Smoking
HPN
DM
Oral contraceptive prolonged
Sedentary lifestyle
Obesity
Hypothyroidism

Created by Nia E. Tubio

Precipitating Factors:

4 Es

1. Excessive physical exertion


2. Exposure to cold environment
(vasoconstriction)
3. Extreme emotional response
Angina
4. Sx:
Excessive intake of foods high in
S sudden onset
1st: Levines Sx: hand clutching chest
A anterior or substernal pain
Type: sharp, stabbing, excruciating pain
Radiates to back, shoulders, axilla,
arms & jaw muscles
V vague discomfort
E exercise will intensify the pain
R rest
Relieved by rest or NGT

93

Sx:
Others:
1. Dyspnea
2. Tachycardia
3. Palpitation
6. Diaphoresis
Dx:
1.History taking & PE
2. ECG ST segment depression
3. Stress test treadmill = abnormal ECG
4. Serum cholesterol & uric acid - increase.
5. Cardiac Catherization

If chest pain does not


radiate:
Cause: Pulmonary

Nsg Mngt: To decrease Myocardial Demand


1. Administer prescribed medications
Nitrates- to dilate the venous vessels decreasing venous return and to some extent dilate the coronary arteries
NTG small doses Venodilator (sublingual)
Large dose vasodilator
1st dose NTG give 3 5 min
2nd dose NTG 3 5 min
Given 3x at 3-5 minutes interval
3rd & last dose 3 5 min
Still painful after 3rd dose notify doc. MI!
Exercise:
55 yrs old with chest pain:
1st question to ask pt: what did you do before you had chest pain.
2nd question: does pain radiate? If radiate heart in nature. If not radiate pulmonary origin
Venodilator veins of lower ext increase venous pooling lead to decrease venous return.
Nsg Mgt For NGT:
1.

Keep in a dry place. Avoid moisture & heat, may inactivate the drug.

2.

Monitor S/E:
Vasodilation
Orthostatic hypotension
Transient headache
Dizziness

3.

Rise slowly from sitting position

4.

Assist in ambulation.

5.

If giving NTG via Patch:

a. Avoid placing it near hairy areas-will decrease drug absorption


b. Avoid rotating transdermal patches- will decrease drug absorption
c. Avoid placing near microwave oven or during defibrillation-will burn pt d/t aluminum foil in patch
(color: blue & white)
Aspirin- to prevent thrombus formation
Beta-blockers- to reduce BP & HR (Propanolol)
Calcium-channel blockers- to dilate coronary artery & reduce vasospasm
ACE inhibitors Captopril
Ca antagonist Nefedipine (anti-hypertensive)
2. Teach the patient management of anginal attacks
Advise patient to stop all activities
Created by Nia E. Tubio

Nursing Diagnoses For


Angina Pectoris:
Decreased cardiac output
Altered comfort
Impaired gas exchange
Activity intolerance
Anxiety

94

3. Enforce CBR
4. Administer O2 inhalation
5. Semi-fowler
6. Diet- Decrease Na & saturated fats, low caffeine
7. Monitor VS, I&O, ECG
8. HT:
Discharge Planning:
a.
b.

c.
d.

Avoid precipitating factors 4 Es


Prevent complications MI
Instruct client to take meds before physical exertion-to achieve maximum therapeutic effect of drug
Importance of follow-up care.

3. MYOCARDIAL INFARCTION (MI)

Anatomy:

A terminal stage of CAD characterized by necrosis & scarring leading to permanent mal-occlusion

Coronary Artery
1.
2.

Right CA ---supply blood------ RA, RV, Posterior Wall


Left CA

i.
j.

Anterior Descending LCA --- supply--- RV, LV, Septum, Anterior Wall
Circumflex LCA -------------- supply --- LA, LV, Lateral Wall

2 Blood vessels supplying ventricles------ventricles receive higher blood than atria


LV needs more blood to pump to pulmonary circulation
RV pump blood to systemic
Ex. If occlusion is in Circumflex LCA-------affected LA, LV so basis of nursing DX----- systemic Circumflex----

CO2

TYPES OF MI:
1. Clot RCA

Zone
RA, RV
Posterior Wall

ECG
Inferior Wall MI
Posterior Wall MI

2. Anterior Descending LCA

RV, LV

Anterior Wall MI

3. Circumflex LCA

Septum
LA
LV lateral wall

Antero-Septal MI
Lateral Wall MI

TYPES OF MI BY LAYERS:
1. Sub-endocardial MI
2. Myocardial Infarction
3. Trasmural MI

Mal-occlusion of either R & L coronary artery, Ischemia of the inner part


muscle layer affected: most common
Most dangerous MI Mal-occlusion of both R&L coronary artery, Involves all layers

PATHOLOGY OF CHEST PAIN IN MI & Sx:


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Myocardial Ischemia

Anaerobic Metabolism

reverse effect if occluded (KREBs CYCLE)

causes
Increased BP Vasodilation

Metabolite will release enzyme


LACTIC ACID

Alters conduction of electrical impulses


Dysrrythmia
Weakness:

PR or

Irritate sensory nerve endings


PR

CHEST PAIN

Ensuing inflammatory process


Causes release of increased neutrophils (1st cells to migrate when inflammation occurs)
LEUKOCYTOSIS
LOW GRADE FEVER (38 degree C) lasts for 3-5 days---best indicator for monitoring of MI
progression or healing
If responding to treatment & N.I.
Neutrophils will be replaced by fibroblastic cells----result to scarring/fibrolysis---- the healing process---- Normal Temperature
MYOCARDIAL INFARCTION
Predisposing
Factors
Sex male
Black raise
Hyperlipidemia
Smoking
HPN
DM
Oral
contraceptive
Sedentary
lifestyle
Obesity
Hypothyroidism

S/Sx

Dx Exam

1. CHEST PAIN

1. Cardiac Enzymes
Go to blood following cardiac death

S sudden onset of pain

a. CPK MB Creatinine Phosphokinase

A anterior/substernal/precordial
area
Excruciating, vice like, visceral
pain
Radiates back, arm, shoulders,
axilla, jaw

b. LDH lactic acid dehydrogenase

via afferent nerve cells


pain

w/ referred epigastric

V vague discomfort
Feeling of tightness or heavy
chest
E exercise increases pain
R rest does not relieved the pain
or by NGT
2. Dyspnea
3. Erthermia
4. Initial increase in BP
5. Mild restlessness &
apprehensions
6. Cool, moist, ashen skin

c. SGPT (ALT)
Serum Glutamic Pyruvate Transaminase
d. SGOT (AST) Serum Glutamic Oxaloacetic
2. Troponin test increase
3. ECG Tracing ST segment elevation,
Widening of QRS complexes means
arrhythmia in MI indicating PVC
4. Serum Cholesterol & Uric acid
5. CBC increase WBC

Myocardial Infarction
Nursing Diagnoses
Pain (Altered comfort)
Decreased cardiac output
Impaired gas exchange
Activity intolerance
Altered tissue perfusion

7. Occasional findings
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a. Split S1 & S2
b. Pericardial friction rub
(inspiration)
c. Rales /crackles
d. S4 (atrial gallop)

*Most critical period after Dx of MI 6-8 hrs. d/t arrhythmia, a type of PVC premature ventricular contraction.
COMPLICATIONS:
(Refer to Pathophysiology of Atherosclerosis)

1. Cardiogenic Shock d/t poor contraction/akinesia .


2.

Renal Failure decreased CO2----decreased renal failure---renal ischemia----cessationRF

3. Ventricular Fibrillation--- heart beat very irregular, erratic & very rapid 180 bpm
4.

5.
6.
7.
8.

9.
10.

Pulmonary Edema
Right Ventricular Hypertrophy
Left-sided HF
Late Sx of Cardiogenic
Right-sided HF
Shock In MI
Thrombophlebitis DVT
Oliguria
Arrhythmias PVC
Dresslers Syndrome post MI syndrome
- Non-resistant to Pharmacological agents
-Administer 150,000 450,000 units of streptokinase

Management of Myocardial Infarction:


1. Increase Myocardial O2 supply
- Administer O2 inhalation (low-flow)
- Also to prevent extension of necrosis
- Monitor VS, I&O & ECG tracings
2. Relieve pt. of chest pain
- Give drug of choice: Narcotic Analgesic
Morphine SO4 ------ Action: Decreased preload & afterload through vasodilation
Decrease level of anxiety
Relieves severe intensity of pain
Longer sustained effect
If not available: Demerol but S/E: Hypotension
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3. Relieve pt. of anginal pain


- *Give NITRITES or NITRATES
Action: Relax smooth muscles of the coronary artery/ also as vasodilators
Ex.

a. Isosorbade (Isordil)
b. Isosorbide Mononitirite (Indur)
c. NGT (Nitroglycerine)
5 mg SL
Ex. Nitrostatic
10 mg - P.O.
Patch, cream Topical Ex> Nitral Patch, Transderm

Nsg. Mgnt For Nitroglycerine:


1. Explain that drug may cause S/E :
Throbbing headache
Flushing of skin
Warm sensation & stringing, biting
Burning sensation under tongue if taken SL

*continue taking the drug s/s will


disappear w/ the continued
medication

2. S/E : Postural hypotension d/t vasodilation


Give drugs while on bed or in a sitting position
3. Keep drug in dark, opaque container because exposure to light/sun will reduce potency of nitrates
4. If topical administration: Cleanse area w/ H2O only, Avoid hairy areas, rotate administration
Place on precardium: 5th ICS or site of pain
5. If SL : Advise pt. to place under tongue, allow to dissolve, swallow saliva
NEVER follow it w/ H2O (interrupt sustained effect)
6. Keep away from your own skin, causes vasodilation & headache
4. R - rest
- To decrease cardiac workload
- To decrease work for breathing
- To decrease myocardial O2 demand
- To increase cardiac reserve
- Enforce CBR without BRP
- Provide Bedside commode
- Abstain from sexual activity (4-6 wks. After MI attack)
- Take nitrate prior to sex & if w/ insomnia, chest pain, SOB-----seek medical advice
- Avoid valsalva maneuver
- Semi fowler
- Resume ADL activity
- Post-cardiac rehab:
1.)Sex as an appetizer rather then dessert
Before meals not after, after meals increase metabolism heart is pumping hard after meals.
2.) Assume a non-weight bearing position.
*When to resume sex/ act: When pt can already use staircase, then he can resume sex.
5. D diet
- To decreased caloric intake in order to decrease cardiac load
- General liquid to soft diet
- Low in Na 2-4 grams/day to get rid of ECF fluid excess
- Avoid food high in saturated fat & avoid gas-forming foods
- Avoid drugs w/ high Na like laxative
- Avoid cardiac stimulant (caffeine, colas)
- Increase fiber intake to avoid constipation
- Avoid too hot drinks ------abdominal distention----- SOB
- Avoid too cold drinks------ vagal stimulation-------- Decreased PR (Bradycardia)
- Take 20 30 ml/week wine, brandy/whisky to induce vasodilation

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6. D- diuretic
- To prevent reabsorption of H20 by the renal tubules-----absorption---Hypokalemia----Use K-sparing diuretics
Ex.
Aldactone
Spironolactone
Ex.

Furosemide (lasix)
Frusema
Diuret
Edecrine
Mercuhydrin

Sign that diuretic is effective?


*Absence of rales indicates (+)
effect of diuretics

7. D- digitalis
- Drug categorized as CARDIAC GLYCOSIDES
Ex.
Digitoxin, Digoxin, Lanoxin, Gdiranid

3-FOLD ACTION OF DIGITALIS


1. Strengthen myocardial contraction-----------(+) Inotropic Effect
Any drug that influences myocardial contraction has an inotropic effect
2. Increase cardiac output -------- Increase renal blood flow/renal perfusion
Increase urinary output (secondary effect: Diuretic)
3. Decrease Cardiac Rate --------- (-) Chronotropic Effect
Any drug that influences cardiac rate has a chronotropic effect (- or +)
Nursing Management in Giving Digitalis:

1. Check CR, if below 60 do not give drug


2.
3.

Monitor serum potassium d/t its secondary effect as a diuretic


Check for DIGITALIS Toxicity:
Anorexia-----------------most common complaint
Headache w/ N/V------ Early Sx of toxicity
Diarrhea
Photophobia
Dysrrythmia
Yellow spots in eyes
Gynecomastia
----- Late Sx of Toxicity
Antidote: DIGIBIND or DIGOXIN IMMUNE Fab ---------bind w/ lanoxin to decrease toxicity of lanoxin

8. If patient undergoes CARDIOGENIC SHOCK:


a. Prepare for vasopressor------

BP

Ex.

Dopamine
Intropine
Aramine --- Metaraminol Bitartrate
Levophed Levartenenol
Adrenalin /Epinephrine

b. Increase rate of impulse formation in SA node


Ex.
Lidocaine 1-2%
Pronestyl --------Procainamide HCI
Quinidine SO4 -- Quinidex
Brethylium ------blocks release of norepenephrine
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c. Dysrrythmia ----------- Give anti-arrhythmic drugs


Ex.
1. Lydocaine
blocks release of norepenephrine
2. Brithylium
S/E: Confusion & Agitation
If not corrected by medications:
- Install artificial pacemaker or when SA node is damaged
- Equipped with wire electrode & pulse generator
PACEMAKER
Type

Insertion

1. Temporary

Antecubital basilic vein

Wire/Electrode

Pulse Generator

Tip rest on RA or RV

Outside

2. Permanent:
Epicardial-------- thru Thoracotomy
RV
Endocardial-----Thoracotomy
RV
(5-6 yrs. )
Permanent SA so attach to chamber w/ thicker myocardium

Implanted in abdominal wall


Implanted subcutaneously
below the device
(subclavicular)

Nursing Management:
1.

Temporary:

2. Permanent:
Both:

Avoid toying w/ the pulse generator


Wrapped w/ rubber gloves
Avoid vigorous arm & shoulder movements
Avoid lifting heavy objects
Do not come closer to a microwave oven, cell site, electrical power
Or any apparatus emitting power voltage
Do not go through X-rays, scanner
Teach pt. how to monitor PR for 1 whole minute
S/S of malfunctioning pacemaker:
HICCUP
Bradycardia
Palpitation
Syncope

9. Prevent other complications. Give medications


a. Beta-blockers lol
1. Propanolol (inderal)
b. ACE inhibitors - pril
1. Captopril (enalapril)
c. Ca antagonist
1. Nifedipine
d. Anti platelet PASA (aspirin)
e. Thrombolitics or fibrinolytics to dissolve clots/ thrombus
S/E allergic reactions/ uticaria
Ex.
Created by Nia E. Tubio

1. Streptokinase--------most common
100

2. Urokinase ----------- S/E: Hypotension


3. Tissue Plasminogen Activating Factor (TPAF) ------- S/E: Chest Pain
Monitor for bleeding:
Anticoagulants
1. Heparin

2. Coumadin delayed reaction 2 3 days

PTT

PT

If prolonged bleeding

Prolonged bleeding

Antidote : Protamine Sulfate

Antidote Vit K

10. For patient w/ VENTRICULAR FIBRILLATION


a. Administer:
DEFIBRILLATION
To terminate a life-threatening dysrrythmia thru unsynchoronous application (anytime) at
any rate (200-360 joules)
CARDIOVERSION
- To correct dangerous dysrrythmia (sinus tachycardia) thru a synchronous application during
R wave w/ 50-200 joules
11. Relieve patient of Sx of PULMONARY EDEMA:
a.

Rotating Tourniquet/ Dry, bloodless Phlebotomy


- To reduce right atrial flow

Indicative of too tight


Tourniquet:
Absence of Peripheral

Nursing Management:

1. Only 3 extremities should be pressed at the same time


2. Tourniquet should not be applied too tight
3. Rotate tourniquet every 15 minutes
4. Rotate clockwise ---use BP cuff if not available (at Pulse pressure)
5. Remove at interval of 15 minutes
6. No single extremity should be compressed for more than 45 minutes
Cause VENOUS STASIS ----- stagnation of blood in 3 extremities
Decrease blood to enter RA----

pulmonary system---- blood will

edema

12. Treatment for patient with CORONARY ARTERY DISEASE:


1. Prepare for Revascularization Surgery to restore myocardial blood flow

a. PTCA
Done to pt with single occluded vessel/simple vessel
- Done under direct fluoroscopic guidance
- Indicated for Angina less than 1 year & coronary artery not calcified
Objective of PTCA:
Created by Nia E. Tubio

PTCA
P
percutaneou
s
T
transluminar
101

1. To revascularize the myocardium


2. To prevent angina
3. Increase survival rate
4. To compress plaque against vessel wall increasing arterial lumen
Procedure: Balloon-tipped catheter to/from femoral to CA to dilate CA or dislodge an atheroma/plaque
b. CABG
- For Multiple occluded vessels:
- Done to improve blood flow to myocardial tissue
- Uses saphinous vein/mammary artery
- Done on an open heart technique & jump-graft from lower extremities
Nsg Mgt Before CABG:
1. Deep breathing cough exercises
2. Use of incentive spirometer
3. Leg exercises
4. Cut at sigmoid process to umbilicus

CABAG
C coronary
A arterial
B bypass
G graft
surgery

Feared
Complications
2 Ps Pneumonia
Pulmonary

- Once thoracic is opened, change in normal pressure (-) intrapleural pressure


lungs will collapse
Prepare for 1 way or 3 way Chest drainage

13.

CHEST DRAINAGE
-Done to restore (-) intrapleural pressure of lungs to prevent collapse
a. One-way H20 Sealed Chest Drainage System
- Maintain an air-tight water-sealed system
To patient

Glass rod 2-3 cm.


Tip below H2O level
Created by Nia E. Tubio

Air vent, above H2O level


(Emerson/Steidmanns Pump)

H2O
102

b. 3-Way Chest Drainage


To suction
provides (-) pressure

To patient

H2O

Output Bottle

H2O

H2O

H2O Sealed Bottle

Vacuum

Controlled
Nursing Management For Chest Drainage:
1. The 3 bottles should be below chest level (18 inches) to prevent backflow
2. Bottles should be taped to the floor to prevent accidental leakage
3. Observe for OSCILLATION fluctuation, Tidalling---- rise & fall of H2O
Important that there is constant communication bet. thoracic cavity & output bottle
a. Observe for OSCILLATION
- Favorable
---- indicates that the lungs has re-expanded
Non-Favorable ---- Absence may mean:
Turn client side to side, if still (-) (To dislodge adhesion to wall)
Tell client to do deep breathing exercise, if still (-)
Stripping/Milking of the tube----an occlusion/clot will come out
b. Observe for BUBBLING
- Normal in vacuum bottle connected to suction machine
- If present in H2O sealed bottle----- indicates PLEURAL LEAKAGE/DAMAGE
- Measure output correctly. Put tape on bottle
- Change bottle when empty
- Do not clamp when changing bottle---- Tension Pneumothorax
- For accidental breakage: Immediately get a bottle w/ sterile H2O & immersed tube
If none available----clamp
- In any set-up: 1st bottle is always the output bottle
- Observe aseptic technique
- Removal:
Do not remove test tube during inhalation.
Inhale deeply then pull during expiratory phase to prevent entry of air & suction residual fluid
Apply petrolatum gauze dressing (non-porous dressing0
After removal, continue observing for S/S of hypoxia
4. CONGESTIVE HEART FAILURE
- Inability of the heart to pump blood towards systemic circulation d/t obstruction.
- Backflow
- A syndrome of congestion of both pulmonary & systemic circulation caused by inadequate cardiac function &
inadequate cardiac output to meet the metabolic demands of tissues
- Inability of the heart to pump sufficiently
- The heart is unable to maintain adequate circulation to meet the metabolic needs of the body
This can happen acutely or chronically
Acute as in Myocardial infarction
Chronic as in cardiomyopathies
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Classified according to the major ventricular dysfunction1.Left Ventricular failure


2. Right ventricular failure
Etiology of CHF
1. CAD
2. Valvular heart diseases
3. Hypertension
4. MI
5. Cardiomyopathy
6. Lung diseases
7. Post-partum
8. Pericarditis & cardiac tamponade
Systemic Circulation
*Inferior Vena Cava

&

Superior Vena cava

UnO2

RSHF
Blood goes back
to TV-circulation

Aorta

Right Atrium

Left Ventricles

Tricuspid Valve

Mitral Valve

Right Ventricles

Left Atrium

Pulmonary Artery

Lungs
(For Oxygenation)

A. RIGHT-SIDED HF
-#1 Cause: Tricuspid Valve Stenosis
S/S:
Jugular Vein Distention
Pitting Edema---IVC from toes
Ascites
Weight Gain
Hepatospleenomegaly
Jaundice
Pruritus---Urticaria
Esophageal Varices
Anorexia

LSHF blood goes


back to PV

Pulmonary Veins

B. LEFT-SIDED HF
-#1 Cause: Mitral Valve Stenosis
S/S:
Pulmonary Edema/ congestion
Dyspnea
Paroxysmal Nocturnal Dyspnea 2 pillows/High-fowlers
Orthopnea
Productive Cough (blood-tinged sputum)
Frothy Salivation
Rales/Crackles
Bronchial Wheezing
Pulsus Alterans (weak-strong pulse)
Anorexia & generalized body malaise
S3 (Ventricular Gallop)
Cyanosis
PMI is displaced laterally : 4th -5th ICSMCL
-----if below 5th ---cardiomegaly

1. LEFT-SIDED HEART FAILURE:


Predisposing Factors:
1. 90% Mitral Valve Stenosis d/t RHD, Aging
RHD affects mitral valve streptococcal infection
Dx:
1. ASO Titer (Anti-Streptolysine O) > 300 total units
- Steroids
- Penicillin
- Aspirin
Complication:
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RS-CHF
Aging degeneration / calcification of mitral valve
Ischemic heart disease
HPN, MI, Aortic stenosis
Dx:

1. CXR Reveals Cardiomegaly


2.
3.

