COMMUNICABLE

DISEASES
Roberto M. Salvador Jr. R.N.,M.D.
Infectious and Tropical Disease
Specialist
Philippines top 10 leading
causes of morbidity & mortality
in the year 2007:
 Diarrhea
 Bronchitis
 Pneumonia
 Influenza
 Hypertension
 Tuberculosis
 Malaria
 Heart diseases
 Cancer
 Accidents
 Chronic obstructive pulmonary disease and other respiratory diseases
 Diabetes and Kidney diseases.
 Host and Microbial Interaction
INTRODUCTION

Although most microorganisms

live in harmony with the human
body, some—called pathogens
—can infect the body and
cause disease. Infectious
diseases range from mild
illnesses, such as a cold, to
fatal illnesses, such as AIDS.
We occasionally come into
contact with people or animals
that are infected and thus
expose ourselves to the
pathogens of their diseases. In
fact, our environment is such
that everyday we live with
some risk of exposure to
diseases.
BLOOD/VECTOR BORNE
DISEASES
Prevention
 Eradicate the source DOH CLEAN

C – chemically treated mosquito net

L - larvae eating fish
E – environmental sanitation
A – anti-mosquito
N – neem tree (oregano, eucalyptus)
Dengue Hemorrhagic Fever
 caused by dengue virus (Flaviridae) with 4 serotypes
 transmitted to a bite of female Aedes aegypti mosquito
 incubation period 2-7 days
Vectors: (day biting)
 Aedes aegypti
(breeds in water
stored in houses)
 Aedes albopictus
 Culex fatigans
Clinical manifestations

 First 4 days – Febrile

or Invasive stage –
high grade fever,
headache, body
malaise, conjuctival
injection, vomiting,
epistaxis or gum
bleeding, positive
tourniquet test.
 4th – 7th day – Toxic or Hemorrhagic Stage – After
the lyze of the fever, this is where the complication
of dengue is expected to come out as manifested
by abdominal pain, melena, indicating bleeding in
the upper gastrointestinal tract, Unstable BP,
narrow pulse pressure and shock.
 7th – 10th day – Convalescent or recovery
stage – after 3 days of afebrile stage and the
patient was properly hydrated and monitored
BP will become stable and laboratory values
of platelet count and bleeding parameters will
begin to normalize.
Classification of Dengue Fever
according to severity

 Grade I – Dengue fever, saddleback fever plus

constitutional signs and symptoms plus positive
tourniquet test
 Grade II – Stage I plus spontaneous bleeding, epistaxis,
GI, cutaneous bleeding
 Grade III – Dengue Shock Syndrome, all of the following
signs and symptoms plus evidence of circulatory failure
 Grade IV – Grade III plus irreversible shock and massive
bleeding
Diagnostics
 Tourniquet test or Rumpel Leads Test –
presumptive test for capillary fragility
- keep cuff inflated for 6-10 mins (child), 10-
15 min (adults)
- count the petechiae formation 1 sq inch
(>20 petechiae/sq inch)
Laboratory Procedures

 CBC
 Bleeding Parameters
 Serologic test
 Dengue blot, Dengue Igm
Other :
 PT (Prothrombin Time)
 APTT (Activated Partial Thromboplastin Time)
 Bleeding time
 Coagulation time

Mgmt: symptomatic and supportive

Management

 Specific Therapy – none

 Symptomatic/Supportive therapy
 Intravenous Fluids (IVF)
 with hemoconcentration, 5-7 ml/kg/hr
 with shock, 10-30ml/kg in <20mins
Use of Blood/Blood Products

Platelet concentrate 1 unit/5-7kg

Cryoprecipitate, 1unit/5kg
FFP, 15ml/kg x 2-4hrs
 given in patient in
impending shock and
unresponsive to isotonic or
colloid transfusion.
 Prolonged PT
FWB 20cc/kg
 active bleeding
 check serum calcium
PRBC 10cc/kg
Nursing Intervention

 Paracetamol (no aspirin)

 Giving of cytoprotectors
 Gastric Lavage
 trendelenburg position for shock
 Nasal packing with epinephrine
 No intramuscular injections
 manage anxiety of patient and family
Preventive measures

 Department of Health program for the

control of Dengue Hemorrhagic Fever
 S eek and destroy breeding places
 S ay no to left and right defogging
 S eek early consultation
FILARIASIS
 The disease often progresses to become
chronic, debilitating and disfiguring
disease since it’s symptoms are unnoticed
or unfamiliar to health workers.
 High rates in region 5(bicol), 8 (samar and
leyte, II (davao)
Filariasis
 Wuchereria bancrofti and Bulgaria malayi
 Transmitted to the bite of infected female
mosquito (Aedes, Anopheles, Mansonia)
 The larvae are carried in the blood stream and
lodged in lymphatic vessels and lymph glands
where they mature in adult form
 Two biological type
 Nocturnal
 microfilaria
circulate in peripheral blood at
night (10pm – 2am)
 Diurnal
 microfilaria circulate in greater concentration
at daytime
Clinical Manifestations
Acute stage
 - filarial fever and lymphatic inflammation that
occurs frequently as 10 times per year and
usually abates spontaneously after 7 days
 - Lymphadenitis (Inflammation of the lymph
nodes)
 - Lymphangitis (Inflammation of the lymph
vessels)
Chronic Stage (10-15 years from the onset of the
first attack)
 - Hydrocele (Swelling of the scotum)
 - Lymphedema (Temporary swelling of the
upper and lower extremities)
 - Elephantiasis (enlargement and thickening of
the skin of the lower or upper extremities)
Laboratory Diagnosis

 Blood smear –
presence of
microfilaria
 Immunochromatograp
hic Test (ICT)
 Eosinophil count
Management Guidelines

 Specific Therapy
 Dietylcarbamazine (DEC) 6mg/KBW in divided doses for
12 consecutive days
 Ivermectine (Mectican)
 Supportive Therapy
 Paracetamol
 Antihistamine for allergic reaction due to DEC
 Vitamin B complex
 Elevation of infected limb, elastic stocking
 DEC should be taken immediately after meals
 It may cause loss of vision, night blindness, or
tunnel vision with prolonged used.
 Ivermectin is best taken as single dose with a
full glass of water in an empty stomach.
 Cannot be used in patient with asthma
Preventive Measures

 Health teachings
 Environmental Sanitation
 Leptospira interrogans
 AKA Red water disease in cattle,
Swineherd’s disease or Weil’s disease in
humans
Leptospirosis (Weil’s disease)

 a zoonotic systemic infection caused by

Leptospires, that penetrate intact and
abraded skin through exposure to water,
wet soil contaminated with urine of
infected animals.
Anicteric Type (without jaundice)
 manifested by fever, conjunctival injection
 signs of meningeal irritation

Icteric Type (Weil Syndrome)

 Hepatic and renal manifestation
 Jaundice, hepatomegaly
 Oliguria, anuria which progress to renal failure
 Shock, coma, CHF
 Convalescent Period
Diagnosis

 Clinical history and manifestation

 Culture
 Blood: during the 1st week
 CSF: from the 5th to the 12th day
 Urine: after the 1st week until convalescent period
 LAAT (Leptospira Agglutination Test)
 other laboratory
 BUN,CREA, liver enzymes
Treatment

 Specific
 Penicillin50000 units/kg/day
 Tetracycline 20-40mg/kg/day

 Non-specific
 Supportive and symptomatic
 Administration of fluids
 Peritoneal dialysis for renal failure
 Educate public regarding the mode of
transmission, avoid swimming or wadding
in potentially contaminated waters and use
proper protective equipment.
Nursing Responsibilities

1. Dispose and isolate urine of patient.

2. Environmental sanitation like cleaning the
esteros or dirty places with stagnant water,
eradication of rats and avoidance of wading or
bathing in contaminated pools of water.
3. Give supportive and asymptomatic therapy
4. Administration of fluids and electrolytes.
5. Assist in peritoneal dialysis for renal failure
patient (The most important sign of renal failure
is presence of oliguria.)
MALARIA
Malaria

 “King of the Tropical Disease”

 an acute and chronic infection caused by
protozoa plasmodia
 Infectious but not contagious
 transmitted through the bite of female anopheles
mosquito
Malaria Exacts Heavy Toll in Africa

Malaria
 There are 300-500m new
cases annually
 Over 1m die every year –
almost 3000 per day
 90% of deaths are in
Sub-Saharan Africa
 Cost of malaria in Africa
is $100bn

Source: World Bank staff estimates

Vector: (night biting)
 Anopheles mosquito

or Minimus flavire

Life cycle:
 Sexual cycle/sporogony (mosquito)
 sporozoites injected into humans
 Asexual cycle/schizogony (human)
 gametes is the infective stage taken up by
biting mosquito
 Plasmodium vivax
 more widely distributed
 causes benign tertian malaria
 chills and fever every 48 hours in 3 days
 Plasmodium falciparum
 common in the Philippines
 causes the most serious type of malaria
because of high parasitic densities in blood.
 causes malignant tertian malaria
 Plasmodium malaria
 much less frequent
 causes quartan malaria, fever and chills
every 72 hrs in 4 days
 Plasmodium ovale
 rarely seen.
Clinical Manifestation

 uncomplicated
 fever, chills, sweating every 24 – 36 hrs
 Complicated
 sporulation or segmentation and rupture of erythrocytes
occurs in the brain and visceral organs.
 Cerebral malaria
 changes of sensorium, severe headache and vomiting
 seizures
 Cold stage – 10-15 mins, chills, shakes
 Hot stage – 4-6 hours, recurring high
grade fever, severe headache, vomiting,
abdominal pain, face is blue
 Diaphoretic stage – excessive sweating
Diagnosis

 Malarial smear
 Quantitative Buffy Coat (QBC)
 Travel in endemic areas
Treatment:

 Determine the species of parasite

 Objectives of treatment
 Destroy all sexual forms of parasite to cure the
clinical attack
 Destroy the excerythrocytes (EE) to prevent
relapse
 Destroy gametocytes to prevent mosquito
infections
 Treatment for P. falciparum
 Chloroquine tablet (150mg/base/tab) Day
1,2,3
 Sulfadoxine/Pyrimethamine 500mg/25mg/tab,
3tabs single dose
 Primaquine (15mg/tab) 3 tabs single dose
 Treatment for P. vivax
 Chloroquine,Day 1,2,3
 Primaquine 1 tab OD for 14 days
 Treatment for mixed
 Chloroquine (4,4,2)
 Sulfadoxine/Pyrimethamine 3 tabs once
 Primaquine 1 tab for 14 days
 Multi-drug resistant P. falciparum
 Quinineplus Doxycycline, or Tetracycline and
Primaquine
Complications

 severe anemia
 cerebral malaria

- hypoglycemia
MENINGOCOCCEMIA

 caused by Neisseria meningitidis, a gram

negative diplococcus
 transmitted through airborne or close contact
 incubation is 1-3 days
 natural reservoir is human nasopharynx
 Clinical Manifestations
 sudden onset of high grade fever, rash and
rapid deterioration of clinical condition within
24 hours
S/sx:
1. Meningococcemia – spiking fever, chills, arthralgia,
sudden appearance of hemorrhagic rash
2. Fulminant Meningococcemia (Waterhouse
Friederichsen) – septic shock; hypotension,
tachycardia, enlarging petechial rash, adrenal
insufficiency
Laboratory
 Blood Culture
 Gram stain of peripheral smear, CSF and
skin lesions
 CBC
Treatment:

 Antimicrobials
 Benzyl Penicillin 250-400000 u/kg/day
 Chloramphenicol 100mg/kg/day
 Symptomatic and supportive
 fever
 seizures
 hydration
 respiratory function
 Chemoprophylaxis
 Rifampicin 300-600mg q 12hrs x 4 doses
 Ofloxacin 400mg single dose
 Ceftriaxone 125-250mg IM single dose
Nursing Intervention
 Provide strict isolation
 Wearing of mask etc
 Health teaching
 Contact tracing
 Prophylaxis
 Meningococcal vaccine for high risk patients
 acute viral encephalomyelitis
 incubation period is 4 days up to 19 years
 risk of developing rabies, face bite 60%, upper
extremities 15-40%, lower extremities 10%
 100% fatal
 pain or numbness at the site of bite
 fear of water
 fear of air
4 STAGES
1. prodrome - fever, headache, paresthesia,
2. encephalitic – excessive motor activity,
hypersensitivity to bright light, loud noise,
hypersalivation, dilated pupils
3. brainstem dysfunction – dysphagia,
hydrophobia, apnea
4. death
 Rabies Virus
The rabies virus is usually transmitted to humans by a bite from an
infected dog, but the bite of any animal (wild or domestic) is suspect in
an area where rabies is present. Symptoms of the disease appear after
an incubation period of ten days to one year and include fever,
breathing difficulties, and muscle spasms in the throat that make
drinking painful. Death almost invariably occurs within three days to
three weeks of the onset of symptoms. For this reason, the emphasis of
treatment is on prevention. In the United States, veterinarians
Diagnosis
 FAT (fluorescent antibody test)
 Clinical history and signs and symptoms
Management
 No treatment for clinical rabies
 Prophylaxis
Postexposure prophylaxis
Category I Observe the dog for 14 days
Licking of intact skin
Category II 1.Active vaccine
Abrasion, laceration, punctured wound 2.Observe dog for 14 days
on the lower extremities
Category III
Abrasion, laceration on upper 1.Active
extremities, head and neck 2.Passive
Dog is killed, lost, died
Active vaccine
 Intradermal (0,3,7,30,90)
 Intramuscular (0,3,7,14,28)
 (0,7,21)
Passive Vaccine
 a. ERIG wt in kg x .2 = cc to be injected
im (ANST)
 b. HRIG wt in Kg x .1333
Pre-exposure Prophylaxis
 Intradermal/Intramuscular (0,7,21)
Infection control
 Patient is isolated to prevent exposure of hospital
personnel, watchers and visitors

Preventive Measures
 Education
 Post-exposure and Pre-exposure Prophylaxis
TETANUS

 caused by Clostridium tetani, grows

anaerobically
 Tetanus spores are introduced into the
wound contaminated with soil.
 Incubation period 4-21 days
 Pathogenesis
> a neurotoxin (tetanoplasmin) and
hemolysin (tetanolysin) are produced
Pathophysiology
Clostridium tetani in puncture wound

Tetanospasmin

attack PNS and CNS

GABA and Glycine inhibited

Tetanic spasm
Clinical manifestation

 Difficulty of opening the mouth (trismus or

lockjaw)
 Risus sardonicus
 Abdominal rigidity
 Localized or generalized muscle spasm
Criteria Stage I Stage II Stage III

Incubation Period > 11 days 8-10 days <7days

Trismus mild moderate Severe

Muscle rigidity mild Pronounced Severe, boardlike

Spasm absent Mild, short Frequent,

prolonged

Dyspnea, cyanosis absent absent Present

Treatment

1. Neutralize the toxin

2. Kill the microorganism
3. Prevent and control the spasm
- muscle relaxants
- Sedatives
- Tranquilizers
4. Tracheostomy
Treatment:
anti-toxin
 Tetanus Anti-Toxin (TAT)
Adult,children,infant 40,000 IU ½ IM,1/2 IV
Neonatal Tetanus 20000 IU, 1/2IM, ½ IV
 TIG
Neonates 1000 IU, IV drip or IM
Adult, infant, children 3000 IU, IV drip or IM
Antimicrobial Therapy
Penicillin !-3 mil units q 4hours
Pedia 500000 – 2mil units q 4 hrs
Neonatal 200000 units IV q 12hrs or
q8hrs
Control of spasms
 diazepam
 chlorpromazine
Nursing care
 Patient should be in a quiet, darkened
room, well ventilated.
 Minimal/gentle handling of patient
 Liquid diet via NGT
 Prevent Injury
Preventive Measures
 Treatment of wounds
 Tetanus toxoid
SCHISTOSOMIASIS

 caused by blood flukes, Schistosoma

 has 3 species, S. haematobium, S.
mansoni, S. japonicum
 S. japonicum is endemic in the Philippines
(Leyte, Samar, Sorsogon, Mindoro,Bohol)
 Intermediate host, Oncomelania quadrasi
cycle
Eggs
Escap
Sex in e into
portal Intesti
vein nal
lumen