PAP Pulmonary Arterial Pressure


PCWP Pulmonary Capillary Wedge Pressure
PAP
PCWP

Measures pressure of R ventricle. Indicates cardiac status.


Measures end systolic/ diastolic pressure

PAP & PCWP:


Swan Ganz Catheterization cardiac catheterization is done at bedside at ICU
(Tracheostomy bedside) - Done 5 20 mins scalpel & tracheostomy set
CVP Indicates fluid or hydration status
Increase CVP decrease flow rate of IV
Decrease CVP increase flow rate of IV
4.

Echocardiography Reveals enlarged heart chamber or cardiomayopathy

5.

ABG PCO2 increase, PO2 decrease = = hypoxemia = respiratory acidosis

Tx:
M

- Morphine SO4 (to induce vasodilation)

- Aminophylline

- Digoxin

- Diuretics

- O2

- Monitor Blood Gases ----------- PO2


Respiratory Acidosis
Hypoxemia
Cyanosis

2. RIGHT-SIDED HEART FAILURE


Predisposing Factor:

1. 90% - Tricuspid Stenosis


2.
3.
4.
5.

COPD
Pulmonary embolism
Pulmonic stenosis
Left sided heart failure

S/Sx:
Venous Congestion
- Neck or jugular vein distension
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Pitting edema
Ascites
Wt gain
Hepatomegaly/ Splenomegaly
Jaundice
Pruritus
Esophageal Varices----- Dilation of the veins of the esophagus
Anorexia, General body malaise, Nausea
Pulsus alternans
Nocturia = urination at night at frequent intervals as the blood moves from interstitial space to
the intravascular space & is excreted

Dx:

CXR Reveals Cardiomegaly


CVP Measures the pressure at R atrium
Normal: 4 to 10 cm of water
Increase CVP > 10 hypervolemia
Decrease CVP < 4 hypovolemia
Flat on bed post of pt when giving CVP
Position during CVP insertion Trendelenburg to prevent pulmonary embolism & promote ventricular
filling.

3. Echocardiography enlarged heart chamber / cardiomyopathy


4.Liver enzyme
SGPT ( ALT)
SGOT AST
Nsg mgt: Increase force of myocardial contraction = increase CO
3 6L of CO
1. Administer meds:
M morphine SO4 to induce vasodilatation
A aminophylline & decrease anxiety
D digitalis (digoxin)
D - diuretics
O - oxygen
G - gases
a.) Cardiac Glycosides
Increase myocardial
= increase CO
Digoxin (Lanoxin)
Antidote: digivine
Digitoxin: metabolizes in liver not in kidneys not given if with kidney failure.
b.) Loop diuretics: Lasix effect with in 10-15 min. Max = 6 hrs
c.) Bronchodilators: Aminophylline (Theophyllin). Avoid giving caffeine
d.) Narcotic analgesic: Morphine SO4 - induce vasodilator & decrease anxiety
e.) Vasodilators NTG
f.) Anti-arrhythmic Lidocaine
2. Administer O2 inhalation high! @ 3 -4L/min via nasal cannula
3. High Fowlers (2-3 pillows)
4. Restrict Na
5. Provide meticulous skin care
6. Weigh pt daily. Assess for pitting edema.
Measure abdominal girth daily & notify MD
7. Monitor V/S, I&O, breath sounds
8. Institute bloodless phlebotomy. Rotating tourniquet or BP cuff rotated clockwise q 15 mins = to promote decrease venous
return
9. Diet decrease salt, fats & caffeine
10. HT:
a) Prevent Complications :
Shock
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Arrhythmia
Thrombophlebitis
MI
Cor Pulmonale RT ventricular hypertrophy
b.) Dietary modifications
c.) Adherence to meds

CLASSIFICATION BASED ON New York Heart Association


Class 1
Ordinary physical activity does NOT cause chest pain & fatigue
No pulmonary congestion
Asymptomatic
NO limitation of ADLs
Class 2
SLIGHT limitation of ADLs
NO symptom at rest
Symptoms with INCREASED activity
Basilar crackles and S3
Class 3
Markedly limitation on ADLs
Comfortable at rest BUT symptoms present in LESS than ordinary activity
Class 4
SYMPTOMS are present at rest

OTHER PROBLEMS ASSOCIATED WITH THE CARDIOVASCULAR SYSTEM


1. CARDIAC TAMPONADE
- A condition where the heart is unable to pump blood d/T accumulation of fluid in the pericardial sac
(pericardial effusion)
- This condition restricts ventricular filling resulting to decreased cardiac output
- Acute tamponade happens when there is a sudden accumulation of more than 50 ml fluid in the pericardial sac
Causative Factors:
1. Cardiac trauma
2. Complication of Myocardial infarction
3. Pericarditis
4. Cancer metastasis
ASSESSMENT FINDINGS
1. BECKs Triad- Jugular vein distention, hypotension & distant/muffled heart sound
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2. Pulsus paradoxus
3. Increased CVP
4. Decreased cardiac output
5. Syncope
6. Anxiety
7. Dyspnea
8. Percussion- Flatness across the anterior chest

Laboratory FINDINGS
1. Echocardiogram= shows accumulate fluid in the pericardial sac
2. Chest X-ray
NURSING INTERVENTIONS
1. Assist in PERICARDIOCENTESIS
2. Administer IVF
3. Monitor ECG, urine output & BP
4. Monitor for recurrence of tamponade
Pericardiocentesis
Patient is monitored by ECG
Maintain emergency equipments
Elevate head of bed 45-60 degrees
Monitor for complications- coronary artery rupture, dysrhythmias, pleural laceration & myocardial trauma

2. CARDIOGENIC SHOCK
- Heart fails to pump adequately resulting to a decreased cardiac output and decreased tissue perfusion
- This shock occurs when the hearts ability to contract & to pump blood is impaired & the supply of oxygen is
inadequate for the heart & tissues
Risk factors: Coronary factor- Myocardial infarction
Risks factors: NON coronary:
Cardiomyopathies
Valvular damage
Cardiac tamponade
Dysrhythmias
Severe CHF

Pathophysiology:
Precipitating factors will cause decreased cardiac contractility Decreased stroke volume & cardiac output
leading to 3 things:
Damming up of blood in the pulmonary vein will cause pulmonary congestion
Decreased blood pressure will cause decreased systemic perfusion
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Decreased pressure causes decreased perfusion of the coronary arteries leading to weaker contractility of the heart
ASSESSMENT FINDINGS
1. HYPOTENSION
2. Oliguria (less than 30 ml/hour)
3. Tachycardia
4. Narrow pulse pressure
5. Weak peripheral pulses
6. Cold clammy skin
7. Changes in sensorium/LOC
8. Pulmonary congestion
LABORATORY FINDINGS
1. Increased CVP due to pooling of blood in the venous system
Normal is 4-10 cmH2O
2. Metabolic acidosis

NURSING INTERVENTIONS
1. Place patient in a modified Trendelenburg (shock ) position
2. Administer IVF, vasopressors and inotropics such as DOPAMINE and DOBUTAMINE
These drugs will increase cardiac contractility
3. Administer O2
4. Morphine is administered to decreased pulmonary congestion & to relieve pain, relieve anxiety
5. Assist in intubation, mechanical ventilation, PTCA, CABG, insertion of Swan-Ganz catherization & IABP
6. Monitor urinary output, BP & pulses
7. Cautiously administer diuretics & nitrates

DIAGNOSTIC PROCEDURES FOR CARDIOVASCULAR DISORDERS


1.

ECG/EKG
-Done To measure the electrical impulses of the heart to Dx heart rate & rhythm
Pathology:
SA node------starts myocardial contractions
Initiates electrical (+) impulses (emikts 60-100 bpm)
Goes into
Intra-atrial Track-------- A-V Node (located at right side of intra-atrial septum)
Bundle of His (L & R)
Purkinje Fibers
Ventricular Contraction

Created by Nia E. Tubio

If below 60---- Sinus Bradycardia


If above 100--- Sinus Tachycardia
If 60-100 ------ Normal Sinus Rhythm

109

DEPOLARIZATION is the myocardial contraction


REPOLARIZATION Refractory Period/relaxation regaining its (-) charge
Normal Refractory Period
0.15-0.30 seconds

SA NODE ----- located at posterior wall of RA close to the entrance to Vena Cava

During depolarization ---- permeable to entry of Na & Cal----- influencing myocardial contraction
During repolarization----- permeable to entry of K & Cl
P Wave Atrial depolarization or contraction
PR interval travel time of impulse from atria to ventricle ( Normal: 0.12-0.20 seconds)
Any delay in flow of impulse ------heart block

QRS Complex Ventricular Repolarization


(From ventricular contraction A---V to time it will be (+) charged
After a brief period of resting----- (-) charge refractory period

ST Segment - completion of depolarization & beginning if repolarization


T Wave ventricular repolarization
QT Interval entire duration of depolarization & repolarization ( lasts for 0.42-0.43 seconds)
(From QRS to T)

5 IMPORTANT ECG TRACINGS


1. MYOCARDIAL INFARCTION
- Inverted T wave
- Elevated ST
-Pathological prominent T wave

area of ischemia ---- reversible with time


area of infarction ----- irreversible, will always appear for life

2. HYPERKALEMIA
- Peaked T wave
- Prolonged PR Interval
- Widened QRS complex
3. HYPOKALEMIA
- Flat T wave
- Depressed ST
- Prominent U wave ----- Pathological--- influences myocardial repolarization
Decreased K ---- weakened contraction or repolarization
Prolonged T wave
Forming an abnormal U wave
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4. HYPERCALCEMIA
- Shortened QT interval
5. HYPOCALCEMIA
- Prologed QT interval
2. 24 HOUR HOLTER MONITORING/DYNAMIC ECG
- Done to monitor 24 hrs. cardiac activity
- Given pen & paper to record 24 hrs.
- Non-invasive
3. STRESS TEST/ THREADMILL TEST/BICYCLE/ERGOMETRIC TEST
- Done to evaluate amount of activities that the heart can tolerate
Nsg Responsibility:
- Avoid smoking the night before the threadmill
- Wear comfortable light material
- Wear rubber-soled shoes
- Avoid heavy meal prior to test
- Allowed light snack 2 hrs. before test
- Avoid hot shower 2 hrs. after test to prevent syncope
- Rest after the exercise
4. PHONO-ECHOCARDIOGRAPHY
- Non-invasive
- Use to detect any abnormal anatomical structure & abnormal heart sounds
5. ECHOCARDIOGRAPHY
- Use to evaluate changes in the cardiac dimension during the cardiac cycle
6. ELECTROLYTE STUDIES
- No NPO
- Na & Ca ------- Depolarization
- K & Cl ------- Repolarization
7. BLOOD TEST
- Use to evaluate atheromatous changes
Serum Cholesterol ------ NPO 6-8 hrs.
Serum Triglyceride ----- NPO 12 hrs
Serum Lipids
-------- NPO 12 hrs.
Nsg. Responsibility:
- No lipid forming drugs
Ex.
Salicylates
Estrogen
Steroids
No alcohol----- influence
8. ENZYMATIC TEST
- No NPO------ it is normally released by the myocardium---- if elevated enzymes----problem to the myocardium
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a. SGOT

(Serum Glutamic Oxaloacitic Aminotransferase)


or
AST (Serum Aspartate Aminotransferase)

b. SGPT (Serum Glutamic Pyruvic Transaminase)


or
ALT ( Serum Alanine Amintransfirase)

SGOT/AST : 5-40 u/L

SGPT/ALT : 4-36 u/L

c. CPK mb ( Creatinine Phosphokinase )


3 Isoenzymes
MB
Increases myocardial insult/damage

BB
Increased brain, bladder, bowel

MM
Increased skeletal muscle

d. SLDH (Serum Lactic Dehydrogenase)

1&2
Myocardial insult
*BEST CONFIRM MI

3
lung parenchymal damage

4&5
liver damage

-------- SGOT

* BEST DIAGNOSED MI -------- CPKmb


*Nsg Intervention prior to blood extraction ----- No IM injection------- Increased CPK when skeletal muscle injury
CARDIOVASCULAR ASSESSMENT
Assessment:
I. During Interview:
1. (+) Family History
2. Smoking
Pathology:
a.)

Nicotine -----stimulates release of Catecholamines--------------------------Epinephrine


Platelet
Aggregation

Increased Myocardial O2 demand

Vasoconstrictor

Increased cardiac workload

HPN

Risk for thrombus formation


Increased cardiac workload
b.) Carbon Monoxide ------ + Hgb (blood) ------interfere w/ O2 transport (carboxyhgb)
Tissue hypoxia/hypoxemia
3. Stress
4. DM------can lead to MI
5. Atherosclerosis
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6. HPN
7. Age ------- above 40 y/o
8. Sex ------- M: high risk
F: high risk after menopause
9. Personality ---- high among Type A individual
10. Assess for history of easy fatigability----- 1st sign of poor cardiac reserve
Ability of the heart to adjust to cardiac demand
11. History of Palpitations
2 Types:
a. Physiologic ------ diet (coffee), strenuous activity, strong emotion, after eating
b. Pathologic ------- clients w/ hyperthyroidism
clients w/ cardiomegaly ( enlarged heart)
contractions----hit cardiac wall----- palpitations
Palpitations---pounding, jumping sensations for every myocardial contractions
12. Listen for normal & abnormal sounds
S1 lubb ----systole
S2 dub ----- diastole
Abnormal:

Best heard at PMI ( Point of Maximum Impulse) on the 4th-5th ICSMCLL

S3 sound -----heard on early part of diastole------ Sign of Ventricular Dysfunction


Sign of Left Ventricular Hypertension
S4 sound ----- heard on late part of diastole------- Seen in MI, HPN, Pulmonic Stenosis
*S3 sound-----normal to children

Assess for audible sound: Murmur ------ audible vibration


Thrill --------- palpable vibration
Heave --------- visible vibration

Stenotic Valvular Opening/narrowing


Increased velocity of bloodflow
Abnormal vibrations

13. Lifestyle----- Diet ----- High in calories, saturated fats, Na & heart stimulant like caffeine, alcohol
---- ExerciseSedentary lifestyle----venous stasis---- Risk for thrombus formation
14. Assess for history of chest pain
15. Assess for Dyspnea & its cause
--- Positioning: Orthopnea
Time : Night (Paroxysmal Nocturnal Dyspnea)
16. Check for history of CYANOSIS
2 Types:
a. Central Cyanosis----- circum-oral (lips, oral mucus membrane)
Sign of decreased arterial O2 saturation

(Normal: 95-100%)

b. Peripheral Cyanosis---- cyanosis of nail beds, earlobes


Sign of decreased cardiac output
17. Assess for pitting edema:

a. Elevate 1st the legs w/ edema, if still (+)


b.

Press skin, if indentation is present = (+) Pitting Edema

18. Assess for HPN:


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Systole---- Atrio-ventricular contraction & closure of the A-V valves-----TV & BV


Strength of Myocardial contractions
Diastole Atrio-ventricular relaxation & closure of Semi-lunar valves---- PV & AV
More dangerous because it is systematic

Degree of systolic arterial resistance

TYPES OF HPN:
1. Systolic HPN & Diastolic HPN
2. Primary/Essential/Idiopathic
- Unknown cause
2 Theory:
a. R-A-A
Pathology:

Juxtaglomerular Cells (kidney)


Renin releases
Angiotensin I (activated by enzymes that converts it to)
Angiotensin II ------- stimulates adrenal cortex to release aldosterone

Potent vasoconstrictor

Fx: Fluid & Na retention & K excretion

HPN

Increased IV volume
Hypovolemic Shock

3. Secondary HPN
- Due to pregnancy related to toxemia
- Children w/ coarctation of the aorta
- Pheochromocytoma ( 5 H)
4. Accelerated HPN ----- persistent high BP with signs of retinal hemorrhages + epistaxis
5. Malignant HPN ----- persistent high BP with signs of papilledema (Increased ICP)

FLUIDS & ELECTROLYTES


1. WATER
Adult:
Child:

50-60% TBS
70-80% TBS

*Volume of Distribution Depends On:


1. Age - H2O decreases with age
2. Sex Male with more muscles so increase H2O
3. Adipose Tissues More Obese so more H2O
*Fluid Intake:

2 2.5 L/day 24 hrs.

Fluid:
Food

1 -1.5 L/24 hrs.


1 L/24 hrs.

By-product of oxidation-nitrogen process = 100 ml/24 hrs.


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*Avenues Of Losses/Routes:
1. Kidney
2. Skin
3. Lungs
4. GIT

= 1-1.5 L/24 hrs


= 600-700 ml/24 hrs
= 400-500 ml/24 hrs
= 100 ml/24 hrs

CELLS
Intracellular
Extravascular

BLOOD
ICF
ECF

= 2/3 of BF 70 %
= 1/3 of BF 30 %

Intravascular (blood, lymph vessels)


Intercellular ( interstitial space)

2. ELECTROLYTES

1. CATION (+) =

Sodium
Potassium
Calcium
Magnesium

Na
K
Cal
Mg

2. ANION (-)

Chloride
Phosphorus
Sulfate
Bicarbonate

Cl
PO4
SO4
HCO3

3.