Adult
in 2 (Miraci
days dia)

Oncol
omela
Portal
nia
veins
Quadr
asi

Skin
penetr Sporo
ate zyst
Cercar
ia
 Diagnosis:
 Schistosoma eggs in stool
 Rectal bipsy
 Kato Katz
 Ultrasound of HBT
Clinical Manifestation

 severe jaundice
 edema
 ascites
 hepatosplenomegaly
 S/S of portal hypertension
Management

 Praziquantel 60mg/kg once dosing

 Supportive and symptomatic
Methods of Control
 Educate the public regarding the mode of
transmission and methods of protection.
 Proper disposal of feces and urine
 Prevent exposure to contaminated water. To
minimize penetration after accidental water
exposure, towel dry and apply 70% alcohol.
 The organism is pathogenic only in man
 Spread chiefly by carriers, ingestion of infected
foods
 Endemic particularly in areas of low sanitation
levels
 Occurs more common in may to august
MOT: oral fecal route

S/sx: Rose spot

(abdominal rashes),
more than 7days Step
ladder fever 40-41 deg,
headache, abdominal
pain, constipation
(adults), mild diarrhea
(children)
Pathophysiology
Oral ingestion

Bloodstream

RES (lymph node, spleen, liver)

Bloodstream

Gallbladder

Peyer’s patches of SI necrosis and

ulceration
Diagnosis
 Blood examination WBC usually leukopenia
with lymphocytosis
 Isolation
- Blood culture 1st week\
- Urine culture 2nd week
- Stool culture 3rd week
 Widal test O or H
- Becomes positive at the end of the 2nd week
 1st week step ladder fever (BLOOD)
 2nd week rose spot and fastidial
 typhoid psychosis (URINE & STOOL)
 3rd week (complications) intestinal bleeding, perforation,
peritonitis, encephalitis,
 4th week (lysis) decreasing S/SX
 5th week (convalescent)
 Typhoid Fever
Ulceration of the Peyer's Patches
Mgmt: Chloramphenicol, Amoxicillin,
Sulfonamides, Ciprofloxacin, Ceftriaxone
 Watch for complications
a. Perforation – symptoms of sharp
abdominal pain, abdominal rigidity and
absent of bowel sounds.
- prepare for intestinal decompression or
surgical intervention
b. Intestinal hemorrhage
- withold food and give blood transfusion
Nursing Interventions
 Environmental Sanitation
 Food handlers sanitation
permit
 Supportive therapy
 Assessment of
complication (occuring on
the 2nd to 3rd week of
infection )
- typhoid psychosis,
typhoid meningitis
- typhoid ileitis
Hepatitis
 Hepa A – fecal oral route
 Hepa B – body fluids
 Hepa C – non A non B, BT, body fluids
 Hepa D – hypodermic, body fluids
 Hepa E – fecal oral route, fatal and common
among pregnant women
 Hepa G – BT, parenteral
Hepatitis A
 Infectious hepatitis, epidemic hepatitis
 Young people especially school children are
most commonly affected.

Predisposing factors:
- Poor sanitation, contaminated water supply,
unsanitary preparation of food, malnutrition,
disaster conditions
Incubation Period: 15-50 days
Signs/Symptoms:
- Influenza
- Malaise and easy fatigability
- Anorexia and abdominal discomfort
- Nausea and vomiting
- Fever, CLAD
- jaundice
Dx: Anti HAV IgM – active infection
Anti HAV IgG – old infection; no active disease

Management:
- Prophylaxis
- Complete bed rest
- Low fat diet but high sugar
 Ensure safe water for drinking
 Sanitary method in preparing handling and
serving of food.
 Proper disposal of feces and urine.
 Washing hands before eating and after toilet
use.
 Separate and proper cleaning of articles used by
patient
Hepatitis B
 DNA, Hepa B virus
 Serum hepa
 Worldwide distribution
 Main cause of liver cirrhosis and liver
cancer

IP: 2-5 months

Mode of Transmission
 From person to person through
- contact with infected blood through broken
skin and mucous membrane
- sexual contact
- sharing of personal items
 Parenteral transmission through

- blood and blood products

- use of contaminated materials
 Perinatal transmission
High Risk group
 Newborns and infants of infected mothers
 Health workers exposed to handling blood
 Persons requiring frequent transfusions
 Sexually promiscous individuals
 Commercial sex workers
 Drug addicts
Possible Outcome

 Some become carriers of the virus and

transmit disease to others.
 Almost 90% of infected newborns become
carriers
Hepatitis C
 Post transfusion Hepatitis
 Mode of transmission – percutaneous, BT
 Predisposing factors – paramedical teams
and blood recipients
 Incubation period – 2weeks – 6 months
Hepatitis D
 Dormant type
 Can be acquired only if with hepatitis B

 Hepatitis E
 If hepatitis E recurs at age 20-30, it can lead to
cancer of the liver
 Enteric hepatitis
 Fecal-oral route
DX:
 Elevated AST or SGPT (specific) and ALT or SGOT
 Increased IgM during acute phase
 (+) or REACTIVE HBsAg = INFECTED, may be acute,
chronic or carrier
 (+) HBeAg = highly infectious
 ALT – 1st to increase in liver damage
 HBcAg = found only in the liver cells
 (+) Anti-HBc = acute infection
 (+) Anti-HBe = reduced infectiousness
 (+) Anti-HBs = with antibodies (FROM vaccine or
disease)
 Blood Chem. Analysis (to monitor progression)
 Liver biopsy (to detect progression to CA)
Mgmt:
 Prevention of spread – Immunization and
Health Education
 Enteric and Universal precautions
 Assess LOC
 Bed rest
 ADEK deficiency intervention
 High CHO, Moderate CHON, Low fat
 FVE prevention
Respiratory System
 Mumps
 RNA, Mumps virus
 Mumps vaccine - > 1yo
 MMR – 15 mos
 Lifetime Immunity

IP: 12-16 days

MOT: Droplet, saliva, fomites

S/sx: Unilateral or bilateral
parotitis, Orchitis - sterility if bilateral,
Oophoritis, Stimulating food cause
severe pain, aseptic meningitis

Dx: serologic testing, ELISA

Mgmt: supportive
Nursing care
 Respiratory precautions
 Bed rest until the parotid gland swelling subsides
 Avoid foods that require chewing
 Apply hot or cold compress
 To relieve orchitis, apply warmth and local
support with tight fitting underpants
 Diptheria
 Acute contagious disease
 Characterized by generalized systemic
toxemia from a localized inflammatory
focus
 Infants immune for 6 months of life
 Produces exotoxin
 Capable of damaging muscles especially
cardiac, nerve, kidney and liver
 Increase incidence prevalence during
cooler months
 Mainly a disease of childhood with peak at
2-5 years, uncommon in >6months
Diphtheria
 Corynebacterium diphtheriae, gram (+),
slender, curved clubbed organism “Klebs-
Loeffler Bacillus”
 IP: 2-6 days

 Mode of transmission is direct or indirect

contact
Pathogenesis
 Pseudomembrane is formed by
leukocytes, necrotic tissue and
microorganism which is adherent to the
tissues and leaves a raw bleeding when
detached
 Further development of toxins causing
attack to the heart, kidney, liver and
cranial nerve
1. Nasal – invades nose by extension from
pharynx
2. Pharygeal
- sorethroat causing dysphagia
- Pseudomembrane in uvula, tonsils, soft
palate
- Bullneck – inflammation of cervical LN
3. Laryngeal
- increasing hoarseness until aphonia
- wheezing on expiration
- dyspnea
Diagnosis
 Nose and throat swab using Loeffler’s
medium
 Schick test – determine susceptibility or
immunity in diptheria
 Maloney test – determines hypersensitivity
to diptheria toxoid
Complications
 Toxic myocarditis – due to action of toxin in the
heart muscles (1st 10-14 days)
 Neuritis caused by absorption of toxin in the
nerve
- Palate paralysis (2nd week)
- Ocular palsy (5th week)
- Diaphragm paralysis (6-10wk causing GBS)
- Motor and skeletal muscle paralysis
Treatment
 Neutralize the toxins – antidiptheria serum
 Kill the microorganism – penicillin
 Prevent respiratory obstruction –
tracheostomy, intubation
Treatment
 Serum therapy (Diptheria antitoxin)
- early administration aimed at neutralizing
the toxin present in the general circulation
 Antibiotics

- Penicillin G 100000mg/kg.day
- Erythromycin 40mg/kg
Nursing Intervention
 Rest.
- Patient should be confined to bed for at
least 2 weeks
- Prevent straining on defecation
- vomiting is very exhausting, do not do
procedures that may cause nausea
 Care for the nose and throat
 Ice collar to reduce the pain of sorethroat
 Soft and liquid diet
Whooping Cough, 100 day fever
 Bordetella pertussis, B. parapertussis, B.
bronchiseptica, gram (-)
IP: 3-21 days
MOT: airborne/droplet
Signs and symptoms
 Invasion or catarrhal stage (7-14days) starts
with ordinary cough
 Spasmodic or paroxysmal

- 5-10 spasms of explosive cough (no time to

catch breath. A peculiar inspiratory crowing
sound followed by prolonged expiration and a
sudden noisy inspiration with a long high
pitched “whoop”
 During attack the
child becomes
cyanotic and the eyes
appear to bulge or
popping out of the
eyeball and tongue
protrudes
Diagnosis
 WBC count 20000-50000
 Culture with Bordet Gengou Agar
Treatment

 Erythromycin shorten the period of

communicability
 Ampicillin if with allergy to erythromycin
 Heperimmune pertusis gamma globulin in
<2 years old (1.25ml IM)
 Control of cough with sedatives
Dx: WHO - >21 days
cough + close
contact w/
pertussis px + (+)
culture OR rise in
Ab to FHA or
pertussis toxin
* throat culture w/
Bordet gengou
agar
Management
 CBR to conserve energy
 Prevent aspiration
 High calorie, bland diet
 Omit milk and milk product because it
increases the mucous
 Refeeding of infants 20 min after vomiting
 Milk should be given at room temperature
complications
 Bronchopneumonia
 Abdominal hernia
 Severe malnutrition
 TB, asthma
 encephalitis
Pre exposure prophylaxis for
Diphtheria, Pertussis, Tetanus
 DPT- 0.5 ml IM
1 - 1 ½ months old
2 - after 4 weeks
3 - after 4 weeks
1st booster – 18 mos
2nd booster – 4-6 yo
subsequent booster – every 10 yrs thereafter
 Household contacts
(+) primary immunization and (-) culture - booster dose
(+) culture and (-) immunization – treated as a case of
Diptheria
 The world’s deadliest disease and remains as a
major public health problem.
 Badly nourished, neglected and fatigued
individuals are more prone
 Susceptibility is highest in children under 3 years
 AKA: Koch’s disease: Galloping consumption
 Pulmonary Tuberculosis
S/sx:
 Wt loss
 night sweats
 low fever,
 non productive to productive cough
 anorexia,
 Pleural effusion and hypoxemia
 cervical lymphadenopathy
 Pathophysiology
Inhalation

Local infiltration of neutrophils and macrohage

Multiply and survive in macrophage

Destroy bacteria

present it to T helper cells in LN

Sensitized T cells searches bacteria and release lymphokines

Attract macrophages w/c attack bacteria caseous necrosis

bacteria dormant
Heal w/ fibrosis, calcification
and granuloma; Primary If TBreactivated, Secondary TB
PPD – ID
macrophages in skin take
up Ag and deliver it to T
cells

T cells move to skin site,

release lymphokines

activate macrophages and

in 48-72 hrs, skin becomes
indurated

- > 10 mm is (+)
Dx:
Chest xray - cavitary lesion
Sputum exam
sputum culture
The National Tuberculosis Control
Program
Vision: A country where TB is no longer a
public health problem.
Mission: Ensure that TB DOTS services are
available to the communities.

Goal: To reduce the prevalence and

mortality from TB by half by the year 2015
Targets:
1. To cure at least 85% of the sputum
smear positive TB patient discovered.
2. Detect at least 70% of the estimated new
sputum smear positive TB cases.
Category TB patient Intensive Maintainance
New smear (+)
I New smear (-) 2HRZE 4 HR
PTB with ext
parenchymal
Treatment
II Failure, 2HRZES/ 5 HRE
Relapse, return 1HRZE
after Default
 New Smear (-)
III PTB, with 2HRZE 4HRE
minimal CXR
lesion

Chronic (still
IV smear (+) after MDRTB
supervised
treatment
Mgmt:
 short course – 6-9 months
 long course – 9-12 months
 DOTS- direct observe treatment short course
 Case finding
 Home meds (members of the family)
 Referrals
 Follow-up

* 2 wks after medications – non communicable

3 successive (-) sputum - non communicable
rifampicin - prophylactic
MDT side effects
 r-orange urine
 i-neuritis and hepatitis
 p-hyperuricemia
 e-impairment of vision
 s-8th cranial nerve damage
Methods of Control
 Prompt treatment and diagnosis
 BCG vaccination
 Educate the public in mode of transmission
and importance of early diagnosid
 Improve social condition
GIT
Amoebiasis
 Entamoeba histolytica, protozoa
 IP: few days to months to years,

usually 2- 4 weeks
MOT: Ingestion of cysts from fecally
contaminated sources (Oro- fecal route)
oral and anal sexual practices
 Extraintestinal amoebiasis- genitalia,
spleen, liver, anal, lungs and meninges
s/sx:
 Blood streaked, watery mucoid diarrhea,
foul smelling,
 abdominal cramps
 Pain on defecation (tenesmus)
 Hyperactive bowel sounds
Diagnostic test
 Stool culture of 3 stool specimens
 Sigmoidoscopy
 Recto-sigmoidoscopy and coloscopy for
intestinal amoebiasis
Medical treatment
 Metronidazole – trichomonocide and
amoebicide for intestinal and extra
intestinal sites (monitor liver function test)
 Diloxanide furoate – luminal amoebicide
 Paromomycin – eradicate cyst of
histolytica
 Tinidazole – hepatic amebic abscess
Bacillary Dysentery
Shigellosis
 Shiga bacillus: dysenteriae (fatal), flexneri
(Philippines), boydii, sonnei; gram (-)
 Shiga toxin destroys intestinal mucosa
 Humans are the only hosts
 Not part of normal intestinal flora

IP: 1-7 days

MOT : oral fecal route

S/sx: fever, severe abdominal pain,
diarrhea is watery to bloody with pus,
tenesmus

Dx: stool culture

Mgmt: Oresol, Ampicillin, Trimethoprim-
Sulfamethoxazole, Chloramphenicol,
Tetracycline, Ciprofloxacin
Cholera
 Vibrio coma (inaba, ogawa, hikojima),
Vibrio cholerae, Vibrio el tor; gram (-)
 Choleragen toxin induces active secretion
of NaCl
 Active Immunization

IP: few hours to 5 days

MOT: oral fecal route
S/sx: Rice watery stool with flecks of mucus, s/sx
of severe dehydration ie Washerwoman’s skin,
poor skin turgor
Dx: stool culture
mgmt: IV fluids, Tetracycline, Doxycycline,
Erythromycin, Quinolones, Furazolidone and
Sulfonamides (children)
Hookworm (Roundworm)

 Necator americanus, Ancylostoma

duodenale
 Leads to iron deficiency and hypochromic
microcytic anemia
 Gain entry via the skin
Dx: microscopic exam (stool
exam)

Mgmt: Pyrantel Pamoate and

Mebendazole
 don’t give drug without (+)
stool exam
 members of the family
must be examined and
treated also
Paragonimiasis
 Chronic parasitic infection
 Closely resembles PTB
 Endemic areas: mindoro, camarines sur,
norte, samar, sorsogon, leyte, albay,
basilan
Paragonimiasis