=
=

K & PO4
Na & Cl

ICF
ECF

Homeostasis--- continuous shifting of fluids in Intravascular compartment

FLUID SHIFTING
1. IV-ITS-IV

(Normally exercised by circulatory blood)

Arteriolar End

COP = 22 mmHg

Venular End

HP = 40 mmHg

HP = 12 mmHg

Start: Fluid pushed into ITS


COP> HP
Fluid drawn back into capillaries
ITS

HP greater than COP so that fluid movement occurs


2 Governing forces for IV-ITS Shifting

1. COLLOID OSMOTIC PRESSURE


- Pressure exerted by plasma protein/albumin on semi-permeable membrane
2. HYDROSTATIC PRESSURE
- Pressure exerted by fluid against wall of BV
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Example:
1. MALNUTRITION

(Protein)

Less COP----venous HPN congestion-----fluids remains in ITS---Edema, Anasarca, Ascites


2. ABNORMAL
If HP less than COP---fluid stays in the VC------ Circulatory Overload------ Hypovolemia
3. BLOOD TRANSFUSION
BT/Protein/Albumin----- High COP----fluid stays in capillary---- Circulatory Overload
4. FLUID SHIFTING IC ----TO----- EC
*Movement of fluids governed by Osmosis & Diffusion
Solvent (H2O)

Solute (Electrolyte)

* High H2O EC------ Low Na concentration-------- H2O will enter the cell
If continues
Cell will Swell/Burst
H2O Intoxication/ Hypo-Osmolar Imbalance
* Less H20 E ----- High Na-----leave the cell-----cell shrink-----Dehydration

3. BURNS
Direct tissue injury caused by thermal, electric, chemical & smoke inhalation (TECS)
Nursing Priority infection (all kinds of burns)
Head burn-priority- a/w
2nd priority for 1st & 2nd - pain
2nd priority for 3rd - F&E
CLASSIFICATION:
1. CAUSE
a. Thermal
b. Electric
c. Chemical
4. Smoke

- direct contact flames, hot grease, sunburn. -- wrapped


wires
direct contact corrosive materials acids-------flush with saline solution
gas / fume inhalation

2. DEPTH OF TISSUE DAMAGE & AREA


I. Partial Thickness Burn
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1. 1st degree
Superficial Partial Thickness Burns
- Affects epidermis
- Cause: Thermal burn/sun burn
- Painful
-No edema
- Redness (erythema) & (+) blanching upon pressure with no fluid filled vesicles
- Healing Duration : 1-2 wks. w/ any residual evidence of tissue damage
2. 2nd degree
Deep Partial Thickness Burns
- Affects epidermis & dermis
- Cause chem. Burns
- With edema
- (+) Very painful
- (+) Erythema & fluid filled vesicles (blisters)
- Mottled (bluish & reddish)
- Healing duration: 2-3 wks. w/ signs of minimal scarring
II . Full Thickness Burns
1. Third & 4th Degrees Burn
- Affects all layers of skin, muscles, bones
- Cause electrical
- Without pain or less painful
- Blanched, pale, charred
- Dry, thick, leathery wound surface known as ESCHAR devitalized or necrotic tissue.
- Healing duration: No exact time-frame. Depends on the actual depth of tissue damage, infection

3. ACCORDING TO EXTENT OF BODY SURFACE BURNED


Rule of 9
Head & Neck & Face
Upper Anterior Trunk/Chest
Upper Posterior Trunk/Chest
@ Arm 9+9
Lower Anterior Extremity (leg)
Upper Posterior Extremity (leg)
Genitalia/ perineum
Total

= 9%
= 18%
= 18%
= 18%
= 18%
= 18 %
= 1%
100%

4. CLASSIFICATION AS MINOR & MAJOR


1. Minor :
2nd Degree :
2nd Degree:
3rd Degree:

10-20% BSA (C)


15-25 % BSA (A)
2-10 % BSA

2. Major:
2nd Degree:
2nd Degree:
3rd Degree:

10-20 % (C)
15-25 % (A)
2-10 %

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3. Critical:
2nd Degree:
2nd Degree:
3rd Degree

> 21 % ( C)
> 25 % (A)
> 10 %

STAGES:

1. Emergent Phase Removal of pt from cause of burn. Determine source or loc or burn
2. Shock Phase

24 - 48. Characterized by shifting of fluids from intravascular to interstitial space = Hypovolemia

S/Sx:

BP
Decrease
Urine output
HR
Increase
Hct
Elevated
Serum Na
Decrease
Serum K
Increase
Metabolic Acidosis

Priority To All Types of Burn:


INFECTION

3. Diuretic/ Fluid Remobilization Phase - 3 to 5 days. Return of fluid from interstitial to intravascular space
4. Recovery/ Convalescent Phase complete diuresis. Wound healing starts immediately after burn injury.

Pathophysiology Of THERMAL BURN:


(2ND Stage in the 1st 24-48 hrs.)
Intense heat ------------- activates a sympatho-adrenal medullary response
Tissue Trauma
Release of Histamine
Vasodilation
Increased Capillary Permeability
Fluid shifts from IV to ITS (seepage of plasma fluid to ITS)
1

Edema formation
HYPOVOLEMIA 3

Hyponatremia

Decreased Cardiac Output


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Sluggish BF
118

Thrombus Formation
Hypovolemic Shock

Renal Perfusion

Hourly Urine Output

BUN

Tissue Ischemia
Evaluate:
1. Decreased BP
Creatinine Hematuria
Hyperkalemia2. Increase Hct
(Evaluate vol. % of
RBC in plasma
Ventricular Fibrillation
hemoconcentration)
3. Decreased CVP
Sudden Cardiac Arrest

Weight loss

Tissue Starvation

Anaerobic Metabolism

(-) Nitrogen balance

Lactic Acid Production

Weakness

METABOLIC ACIDOSIS
(Common problem)

Legend:
1 - Stage of Neurogenic Shock
2 Stage of Hypovolemic Shock/ Oligenic Shock
3 Stage of Diuresis
4 Stage of Repair
COMPLICATIONS OF BURNS:
1. SODIUM (Na)
(Normal: 135-145 mEq/L)
a. Decrease Na system of burn victim d/t Hyponatremia
Edema----- trapping of Na----------------- Na activated in 3 Ways/Causes
Hyponatremia
S/Sx:

- Decreased BP
- Increased rapid, weak pulse
- Diaphoresis
- Poor memory
- Hypoactive
- (-) reflexes
- Oliguria-Anuria

1. R-AAldosterone --- Na reabsorption &


K excretion
2. Prostaglandin-Renin
3. Kallikreen---Kinin--- Increase urination,
Na excretion
Distal tubules of the kidneys

b. Hypernatremia
S/Sx:
- Thirst
- Flushed Skin
- Increase temperature
- Dry tongue
- Dry & sticky mucus membrane
- Hyperactive reflexes

Normal CVP
6-12 mmHg

c. Hypovolemia
- Assess for BP, Hct, CVP
d. CVP
- Pressure exerted by blood appropriately at the right atrium of the heart
- Done to evaluate cardiac efficiency
- Done to evaluate state of hydration
- CVP: decrease in burn victims
-If CVP, prepare for Cut-down or Venesection------prior insert 3-way polyethylene tubing
e. Hypovolemic Shock (Oligenic)
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Normal Hourly Urine


Output:
30 60 ml/hour

119

- Evaluate BP, Hct, CVP


- LOC decreased
- PR increased
- RR increased but shallow
- Skin cold & clammy (Hypo, Tachy, Tachy)
BUN
Creatinine

2. POTASSIUM (K)
b.
c.

------ 10-20 mg% w/ NPO


------ 0.9 -1.5 mg % w/o NPO--- Reliable indicator of renal function
Not influenced by protein content & diet
Product of muscle metabolism

(Normal: 3-5 5.5 mEq/L)

causes
R-A-A
Insulin/Glucose/ Glucagon ----- Increase Uptake of K----- cell

Ex. In DM pt.--- insulin decrease or none--- potassium will leave the cell (EC to IV)--- K in blood (Hyperkalemia)
a. Increased K in Burns
S/Sx:
- Decreased PR
- Abdominal cramps
- Diarrhea
- Muscular weakness
- ECG changes
b. Decreased K in Diarrhea
S/Sx:
- Increased PR followed by decreased PR
- Weakness
- Weak respiratory muscle
- Shallow respiration------- Paralytic Ileus
Hypo-active bowel sound
(K influences intestinal tone)

Abdominal distention

3. Evaluate METABOLIC ACIDOSIS: ABG Interpretation


S/Sx:
Acidosis
= CNS depression + Increased K
Alkalosis
= CNS excitability + Decreased K
MANAGEMENT OF BURN VICTIMS:
1. Extinguish the flame
- Roll over the pt.
- If burn w/in the eyes, irrigate the eyes.
- Remove clothing that can impede circulation
- Get piece of cloth & place on wound
2. Hospital:
- Establish patent airway
- Make initial assessment including body weight---needed for fluid replacement
- If (+) for hypokalemia: hook patient to a cardiac monitor
- Get an open IV line for cardiac replacement
- If veins are collapsed, do a cut-down or venisection
- Prepare for insertion of indwelling catheter to monitor urine output
- Prepare for NGT ----- to evacuate/decompress gastric content to prevent aspiration
3. Administer isotonic fluid solution
4. Strict aseptic technique
5. Diet increase CHO, increase CHON, increase Vit C, and increase K- orange
6. If (+) to burns on head, neck, face - Assist in intubation
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7. Assist in surgical wound debridement. Administer analgesic 15 30 minutes before debridement


8. Prevent Complications:
1. Infection ------ Increase anerobic circulation, risk for anaerobic infection
a. Prepare Tetanus Toxoid Injection------ .5 ml IM
- Prevent Tetanus: Burn surface area is source of anaerobic growth Clostridium tetany
Tetanus
Tetanolysin

Tetanospasmin

Hemolysis

Muscle Spasm
b. Morphine SO4

2. Hypovolemic Shock
- Replace fluid losses. Use solution
a. EVANS FORMULA

Colloid

Non-Electrolyte
Electrolyte

1 ml x kgBW x % BSA
Ex. Isotonic solution---- NSS, LRS
- 2,000 ml of glucose in H2O
- 1 ml x Kg BW x % BSA

b. BROOKES FORMULA

Colloid
Electrolyte

- 0.5 ml x Kg BW x % BSA
- 1.5 ml x kg BW x % BSA

c. PARKLAND/BAXTER FORMULA

Ex.

4 ml LRS x KgBW x % BSA

Colloid Plasma Expanders ------ will increase IV volume


Dextran
Polyrpan
Electrolyte

- Isotonic solution--- NSS, LRS------ will increase IV volume

Non- Electrolyte - Glucose in H2O


- D5 in H2O
INDICATIONS FOR FLUID RESUSCITATION/REPLACEMENT
1. Child below 2 y/o ----- resuscitate ---- Increase 10 % BSA
2. Adult
60 y/o ------ resuscitate ------- Increase 10 % BSA
Ex.
Face & Neck
= 45
Abdomen
=9
Posterior forearm = 2.25
Whole RLE
= 18
Buttocks
=6
Perineum
=1
Total
40.75 = 41%
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33 y/o with BW 60
Using Evans Formula:

Colloid
= 1 x 60 x 41 = 2,460 ml/24 hrs.
Electrolyte
= 1 x 60 x 41 = 2,460 ml/24 hrs.
Non-electrolyte = 2,000 ml/24 hrs.
*Replace losses 1 hr. after incident to prevent hypovolemic shock
Time
12-8pm
8-4 pm
4-12

%
1st 8 hrs. 50%
2nd 8 hrs. 25 %
3rd 8 hrs. 25 %

Colloid
1,230 ml
615
615

Electrolyte
1,230 ml
615
615

Non-Electrolyte
1,000 ml
500
500

*If only 1 IV line (cut-down) ---- transfuse LRS, NSS---- piggyback glucose H2O
*Maximum volume in 24 hrs. is only 10 liters (divided)
* Should replaced only 50 % of body losses
* No plasma in cut-down
* WBC---- FWB given only to burn pt. 1 unit = 500 ml to run for 4 hrs. to prevent hemolysis
3. Paralytic ileus d/t hypovolemia & hypokalemia
4. Curlings ulcer H2 receptor antagonist
5. Septicemia blood poisoning
6. Surgery: Skin grafting
9. Management to promote wound healing:
a. Diet : Increase CHON replacements & K-orange for repair of tissue damage &o promote wound healing
Vitamin C ----- for formation of collagen fibers
Granulation of tissue
Scarring/ fibrosis
Healing Process
b. Cleanse wound/ dress
- Use aseptic technique, use betadine or NSS
c. Apply ointment as anti-microbic agent
Topical antibiotic :
1. Silver Sulfadiazine (silvadene) ----- anti-microbic---promote re-epithelization of wound tissue
2. Sulfamylon
3. Silver nitrate
4. Povidone iodine (betadine)
d. Systemic Antibiotic
Ex.
1. Ampicillin
2. Cephalosporin
3. Tetracycline
e. Dressing
1. Open/Exposure Method
2. Closed/Occlusive
*Reverse isolation if open wound/method (bed cradle)
f. Do hydrotherapy/Tubbing ------ to loosen the eschar
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- In Hubbard Tank
Done only when VS are stable & level of electrolyte is normal
2 to 3x/day for 15-20 minutes
Prior to tubbing, check temperature of solution
Give analgesic 30 minutes before tubbing
Take VS prior to tubbing
While pt. in tub, encourage ROM exercises to prevent contracture deformity
If wound is severely infected, mix betadine solution

4. RELATED TO F & E BALANCE


1. BLOOD GASES

pH
pH

HCO3
PCO2

Respiratory Alkalosis

ph

PCO2

Respiratory Acidosis

ph

HCO3

Metabolic Alkalosis

ph

HCO3

Metabolic Acidosis

RESPIRATORY
ALKALOSIS

RESPIRATORY
ACIDOSIS
Chronic
Bronchitis

METABOLIC
ALKALOSIS
Vomiting

METABOLIC
ACIDOSIS
Ileostomy

Pyloric Stenosis

Intestinal
Tubing
DM
Diarrhea

Cushing

VASCULAR DISEASES
I. HYPERTENSION
CLASSIFICATION OF HYPERTENSION by JNC-VII
Pathophysiology:
Multi-factorial etiology
BP= CO (SV X HR) x TPR
Any increase in the above parameters will increase BP
1. Increased sympathetic activity
2. Increased absorption of Sodium & water in the kidney
Risk factors for Cardiovascular Problems in
3. Increased activity of the RAAS
Hypertensive patients
4. Increased vasoconstriction of the peripheral vessels
5. Insulin resistance
Major Risk factors
ASSESSMENT FINDINGS
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1. Smoking
2. Hyperlipidemia
3. DM
4. Age older than 60
5. Gender- Male & post menopausal Women
6. Family History

123

1. Headache
2. Visual changes
3. chest pain
4. dizziness
5. N/V
DIAGNOSTIC STUDIES
1. Health history & PE
2. Routine laboratory
- Urinalysis, ECG, lipid profile, BUN, serum creatinine , FBS
3. Other lab- CXR, creatinine clearance, 24-huour urine protein
MEDICAL MANAGEMENT
1. Lifestyle modification
2. Drug therapy
3. Diet therapy
4. Drug therapy

NURSING INTERVENTIONS

Drug Therapy For


HPN:
Diuretics
Beta blockers
Calcium channel
blockers
ACE inhibitors

1. Provide health teaching to patient


Teach about the disease process
Elaborate on lifestyle changes
Assist in meal planning to lose weight
Provide list of LOW fat , LOW sodium diet of less than 2-3 grams of Na/day
Limit alcohol intake to 30 ml/day
Regular aerobic exercise
Advise to completely Stop smoking
2. Provide information about anti-hypertensive drugs
Instruct proper compliance and not abrupt cessation of drugs even if pt becomes asymptomatic/ improved condition
Instruct to avoid over-the-counter drugs that may interfere with the current medication
3. Promote Home care management
Instruct regular monitoring of BP
Involve family members in care
Instruct regular follow-up
4. Manage hypertensive emergency & urgency properly
II. ANEURYSM
- Dilation involving an artery formed at a weak point in the vessel wall
Types:
1. Saccular= when one side of the vessel is affected
2. Fusiform= when the entire segment becomes dilated

RISK FACTORS
1. Atherosclerosis
2. Infection= syphilis
3. Connective tissue disorder
4. Genetic disorder= Marfans Syndrome
PATHOPHYSIOLOGY
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Damage to the intima and media weakness outpouching


Dissecting aneurysm tear in the intima and media with dissection of blood through the layers
ASSESSMENT
1. Asymptomatic
2. Pulsatile sensation on the abdomen
3. Palpable bruit
LABORATORY:
1. CT scan
2. Ultrasound
3. X-ray
4. Aortography
Medical Management:
1. Anti-hypertensives
2. Synthetic graft
Nursing Management:
1. Administer medications
2. Emphasize the need to avoid increased abdominal pressure
3. No deep abdominal palpation
4. Remind patient the need for serial ultrasound to detect diameter changes

III. PERIPHERAL VALVULAR DISEASES


A. PERIPHERAL ARTERIAL OCCLUSIVE DISEASE (PAOD)
- Refers to arterial insufficiency of the extremities usually secondary to peripheral atherosclerosis.
- Found in males age 50 & above
- The legs are most often affected
Risk factors for Peripheral Arterial occlusive disease
Non-Modifiable
1. Age
2. gender
3. family predisposition
Risk factors for Peripheral Arterial occlusive disease
Modifiable
1. Smoking
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2. HPN
3. Obesity
4. Sedentary lifestyle
5. DM
6. Stress
ASSESSMENT FINDINGS:
1. INTERMITTENT CLAUDICATION- the hallmark of PAOD
This is PAIN described as aching, cramping or fatiguing discomfort consistently reproduced with the same
degree of exercise or activity
This pain is RELIEVED by REST
This commonly affects the muscle group below the arterial occlusion
2. Progressive pain on the extremity as the disease advances
3. Sensation of cold and numbness of the extremities
4. Skin is pale when elevated and cyanotic/ruddy when placed on a dependent position
5. Muscle atrophy, leg ulceration and gangrene
Diagnostic Findings
1. Unequal pulses between the extremities
2. Duplex ultrasonography
3. Doppler flow studies
Medical Management
1. Drug therapy
Pentoxyfylline (Trental) reduces blood viscosity and improves supply of O2 blood to muscles
Cilostazol (Pletaal) inhibits platelet aggregation and increases vasodilatation
2. Surgery- Bypass graft and anastomoses
Nursing Interventions
1. Maintain Circulation to the extremity
Evaluate regularly peripheral pulses, temperature, sensation, motor function and capillary refill time
Administer post-operative care to patient who underwent surgery
2. Monitor and manage complications
Note for bleeding, hematoma, decreased urine output
Elevate the legs to diminish edema
Encourage exercise of the extremity while on bed
Teach patient to avoid leg-crossing
3. Promote Home management
Encourage lifestyle changes
Instruct to AVOID smoking
Instruct to avoid leg crossing
B. ARTERIAL ULCERS
1. BUERGERS DISEASE / THROMBOANGIITIS OBLITERANS
-Acute inflammatory disorder characterized by recurring inflammation of the medium sized small arteries & veins of the
lower extremities
- Occurs in MEN ages 30 y/o /FEET
- SMOKING!
Pathophysiology:
Cause is UNKNOWN
Probably an Autoimmune disease
Inflammation of the arteries thrombus formation occlusion of the vessels
Sx:

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1. INTERMITTENT CLAUDICATION
Leg PAIN upon walking but relieved by rest
Foot cramps in the arch (instep claudication) after exercise
Aggravated by smoking, emotional disturbance & cold chilling
2. Digital rest pain not changed by activity or rest
3. Cold sensitivity & skin color changes
Intense RUBOR (reddish-blue discoloration), progresses to CYANOSIS as disease advances
FEET----becomes White
Pallor
d/t vasoconstriction

Bluish

Red (W-B-R)

Cyanosis
d/t pooling of deoxygenated blood

Rubor with dependency (+) especially post-smoking


d/t exaggerated reflow/hyperemia

4. Paresthesia
5. Decrease or diminished peripheral pulses - Post tibial, Dorsalis pedis
6. Tropic changes
7. Ulcerations
8. Gangrene formation
Dx:

1. Oscillometry
2. Doppler UTZ
3.

Reveals a decrease peripheral pulse volume.


(Duplex ultrasnography) Reveals a decrease blood flow to affected extremities.
Angiography (Contrast angiography) reveals site & extent of mal-occulsion.