 AKA: Lung fluke disease

 causative agent: Paragonimus
westermani; Trematode
 Eating raw or partially cooked fish or fresh
water crabs
Signs and symptoms
 Cough of long duration
 Hemoptysis
 Chest/back pain
 PTB not responding to anti-koch’s meds
 Diagnosis
- sputum examination – eggs in brown
spots
 Treatment
1. Praziquantel (Biltrizide)
2. Bithionol
Ascariasis
 Common worldwide with greatest
frequency in tropical countries.
 Has an infection rate of 70-90% in rural
areas
 MOT: ingestion of embryonated egss
(fecal-oral)
 Worms reach maturity 2 months after
ingestion of eggs.
 Adult worms live less than 10 months(18
months max.)
 Female can produce up to 200000 eggs
per day
 Eggs may be viable in soils for months or
years
 Worms can reach 10-30cm in length
MOT: ingestion of food contaminated
by ascaris eggs larvae in
large intestine penetrate wall
lung where larvae grow and coughed
up intestine
larvae mature and passed out
in feces
 Initial symptom: loss of appetite
 Worms in the stool
 Fever
 Wheezing
 Vomiting
 Abdominal distention
 Diarhea
 dehydration
Medical Management
 Mebendazole (antihelmintic) effect occurs by
blocking the glucose uptake of the organisms,
reducing the energy until death
 Pyrantel pamoate: neuromuscular blocking
effect which paralyze the helminth, allowing it to
be expelled in the feces
 Piperazine citrate: paralyze muscles of parasite,
this dislodges the parasites promoting their
elimination
Nursing Intervention
 Environmental sanitation
 Health teachings
 Assessment of hydration status
 Use of ORS
 Proper waste disposal
 Enteric precautions
Complications
 Migration of the worm to different parts of
the body Ears, mouth,nose
 Loefflers Pneumonia
 Energy protein malnutrition
 Intestinal obstruction
Tapeworm (Flatworms)
 Taenia saginata (cattle), Taenia solium (pigs)

MOT: fecal oral route

(ingestion of food contaminated by the agent)
s/sx: neurocysticercosis – seizures, hydrocephalus

Dx: Stool Exam

Mgmt: Praziquantel, Niclosamide

Nursing Intervention
 Promote hygiene
 Environmental Sanitation
 Proper waste and sewage disposal
 Antihelmintic medications repeated after 2
weeks (entire family)
PARALYTIC SHELLFISH
POISONING
 A syndrome of characteristic symptoms
predominantly neurologic which occurs
within minutes or several hours after
ingestion of poisonous shellfish
 Single celled dinoflagellates (red
planktons) become poisonous after heavy
rain fall preceded by prolonged summer
 Common in seas around manila bay,
samar, bataan and zambales
 MOT = Ingestion of contaminated bi-valve
shellfish

 IP = within 30 minutes
CLINICAL MANIFESTATIONS:

 NUMBNESS OF THE FACE ESPECIALLY

AROUND THE MOUTH
 VOMITING, DIZZINESS, HEADACHE
 TINGLING SENSATION, WEAKNESS
 RAPID PULSE, DIFFICULTY OF SPEECH
( DYSPHAGIA, RESPI PARALYSIS,
DEATH.
MANAGEMENT AND CONTROL
MEASURES:
 NO DEFINITE MEDICATIONS
 INDUCE VOMITING (EARLY INTERVENTION)
 DRINKING PURE COCONUT MILK
(WEAKENS TOXIC EFFECT) DON’T GIVE
DURING LATE STAGE IT MAY WORSEN THE
CONDITION.
 NaHCO3 SOLUTION (25 GRAMS IN ½ GLASS
OF WATER)
 RESPIRATORY SUPPORT

 AVOID USING VINEGAR IN COOKING SHELLFISH

AFFECTED BY RED TIDE (15X virulence)
 TOXIN OF RED TIDE IS NOT TOTALLY
DESTROYED IN COOKING.
 AVOID TAHONG, TALABA, HALAAN, KABIYA,
ABANIKO. WHEN RED TIDE IS ON THE RISE.
Contact
Pediculosis
 Blood sucking lice/Pediculus humanus
p. capitis-scalp
p. palpebrarum-eyelids and eyelashes
p. pubis-pubic hair
p. corporis-body

MOT: skin contact, sharing of grooming implements

s/sx: nits in hair/clothing, irritating maculopapular or urticarial
rash

Mgmt: disinfect implements, Lindane (Kwell) topical

Permethrin (Nix) topical
Dr. Salvador
Dr. Salvador
Dr. Salvador
Dr. Salvador
Scabies  Sarcoptes scabiei
 Pruritus (excreta of mites)
 Mites come-out from burrows to
mate at night

MOT: skin contact

s/sx: itching worse at night and after
hot shower; rash; burrows (dark
wavy lines that end in a bleb w/
female mite) in between fingers,
volar wrists, elbow, penis; papules
and vesicles in navel, axillae, belt
line, buttocks, upper thighs and
scrotum

Dr. Salvador
Dr. Salvador
Dr. Salvador
Dx: biopsies/scrapings of lesions

Mgmt: Permethrin (Nix) cream, crotamiton

cream, Sulfur soap, antihistamines and
calamine for pruritus, wash linens with hot
water, single dose of Ivermectin, treat
close contacts

Dr. Salvador
Dx: biopsies/scrapings of lesions

NURSING CARE
a. Administer antihistamines or topical steroids to
relieve itching.
b. Apply topical antiscabies creams or lotion like
lindane(kwell), Crotamiton (Eurax), permithrin

Dr. Salvador
d. Lindane (kwell) not used in <2 years old,
causes neurotoxicity and seizures
e. Apply thinly from the neck down and
leave for 12-14hrs then rinse
f. Apply to dry skin, moist skin increases
absorption
g. All family members and close contacts
h. Beddings and clothings should be
washed in very hot water and dried on hot
dryer

Dr. Salvador
Leprosy
 Chronic infectious and communicable disease
 No new case arises without previous contact
 Majority are contracted in childhood,
manifestation arises by 15 yrs old and will
definitely diagnose at 20
 it is not hereditary
 Does not cross placenta

Dr. Salvador
Cardinal Sign
 Presence of Hansen’s bacilli in
stained smear or dried biopsy
material.
 Presence of localized areas of
anesthesia

Dr. Salvador
Leprosy/Hansen’s disease

* Lepromatous or malignant
- many microorganisms
- open or infectious cases
- negative lepromin test
* Tuberculoid or benign
- few organism
- noninfectious
- positive reaction to lepromin test
Dr. Salvador
s/sx:
• Early/Indeterminate – hypopigmented /
hyperpigmented anesthetic macules/plaques

• Tuberculoid – solitary hypopigmened

hypesthetic macule, neuritic pain, contractures
of hand and foot, ulcers, eye involvement ie
keratitis

• Lepromatous – multiple lesions, Loss of lateral

portion of eyebrows (madarosis), corugated skin
(leonine facies), septal collapse (saddlenose)
Dr. Salvador
Diagnosis
 Skin smear test
 Skin lesion biopsy
 Lepromin test -

Dr. Salvador
Mgmt:
 MDT-RA 4073 (home meds)
 Paucibacillary - 6-9 months
1. Dapsone
2. Rifampicin
 Multibacillary- 12-24 months

1. Dapsone – mainstay; hemolysis, agranulocytosis

2. Clofazimine – reddish skin pimentation, intestinal
toxicity
3. Rifampicin – bactericidal; renal and liver toxicity

Dr. Salvador
Nursing Intervention
 Health teachings
 Counseling involving the family members
and even the community
 Prevention of transmission ( use of mask )

Dr. Salvador
Leprosy
 Chronic infectious and communicable disease
 No new case arises without previous contact
 Majority are contracted in childhood,
manifestation arises by 15 yrs old and will
definitely diagnose at 20
 it is no hereditary
 Does not cross placenta
Cardinal Sign
 Presence of Hansen’s bacilli in
stained smear or dried biopsy
material.
 Presence of localized areas of
anesthesia
Leprosy/Hansen’s disease