Nsg Mgt:
1. Encourage a slow but progressive physical activity
a.) Walk 3 -4 x / day
b.) Out of bed 2 3 x a / day
2. Meds
a.) Analgesic
b.) Vasodilator
c.) Anticoagulant
3. Foot care mgt like DM to prevent gangrene formation
a.) Avoid walking barefoot
b.) Cut toe nails straight
c.) Apply lanolin lotion prevent skin breakdown
d.) Avoid wearing constrictive garments
4. Avoid smoking & exposure to cold environment
5. Assist in the medical and surgical management
Surgery: BKA (Below the knee amputation) Bypass graft/amputation
Post-operative care: after amputation
Elevate stump for the FIRST 24 HOURS to minimize edema & promote venous return
Place patient on PRONE position after 24 hours
Assess skin for bleeding and hematoma
Wrap the extremity with elastic bandage
2. RAYNAUDS DISEASE/

- A form of intermittent arteriolar VASOCONSTRICTION that results in coldness, pain & pallor of the fingertips or toes
- Acute episodes of arterial spasm affecting digits of hands & fingers

Cause : UNKNOWN
Predisposing Factors:

1. WOMEN 16- 40 yrs


2.

Smoking

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1. SLE Pathognomonic sign butterfly rash on face


Chipmunk face
bulimia nervosa
Cherry red skin
carbon monoxide
poisoning
Spider angioma
liver cirrhosis
Caput medusae
leg & trunk umbilicus-127
Liver cirrhosis
Lion face
leprosy

2. Rheumatoid Arthritis

- Direct hand trauma

3. Collagen Disease

Sx:
1. RAYNAUDS PHENOMENON
- A localized episode of vasoconstriction of the small arteries of the hands that causes color & temperature
changes
2. Intermittent claudication - leg pain upon walking - Relieved by rest
3. Cold sensitivity (same with buergers) W-B-R
4. Paresthesia
5. Decrease or diminished peripheral pulses - Post tibial, Dorsalis pedis
6. Ulcerations
7. Gangrene formation
8. Tingling sensation
9. Burning pain on the hands and feet
Nsg Mgt:
a. Analgesics to relieve pain
Vasodilators -----CALCIUM channel blockers
To prevent vasospasms
b. Encourage to wear gloves especially when opening a refrigerator.
c. Avoid smoking & exposure to cold environment
Instruct patient to avoid situations that may be stressful
Instruct to avoid exposure to cold & remain indoors when the climate is cold
g. Instruct to avoid all kinds of nicotine
h. Instruct about safety. Careful handling of sharp objects

DIFFERENTIATION:
PERIPHERAL VALVULAR DISEASE

Arterial Ulcers
1. Thromboangiitis Obliterans male/ feet
2. Raynauds
female/ hands

Venous Ulcer
1. Varicose veins
2. Thrombophlebitis

C. VENOUS ULCERS
1. VARICOSE VEINS / Varicosities
- Abnormal dilation of veins usually in the lower extremities & trunk
Pathophysiology
Factors venous stasis increased hydrostatic pressure edema

Veins in valve
Fx: To increase
venous return
If incompetent

Due to:
a.) Incompetent valves leading to

valve

b.) Increase venous pooling & stasis leading to

down

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Pump blood
128

Pooling of blood
in veins
heart

Cannot return to

c.) Decrease venous return


Predisposing Factors:
a.
b.
c.
d.
e.
f.

g.
h.
i.

Hereditary
Congenital weakness of veins
Thrombophlebitis
Cardiac diseases
Pregnancy
Obesity
Prolonged immobility - Prolonged standing/sitting -------dorsiflex feet
Constipation (for hemorrhoids)
Incompetent venous valves

Sx:
-

Pain especially after prolonged standing


Dilated tortuous superficial skin veins on the legs
Warm to touch
Leg pain & Heaviness in legs
Dependent edema

Dx:
1.

Venography

2. Trendelenbergs Test Reveals that veins distends quickly in < 35 secs.


How: Elevate legs in 45 degrees angle. After 15-30 minutes, let pt. stand & see the varicosities
Medical Management:
1. Pharmacological therapy
2. Leg vein stripping/ligation
Sclerotherapy----------Spider Wed Varicosities (small-like)
(Cold-solution injection)
S/E: Thrombosis
3. Anti-embolic stockings
Nsg Mgt: Consistent to all venous ulcers
1.
2.

Elevate legs above heart level to promote venous return 1 to 2 pillows


Measure circumference of leg muscles to determine if swollen.
3. Wear anti embolic or knee high stockings. Women full panty hose
4. Meds: Analgesics for pain
5. Caution patient to avoid prolonged standing or sitting
6. Provide high-fiber foods to prevent constipation
7. Teach simple exercise to promote venous return
8. Caution patient to avoid knee-length stockings & constrictive clothings
9. Avoid massage on the affected area
2. THROMBOPHLEBITIS / DVT- Deep Vein Thrombosis
- Inflammation of the deep veins of the lower extremities & the pelvic veins
- The inflammation results to formation of blood clots in the area

Predisposing Factors:
1.
2.
4.
-

Smoking
Obesity
2.
Hyperlipedemia
Prolonged use of oral contraceptives
Chronic anemia
DM

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MI
CHF
Post-surgical complications
Post cannulation insertion of various cardiac catheters
Prolonged immobility
Varicosities
Traumatic procedures
Diet high in saturated fats

Complication:

Pulmonary Embolism:
Sx:
- Sudden sharp chest pain
- Dyspnea
- Tachycardia
- Palpitation
- Diaphoresis
- Mild restlessness

Sx:
1.
2.

3.
4.
5.
6.

Pain at affected extremities


Cyanosis
(+) HOMANS SIGN - Pain at leg muscles upon dorsiflexion of foot ---- Pathognomonic sign
Leg tenderness
Leg pain & edema
Dilated tortous vein

Dx:
1.
2.
3.

Angiography
Doppler UTZ
Duplex Scan

Medical Management:
Antiplatelets
Vein stripping & grafting
Anti-embolic stockings
Analgesics.
Anticoagulant: Heparin
Nsg Mgt:
1. Elevate legs above heart level.
2. Apply warm, moist packs to reduce lymphatic congestion.
3. Measure circumference of leg muscles to detect if swollen.
4. Use anti embolic stockings.
5. Provide measures to avoid prolonged immobility
Repositioning Q2
Provide passive ROM
Early ambulation
6. Provide skin care to prevent the complication of leg ulcers
7. Monitor for signs of pulmonary embolism (sudden respiratory distress)

GASTROINTESTINAL TRACT
Overview:
The GIT is composed of two general parts
The main GIT starts from the mouthEsophagusStomachSILI
I. Upper Alimentary Canal: Function for digestion

a. Mouth ------------------------ where digestion starts


Contains the lips, cheeks, palate, tongue, teeth, salivary glands, masticatory/facial muscles & bones
Anteriorly bounded by the lips
Posteriorly bounded by the oropharynx
Important for the mechanical digestion of food
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The saliva contains SALIVARY AMYLASE or PTYALIN that starts the INITIAL digestion of CHO
b.
c.

Pharynx (throat)
Esophagus
A hollow collapsible tube
Length- 10 inches
Made up of stratified squamos epithelium
The upper third contains skeletal muscles
The middle third contains mixed skeletal and smooth muscles
The lower third contains smooth muscles and the esophago-gastric/ cardiac sphincter is found here
Functions to carry or propel foods from the oropharynx to the stomach

d. Stomach ---------------------- widest section of UAC: Digestion ends here


e. 1st half of duodenum
II. Middle Alimentary canal Function: For Absorption

a.
b.
c.

d.

* Small Intestine Absorption starts


* Large Intestine - Complete absorption / 90% of water absorbed
2nd half of duodenum
Jejunum
Ileum
1st half of ascending colon

III. Lower Alimentary Canal Function: Elimination

a. 2nd half of ascending colon


b.
c.
d.
e.

Transverse
Descending colon
Sigmoid
Rectum

IV. Accessory Organ

a. Salivary Gland
b. Verniform Appendix ---------------------- commonly inflammed
c. Liver
---------------------- site of bile production
d.
e.

Pancreas auto digestion


Gallbladder storage of bile

The GIT Physiology


Absorbs water
Eliminates wastes
Bacteria in the colon synthesize Vitamin K
Appendix participates in the immune system
SYMPATHETIC
Generally INHIBITORY!
Decreased gastric secretions
Decreased GIT motility
But: Increased sphincteric tone and constriction of blood vessels
PARASYMPATHETIC
Generally EXCITATORY!
Increased gastric secretions
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Increased gastric motility


But: Decreased sphincteric tone and dilation of blood vessels

Gastrointestinal Assessment : Physical Exam Sequence


Inspection
Auscultation
Percussion
Palpation

The ABDOMINAL examination


The sequence to follow is:
Inspection
Auscultation
Percussion
Palpation

COMMON LABORATORY PROCEDURES


1. FECALYSIS
Examination of stool consistency, color and the presence of occult blood.
Special tests for fat, nitrogen, parasites, ova, pathogens and others
FECALYSIS: Occult Blood Testing
Instruct the patient to adhere to a 3-day meatless diet
No intake of NSAIDS, aspirin and anti-coagulant
Screening test for colonic cancer
2. Upper GIT study: barium swallow
Examines the upper GI tract
Barium sulfate is usually used as contrast
Pre-test: NPO post-midnight
Post-test: increase pt fluid intake, instruct that stools will turn white, monitor for obstruction, laxative is also
ordered
3. Lower GIT study: barium enema
Examines the lower GI tract
Pre-test: Clear liquid diet and laxatives, NPO post-midnight, cleansing enema prior to the test
Post-test: Laxative is ordered, increase patient fluid intake, instruct that stools will turn white, monitor for obstruction
4. Gastric analysis
Aspiration of gastric juice to measure pH, appearance, volume and contents
Pre-test: NPO 8 hours, avoidance of stimulants, drugs and smoking
Post-test: resume normal activities
5. EGD (Esophagogastroduodenoscopy)
Visualization of the upper GIT by endoscope
Pre-test: ensure consent, NPO 8 hours, pre-medications like atropine and anxiolytics
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Intra-test: position : LEFT lateral to facilitate salivary drainage and easy access
Post-test: NPO until gag reflex returns, place patient in SIMS position until he awakens, monitor for complications, saline
gargles for mild oral discomfort
6. Lower GI- scopy
Use of endoscope to visualize the anus, rectum, sigmoid and colon
Pre-test: consent, NPO 8 hours, cleansing enema until return is clear
Intra-test: position is LEFT lateral, right leg is bent and placed anteriorly
Post-test: bed rest, monitor for complications like bleeding and perforation
7. Cholecystography
Examination of the gallbladder to detect stones, its ability to concentrate, store and release the bile
Pre-test: ensure consent, ask allergies to iodine, seafood and dyes; contrast medium is administered the night prior, NPO
after contrast administration
Post-test: Advise that dysuria is common as the dye is excreted in the urine, resume normal activities
8. Paracentesis
Removal of peritoneal fluid for analysis
Pre-test: ensure consent, instruct to VOID and empty bladder, measure abdominal girth
Intra-test: Upright on the edge of the bed, back supported and feet resting on a foot stool
9. Liver biopsy
Pretest
Consent
NPO
Check for the bleeding parameters
Intratest
Position: Semi fowlers LEFT lateral to expose right side of abdomen
Post-test: position on RIGHT lateral with pillow underneath, monitor VS and complications like bleeding, perforation.
Instruct to avoid lifting objects for 1 week

I. ACCESSORY ORGANS DISORDER


SALIVARY GLANDS
Function: Produces saliva for mechanical digestion
1200 -1500 ml/day - saliva produced
3 Types of Saliva produced:
Parotid below & front of ear
Sublingual
Submaxillary

1. PAROTITIS
- Endemic Mumps
- Inflammation of the parotid gland
- Contagious
Causative Agent: Paramyxo Virus --------- Target:

Parotid Glands, Respiratory Glands & Meninges


Swollen Parotid Glands
Ear Ache
(Otalgia)

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Fever

Dysphagia

133

S/Sx:
1. Fever, chills anorexia, gen body malaise
2. Swelling of parotid gland
3. Dysphagia
4. Ear ache Otalgia
MOT: Direct transmission & droplet nuclei
Incubation Period: 14 21 days
Period of Communicability 1 week before swelling & immediately when swelling begins.
Nsg Mgt:
1.

CBR

2. Strict isolation (Gentan Violet for aesthetic purposes only)


3. Meds: Analgesic
4.

5.
6.

Antipyretic
Antibiotics to prevent 2 complications
Alternate warm & cold compress at affected part
General liquid to soft diet
Prevent Complications :
1.Women Cervicitis, Vaginitis, Oophoritis
2.Both sexes meningitis & encephalitis/ reason why antibiotics is needed
3. Men Orchitis (inflammation of testes) might lead to sterility if it occur during / after puberty.

VERNIFORM APPENDIX
Location: Right Iliac or Right Inguinal area
Function : As a Lymphatic organ that produces WBC during fetal life - ceases to function upon birth of baby
1. APENDICITIS
Inflamation of verniform appendix
Predisposing Factor:

1.
2.
3.
4.

Microbial infection cause by bacteria


Fecalith undigested food particles Ex. Tomato seeds, guava seeds
Intestinal obstruction, lymphoid hyperplasia, foreign body & helminthic obstruction
Kinking & external occlusion by adhesions, fibrous conditions of abdomen

Pathophysiology:
Obstruction of lumen increased pressure decreased blood supply bacterial proliferation and mucosal inflammation
ischemia necrosis rupture
Stages: 1. Congestive
2. Suppurative
3. Gangenous
4. Perforation
S/Sx:

1. Pathognomonic sign: (+) REBOUND TENDERNESS


2.

Low grade fever, anorexia, n/v

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134

3.
4.

5.
6.

7.

Diarrhea / & or constipation


Pain at Rt iliac region
Late sign : Tachycardia D/T pain
Abdominal pain: begins in the umbilicus then localizes in the RLQ (Mc Burneys point)
Abdominal rigidity (if perforated)

Dx:

1. CBC : Reveals mild leukocytosis increase WBC---------- Confirmatory DX


2. PE
: (+) Rebound Tenderness (flexion of Rightt leg, palpate Rt iliac area rebound)
3. Urinalysis --- Reveals (+) to acetone
4.
5.

Ultrasound
Abdominal X-ray

Treatment:
1. Surgical Intervention
Appendectomy- Should be operated 24 48 to prevent rupture---- Peritonitis
* MC BURNEYS POINT site of surgical incision for appendectomy
Nsg Mgt: PRE- OPERATIVE
1.
2.
3.

Consent
Notify MD----- local anesthesia
Routinary nursing measures:
a.) Skin preparation
b.) NPO
c.) Avoid enema lead to rupture of appendix
4. Meds:
Antipyretic
Antibiotics to prevent secondary infection
*Dont give analgesic will mask the pain
- Presence of pain means appendix has not ruptured.
4. Avoid heat application, enemas & laxative will rupture appendix.
5. Monitor VS, I&O bowel sound, fever & hydration status
6. Monitor for perforation and signs of shock
7. POSITION of Comfort: RIGHT SIDELYING in a low FOWLERS

PAIN sensation an important


parameter:
(-) to pain : Ruptured appendix
(+) to pain : Inflammation

Nursing Mgt: POST-OPERATIVE

1. If (+) to Pendrose Drain indicates rupture of appendix


Position- affected side to drain
If no Penrose Drain, position based on pt. comfort
2.
3.
4.

Meds: analgesic due post op pain


Antibiotics, Antipyretics PRN
Monitor VS, I&O, bowel sound
Maintain patent IV line

5. Complications: Peritonitis & Septicemia


6. Monitor VS and signs of surgical complications
7. Maintain NPO until bowel function returns
8. If rupture occurred, expect drains and IV antibiotics
9. POSITION post-op: RIGHT side-lying, SEMI- FOWLERS to decrease tension on incision & legs flexed to promote
drainage
10. Administer prescribed pain medications

COMMON GIT SYMPTOMS AND MANAGEMENT


1. CONSTIPATION
- An abnormal infrequency and irregularity of defecation
- Multiple causations
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135

Pathophysiology
Interference with three functions of the colon
1. Mucosal transport
2. Myoelectric activity
3. Process of defecation
NURSING INTERVENTIONS
1. Assist physician in treating the underlying cause of constipation
2. Encourage to eat HIGH fiber diet to increase the bulk
3. Increase fluid intake
4. Administer prescribed laxatives, stool softeners
5. Assist in relieving stress
2. DIARRHEA
-Abnormal fluidity of the stool
Multiple causes
Gastrointestinal Diseases
Hyperthyroidism
Food poisoning
Nursing Interventions
1. Increase fluid intake- ORESOL is the most important treatment!
2. Determine and manage the cause
3. Anti-diarrheal drugs

LIVER

In locating organs of the


abdomen:
Use the 9 regions

The largest internal organ


Located in the right upper quadrant/ Right Hypochondriac Region
Contains two lobes- the right & the left
Color: Scarlet Red
Covered by a fibrous capsule--------- GLISSONS CAPSULE
The hepatic ducts join together with the cystic duct to become the common bile duct
Functions to store excess glucose, fats and amino acids
Also stores the fat soluble vitamins- A, D and the water soluble- Vitamin B12
Produces the BILE for normal fat digestion
The Von Kupffer cells remove bacteria in the portal blood
Detoxifies ammonia into urea
Functional Unit Liver Lobules

Function:
1.

Produces bile
Bile: Function is to emulsifies fats
Gives color to urine Urobilin (light yellow)
Stool Stircobilin (brown)

2. Detoxifies toxic substances from drugs


3. Promotes synthesis of Vit A, D, E, K
Created by Nia E. Tubio

Precursor:
Cholesterol
water

Bile salt +

Vitamin A = Retinol
Vitamin D = Cholecalciferol
Vitamin E = Tococalciferol
Vitamin K = Phetione
Excess Vit. D & K =
Hypervitaminosis
Deficiency Vit. A = Night
Blindness

136

(Fat soluble vitamins)


4. It destroys excess estrogen hormone
5. For metabolism of:
A. CHO
1. Glycogenesis synthesis of glycogens
2. Glycogenolysis breakdown of glycogen
3. Gluconeogenesis formation of glucose from non- CHO sources
B. CHON
1. Promotes synthesis of albumin & globulin
Cirrhosis decrease albumin
Albumin maintains osmotic pressure, prevents edema
2. Promotes synthesis of prothrombin & fibrinogen
3. Promotes conversion of ammonia to urea.
Ammonia like breath fetor hepaticus
C. FATS
1. Promotes synthesis of cholesterol to neutral fats called triglycerides

1. LIVER CIRRHOSIS / Laennecs Cirrhosis

Lost of architectural design of liver leading to fat necrosis & scarring


A chronic, progressive disease characterized by a diffuse damage to the hepatic cells
The liver heals with scarring, fibrosis and nodular regeneration

Predisposing Factor:
Laennacs Cirrhosis caused by alcoholism
1. Chronic alcoholism ------ Common Cause
2. Malnutrition DecreaseVit B- Thiamine - main cause
3. Virus
4. Toxicity to Carbon Tetrachloride
5. Use of hepatotoxic agents
6. Post-infection
7. Cardiac diseases
8. Schistosomiasis
9. Biliary obstruction
10. Portal Hypertension
Compression of the intra-liver vessels
Decreased protein (colloid pressure)
Increased hydrostatic pressure
S/Sx:
Early signs:

a.) Weakness & Fatigue


b.) Anorexia, Early mornig Nausea & vomiting, Weight loss
c.) Stomatitis
d.) Urine Tea color / Stool Clay color
e.) Amenorrhea
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137

f.) Decrease sexual urge


g.) Loss of pubic & axilla hair
h.) Hepatomegaly
i.) Jaundice
j.) Pruritus or Urticaria
k.) RUQ abdominal pain
2. Late signs
a.) Hematological changes all blood cells decrease---- Pancytopenia
Leukopenia- decrease
Thrombocytopenia- decrease
Anemia- decrease
b.) Endocrine changes
Spider Angiomas (Teleangectasis---nose), Gynecomastia
Caput medusae (Abdomenloss of tortousity of the umbilicus) , Palmar errythema (redness)
c.) GIT changes
Ascitis, bleeding esophageal varices due to portal HPN
d.) Neurological Changes: Hepatic Encephalopathy
Dx:
Liver enzymes- increase
SGPT (ALT)
SGOT (AST)
Serum cholesterol & ammonia
= Iincrease
Indirect Bilirubin or Unconjugated Bilirubin = Increase
CBC
= Pancytopenia
PTT
= Prolonged
Hepatic Ultrasonogram = Reveals fat necrosis of liver lobules
Pathophysiology:
CIRRHOSIS
* 1-3 : Complications
No production of albumin
Decreases Osmotic Pressure
Edema to Liver
ASCITES 2
ASCITES
(Fluid Accumulation in the
Peritoneal cavity)
Nsg Mgt:
1. Medication:
Loop Diuretics (10-15
minutes)
K- sparing diuretics
2. Assist in abdominal
Paracentesis
(Aspiration of fluid in the
peritoneum)
*Void before paracentesis
to prevent accidental
puncture
of bladder
Created by Nia
E. Tubio as

No convertion of Ammonia to urea


Ammonia reabsorb back to blood

No Prothrombin & Firinogen


No clotting Factor

HEPATIC ENCEPHALOPATHY 1
HEPATIC ENCEPHALOPATHY
(accumulation of ammonia-a
cerebral toxin)

BLEEDING 3

1st Sign: Asterixis


(Flapping Hand
Tremors)

BLEEDING ESOPHAGEAL
VARICES
(d/t Portal HPNdilation of
esophageal veins)
Sx:
Vomiting---- accompanied by
blood

Late Signs:
Headache
Fetor Hepaticus
Restlessness
Disorientation/ Confusion
Decrease LOCcan lead to
Hepatic Coma
Nsg. Priortity:
Assist In Mechanical
Ventilation
Nsg. Mgt:
1. Assist in mechanical
ventilation d/t coma
2. Monitor VS, neuro check
3. Siderails d/t restless
4. Meds:

Nsg Mgt:
1. Medication:
Vit. K
Pitressin or Vasopressin (IM)
2. NGT DecompressionLavage
Give before lavage
- ice or cold saline
solution
Monitor NGT output
3.Assist in Mechanical

138

Liver cirrhosis bedside


scissor if pt complaints of
DOB
Nsg Mgt:
Cut cystachean tube to
1. CBR ---- Elevate the head of the bed to minimize dyspnea
2. Restrict Na before fluids
3. Monitor VS, I&O, weight, LOC & bleeding
4. With pt daily & assess pitting edema
5. Measure abdominal girth daily notify MD
6. Meticulous skin care
7. Provide Moderate to LOW-protein (1 g/kg/day) & LOW-sodium diet
DIET
8. Diet Increase CHO, Vit. & minerals. Moderate fats. Well balanced diet
Early Stage
9. Provide supplemental Vit. (especially K) & minerals
10. Administer prescribed:
High in:
CHO
Diuretics= to reduce ascites & edema
CHON
Lactulose= to reduce NH4 in the bowel
Vitamins
Antacids= to prevent ulcer & bleeding
Minerals
Neomycin= to kill bacterial flora that cause NH production
Low in : Fats
11. Avoid hepatotoxic drugs
Paracetamol
Late Stage:
Anti-tubercular drugs
High in:
CHO
12. Reduce the risk of injury
Vit. &
Side rails reorientation
Minerals
Assistance in ambulation
Low in :
CHON
Use of electric razor & soft-bristled toothbrush
13. Keep equipments ready including Sengstaken-Blakemore tube, IV fluids, Medications to treat hemorrhage
PANCREAS
- Mixed gland (Functions as an exocrine & endocrine gland)
- A retroperitoneal gland
The pancreatic duct (major) joins the common bile duct in the sphincter of Oddi
The exocrine function of the pancreas is the secretion of digestive enzymes for carbohydrates, fats & proteins
Pancreatic amylase carbohydrates
Pancreatic lipase (steapsin) fats
Trypsin, Chymotrypsin and Peptidases proteins
Bicarbonate to neutralize the acidic chyme. Stimulated by SECRETIN!
Pancreas----- with acinar cells----secretes pancreatic juice going to--- pancreatic duct--- to--stomach
1. PANCREATITIS

An Inflammation of pancreas leading to pancreatic edema, hemorrhage & necrosis due to auto digestion
Can be acute or chronic

Predisposing Factors:
1.
2.
3.
4.
5.

6.
7.
8.

Chronic alcoholism
Hepatobilary disease
Obesity
Hyperlipidemia
Hypoparathyroidism
Drugs Thiazide diuretics, pills, Pentamidine HCL (Pentam)---for AIDS
Diet increase saturated fats
Hypercalcemia

Created by Nia E. Tubio

Cullens Sign at the


Umbilicus:
Bleeding of

139

9.
10.
11.
12.
13.

Trauma
Biliary tract disease
Bacterial disease
PUD
Mumps

- cholelithiasis

Pathophysiology of Acute Pancreatitis:


Self-digestion of the pancreas by its own digestive enzymes principally TRYPSIN
Spasm, edema or block in the Ampulla of Vater reflux of proteolytic enzymes Auto digestion of the Pancreatic Tissue
INFLAMMATION
Hemorrhage----- Necrosis
KININ ACTIVATION will result to increased permeability
Loss of Protein-rich fluid into the peritoneum
HYPOVOLEMIA
S/Sx:

1. Severe Left epigastric pain radiates from back &flank area


Abdominal pain- acute onset, occurring after a heavy meal or alcohol intake
2. Aggravated by eating, with DOB---- rest the GIT
2. N/V, Jaundice, Anorexia
3. Tachycardia
4. Palpitation due to pain
5. Dyspepsia indigestion
6. Decrease bowel sounds
7. (+) Cullens sign - ecchymosis of umbilicus
Hemorrhage------ Chronic Hemorrhagic Pancreatitis
8. (+) Grey Turners spots ecchymosis of flank area
Confirmatory Dx
9. Hypocalcemia
10. Hypotension & Hypovolemia
11. Signs of Shock
Dx:
1. Serum amylase & lipase Increase---- Confirm the presence of pancreatitis
2. Urine lipase Increase
3. Serum Ca Decrease
4. Ultrasound
5. WBC
6. CT scan
7. Hemoglobin and hematocrit
Nursing Mgt:
1. Meds:
Assist in pain management. Usually, Demerol is given. Morphine is AVOIDED
a.) Narcotic analgesic - Meperidine Hcl (Demerol)
Dont give Morphine SO4 will cause spasm of sphincter.
b.) Smooth muscle relaxant/ anti cholinergic
Ex.
Papavarine Hcl
Prophantheline Bromide (Profanthene)
c.) Vasodilator NTG
d.) Antacid Maalox
e.) H2 receptor antagonist - Ranitidine (Zantac)
To decrease pancreatic stimulation
*Ranitidine ---- more common & with less S/E
f.) Ca gluconate
A Phosphate binder---- Antacid-----Constipation---- Amphogel
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140

2. Withold food & fluid aggravates pain


3. Assist in Total Parenteral Nutrition (TPN) or hyperalimentation
Complications of TPN:
1. Infection
2. Air Embolism -----Tape all connections to the system
3. Hyperglycemia
4. Hyponatremia
4. Institute stress mgt tech
a.) DBE
b.) Biofeedback
5. Comfy position - Knee chest or fetal like position to decrease pain
Position patient in SEMI-FOWLERs to decrease pressure on the diaphragm
6. If pt can tolerate food, give increase CHO, decrease fats, and increase CHON
7. Assist in correction of Fluid and Blood loss
8. lace patient on NPO to inhibit pancreatic stimulation
9. NGT insertion to decompress distention and remove gastric secretions
10. Maintain on bed rest
11. Deep breathing and coughing exercises
12. Introduce oral feedings gradually- HIGH carbo, LOW FAT
13. Maintain skin integrity
14. Manage shock and other complications:
Chronic hemorrhagic pancreatitis
Shock
Pulmonary Complications---- Pneumonia, Air embolism & Pleural effusion
GALLBLADDER
Located below the liver
The cystic duct joins the hepatic duct to become the bile duct
The common bile duct joins the pancreatic duct in the sphincter of Oddi in the first part of the duodenum
Storage of bile (made of cholesterol) & concentrates bile
Contracts during the digestion of fats to deliver the bile
Cholecystokinin is released by the duodenal cells, causing the contraction of the gallbladder & relaxation of the sphincter
of Oddi
DISORDER OF THE GALLBLADDER
1. CHOLECYSTITIS
Inflammation of the gallbladder
Can be acute or chronic:
1. Acute cholecystitis usually is due to gallbladder stones
2. Chronic cholecystitis is usually due to long standing gall bladder inflammation
CHOLELITHIASIS
- Inflammation of the gallbladder with Formation of GALLSTONES in the biliary apparatus
Predisposing FACTORS:
1.

5 F
Female
Fat (Obesity)
Forty (High Risk : 40 y/o)
Fertile

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141

Fair
2. Post menopausal women undergoing estrogen therapy
3. Sedentary lifestyle
4. Hyperlipidemia
5. Neoplasm
Pathophysiology:
Supersaturated bile, Biliary stasis
Stone formation
Blockage of Gallbladder
Inflammation, Mucosal Damage and WBC infiltration
S/Sx:
1.

Severe Right abdominal pain (after eating fatty food). Occurring especially at night
Epigastric pain that radiates to the scapula or localized at the RUQ
Mass at the RUQ
2. Fatty intolerance
3. Anorexia, n/v
4. Jaundice
5. Pruritus
6. Easy bruising
7. Tea colored urine / Dark-orange & foamy urine
8. Steatorrhea
9. Indigestion, belching and flatulence
10. Murphys sign
Dx:

1. Oral cholecystogram (or gallbladder series)- Confirms presence of stones but cannot visualize the gallbladder
2. Ultrasonography- can detect the stones
3. Abdominal X-ray
4. Cholecystography
WBC count increased
ERCP: Revaels inflamed gallbladder with gallstone
5. Serum Lipase Increase
6. Indirect Bilirubin - Increase
Tx:
Analgesic- Meperidine
Chenodeoxycholic acid= to dissolve the gallstones
Antacids
Anti-emetics
Nursing Mgt:
1.

Medications:
Administer prescribed medications to relieve pain.
a.) Narcotic Analgesic - Usually Demerol (MEPERIDINE)
NOT Codeine & Morphine may cause spasm of the Sphincter increased pain.
Morphine cause MOREPAIN
b.) Anti cholinergic - Atropine SO4
c.) Anti emetic Metoclopramide (Plasil)
Phenergan Phenothiazide with anti emetic properties

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142

2. Diet increase CHO, moderate CHON, decrease fats


3. Meticulous skin care d/t Urticaria
4. Maintain NPO in the active phase
5. Maintain NGT decompression
6. Instruct patient to AVOID HIGH- fat diet & GAS-forming foods
7. Surgical Procedures :
Cholecystectomy---removal of gallbladder
Choledochotomy
Laparoscopy
Post-operative Nursing Interventions Cholecystectomy:
1. Monitor for surgical complications
2. Post-operative position after recovery from anesthesia- LOW FOWLERs
3. Encourage early ambulation
4. Administer medication before coughing and deep breathing exercises
5. Advise client to splint the abdomen to prevent discomfort during coughing
6. Administer analgesics, antiemetics, antacids
7. Care of the biliary drainage or T-tube drainage
8. Fat restriction is only limited to 4-6 weeks. Normal diet is resumed
IMPORTANT:
-Maintain patency of T-tube . Check if intact & drain to prevent infection
Purpose: To prevent entry of bile into the peritoneal cavity

STOMACH

A J-shaped structure organ in the epigastrium


- Capacity is 1,500 ml
Contains 4 Parts:
Fundus/ Anthrum
Cardia
Body
Pylorus

Valves ------ prevents reflux or regurgitation of food


1. Cardiac Sphincter - prevents the reflux of the contents into the esophagus (bet. esophagus & stomach)
2. Pyloric Sphincter - regulates the rate of gastric emptying into the duodenum (bet. stomach & half of pylorus)

The glands & cells in the stomach secrete digestive enzymes:


1. Parietal / Oxyntic Cells
Function:
a. Produces intrinsic factor - promotes reabsorption of Vit. B12 promotes maturation of
RBC
b.

HCl Acid - Aids in digestion

2. Chief Cells/ Zymogenic Cells : Secretes


a.
b.
Created by Nia E. Tubio

Ph of Hydrocholoric
Acid: 1-2

Gastric amylase - digest CHO


Gastric lipase digest fats
143

c.
d.

Pepsin digests PROTEIN


Rennin digests milk products

3. Antral G-cells- gastrin


4. Argentaffin cells- serotonin
5. Mucus neck cells- mucus
6. Endocrine cells - Secrets gastrin increase Hcl acid secretion
Function of the Stomach:
Generally to digest the food (proteins) & to propel the digested materials into the SI for final digestion
1.Mechanical
2.Chemical
Digestion
3.Storage of food

CHO & CHON : Stored in the stomach for 1 -2 hrs.


FATS

: Stored in stomach for 2 3 hrs

DISORDERS OF THE STOMACH


1. PEPTIC ULCER DISEASE (PUD)

An ulceration of the gastric & duodenal lining characterized by excoriation / erosion of submucosa &
mucosal lining due to:
a.) Hypercecretion of acid pepsin
b.) Decrease resistance of mucosal barrier to HCl acid secretion
- May be referred as to location as Gastric ulcer in the stomach, or Duodenal ulcer in the duodenum
- Most common Peptic ulceration: anterior part of the upper duodenum
Incidence Rate:

1. Men : 40 55 yrs old


2.

Aggressive persons

PATHOPHYSIOLOGY of PUD:
Disturbance in acid secretion & mucosal protection
Increased acidity or decreased mucosal resistance erosion & ulceration
Infection with H. pylori------ # 1 cause of ULCER
Predisposing Factors:
1. Hereditary
2. Emotional Stress
3. Smoking vasoconstriction GIT ischemia---lead to resistance of HCl----- ulceration
4. Alcoholism stimulates release of histamine = stimulates Parietal cell release Hcl acid = Hypersecretion ----Ulceration
5. Caffeine tea, soda, chocolate
6. Irregular diet
7. Rapid eating
8. Ulcerogenic drugs NSAIDS, aspirin, steroids, indomethacin, ibuprofen
Indomethacin - S/E corneal cloudiness. Needs annual eye check up.
9. Gastrin producing tumor or Gastrinoma Zollinger Ellison Syndrome
10. Microbial invasion R/T helicobacter pylori. Metromidazole (Flagyl)
Created by Nia E. Tubio

144

TYPES OF ULCERS
I. Ascending to severity:
1. Acute affects submucosal lining
2. Chronic affects underlying tissue heals & forms a scar

Most feared
complications of Bruns
in GIT : Curlings Ulcer

II. According to location:

1. Stress ulcer ---common among critically-ill patients


2.

3.

Gastric ulcer
Duodenal ulcer most common----- 90% of ulcers because it has less bicarbonate ions
Buffers that neutralizes acidity

A. STRESS ULCER
2 Types Of Stress Ulcer
2. CUSHINGS ULCER:

1. CURLINGS ULCER :
Cause: Trauma & Burns

Cause:

Bleeding

Stroke/ CVA / Head Injury


Increase vagal stimulation

Hypovolemia

Hyperacidity

GIT schemia

Ulcerations

Decrease resistance of mucosal barriers to Hcl acid

B.

Ulcerations
Drug Of Choice: Ranitidine (Zantax)
GASTRIC ULCER
DEFINITION

- Ulceration of the gastric mucosa,


submucosa & rarely the muscularis
d/t break in the mucosal barrier w/
reduced production 2nd to
incompetent pylorus.

DUODENAL ULCER
- Ulceration of duodenal mucosa &
submucosa
- Usually d/t increased gastric acidity

- Hypoperfusion-ischemia to gastric
mucosa is also a factor. H.pylori in
>90% cases
RISK FACTORS
(same)
PATHOLOGY
SITE
Other Sx

EPIGASTRIC
PAIN

Created by Nia E. Tubio

Stress
Smoking
Alcohol
History of gastritis
Decreased mucosal protection---------Infection with H. pylori-----Decreased
blood supply to the stomach
Antrum or lesser curvature
1. Nausea
2. Vomiting is more common
3. Hematemesis>melena
4. Weight loss
-30 min 1 hr AFTER EATING
- epigastrium
- Hot , gaseous & burning
- not usually relieved by food & antacid
- Gnawing, sharp pain in the midepigastrium
- NOT RELIEVED by food intake,

Helicobacter pylori infection


NSAIDS abuse
Type A personality
Increased gastric acidity------Infection
with H pylori
Duodenal bulb

-2-4 hrs after eating or during the night


- mid epigastrium
- Cramping & Burning PAIN
- usually relieved by food intake &
antacid
- 12 MN 3am pain
145

sometimes AGGRAVATING the pain!

GASTRIC
SECRETION
VOMITING
HEMORRHAGE
WT
COMPLICATION
S
HIGH RISK

Normal gastric acid secretion

Increased gastric acid secretion

common

Not common

Hematemesis

Melena

Wt loss

Wt gain

a. Stomach Cancer
b. Hemorrhage

a. Perforation

40 - 60 y/o
Incidence is high in older adults,
male>female,

20 y/o

1. EGD to visualize the ulceration


2. Urea breath test for H. pylori infection
3. Biopsy- to rule out gastric cancer d/t
malignancy risk
4. Barium swallow
5. Gastric analysis = NORMAL

1. EGD & Biopsy


2. Endoscopic exam
3.Stool from occult blood
4.Gastric analysis = INCREASE
5. Upper GI series confirms presence
of ulceration

Dx

NURSING INTERVENTIONS:
1. Give BLAND diet, small frequent meals during the active phase of the disease
a.

b.

Diet bland, non irritating, non spicy


Avoid caffeine & milk/ milk products, carbonated drinks
Increase gastric acid secretion

2. Administer prescribed medications- H2 blockers, Protein pump inhibitor, mucosal barrier protectants & antacids
a.) Antacids
ACA
Aluminum Containing Antacids
Ex. Aluminum OH gel
(Ampho-gel)
S/E constipation

MA
Magnesium Containing Antacids
Ex. Milk Of Magnesia
S/E diarrhea

Maalox (fewer S/E)

b.) H2 Receptor Antagonist


Ex.

1. Ranitidine (Zantac) lesser S/E---- Best given if OD = AM


or BID = AM & Nightime to prevent nocturnal acid gastric secretion

2. Cimetidine (Tagamet) more S/E


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146

3. Famotidine (Pepcid)
3.

Avoid smoking decrease effectiveness of drug

Nursing Mgt For Both:


1.

Administer antacid & H2 receptor antagonist 1hr apart


-Cimetidine decrease antacid absorption & vise versa
- Instruct client to avoid smoking because it decreases effectiveness of the drug

c.) Cytoprotective Agents


Ex.
1. Sucralfate (Carafate) - Provides a paste-like substance that coats mucosal lining of stomach
2. Cytotec - causes severe spasm ( abortive effect)
d.) Sedatives/ Tranquilizers - Valium, lithium
e.)Anticholinergics / Anti-spasmodic Agent
1. Atropine SO4
2. Prophantheline Bromide (Probanthine)
(Pt has history of HPN crisis With peptic ulcer disease. Rn should not administer alka seltzer- has large amount of Na.
4. Provide teaching about stress reduction & relaxation techniques
5. Surgery: Subtotal Gastrectomy - Partial removal of stomach
Billroth I (Gastroduodenostomy)
-Removal of 1/3 of stomach & anastomoses of gastric
stump to the duodenum.

Billroth II (Gastrojejunostomy)
- Removal of 1/2 -3/4 of stomach & duodenal bulb & anastomostosis
of gastric stump to jejunum.

Before surgery for BI or BII - Do vagotomy (severing of vagus nerve) & pyloroplasty (drainage) first.
`

Nursing Mgt For B1 or B II:


1.

2.

3.
4.

5.