* Lepromatous or malignant
- many microorganisms
- open or infectious cases
- negative lepromin test
* Tuberculoid or benign
- few organism
- noninfectious
- positive reaction to lepromin test
s/sx:
• Early/Indeterminate – hypopigmented /
hyperpigmented anesthetic macules/plaques

• Tuberculoid – solitary hypopigmened

hypesthetic macule, neuritic pain, contractures
of hand and foot, ulcers, eye involvement ie
keratitis

• Lepromatous – multiple lesions, Loss of lateral

portion of eyebrows (madarosis), corugated skin
(leonine facies), septal collapse (saddlenose)
Diagnosis
 Skin smear test
 Skin lesion biopsy
 Lepromin test -
Mgmt:
 MDT-RA 4073 (home meds)
 Paucibacillary - 6-9 months
1. Dapsone
2. Rifampicin
 Multibacillary- 12-24 months

1. Dapsone – mainstay; hemolysis, agranulocytosis

2. Clofazimine – reddish skin pimentation, intestinal
toxicity
3. Rifampicin – bactericidal; renal and liver toxicity
Acne Vulgaris
 Common, self limiting, multifactorial skin disease
 Over production of sebum, propionibacterium
acnes, hormonal,
 Closed comedones – whiteheads
 Open comedones – blackheads
 Requires active treatment
 Intervention: don’t squeeze, prick or pick,
Isotretinoin Accutane (avoid sunlight and vit A,
may increase triglycerides), antibiotics

Dr. Salvador
Dr. Salvador
 No evidence that chocolate, nuts, fatty
foods or cosmetics affects acne
 Exacerbation coincides with menstrual
activity.
 Heat, increase sweat increase acne

Dr. Salvador
Nursing care
 Use of topical or oral antibiotics
 Instruct in the use of isotretinoin
(ACCUTANE) to decrease sebum
production
 Adverse effect, cheilitis, skin dryness,
elevated triglycerides and eye discomfort

Dr. Salvador
 Stop Vit A supplement during treatment
 Instruct not to squeeze, prick or pick at
lesions
 Use products labeled noncomedogenic
and cosmetics that are water based

Dr. Salvador
Dr. Salvador
Decubitus Ulcer
 Skin impairment secondary to immobility
 Common to immobilized and with
decreased sensory perception patient

Dr. Salvador
Stage 1 Stage 2 Stage 3 Stage 4

-Skinis intact -Top layer -Deep ulcer -Ulcer

-Reddened is missing extends to extend to
area -Ulcer is dermis and muscle and
shallow, subcutaneou bones
wih pink or s areas - foul
red base - white, gray smelling
- white or or yellow - brown or
yellow eschar black eschar
eschar - purulent - purulent
discharge discharge

Dr. Salvador
Dr. Salvador
Risk Factors
 Malnutrition
 Incontinence
 Immobility
 Skin shearing
 Decreased sensory perception

Dr. Salvador
Nursing care
 Institute measures to prevent decubitus
ulcer
 Assess the nutritional status
 Provide adequate nutritional intake to
promote skin integrity
 Monitor for alteration in skin integrity
 Relieve or remove pressure on skin

Dr. Salvador
 Turn every 2 hours
 Ambulate the patient
 Provide active and passive exercise q
8hrs
 Keep skin clean and dry and bed wrinkle
free
 Apply medications or dressing on the
wound

Dr. Salvador
ERUPTIVE FEVER
 MEASLES
 Extremely contagious
 Breastfed babies of mothers have 3
months immunity for measles
 The most common complication is otitis
media
 The most serious complications are
bronchopneumonia and encephalitis
Measles, Rubeola, 7 Day Fever,
Hard Red Measles
 RNA, Paramyxoviridae
 Active MMR and Measles vaccine
 Passive Measles immune globulin
 Lifetime Immunity

IP: 7-14 days

MOT: droplets, airborne

*Contagious 4 days before rash and 4 days after rash
Clinical Manifestation
 Pre eruptive stage
- Patient is highly communicable
- 4 characteristic features
a. Coryza
b. Conjunctivitis
c. Photophobia
d. Cough
- Koplik’s spots
- Stimsons line

 Eruptive stage
- Maculopapular rashes appears first on the
hairline, forehead, post auricular area the
spread to the extremities (cephalocaudal)
- Rashes are too hot to touch and dry
- High grade fever and increases steadily at
the height of the rashes
 Stage of convalescence
- Rashes fade in the same manner leaving
a dirty brownish pigmentation
(desquamation)
- Black measles – severe form of measles
with hemorrhagic rashes, epistaxis and
melena
Rashes: maculopapaular, cephalocaudal
(hairline and behind the ears to trunk and
limbs), confluent, desquamation, pruritus
Complication
 Bronchopneumonia
 Secondary infections
 Encephalitis
 Increase predisposition to TB
 MANAGEMENT
1. Supportive
2. Hydration
3. Proper nutrition
4. Vitamin A
5. Antibiotics
6. Vaccine
Nursing Care
 Respiratory precautions
 Restrict to quite environment
 Dim light if photophobia is present
 Administer antipyretic
 Use cool mist vaporizer for cough
German Measles (rubella)
 Acute infection caused by rubella virus
characterized by fever, exanthem and
retroauricular adenopathy.
 Has a teratogenic potential on the fetus of
women in the 1st trimester
s/sx: forscheimer’s (petechial lesion on buccal cavity
or soft palate),
- cervical lymphadenopathy, low grade fever
- “ Oval, rose red papules about the size of pinhead

Dx: clinical
CX: rare; pneumonia, meningoencephalitis
CX to pregnant women:
 1st tri-congenital anomalies
 2nd tri-abortion
 3rd tri-pre mature delivery
Rashes: Maculopapular,
Diffuse/not confluent, No
desquamation, spreads
from the face downwards

Chicken Pox, Varicella
Herpes zoster virus (shingles),
varicella zoster virus(chicken pox)
 Active : Varicella vaccine
 Passive: VZIG, ZIG – given 72-96 hrs
w/n exposure
 Lifetime Immunity
IP: 14-21 days
MOT: Respiratory route
* Contagious 1 day before rash and 6 days after first crop of
vesicles

S/sx:
fever, malaise, headache
Rashes:
Maculopapulovesicular
(covered areas),
Centrifugal, starts on
face and trunk and
spreads to entire body

 Leaves a pitted scar

(pockmark)
CX furunculosis, erysipelas,
meningoencephalitis

 Dormant: remain at the dorsal root ganglion

and may recur as shingles (VZV)
Maxillary division of the trigeminal nerve
Mgmt:
a. oral acyclovir
b. Tepid water and wet compresses for
pruritus
c. Aluminum acetate soak for VZV
d. Potassium Permanganate (ABO)
a. Astringent effect
b. Bactericidal effect
c. Oxidizing effect (deodorize the rash)
 Small Pox,
 DNA, Pox virus
Variola
 Last case 1977
 spreads from man-to-man
only
 Active: Vaccinia pox virus

IP: 1-3 weeks

S/sx:
Rashes:
Maculopapulovesiculopustular
 Centripetal
 contagious until all crusts disappeared

Dx:
 Paul’s test - instilling of vesicular fluid
w/ small pox into the cornea; if keratitis
develops, small pox
Cx: same with chicken pox
Emerging Diseases
Severe Acute Respiratory Syndrome
 Coronavirus
 Severe acute respiratory syndrome

IP: 2-7 days

Mortality rate – 5% only

 1 Mainland
Visitor
2/15/03

3 Singapore 1 American
Visitors Metropole Chinese
Hotel
Singapore Outbreak Hanoi Outbreak
2 Canadian
Visitor

Hongkong Outbreak
Toronto, Canada Outbreak
A.C (Canada) Narita, Japan

Philippines Pangasinan
Tarlac
Cordillera
MetroManila

San Lazaro Hospital

(SARS UNIT)
Risk Factors:
 history of recent travel to China, Hong Kong,
singapore Taiwan, vietnam, canada. or close contact
w/ ill persons with a hx of recent travel to such areas,
OR
 Is employed in an occupation at particular risk for
SARS exposure, healthcare worker with direct
patient contact or a worker in a laboratory that
contains live SARS, OR
 Is part of a cluster of cases of atypical pneumonia
without an alternative diagnosis
Clinical Manifestations
 History of travel to SARS affected country or
close contact with persons suspected of
having SARS and within 14 days manifest
the ff
 High grade fever (>38.0 c)
 Headache, body malaise, muscle pain
 Cough, sneezing, nasal congestion
 Difficulty of breathing after 2-7 days
 SARS suspect
 Probable SARS

Diagnosis:
Chest X-ray, CBC, Isolation of virus

Mgt:
Supportive
Treat as Atypical Pneumonia
Quarantine
AVIAN INFLUENZA

Serious consequences for

ASIA
Avian Influenza…..
 Is an infectious disease of birds caused by
Type A strains of the influenza virus
 First identified in Italy more than 100 years
ago
 Occurs worldwide
 Infection causes a wide spectrum of
symptoms in birds, ranging from mild
illness to a highly contagious and
rapidly fatal disease resulting in severe
epidemics
 “ highly pathogenic avian influenza”
Pathogenesis
 Avian influenza do not
normally infect species other
than birds and pigs
 First documented infection of
humans with avian flu
occurred in Hong Kong in
1997
 Affected 18 humans, 6 died
Bird Flu
 Human cases of influenza A (H5N1)
infection have been reported in
Cambodia, China, Indonesia, Thailand,
and Vietnam.
Clinical manifestations
 Patients develop
fever, sore throat,
cough, in fatal
cases, severe
respiratory distress
may result
secondary to
pneumonia
 A constantly mutating virus
 All type A influenza
virus, including
those that regularly
cause seasonal
epidemics of
influenza in humans
are genetically labile
and well adapted to
elude host defenses
 So far bird flu is mainly
transmitted between
birds, but experts fear
the H5N1 virus could
be devastating to
humans if it genetically
mutates and develops
the capacity to be
transmitted from
human to human.
 Novel influenza A (H1N1) is a new flu virus of
swine origin that was first detected in April, 2009.

 Reassortment of 4 viruses from pigs, humans and

birds

 The virus is infecting people and is spreading from

person-to-person, and has sparked a growing
outbreak of illness in the United States with an
increasing number of cases being reported
internationally as well.

Dr. Salvador
Why is this new H1N1 virus
sometimes called “swine flu”?
 This virus was originally referred to as “swine flu”
because laboratory testing showed that many of the
genes in this new virus were very similar to influenza
viruses that normally occur in pigs in North America.
 But further study has shown that this new virus is very
different from what normally circulates in North
American pigs. It has two genes from flu viruses that
normally circulate in pigs in Europe and Asia and avian
genes and human genes. Scientists call this a
“quadruple reassortant” virus.
 How does this new H1N1 virus spread?
Spread of this H1N1 virus is thought to be happening in
the same way that seasonal flu spreads. Flu viruses are
spread mainly from person to person through coughing
or sneezing by people with influenza. Sometimes people
may become infected by touching something with flu
viruses on it and then touching their mouth or nose.
How severe is illness associated
with this new H1N1 virus?
 It’s not known at this time how severe this virus will
be in the general population. In seasonal flu, there
are certain people that are at higher risk of serious
flu-related complications.
 This includes people 65 years and older, children
younger than five years old, pregnant women, and
people of any age with chronic medical conditions.
WHO Pandemic Levels
Here is a quick look at the WHO's pandemic alert
phases:
Phase 1: A virus in animals has caused no
known infections in humans.
Phase 2: An animal flu virus has caused
infection in humans.
Phase 3: Sporadic cases or small clusters of
disease occur in humans. Human-to-human
transmission, if any, is insufficient to cause
community-level outbreaks.
Phase 4: The risk for a pandemic is greatly
increased but not certain. The disease-causing
virus is able to cause community-level
outbreaks.
Phase 5: Still not a pandemic, but spread of
disease between humans is occurring in more
than one country of one WHO region.
Phase 6: This is the pandemic level.
Community-level outbreaks are in at least one
additional country in a different WHO region
from phase 5. A global pandemic is under way.
“In response to the intensifying
outbreak, the World Health
Organization raised the worldwide
pandemic alert level to Phase 5”

A phase 5 alert means there is

sustained human to human spread in at
least two countries. It also signals that
efforts to produce a vaccine will be
ramped up.
Case Definitions for H1N1
Clinical case description:
 Acute febrile illness (fever >38C)
1. Suspected case – individual with influenze like illness who has close
contact with an ill confirmed case of influenza virus infection OR
a person with influenza like illness with recent history of contact with an
animal with confirmed or suspected H1N1 virus OR
a person with influenza like illness who has traveled to an area where
there are confirmed cases of H1N! Within 7 days of onset of illness
 Close contact
- within 6 feet for an ill person who is
confirmed case of swine influenza
 Probable Case – an individual with an
influenza test that is positive for influenza
A, but non subtypable by reagents used to
detect seasonal influenza virus

An individual with a clinically compatible

illness or who died of an unexplained
acute respiratory illness who is considered
to be an epidemiologically linked to a
probable or confirmed case
 Confirmed case – an individual with
laboratory confirmed H1N1 virus by 1 or
more of the ff:
a. real time TR-PCR
b. Viral culture
c. Four-fold rise in influenza A (H1N1)
specific antibodies
Signs and Symptoms
 Fever and chills
 cough
 sore throat
 Nasal congestion
 Myalgia
 Pneumonia
 Respiratory failure
 For interview of an ill, suspected or
confirmed case;
a. keep distance of at least 6 feet from the
ill person
b. Personal protective equipment: fit tested
N95 respirator
 For collecting respiratory specimens
a. Personal protective equipment
b. When completed place all PPE in
biohazard bag for appropriate disposal
c. Wash hands thoroughly with soap and
water or alcohol based gel
 How long can influenza virus remain
viable on objects (such as books and
doorknobs)?
Studies have shown that influenza virus
can survive on environmental surfaces
and can infect a person for up to 2-8 hours
after being deposited on the surface
Treatment:
 If you get sick, antiviral drugs can make your
illness milder and make you feel better faster.
They may also prevent serious influenza
complications. For treatment, antiviral drugs
work best if started as soon after getting sick
as possible, and might not work if started
more than 48 hours after illness starts.
Prevention:
 Influenza antiviral drugs also can be used to prevent
influenza when they are given to a person who is not ill,
but who has been or may be near a person with swine
influenza. When used to prevent the flu, antiviral drugs
are about 70% to 90% effective. When used for
prevention, the number of days that they should be used
will vary depending on a person’s particular situation.
Recommendation for Prophylaxis
 Priority groups to receive antiviral agents for
prophylaxis are those who have potential
contact with droplets from a patient without
having an adequate PPE
- Health worker
- First responders
- Workers providing essential services
 Other people like household contacts of
probable or confirmed case
Anti-viral treatment should be given to:
 Confirmed case
 Probable case
 Suspected case at high risk of severe
disease
Antiviral treatment
 Oseltamavir (Tamiflu) 75mg/cap or 12mg/ml
- <15kg 30mg BID for 5 days
- >15-23kg 45mg BID
- >23-40kg 60mg BID
- >40kg 75mg BID