Monitor NGT output


a.) Immediately post op should be bright red drainage
b.) Within 6-8 hrs output is greenish in color
c.) After 24h output is dark red d/t influence of HCI acid
Administer meds:
a.) Narcotic Analgesic
b.) Antibiotic
c.) Antiemetics
Maintain patent IV line
VS, I&O & bowel sounds
Monitor for Complications:

SURGICAL PROCEDURES FOR PUD


Total gastrectomy, vagotomy,
gastric resection, Billroth I &
II, pyloroplasty
Post-operative Nursing
management
1. Monitor VS
2. Post-op position: FOWLERS
3. NPO until peristalsis returns
4. Monitor for bowel sounds
5. Monitor for complications of
surgery
6. Monitor I & O- report
U.O:<.5cc/kg/hr, IVF, hydrate

a. HEMORRHAGE Hypovolemic shock


Late signs anuria
Nsg Interventions For BLEEDING:
1. Maintain on NPO
2. Administer IVF & medications
3. Monitor hydration status, Hct & Hgb
4. Assist with room temperature SALINE lavage
(iced may lead to more mucosal damage via severe vasoconstriction-ischemia,vagal stimulation)
5. Insert NGT for decompression & lavage & assessment of GI bleeding
6. Prepare to administer blood transfusion
7. Prepare to give VASOPRESSIN to induce vasoconstriction to reduce bleeding
8. Prepare patient for SURGERY if warranted
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b. PERITONITIS
c. PARALYTIC ILEUS Most feared complication in all types of abdominal surgery (absence of peristalsis)
d.
e.

f.

Hypokalemia
Thromobphlebitis
Pernicious anemia

g. DUMPING SYNDROME

Common complication
Rapid gastric emptying of hypertonic food solutions CHYME leading to hypovolemia.
A postprandial condition of rapid emptying of the gastric contents into the small intestine (jejunum) usually
after a gastric surgery (gastrojejunostomy) without proper mixing of chyme & the normal duodenal
digestive process
- Symptoms occur 5-30 minutes after eating

Pathophysiology:
Foods high in CHO & electrolytes must be diluted in the jejunum before absorption takes place.
The rapid influx of stomach contents will cause distention of the jejunum early symptoms
The hypertonic chyme will draw fluid from the blood vessels to dilute the high concentrations of CHO and electrolytes
Later, there is increased blood glucose stimulating the increased secretion of insulin
Then, blood glucose will fall causing reactive hypoglycemia
Sx of Dumping syndrome:
EARLY Sx: d/t rapid movement of extracellular fluids into the bowel to convert the hypertonic bolus to
isotonic
1. Nausea and Vomiting, syncope
2. Abdominal fullness
3. Abdominal cramping
4. Palpitation, tachycardia
5. Diaphoresis, Pallor
LATE Sx:
1. Drowsiness
2. Weakness & Dizziness
3. Hypoglycemia
4. Diarrhea
Nursing Mgt:
1. Avoid fluids in chilled solutions
Instruct to eat SMALL frequent meals, include MORE dry food items in 6 equally divided feedings
Advise patient to eat LOW-carbohydrate HIGH-fat and HIGH-protein diet
2. Flat on bed 15 -30 minutes after q feeding
5. Instruct to AVOID consuming FLUIDS 1 hr before, with, 2 hrs after meals
6. Instruct to eat in semi recumbent position, LIE DOWN after meals
7. Administer sedative, anti-spasmodic medications to delay gastric emptying
2. GASTRO-ESOPHAGEAL REFLUX DISEASE (GERD)
- Backflow of gastric contents into the esophagus
FACTORS:
- Usually due to incompetent lower esophageal sphincter , pyloric stenosis or motility disorder
- Symptoms may mimic ANGINA or MI

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Pathophysiology:
incompetent lower esophageal sphincter
regurgitation of acidic contents
Erosion of esophageal mucosa
Pain
Sx:

Heartburn
Dyspepsia
Regurgitation
Epigastric pain
Difficulty swallowing
Ptyalism

Dx:
1. Endoscopy or barium swallow
2.Gastric ambulatory pH analysis
Note for the pH of the esophagus, usually done for 24 hours
The pH probe is located 5 inches above the lower esophageal sphincter
The machine registers the different pH of the refluxed material into the esophagus
NURSING INTERVENTIONS
1. Instruct the patient to AVOID stimulus that increases stomach pressure & decreases GES pressure
2. Instruct to avoid alcohol , spices, coffee, tobacco & carbonated drinks
3. Instruct to eat LOW-FAT, HIGH-FIBER diet, BLAND DIET
4. Avoid foods and drinks TWO hours before bedtime
5. Elevate the head of the bed with an approximately 8-inch block
6. Administer prescribed H2-blockers & prokinetic meds like cisapride, metochlopromide
7. Advise proper weight reduction
3. GASTRITIS
- Inflammation of the gastric mucosa
May be Acute or Chronic
Etiology:
Acute- bacteria, irritating foods, NSAIDS, alcohol, bile & radiation
Chronic- Ulceration, bacteria, Autoimmune disease, diet, alcohol, smoking
Pathophysiology:
Insults cause gastric mucosal damage inflammation, hyperemia and edema superficial erosions decreased
gastric secretions, ulcerations & bleeding
Dx:
1. EGD- to visualize the gastric
mucosa for inflammation
2. Low levels of HCl
3. Biopsy to establish correct
diagnosis whether acute or
chronic

Sx:
(Acute)
Dyspepsia
Headache
Anorexia
Nausea/Vomiting
Chronic)
Pyrosis
Singultus
Sour taste in the mouth
Dyspepsia, N/V/anorexia, Pernicious anemia
UPPER GIT

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NURSING INTERVENTIONS
1. Give BLAND diet
2. Monitor for signs of complications
like bleeding, obstruction and
pernicious anemia
3. Instruct to avoid spicy foods,
irritating foods, alcohol and
caffeine
4. Administer prescribed medicationsH2 blockers, antibiotics,

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1. HERNIATIONS
- Abnormal protrusion of an organ/tissue/part of an organ through a structure that normally contains it through
a congenital or acquired weakness of the enclosing wall
(eg. Abdominal musculature) with accompanying increased pressure (valsalva, lifting, crying).
Wall defect
Intraabdominal
Pressure
Tissue/organ
Protrusion
Types:
Descriptors:

- Reducible
- Incarcerated/Irreducible
- Strangulated (emergency)

Medical management:
- Truss
Surgery:
- Herniorrhapy, mesh
- Laparoscopic ExtraPeritoneal herniorrhapy
Nursing Management:
- Preop: Health instructions, consent, let patient void
- Postop: Vital signs, urine output & urine bladder status
- Scrotal swelling. Ice pack over the incision.
- General diet as soon tolerated by the patient. Advise no lifting for 4-6 wks
- Postop Scrotal support.
ESOPHAGUS
1. ESOPHAGEAL VARICES
- Dilation &tortuosity of the submucosal veins in the distal esophagus
ETIOLOGY: commonly caused by PORTAL hypertension secondary to liver cirrhosis
This is an Emergency condition!
Sx:
1. Hematemesis
2. Melena
3. Ascites
4. Jaundice
5. Hepatomegaly/splenomegaly
Signs of Shock- tachycardia, hypotension, tachypnea, cold clammy skin, narrowed pulse pressure
Dx:

1. Esophagoscopy

NURSING INTERVENTIONS FOR EV


1. Monitor VS strictly. Note for signs of shock
2. Monitor for LOC
3. Maintain NPO
4. Monitor blood studies
5. Administer O2
6. Prepare for blood transfusion
7. Prepare to administer Vasopressin and Nitroglycerin
8. Assist in NGT and Sengstaken-Blakemore tube insertion for balloon tamponade (scissors pls!)
9. Prepare to assist in surgical management: Endoscopic sclerotherapy, Variceal ligation, Shunt procedures
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2. HIATAL HERNIA (Diaphragmatic Hernia)


-Protrusion of the esophagus into the diaphragm thru an opening (esophageal hiatus)
Two types:
- Sliding hiatal hernia ( most common)
- Axial hiatal hernia
Factors:
History: >/=60 y/o, female>male, history of trauma, increased intraabdominal pressure conditions
Sx:
1. Heartburn (30-60min after meal) in sliding type, (-) in rolling type.
2. Regurgitation
3. Dysphagia, chestpain
4. 50%- without symptoms
Pathophysiology:
Weakness/ Enlarged Esophagial hiatus
Increased intraabdominal pressure
Protrusion of the stomach

sliding hernia

rolling hernia

LES exposed to low


thoracic pressure

Obstruction
Strangulation
Volvulus

Reflux/regurgitation &
motor dysfunction
manifestations
Dx:
1. Barium swallow & Fluoroscopy
NURSING INTERVENTIONS
1. Provide small frequent feedings
2. AVOID supine position for 1 hour after eating
3. Elevate the head of the bed on 8-inch block
4. Provide pre-op and post-op care
Surgical Management: -Nissen fundoplication (suturing the fundus around esophagus, most common procedure)
- Angelchick prosthesis insertion
Pre-op nursing: Health teaching, consent
Post-op nursing:
Monitor respi distress especially if chest tubes are in place.
Instruct coughing and deep breathing exercises, ambulation
Assess for bleeding, thrombosis and infection
NGT maintained patent
Diet transition, starts with fluids after 24hrs, then small frequent feeding,
avoid carbonated beverages

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LOWER GIT
The Small Intestine
Grossly divided into the Duodenum, Jejunum & Ileum
The duodenum contains the two openings for the bile & pancreatic ducts
The ileum is the longest part (about 12 feet)
The intestinal glands secrete digestive enzymes that finalize the digestion of all foodstuff
Enzymes for carbohydrates disaccharidases
Enzymes for proteins dipeptidases & aminopeptidases
Enzyme for lipids intestinal lipase
The Large intestine
Approximately 5 feet long, with parts:
1. The cecum widest diameter, prone to rupture
2. The appendix
3. The ascending colon
4. The transverse colon
5. The descending colon
6. The sigmoid most mobile, prone to twisting
7. The rectum
1. CROHNS DISEASE
-Also called Regional Enteritis
- An inflammatory disease of the GIT affecting usually the small intestine
Inflammatory Bowel Disease
ETIOLOGY: unknown, genetics,environmental, immune defect
1. CROHNS DISEASE
The terminal ileum thickens, with scarring, ulcerations, abscess formation and narrowing of the lumen
Sx:
1. Fever
2. Abdominal distention
3. Diarrhea
4. Colicky abdominal pain
5. Anorexia/N/V
6. Weight loss
7. Anemia
CONDITIONS OF THE LARGE INTESTINE
2. ULCERATIVE COLITIS
- Ulcerative and inflammatory condition of the GIT usually affecting the large intestine
- The colon becomes edematous and develops bleeding ulcerations
- Scarring develops overtime with impaired water absorption and loss of elasticity
Sx:
1. Anorexia
2. Weight loss
3. Fever
4. SEVERE diarrhea with Rectal bleeding
5. Anemia
6. Dehydration
7. Abdominal pain and cramping
NURSING INTERVENTIONS for CD & UC
1. Maintain NPO during the active phase
2. Monitor for complications like severe bleeding, dehydration, electrolyte imbalance
3. Monitor bowel sounds, stool and blood studies
4. Restrict activities= rest and comfort
5. Administer IVF, electrolytes and TPN if prescribed
Monitor complications of diarrhea
6. Instruct the patient to AVOID gas-forming foods, MILK products and foods such as whole grains, nuts, RAW fruits and
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vegetables especially SPINACH, pepper, alcohol and caffeine


7. Diet progression- clear liquid LOW residue, high protein diet
8. Administer drugs- anti-inflammatory, antibiotics, steroids, bulk-forming agents and vitamin/iron supplements
3. HEMORRHOIDS
- Abnormal dilation and weakness of the veins of the anal canal
- Variously classified as Internal or External, Prolapsed, Thrombosed and Reducible
PATHOPHYSIOLOGY
-Increased pressure in the hemorrhoidal tissue due to straining, pregnancy, etc dilatation of veins
Internal hemorrhoids
These dilated veins lie above the internal anal sphincter
Usually, the condition is PAINLESS
External hemorrhoids
These dilated veins lie below the internal anal sphincter
Usually, the condition is PAINFUL
Sx:
1. Internal hemorrhoids- cannot be seen on the peri-anal area
2. External hemorrhoids- can be seen
3. Bright red bleeding with each defecation
4. Rectal/ perianal pain
5. Rectal itching
6. Skin tags
Dx:
1. Anoscopy
2. Digital rectal examination
NURSING INTERVENTIONS
1. Advise patient to apply cold packs to the anal/rectal area followed by a SITZ bath
2. Apply astringent like witch hazel soaks
3. Encourage HIGH-fiber diet and fluids
4. Administer stool softener as prescribed
Post-operative care for hemorrhoidectomy
1. Position: Prone or Side-lying
2. Maintain dressing over the surgical site
3. Monitor for bleeding
4. Administer analgesics and stool softeners
5. Advise the use of SITZ bath 3-4 times a day

BOWEL OBSTRUCTION
Condition where the segment of the intestine is obstructed by:
Tumors
Paralysis
Volvolus
Signs and Symptoms
Abdominal pain
Abdominal rigidity
Increased BOWEL sound in early stage and ABSENT BOWEL sound in late stage
Abdominal distention
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Vomiting and fluid imbalance


DX:
1. Abdominal x-ray
Management:
Surgery
Nursing care of abdominal surgery

Quick Summary
Peptic Ulcer
Ulceration of mucosa; In the stomach or duodenum
Outstanding Symptom: PAIN
Nursing Goal: Allow ulcer to heal, prevent complication
Rest: physical and Mental
Eliminate certain foods
Medications: antacid, H2 blockers, Proton Pump inhibitors, antibiotics, mucosal protectants
Surgery: Vagotomy, Billroth 1 and 2
Quick Summary
Liver Cirrhosis
Destruction of liver with replacement by scars
Common causes: alcoholism, post-hepatitic
Manifestations related to liver derangements
Jaundice, Ascites, splenomegaly, bleeding, enceph
Nursing goal: Control manifestations and maximize liver function

GENITO-URINARY TRACT
Overview:
Function:
1.
2.

Promote excretion of nitrogenous waste products


Maintain F&E & acid base balance

I. KIDNEYS:
Pair of bean shaped organ
- Located Retro peritonially (back of peritoneum) on either side of vertebral column. Encased in Bowmanss Capsule.
Parts:
1. Renal pelvis --------If theres inflammation----Pyelonephritis
2. Cortex
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3.

Medulla

* Nephrons = Basic living unit


* Glomerulus = Filters blood going to kidneys
Function of Kidneys:
1.

Urine formation
Urine formation 25% of total CO (Cardiac Output) is received by kidneys

1. Filtration -------------any disorder affecting filtration results to decreased renal output


*Normal GFR/ min is 125 ml of blood /minute filtered by glomerulus
2.

Tubular Reabsorption
Tubular reabsorption 124ml of ultra infiltrates (Na,K,Mg,Cl, H2O)
(H2O & electrolytes is for reabsorption)

3. Tubular Excretion
Tubular Excretion 1 ml is excreted in urine/minute
2. Regulation of BP:
Predisposing Factor:
Ex. CS hypovolemia decrease BP going to kidneys
Activation of RAAS
Release of Renin (hydrolytic enzyme) at juxtaglomerular apparatus
Angiotensin I mild vasoconstrictor
Angiotensin II Vasoconstrictor
Adrenal cortex

increase CO

increase PR

Aldosterone
Increase BP
Increase Na &
H2O reabsorption
Hypervolemia

II. URETERS

25 30 cm long, passageway of urine to bladder


Capable of peristalis movement

III. BLADDER
Located behind the symphysis pubis. Consists of muscular & elastic tissue that is distensible
Function: Reservoir of urine
Maximum capacity: 1200 1800 ml Normal adult can hold
250 500 ml needed to initiate micturition reflex
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NORMAL COMPOSITION OF URINE:


Color
=
Odor
=
Consistency
=
Ph
=
Specific Gravity =
WBC/ RBC
=
Albumin
=
E coli
=
Mucus thread
=
Amorphous urate =
CHON
=

Pale yellow toAmber


Faint Aromatic
Clear or slightly turbid
48
1.015 1.030
(-)
(-)
(-)
few
(-)
None

Catheters:
Pediatric
Female
Male

=
=
=

8-10 french
12-14 french
16-18 french

IV. URETHRA
Extends to external surface of body. Passage of urine, seminal & vaginal fluids.
Female :
Male:

3 5 cm or 1 to 1
20 cm or 8

Urological Assessment
I. Nursing History
Reason for seeking care
Current illness
Previous illness
Family History
Social History
Sexual history
II. Key Signs & Symptoms of Urological Problems
1. EDEMA
Associated with fluid retention
Renal dysfunctions usually produce ANASARCA
2. PAIN
Suprapubic pain= bladder
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Colicky pain on the flank= kidney


3. HEMATURIA
Painless hematuria may indicate URINARY CANCER!
Initial/Early-stream hematuria= urethral lesion,prostatic,seminal vesicle
Terminal/Late-stream hematuria= bladder lesion,post urethra
Throughout: glomerulonephritis
Pneumaturia: gas in urine;bladder-bowel fistula
4. DYSURIA
Pain with urination= lower UTI
Normal urine output: 1cc/kg/hr or 800-1800ml/24hr
5.POLYURIA
More than 2 Liters urine per day
6. OLIGURIA
100- 400 mL per day
7. ANURIA
Less than 100 mL per day
8.

Urinary Urgency: sudden controllable strong desire to void


Urinary retention: sense of incomplete bladder emptying(100ml left)
Urinary frequency: voiding more often than every 2hrs
Urinary Hesitancy: at least 10 sec delay in initiation of urination
Urinary incontinence: involuntary loss of urine
Nocturia: excessive urination at night
Implementation Steps for selected
III. PHYSICAL EXAMINATION
problems
Inspection
Auscultation
Percussion
Palpation
IV. Laboratory examination
Urinalysis
BUN and Creatinine levels of the serum
Serum electrolytes
Radiographic
IVP
KUB x-ray
KUB ultrasound
CT and MRI
Cystography
DISORDERS OF THE GUT

1. Provide PAIN relief


Assess the level of pain
Administer medications usually narcotic
ANALGESICS
2. Maintain Fluid and Electrolyte Balance
Encourage to consume at least 2 liters of
fluid per day
In cases of ARF, limit fluid as directed
Weigh client daily to detect fluid retention
3. Ensure Adequate urinary elimination
Encourage to void at least every 2-3 hours
Promote measures to relieve urinary
retention:
Alternating warm and cold compress
Bedpan
Open faucet

1. URINARY TRACK INFECTION (UTI)


- Bacterial invasion of the kidneys or bladder (CYSTITIS) usually caused by Escherichia coli
- Bacteria (+) 10 to the 5th in culture
Predisposing Factors:
Poor hygiene
Irritation from bubble baths
Urinary reflux
Instrumentation
Residual urine, urinary stasis
Dehydration

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Pathophysiology:
The invading organism ascends the urinary tract, irritating the mucosa & causing characteristic symptoms:
Ureter= ureteritis
Bladder= cystitis
Urethra=Urethritis
Pelvis= Pyelonephritis
Sx:
Low-grade fever
Abdominal pain
Enuresis
Pain/burning on urination
Urinary frequency
Hematuria
Upper UTI
Fever and CHIILS
Flank pain
Costovertebral angle tenderness
Laboratory Examination
Urinalysis
Urine Culture
Nursing interventions:
Administer antibiotics as ordered
Provide warm baths and allow client to void in water to alleviate painful voiding.
Force fluids. Nurses may give 3-4 liters of fluid per day if not contraindicated
Encourage measures to acidify urine (cranberry juice, acid-ash diet).
Provide client teaching and discharge planning concerning
a. Avoidance of tub baths
b. Avoidance of bubble baths that might irritate urethra
c. Importance for girls to wipe perineum from front to back
d. Increase in foods/fluids that acidify urine.
Pharmacology for urine bacteria >100,000/ml
1. Sulfa drugs
Highly concentrated in the urine
Effective against E. coli!
Can cause CRYSTALLURIA
2. Quinolones
Not given to less than 18 because they can cause cartilage degradation
3. Pyridium= urinary antiseptic
Can cause urine discoloration
a. CYSTITIS
Inflammation of bladder
Predisposing Factors:
1.
2.
3.

4.
5.
6.

Microbial invasion E. coli


High risk women
Obstruction
Urinary retention/stagnation
Increase estrogen levels
Sexual intercourse

S/Sx:

1. Hypogastric Pain flank area


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2.
3.
4.
5.

Urinary frequency & urgency


Burning upon urination
Dysuria & hematuria
Fever, chills, anorexia, gen body malaise

Dx:

1. Urine culture & sensitivity = (+) to E. coli (80-90% cause)


Nursing Mgt:

1. Force fluid = 2000 ml-3000 ml/day


2.

Warm sitz bath to promote comfort

3. Monitor & assess for gross hematuria, assess odor of urine


4. Acid Ash Diet cranberry, vit C -OJ to acidify urine & prevent bacterial multiplication
5.

Meds:
a. Systemic antibiotics
Ampicillin
Cephalosporin
b. Sulfonamides cotrimaxazole (Bactrim)
- Gantrism (ganthanol)
c. Urinary Antiseptics Nitrofurantoin (Macrodantin)
S/E:
Staining of Teeth
Peripheral Nephropathy
GIT irritants
Hemolytic Anemia ----- 1st Sign: Fever
d. Urinary analgesic- Pyridum

6. Health Teaching
a.) Importance of Hydration
b.) Void after sex
c.) Female avoids cleaning front to back
Do not use Bubble bath, Tissue paper, Powder, perfume----alters the ph of vagina & irritants
d.) Complications:
Pyelonephritis
*Ph = measures acidity of solution

b. PYELONEPHRITIS
- Acute/Cchronic inflammation of 1 or 2 renal pelvis of kidneys leading to tubular destruction, interstitial abscess
formation & can leadt to Renal Failure
Predisposing Factor:
1. Microbial invasion
a. E. Coli
b. Streptococcus
2. Urinary retention /obstruction
3. Pregnancy
4. DM
5. Exposure to renal toxins
S/Sx:
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Acute Pyelonephritis:

a. Costovertibral angle pain & tenderness FLANK PAIN


b.
c.
d.
e.

Fever, anorexia, gen body malaise


Urinary frequency, urgency
Nocturia, dsyuria, hematuria
Burning on urination

Chronic Pyelonephritis:
a.
b.
c.

Fatigue, wt loss
Polyuuria, polydypsia
HPN

Dx:

1. Urine culture & sensitivity (+) E. coli & streptococcus---- (+) Cultured Microorganisms
2.

3.

Urinalysis
Increase WBC, CHON & pus cells
Cystoscopic exam Reveals urinary obstruction

Nursing Mgt:

1. Provide CBR acute phase. Especially during acute attack


2.
3.
4.

Force fluid
Acid ash diet
Meds:
a.) Urinary antiseptic nitrofurantoin (macrodantin)
SE: peripheral neuropathy
GI irritation
Hemolytic anemia
Staining of teeth

b.) Urinary analgesic Pyridium


2.

Complication- Renal Failure

2. NEPHROLITHIASIS/ UROLITHIASIS
- Formation/ Presence of stones elsewhere in the urinary tract
3 Major Types of Stone
1. Calcium

2. Oxalate

3. Uric Acid

Milk

Cabbage
Cranberries
Nuts tea
Chocolates

Anchovies
Organ meat
Nuts
Sardines

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Predisposing Factors:

1. Diet large amounts of Ca & oxalate


2.
3.
4.
5.
6.

7.

Hereditary gout
Obesity
Sedentary lifestyle, immobility
Hyperparathyroidism
Increased uric acid levels(diet)
Dehydration,urinary stasis

Pathophysiology:
Supersaturation of crystals due to stasis
Stone formation
May pass through the urinary tract
OBSTRUCTION, INFECTION & HYDRONEPHROSIS
S/Sx:

1. Renal Colic radiating to the groin


2. Cool moist skin (shock)
3. Burning upon urination
4. Hematuria
5. Anorexia, n/v
Abdominal or flank pain
Dx:

1.
2.
3.
4.

IVP (Intravenous Pyelography) = Identifies site of obstruction and presence of non-radiopaque stones
KUB Ultrasound & X-ray = Reveals location of stone, number & size
Cytoscopic exam = Reveals urinary obstruction
Stone analysis = Reveals composition & type of stone
5. Urinalysis = Indicates presence of bacteria, increased protein, increased WBC and RBC (hematuria)
Medical Mgt:
1. Surgery
a. Percutaneous Nephrostomy: tube is inserted through skin & underlying tissues into renal pelvis to remove calculi.
b. Percutaneous Nephrostolithotomy: delivers ultrasound waves through a probe placed on the calculus.
2.

Extracorporeal shock-wave lithotripsy: delivers shock waves from outside the body to the stone, causing pulverization
- Non-invasive
- Dissolves stone through shock wave application
Pain management : Morphine or Meperidine
Diet modification

3. Nephrectomy Removal of affected kidney


4. Litholapoxy removal of 1/3 of stones- Stones will recur. Not advised for pt with big stones
Nursing interventions
1. Strain all urine through gauze to detect stones and crush all clots.
2. Force fluids (30004000 cc/day).
3. Encourage ambulation to prevent stasis.
4. Relieve pain by administration of analgesics as ordered and application of moist heat to flank area.
5. Monitor I & O
6. Warm sitz bath for comfort
7. Alternate warm compress at flank area
8. Medications:
a.) Narcotic analgesic- Morphine SO4
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b.) Allopurinol (Zyloprim) to decrease uric acid production


S/E : Allergic Reactions-----rashes, nasal congestion
9. Patent IV line
10. Provide modified diet, depending upon stone consistency: Calcium, Oxalate and Uric acid stones
1. Calcium Stones
Limit milk/dairy products
Acid-Ash Diet to acidify urine (cranberry or prune juice, meat, eggs, poultry, fish, grapes & whole grains)
2. Oxalate Stones
Avoid excess intake of foods/ fluids high in oxalate (tea, chocolate, rhubarb, spinach)
Alkaline-Ash Diet to alkalinize urine (Milk, milk products, vegetables; fruits except prunes, cranberries & plums)
3. Uric Acid Stones
Reduce foods high in purine (liver, beans, kidneys, venison, shellfish, meat soups, gravies, legumes)
Maintain alkaline urine
11. Provide client teaching and discharge planning concerning
Prevention of Urinary stasis by maintaining increased fluid intake especially in hot weather & during illness; mobility;
voiding whenever the urge is felt and at least twice during the night
12. Provide client teaching & discharge planning concerning:
Adherence to prescribed diet
Need for routine urinalysis (at least every 34 months)
Need to recognize and report signs/ symptoms of recurrence (hematuria, flank pain).

3. ACUTE RENAL FAILURE (ARF)


Sudden inability of the kidneys to excrete nitrogenous waste products & maintain F&E balance d/t a decrease in GFR.
Most important manifestation: OLIGURIA
Pathophysiology:
3 Stages/Causes:

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Normal GFR = 125 ml/min

162

1. Pre-Renal Cause:
Decrease in GFR
Causes:
1.
2.

3.
4.
5.
6.
7.
8.
9.

Septic shock
Hypovolemia
Hypotension
CHF
Hemorrhage
Chronic Diarrhea
Burns
Cardiogenic Shock
Anaphylaxis

Decrease flow to kidneys

2. Intra-Renal Cause:
Involves renal pathology Kidney Problem
Conditions that cause damage to the nephrons:
Acute tubular necrosis (ATN
Endocarditis
DM
Malignant HPN
AGN
Ttumors
BT Reactions
Hypercalcemia
Nephrotoxins (certain antibiotics, x-ray dyes, pesticides, anesthetics)
Pyelonephritis
3. Post-Renal Cause:
Mechanical Obstruction anywhere from the tubules to the urethra
Calculi
BPH
Tumors
Strictures
Blood clots
Trauma
Anatomic malformation
Urolithiasis
Laboratory Findings:
1. Urinalysis: Urine osmo and sodium
2. BUN & Creatinine levels increased
3. Hyperkalemia
4. Anemia
5. ABG: Metabolic Acidosis

3 Phases of Acute Renal Failure


1. Oliguric Phase
Urine output less than 400 cc/24 hours
Duration 12 weeks
Manifested by
a. Dilutional Hyponatremia
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4 Phases of Acute Renal Failure


(Brunner & Suddarth)
Initiation phase ( 0-2 days)
Oliguric phase
Diuretic phase
Convalescence or recovery phase

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b. Hyperkalemia
c. Hyperphosphatemia
d. Hypocalcemia
e. Hypermagnesemia
f. Metabolic Acidosis
Dx: BUN & creatinine elevated
2. Diuretic Phase
Diuresis may occur (output 35 liters/day) d/t partially regenerated tubules inability to concentrate urine
Duration: 23 week
Manifested by:
a. Hyponatremia
b.Hyperkalemia
c. Hypovolemia
d. Metabolic Acidosis
Dx: BUN & Creatinine slightly elevated
3. Convalescence or Recovery Phase
Renal function stabilizes with gradual improvement over next 312 months. Complete Diuresis

Nursing Interventions:
1. Monitor & maintain fluid & electrolyte balance.
Measure l & O every hour. note excessive losses in diuretic phase
Administer IV F & E supplements as ordered.
Weigh daily & report gains.
Monitor lab values; assess/treat F & E & acid-base imbalances as needed
2. Monitor alteration in fluid volume.
Monitor vital signs, PAP, PCWP, CVP as needed.
Weigh client daily.
Maintain strict I & O records.
3. Assess every hour for hypervolemia
Maintain adequate ventilation.
Restrict FLUID intake
Administer diuretics & antihypertensives
4. Promote optimal nutritional status.
Administer TPN as ordered.
With enteral feedings, check for residual & notify physician if residual volume increases.
Restrict protein intake to 1 g/kg/day
Restrict POTASSIUM intake
HIGH CARBOHYDRATE DIET, calcium supplements
5. Prevent complications from impaired mobility (pulmonary embolism, skin breakdown & atelectasis)
6. Prevent fever/infection.
Assess for signs of infection.
Use strict aseptic technique for wound & catheter care.
7. Support client/significant others & reduce/ relieve anxiety.
Explain pathophysiology & relationship to symptoms.
Explain all procedures and answer all questions in easy-to-understand terms
Refer to counseling services as needed
8. Provide care for the client receiving dialysis
9. Provide client teaching & discharge planning concerning
Adherence to prescribed dietary regimen
Signs and symptoms of recurrent renal disease
Importance of planned rest periods
Use of prescribed drugs only: Sx of UTI or respiratory infection need to report to physician immediately
4. CHRONIC RENAL FAILURE (CRF)
Irreversible loss of kidney function
- Gradual, Progressive irreversible destruction of the kidneys causing severe renal dysfunction.
The result is azotemia to UREMIA
Predisposing Factors:

1. DM worldwide leading cause


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Hallmark of Renal Failure:


AZOTEMIA & OLIGURIA

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2. HPN -2nd cause


3. Recurrent UTI/ Pyelonephritis
4.
5.

6.

Exposure to renal toxins


Recurrent infections
Urinary tract obstruction

Pathophysiology:

As renal functions decline


Retention of end-products of metabolism

STAGE 1= Reduced renal reserve volume (Asymptomatic) 40-75% loss of nephron function
Normal BUN & Creatinine
GFR <10-30%
STAGE 2= Renal insufficiency, 75-90% loss of nephron function
STAGE 3= End-stage renal disease, more than 90% loss. DIALYSIS IS THE TREATMENT!
S/Sx:
1. Urinary System
a. Polyuria
b. Nocturia
c. Hematuria
d. Dysuria
e. Oliguria
3. CNS
a. Headache
b. Lethargy
c. Disorientation/Confusion
d. Restlessness
e. Memory impairment
5. Respiratory
a. Kassmauls resp
b. Decrease cough reflex
c. Pericardial Friction rub
7. Fluid & Electrolytes
a. Hyperkalemia
b. Hypernatermia
c. Hypermagnesemia
d. Hyperposphatemia
e. Hypocalcemia
f. Metabolic Acidosis

2. Metabolic disturbances
a. Azotemia (increase BUN & Crea)
b. Hyperglycemia
c. Hyperinulinemia
4. GIT
a. N/V, Anorexia
b. Stomatitis
c. Uremic breath
d. Diarrhea/ constipation
6. Hematological
a. Normocytic anemia
bleeding tendencies
Pancytopenia/ Leukopenia
8. Integumentary
a. Itchiness/ pruritus
b. Uremic frost accumulation of urea in the
skin
9. Cardiovascular
a. Pulmonary HPN
b. CHF
c. Pericarditis

Diagnostic Tests:
a. 24 hour creatinine clearance urinalysis
b. Protein, sodium, BUN, Crea and WBC elevated
c. Specific gravity, platelets, and calcium decreased
d. CBC = Aanemia
Medical Mgt:
1. Diet restrictions
2. Multivitamins
3. Hematinics and erythropoietin
4. Aluminum hydroxide gels
5. Anti-hypertensive
6. Anti-seizures
7. Assist in DIALYSIS
DIALYSIS
- A procedure that is used to remove fluid & uremic wastes from the body when the kidneys cannot function
Two Methods:
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1. Hemodialysis
2. Peritoneal dialysis
Process of: Diffusion / Osmosis / Ultrafiltration
Nsg. Responsibility:

Weight:
An important
parameter that
indicates effective
hemodialysis

1. Assist in Hemodialysis
1.)
2.)
3.)
4.)

Consent/ explain procedure


Obtain baseline data & monitor VS, I&O, wt, blood exam
Strict aseptic technique
Monitor for signs of complications:
DISEQUILIBRIUM SYNDROME:
B bleeding
E embolism
D disequilibrium syndrome
S septicemia
S shock decrease in tissue perfusion

-Results from rapid removal of


urea & nitrogenous waste prod
leading to:
1. N/V
2. HPN
3. Leg cramps
4. Disorientation
5. Paresthesia
6. Headache

5.) Avoid BP taking, blood extraction, IV, at side of shunt or fistula.


Can lead to compression of fistula.
6.) Maintain patency of shunt by:
Palpate for thrills & auscultate for bruits if (+) patent shunt!
Bedside- Bulldog Clip to prevent embolism
- If with accidental removal of fistula to prevent embolism.
- Infersole (Diastole) Most common type of dialysate used
7. Meet the patient's psychosocial needs
8. Remember to avoid any procedure on the arm with the fistula (HEMO)
9. Monitor WEIGHT, blood pressure & fistula site for bleeding
10. Monitor symptoms of uremia
11. Detect complications like infection, bleeding (Hepatitis B/C and HIV infection in Hemodialysis)
Peritonitis in peritoneal dialysis
12. Warm the solution to increase diffusion of waste products (PERITONEAL)
13. Manage discomfort & pain
14. To determine effectiveness, check serum creatinine, BUN & electrolytes
15. Inform client that minimal bleeding is expected because blood has been heparinized

Nursing Mgt For Chronic Renal Failure:


1.
2.
3.

Enforce CBR
Monitor VS, I&O
Meticulous skin care. Uremic frost assist in bathing pt

DIET:
CHO = Increased
CHON = Decreased
FATS = Decreased

4. Meds:
a.) Na HCO3 = to correct acidosis
b.) Kayexelate Enema = to promote excretion of potassium
c.) Anti HPN = Hydralazine
d.) Vit & minerals
e.) Phosphate binder
(Amphogel) Al OH gel - S/E constipation
f.) To Decrease Ca Ca gluconate
g.) Hematinics
5. Assist in surgery: Renal transplantation : Complication rejection. Reverse isolation: Lifetime steroids
6. Complication
- Peritonitis -------Early Sign: Cloudy Output
- Shock
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Additional Nsg. Interventions For Chronic Renal Failure:


1. Prevent neurological complications.
Assess every hour for signs of uremia (fatigue, loss of appetite, decreased urine output, apathy, confusion, elevated blood
pressure, edema of face and feet, itchy skin, restlessness, seizures).
Assess for changes in mental functioning.
Orient confused client to time, place, date, and persons
Institute safety measures to protect client from falling out of bed.
2. Promote optimal GI function.
Assess/provide care for stomatitis
Monitor nausea, vomiting, anorexia
Administer antiemetics as ordered.
Assess for signs of Gl bleeding
3. Monitor/prevent alteration in fluid and electrolyte balance
4. Assess for hyperphosphatemia (paresthesias, muscle cramps, seizures, abnormal reflexes), and
hydroxide gels (Amphojel) as ordered

administer aluminum

5. Promote maintenance of skin integrity.


Assess/provide care for pruritus.
Assess for uremic frost (urea crystallization on the skin) and bathe in plain water
6. Monitor for bleeding complications, prevent injury to client.
Monitor Hgb, hct, platelets, RBC.
Hematest all secretions.
Administer hematinics as ordered.
Avoid lM injections
7. Promote/maintain maximal cardiovascular function.
Monitor blood pressure and report significant changes.
Auscultate for pericardial friction rub.
Perform circulation checks routinely.
Administer diuretics as ordered and monitor output.
Modify drug doses
8. Provide care for client receiving dialysis

MALE REPRODUCTIVE DISORDERS


1. BPH
2. Prostatic cancer

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DIAGNOSTIC PROCEDURES:
1. DIGITAL RECTAL EXAMINATION- DRE
Recommended for men annually with age over 40 years
Screening test for cancer
Ask patient to BEAR DOWN
2. TESTICULAR EXAMINATION
Palpation of scrotum for nodules and masses or inflammation
BEGINS DURING ADOLESCENCE
3. Prostate specific antigen (PSA)
Elevated in prostate cancer
Normal is 0.2 to 4 nanograms/mL
Cancer= over 4
1. BENIGN PROSTATIC HYPERPLASIA (BPH)
Enlargement of the prostate gland that causes outflow obstruction leading to :
1.
2.
3.
4.

Hydro ureters dilation of ureters


Hydronephrosis dilation of renal pelvis
Kidney stones
Renal failure

Predisposing Factor:

1. High Risk Men 50 years old & above


2.

60 70 (3 to 4 x at risk)
Influence of male hormone

S/Sx:
1.Nocturia - Decrease in the volume & force of urinary stream
2.Dysuria
3.Hematuria
4.Burning upon urination
5.Terminal bubbling
6.Backache
7.Sciatica
8. Increased frequency, urgency & hesitancy
Diagnosis:
1. Digital rectal exam enlarged prostate gland that is rubbery, large & NON-TENDER
2. KUB urinary obstruction
3. Cystoscopic exam obstruction
4. Urinalysis increase WBC, CHON
Medical Mgt:
1. Immediate catheterization
2. Prostatectomy
3. TRANSURETHRAL RESECTION of the PROSTATE (TURP)
4. Pharmacology: alpha-blockers, alpha-reductase inhibitors. SAW palmetto
NURSING INTERVENTION: TURP
Maintain the three way bladder irrigation to prevent hemorrhage
Only initially the drainage is pink-tinged and never reddish
Administer anti-spasmodic to prevent bladder spasms
NURSING INTERVENTION
Nursing Mgt:
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1.
2.

3.
4.

Prostatic message promotes evacuation of prostatic fluid


Limit fluid intake
Provide catheterization
Meds:
a. Alpha-Adrenergic Blockers
b. Terazozine (hytrin) - Relaxes bladder sphincter
c. Finasteride (Proscar) - Atrophy of Prostate Gland

Avoid anticholinergics
Prepare for surgery or TURP
Teach the patient perineal muscle exercises. Avoid valsalva until healing
Surgery: Prostatectomy TURP- Transurethral resection of Prostate- No incision
-Assist in cystoclysis or continuous bladder irrigation.
Nursing Mgt:
1.

Monitor symptoms of infection


2. Monitor symptoms gross/ flank bleeding. Normal bleeding within 24h.
9. Maintain irrigation or tube patent to flush out clots - to prevent bladder spasm & distention

2. PROSTATE CANCER
- A slow growing malignancy of the prostate gland
- Usually an adenocarcinoma
-This usualy spread via blood stream to the vertebrae
Predisposing Factor: Age
Assessment:
1. DRE: hard, pea-sized nodules on the anterior rectum
2. Hematuria
3. Urinary obstruction
4. Pain on the perineum radiating to the leg
Dx:
1. Prostatic specific antigen (PSA)
2. Elevated SERUM ACID PHOSPHATASE indicates SPREAD or Metastasis
Medical & Surgical Mgt:
1.Prostatectomy
2. TURP
3. Chemotherapy: hormonal therapy to slow the rate of tumor growth
4. Radiation therapy
Nursing Interventions:
1.Prepare patient for chemotherapy
2. Prepare for surgery
Nursing Interventions: Post-prostatectomy:
1. Maintain continuous bladder irrigation. Note that drainage is pink tinged w/in 24 hours
2. Monitor urine for the presence of blood clots and hemorrhage
3. Ambulate the patient as soon as urine begins to clear in color
OVERVIEW OF RESPIRATORY SYSTEM:
I. Upper respiratory tract:
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Fx:

a.

b.

1.
Filtering of air
2.
Warming & moistening
3.
Humidification
Nose cartilage
- Parts:
Rt nostril
separated by septum
Lt nostril
2. Consists of anastomosis of capillaries
Kessel Bach Plexus site of epistaxis
Pharynx (throat) muscular passageway for air& food
Branches:
1.
Oropharynx
2.
Nasopharynx
3.
Layngopharynx

c. Larynx voice box


Fx:
1.
2.

For phonation
Cough reflex

Glottis opening
Opens to allow passage of air
Closes to allow passage of food
II. Lower Rt Fx for gas exchange
a. Trachea windpipe
- has cartillagenous rings
- site for permanent/ artificial a/w tracheostomy
b. Bronchus R & L main bronchus
c. Lungs R 3 lobes = 10 segments
L 2 lobes 8 segments
Post pneumonectomy - position affected side to promote expansion of lungs
Post segmental lobectomy position unaffected side to promote drainage
Lungs covered by pleural cavity, parietal lobe & visceral lobe
Alveoli acinar cells
3. site of gas exchange (O2 & CO2)
4. diffusion: Daltons law of partial pressure of gases
Ventilation movement of air in & out of lungs
Respiration movement of air into cells
Type II cells of alveoli secrets surfactant
Surfactant - decrease surface tension of alveoli
Lecithin & spinogometer
L/S ratio 2:1 indicator of lung maturity
If 1:2 adm O2 - < 40% Concentration to prevent atelectasis & retinopathy or blindness.

I. PNEUMONIA inflammation of lung parenchyma leading to pulmonary consolidation as alveoli is filled with exudates.
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Etiologic agents:
1. Streptococcus pneumoniae (pnemococcal pneumonia)
2. Hemophilus pneumoniae(Bronchopneumonia)
3. Escherichia coli
4. Klebsiella P.
5. Diplococcus P.
High risk elderly & children below 5 yo
Predisposing factors:
1. Smoking
2. Air pollution
3. Immuno-compromised
a. AIDS PLP
b. Bronchogenic CA - Non-productive to productive cough
4. Prolonged immobility CVA- hypostatic pneumonia
5. Aspiration of food
6. Over fatigue
S/Sx:

1. Productive cough pathognomonic: greenish to rusty sputum


2.
3.
4.
5.
6.
7.
8.

Dyspnea with prolonged respiratory grunt


Fever, chills, anorexia, gen body malaise
Wt loss
Pleuritic friction rub
Rales/ crackles
Cyanosis
Abdominal distension leading to paralytic ileus

Sputum exam could confirm presence of TB & pneumonia


Dx:
1. Sputum GSCS- gram staining & culture sensitivity - Reveals (+) cultured microorganism.
2. CXR pulmo consolidation
3. CBC increase WBC
Erythrocyte sedimentation rate
4. ABG PO2 decrease
Nsg Mgt:
1.
2.
3.

Enforce CBR
Strict respiratory isolation
Meds:
1. Broad spectrum antibiotics
Penicillin or tetracycline
Macrolides ex azythromycin (zythromax)
2. Anti pyretics
3. Mucolytics or expectorants
4. Force fluids 2 to 3 L/day
5. Institute pulmonary toilet1. Deep breathing exercise
2. Coughing exercise
3. Chest physiotherapy cupping
4. Turning & reposition - Promote expectoration of secretions
6. Semi-fowler
7. Nebulize & suction
8. Comfy & humid environment
9. Diet: increase CHO or calories, CHON & vit C
10. Postural drainage - To drain secretions using gravity
Mgt for postural drainage:
a.) Best done before meals or 2 4 hrs after meals to prevent Gastroesophageal Reflux
b.) Monitor VS & breath sounds
Normal breath sound bronchovesicular
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c.) Deep breathing exercises


d.) Adm bronchodilators 15 30 min before procedure
e.) Stop if pt cant tolerate procedure
f.) Provide oral care it may alter taste sensation
g.) C/I pt with unstable VS & hemoptysis, increase ICP, increase IOP (glaucoma)
Normal IOP 12 21 mmHg
11. HT:
a.) Avoidance of precipitating factors
b.) Complication: Atelectacies & meningitis
c.) Compliance to meds
2. PULMONARY TUBERCULOSIS (KOCH DSE) - Inflammation of lung tissue caused by invasion of mycobacterium TB or
tubercle bacilli or acid fast bacilli gram (+) aerobic, motile & easily destroyed by heat or sunlight.
Predisposing factors:
1. Malnutrition
2. Overcrowding
3. Alcoholism
4. Ingestion of infected cattle (mycobacterium BOVIS)
5. Virulence
6. Over fatigue
S/Sx:
1.
2.
3.
4.
5.
6.
7.

Productive cough yellowish


Low fever
Night sweats
Dyspnea
Anorexia, general body malaise, wt loss
Chest/ back pain
Hempotysis

Diagnosis:
1. Skin test mantoux test infection of Purified CHON Derivative PPD
DOH 8-10 mm induration
WHO 10-14 mm induration
Result within 48 72h
(+) Mantoux test previous exposure to tubercle bacilli
Mode of transmission droplet infection
2. Sputum AFB (+) to cultured microorganism
3. CXR pulmonary infiltrate
caseosis necrosis
4. CBC increase WBC
Nursing Mgt:
1. CBR
2. Strict resp isolation
3. O2 inhalation
4. Semi fowler
5. Force fluid to liquefy secretions
6. DBCE
7. Nebulize & suction
8. Comfy & humid environment
9. Diet increase CHO & calories, CHON, Vit, minerals
10. Short course chemotherapy
5.

Intensive phase
INH isoniazide
Rifampicin

- give before meals for absorption


- given within 4 months, given simultaneously to prevent resistance
-S/E: peripheral neutitis vit B6
Rifampicin -All body secretions turn to red orange color urine, stool, saliva, sweat & tears.

PZA Pyrazinamide given 2 mos/ after meals. S/E: allergic rxn, nephrotoxicity & hepatoxicity
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Standard regimen
1. Injection of streptomycin aminoglycoside
Ex. Kanamycin, gentamycin, neomycin
S/E:
a.)
Ototoxicity damage CN # 8 tinnitus hearing loss
b.)
Nephrotoxicicity monitor BUN & Crea
HT:
a.) Avoid pred factors
b.) Complications:
1.) Atelectasis
2.) Miliary TB spread of Tb to other system
b.) Compliance to meds
- Religiously take meds
3. HISTOPLASMOSIS- acute fungal infection caused by inhalation of contaminated dust with histoplasma capsulatum
transmitted to birds manure.
S/Sx: Same as pneumonia & PTB like
1. Productive cough
2. Dyspnea
3. Chest & joint pains
4. Cyanosis
5. Anorexia, gen body malaise, wt loss
6. Hemoptysis
Dx:
1.
2.

Histoplasmin skin test = (+)


ABG pO2 decrease

Nsg Mgt:
1. CBR
2. Meds:
a.) Anti fungal agents
Amphotericin B (Fungizone)
S/E :
a.) Nephrotoxcicity check BUN
b.) Hypokalemia
b.)Corticosteroids
c.) Mucolytic/ or expectorants
3. O2 force fluids
4. Nebulize, suction
5. Complications:
a.) Atelectasis
b.) Bronchiectasis COPD
6. Prevent spread of histoplasmosis:
a.) Spray breading places or kill the bird.

4. COPD Chronic Obstructive Pulmonary Disease


1. Chronic bronchitis
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2.
3.
4.

Bronchial asthma
Bronchiectasis
Pulmonary emphysema terminal stage

CHRONIC BRONCHITIS - called BLUE BLOATERS inflammation of bronchus due to hypertrophy or hyperplasia of goblet
mucus producing cells leading to narrowing of smaller airways.
Predisposing factors:
1. Smoking all COPD types
2. Air pollution
S/Sx:
1. Prod cough
2. Dyspnea on exertion
3. Prolonged expiratory grunt
4. Scattered rales/ rhonchi
5. Cyanosis
6. Pulmo HPN a.)Leading to peripheral edema
b.) Cor pulmonary respiratory in origin
7. Anorexia, gen body malaise
Dx:
1.

ABG
PO2

PCO2

Resp acidosis

Hypoxemia causing cyanosis


Nsg Mgt:
(Same as emphysema)
2.) BRONCHIAL ASTHMA- reversible inflammation lung condition due to hyerpsensitivity leading to narrowing of smaller
airway.
Predisposing factor:
1. Extrinsic Asthma called Atropic/ allergic asthma
a.) Pallor
b.) Dust
c.) Gases
d.) Smoke
e.) Dander
f.) Lints
2. Intrinsic AsthmaCause:
Herediatary
Drugs aspirin, penicillin, blockers
Food additives nitrites
Foods seafood, chicken, eggs, chocolates, milk
Physical/ emotional stress
Sudden change of temp, humidity &air pressure
3. mixed type: combi of both ext & intr. Asthma
90% cause of asthma
S/Sx:
1.
2.
3.
4.
5.
6.
7.
Dx:
1.
2.

C cough non productive to productive


D dyspnea
W wheezing on expiration
Cyanosis
Mild apprehension & restlessness
Tachycardia & palpitation
Diaphoresis
Pulmo function test decrease lung capacity
ABG PO2 decrease

Nsg Mgt:
1. CBR all COPD
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2.

Meds-

a.) Bronchodilator through inhalation or metered dose inhaled / pump. Give 1st before corticosteroids

2.

3.
4.
5.
6.
6.
7.

b.) Corticosteroids due inflammatory. Given 10 min after adm bronchodilator


c.) Mucolytic/ expectorant
d.) Mucomist at bedside put suction machine.
e.) Antihistamine
Force fluid
O2 all COPD low inflow to prevent resp distress
Nebulize & suction
Semifowler all COPD except emphysema due late stage
HT
a.) Avoid pred factors
b.) Complications:
Status astmaticus- give epinephrine & bronchodilators
Emphysema
c.) Adherence to med

BRONCHIECTASIS abnormal permanent dilation of bronchus resulting to destruction of muscular & elastic tissues of alveoli.
Predisposing factors:
1. Recurrent upper & lower RI
2. Congenital anomalies
3. Tumors
4. Trauma
S/Sx:
1. Productive cough
2. Dyspnea
3. Anorexia, gen body malaise- all energy are used to increase respiration.
4. Cyanosis
5. Hemoptisis
Dx:
1.
2.

ABG PO2 decrease


Bronchoscopy direct visualization of bronchus using fiberscope.
Nsg Mgt: before bronchoscopy
1.
Consent, explain procedure MD/ lab explain RN
2.
NPO
3.
Monitor VS
Nsg Mgt after bronchoscopy
1.
Feeding after return of gag reflex
2.
Instruct client to avoid talking, smoking or coughing
3.
Monitor signs of frank or gross bleeding
4.
Monitor of laryngeal spasm
8.
DOB
9.
Prepare at bedside tracheostomy set
Mgt: same as emphysema except Surgery
Pneumonectomy removal of affected lung
Segmental lobectomy position of pt unaffected side

PULMONARY EMPHYSEMA irreversible terminal stage of COPD


10. Characterized by inelasticity of alveolar wall leading to air trapping, leading to maldistribution of gases.
11. Body will compensate over distension of thoracic cavity
12. Barrel chest
Predisposing factor:
1. Smoking
2. Allergy
3. Air pollution
4. High risk elderly
5. Hereditary - 1 anti trypsin to release elastase for recoil of alveoli.
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S/Sx:
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.

Productive cough
Dyspnea at rest due terminal
Anorexia & gen body malaise
Rales/ rhonchi
Bronchial wheezing
Decrease tactile fremitus (should have vibration) palpation 99. Decreased - with air or fluid
Resonance to hyperresonance percussion
Decreased or diminished breath sounds
Pathognomonic: barrel chest increase post/ anterior diameter of chest
Purse lip breathing to eliminated PCO2
Flaring of alai nares

Diagnosis:
1. Pulmonary function test decrease vital lung capacity
2. ABG
1. Panlobular / centrolobular emphysema
pCO2 increase
pO2 decrease hypoxema
resp acidosis
Blue bloaters
2. Panacinar/ Centracinar
pCO2 decrease
pO2 increase hyperaxemia
resp alkalosis
Pink puffers
Nursing Mgt:
1. CBR
2. Meds
a.) Bronchodilators
b.) Corticosteroids
c.) Antimicrobial agents
d.) Mucolytics/ expectorants
3. O2 Low inflow
4. Force fluids
5. High fowlers
6. Neb & suction
7. Institute
P posture
E end
E expiratory
to prevent collapse of alveoli
P pressure
8. HT
a.) Avoid smoking
b.) Prevent complications
1.) Cor pulmonary R ventricular hypertrophy
2.) CO2 narcosis lead to coma
3.) Atelectasis
4.) Pneumothorax air in pleural space
9. Adherence to meds

5. RESTRICTIVE LUNG DISORDER


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PNEUMOTHORAX partial / or complete collapse of lungs due to entry or air in pleural space.
Types:
1. Spontaneous pneumothorax entry of air in pleural space without obvious cause.
Eg. rupture of bleb (alveoli filled sacs) in pt with inflammed lung conditions
Eg. open pneumothorax air enters pleural space through an opening in chest wall
-Stab/ gun shot wound
2. Tension Pneumothorax air enters plural space with @ inspiration & cant escape leading to over distension of thoracic
cavity resulting to shifting of mediastinum content to unaffected side.
Eg. flail chest paradoxical breathing
Predisposing factors:
1.Chest trauma
2.Inflammatory lung conditions
3.Tumor
S/Sx:
1. Sudden sharp chest pain
2. Dyspnea
3. Cyanosis
4. Diminished breath sound of affected lung
5. Cool moist skin
6. Mild restlessness/ apprehension
7. Resonance to hyper resonance
Diagnosis:
1. ABG pO2 decrease
2. CXR confirms pneumothorax
Nursing Mgt:
1. Endotracheal intubation
2. Thoracenthesis
3. Meds Morphine SO4
13. Anti microbial agents
4. Assist in test tube thoracotomy
Nursing Mgt if pt is on CPT attached to H2O drainage
1. Maintain strict aseptic technique
2. DBE
3. At bedside
1. Petroleum gauze pad if dislodged Hemostan
2. If with air leakage clamp
3. Extra bottle
4. Meds Morphine SO4
Antimicrobial
5. Monitor & assess for oscillation fluctuations or bubbling
1. If (+) to intermittent bubbling means normal or intact
- H2O rises upon inspiration
- H2o goes down upon expiration
b.) If (+) to continuous, remittent bubbling
1. Check for air leakage
2. Clamp towards chest tube
3. Notify MD
c.) If (-) to bubbling
1. Check for loop, clots, and kink
2. Milk towards H2O seal
3. Indicates re-expansion of lungs
When will MD remove chest tube:
1. If (-) fluctuations
2. (+) Breath sounds
3. CXR full expansion of lungs
Nursing Mgt of removal of chest tube
2. DBE
3. Instruct to perform Valsalva maneuver for easy removal, to prevent entry of air in pleural space.
4. Apply vaselinated air occlusive dressing
14. Maintain dressing dry & intact
EAR
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1.
2.
Parts:
1.

Hearing
Balance (Kinesthesia or position sense)
Outera.) Pinna/ auricle protects ear from direct trauma
b.) Ext. auditory meatus has ceruminous gland. Cerumen
c.) Tympanic membrane transmits sound waves to middle ear

Disorders of outer ear


Entry of insects put flashlight to give route of exit
Foreign objects beans (bring to MD)
H2O - drain
2. Middle ear
a.) Ear osssicle
1. Hammer -malleus
2. Anvil
-Incus
3. Stirrups -stapes

for bone conduction

disorder conductive hearing loss

b. Eustachian tube - Opens to allow equalization of pressure on both ears


- Yawn, chew, and swallow
Children straight, wide, short
5. Otitis media
Adult long, narrow & slanted
c. Muscles
1. Stapedius
2. Tensor tympani

3. Inner ear
a. Bony labyrinth for balance, vestibule
Utricle & succule
Otolithe or ear stone has Ca carbonate
Movement of head = Righting reflex = Kinesthesia
b. Membranous Labyrinth
1. Cochlea ( function for hearing) has organ of corti
2. Endolymph & perilymph for static equilibrium
3. Mastoid air cells air filled spaces in temporal bone in skull
Complications of Mastoditis meningitis
Types of hearing loss:
1. Conductive hearing loss transmission hearing loss
Causes:
a.) Impacted cerumen tinnitus & conduction hearing loss- assist in ear irrigaton
b.) Immobility of stapes OTOSCLEROSIS
6. Middle ear disease char by formation of spongy bone in the inner ear causing fixation or immobility of stapes
7. Stapes cant transmit sound waves
Surgery
Stapedectomy removal of stapes, spongy bone & implantation of graft/ ear prosthesis
Created by Nia E. Tubio

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Predisposing factor:
1. Familiar tendency
2. Ear trauma & surgery
S/Sx:
1.
2.

Tinnitus
Conductive hearing loss

Diagnosis:
1. Audiometry various sound stimulates (+) conductive hearing loss
2. Webers test Normal AC> BC
result BC > AC
Stapedectomy
Nursing Mgt post op
1. Position pt unaffected side
2. DBE
No coughing & blowing of nose
- Night lead to removal of graft
3. Meds:
a.) Analgesic
b.) Antiemetic
c.) Antimotion sickness agent. Ex. meclesine Hcl (Bonamine)
4. Assess motor function facial nerve - (Smile, frown, raise eyebrow)
5. Avoid shampoo hair for 1 to 2 weeks. Use shower cap
SENSORY NEURAL HEARING LOSS/ NERVE DEAFNESS
Cause:
1. Tumor on cocheal
2. Loud noises (gun shot)
3. Presbycusis bilateral progressive hearing loss especially at high frequencies elderly
Face elderly to promote lip reading
4. Menieres disease endolymphatic hydrops
8. Inner ear disease char by dilation of endo lympathic system leading to increase volume of endolin
Predisposing factor of MENIERES DISEASE
Smoking
Hyperlipidemia
30 years old
Obesity (+) chosesteatoma
Allergy
Ear trauma & infection
S/Sx:
1.

2.
3.
4.
5.
6.
7.
Diagnosis:
1.

TRIAD symptoms of Menieres disease


a.)
Tinnitus
b.)
Vertigo
c.)
Sensory neural hearing loss
Nystagmus
n/v
Mild apprehension, anxiety
Tachycardia
Palpitations
Diaphoresis
Audiometry (+) sensory hearing loss

Nursing mgt:
1.
Comfy & darkened environment
2.
Siderails
3.
Emetic basin
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4.

Meds:
a.)
b.)
c.)
d.)
e.)
f.)

Diuretics to remove endolymph


Vasodilator
Antihistamine
Antiemetic
Antimotion sickness agent
Sedatives/ tranquilizers

5.
Restrict Na
6.
Limit fluid intake
7.
Avoid smoking
8.
Surgery endolymphatic sac decompression- Shunt
*Kawasaki : Drug of Choice : Aspirin, IgG
Common to children 5 y/o below
(desquamation of palms & toes)
*Anatomy :

URT
Nose
Pharynx
Larynx

Created by Nia E. Tubio

LRT
Trachea
Bronchos

180