For prophylaxis 1 cap OD x 10 days

 Zanamavir (relenza)
- alternate drug in patient >7 years old
- 2 inhalations BID for 5 days
Discharge Guidelines
 7 days after the resolution of fever
 Children can shed virus for 21 days after
onset of illness
 Family should be educated on personal
hygiene and infection control measures.
Infection control
 Main route of human to human
transmission is via respiratory droplets
which are expelled by speaking, sneezing
or coughing
Public health measures
 Suspension of public events
 limitation of movement from one area
 Suspension of travel to a country with
outbreaks of influenza
 Closure or limitation of people in public
places or establishments
 Cancellation of mass gatherings
Personal Protective Equipment
 Health care personnel
Key elements
1. Use of medical or surgical gloves
2. Emphasize hand hygiene and provide
hand hygiene facilities and supplies
General public
 Promote physical distance (1 meter)
 Avoid crowded situations
 Refrain from touching mouth and nose
 Perform hand hygiene frequently
 Improve airflow in living space
 People who have contact with influenza
cases shall stay in their homes
Guidelines in use of mask
 Place mask carefully to cover the mouth
and nose and tie securely to minimize
gaps between the face and the mask
 While in use, avoid touching the mask
 Replaced the mask with new clean, dry
mask as soon it become damp/humid
 Discard single use of mask
 Can H1N1 influenza virus be spread at recreational water
venues outside of the water?
Yes, recreational water venues are no different than any other
group setting. The spread of this novel H1N1 flu is thought to
be happening in the same way that seasonal flu spreads. Flu
viruses are spread mainly from person to person through
coughing or sneezing of people with influenza. Sometimes
people may become infected by touching something with flu
viruses on it and then touching their mouth or nose.
 What can I do to protect myself from
getting sick?
There is no vaccine available right now to
protect against this new H1N1 virus. There
are everyday actions that can help prevent
the spread of germs that cause respiratory
illnesses like influenza.
Take these everyday steps to protect
your health:

 Cover your nose and mouth with a tissue when you cough or
sneeze. Throw the tissue in the trash after you use it.
 Wash your hands often with soap and water, especially after
you cough or sneeze. Alcohol-based hand cleaners are also
effective.
 Avoid touching your eyes, nose or mouth. Germs spread this
way.
 Try to avoid close contact with sick people.
 Stay home if you are sick for 7 days after your symptoms
begin or until you have been symptom-free for 24 hours,
whichever is longer. This is to keep from infecting others and
spreading the virus further
What is the best technique for washing
my hands to avoid getting the flu?

Washing your hands often will help protect you from

germs. Wash with soap and water or clean with alcohol-
based hand cleaner. CDC recommends that when you
wash your hands -- with soap and warm water -- that you
wash for 15 to 20 seconds. When soap and water are not
available, alcohol-based disposable hand wipes or gel
sanitizers may be used. You can find them in most
supermarkets and drugstores. If using gel, rub your hands
until the gel is dry. The gel doesn't need water to work; the
alcohol in it kills the germs on your hands.
What should I do if I get sick?
 If you live in areas where people have been identified with
new H1N1 flu and become ill with influenza-like symptoms,
including fever, body aches, runny or stuffy nose, sore throat,
nausea, or vomiting or diarrhea, you should stay home and
avoid contact with other people, except to seek medical care.
 If you have severe illness or you are at high risk for flu
complications, contact your health care provider or seek
medical care. Your health care provider will determine
whether flu testing or treatment is needed
 If you become ill and experience any of the following warning
signs, seek emergency medical care
 In children emergency warning signs that need urgent
medical attention include:
 Fast breathing or trouble breathing
 Bluish or gray skin color
 Not drinking enough fluids
 Severe or persistent vomiting
 Not waking up or not interacting
 Being so irritable that the child does not want to be held
 Flu-like symptoms improve but then return with fever and
worse cough
 In adults, emergency warning signs that need urgent
medical attention include:
 Difficulty breathing or shortness of breath
 Pain or pressure in the chest or abdomen
 Sudden dizziness
 Confusion
 Severe or persistent vomiting
 Flu-like symptoms improve but then return with fever and worse
cough
Health alert Notice
 For travellers
 Monitor health for 10 days
 If become ill with fever accompanied by
cough, sore throat, nasal congestion or
DOB consult a physician
 Gonorrhea, Morning drop, Clap,
Jack
 Neisseria gonorrheae, gram (+)
IP: 3-7 days
S/sx:
Females: usually asymptomatic or minimal
urethral discharge w/ lower abdominal pain
- sterility or ectopic pregnancy
Male: Mucopurulent discharge, Painful urination
- decreased sperm count
Clinical problems
 The most common reportable
communicable disease
 Has a short incubation period which
permits rapid spread and a high
percentage of females are asymptomatic
 It is becoming increasingly resistant to
penicillin
DX:
gram stain and culture of cervical
secretions on Thayer Martin medium
Mgmt: single dose only
 Ceftriaxone (Rocephin)
125 mg IM
 Ofloxacin (Floxin) 400 mg
orally
 treat concurrently with
Doxycycline or
Azithromycin for 50%
infected w/ Clamydia
CX:
PID, ectopic pregnancy
and infertility, peritonitis,
perihepatitis, Ophthalmia
neonatorum, sepsis and
arthritis
 Syphilis
 Treponema pallidum, spirochete
 “ Beautiful” fast moving but delicate spiral
thread

 IP: 10-90 days

Primary (3-6 wks after contact) –
nontender lymphadenopathy and chancre;
most infectious; resolves 4-6 wks
Chancre – painless ulcer with heaped up
firm edges appears at the site where the
treponema enters. Related to pattern of
sexual behavior (genitalia, rectal, oral, lips)
BUBO – swelling of the regional lymphnode
Chancre of the anus Chancre of the fingers Chancre of the lip

Chancre of the labia Chancre on the labia minora

 Secondary – systemic; generalized
macular papular rash including palms and
soles and painless wartlike lesions in
vulva or scrotum (condylomata lata) and
lymphadenopathy
 Tertiary – (6-40 years) -
neurosyphilis/permanent damage
(insanity); gumma (necrotic
granulomatous lesions), aortic aneurysm
DX:
Dark-field examination of lesion- 1st and 2nd stage
Non specific VDRL and RPR

Mgmt
 Primary and secondary - Pen G
 Tertiary - IV Pen G
 The most common STD in the US
 Transmission is thru vaginal or rectal
intercourse, or oral- genital contact with
infected person.
Signs and symptoms
 Usually asymptomatic
 Gray-white discharge with burning or
itchiness at the urethral opening
 Lymphogranuloma venereum, enlarged
unilateral lymphnodes
Chlamydia
 Gram stain
 Antigen detection test on cervical smear
 Urinalysis
Mgmt:
 Doxycycline or Azithromycin

CX:
 PID
 Ectopic pregnancy
 Fetus transmittal (vaginal birth)
Herpes Genitalis
 HSV 2
S/sx: Painful sexual intercourse, Painful vesicles
(cervix, vagina, perineum, glans penis)
Dx:
 Viral culture
 Pap smear (shows cellular changes)
 Tzanck smear (scraping of ulcer for staining)
Mgmt:
Anti viral - acyclovir
(zovirax)

CX:
 Meningitis
 Neonatal infection
(vaginal birth)
Genital Warts,
Condyloma Acuminatum
 HPV type 6 & 11, papilloma virus

S/sx: Single or multiple soft, fleshy painless growth

of the vulva, vagina, cervix, urethra, or anal
area, Vaginal bleeding, discharge, odor and
dyspareunia
DX:
 Pap smear-shows cellular changes (koilocytosis)
 Acetic acid swabbing (will whiten lesion)
 Cauliflower or
hyperkeratotic
papular lesions
 Treatment

- liquid nitrogen
- podophylin resin
Mgmt:
Laser treatment is more
effective

CX:
 Neoplasia
 Neonatal laryngeal
papillomatosis (vaginal birth)
Candidiasis, Moniliasis
 Candida Albicans, Yeast or fungus

S/sx: Cheesy white discharge,

\Extreme itchiness

DX:
 KOH (wet smear indicate positive result)

Mgmt:
 Imidazole, Monistat, Diflucan

CX:
 Oral thrush to baby (vaginal birth)
HIV and AIDS
 Retrovirus (HIV1 & HIV2)

 Attacks and kills CD4+

lymphocytes (T-helper)

 Capable of replicating in
the lymphocytes
undetected by the immune
system

 Immunity declines and

opportunistic microbes set
in
 No known cure
HIV/AIDS Reverses Development and
Poses Serious Threat to Future Generations
 Since 1980s, 60m have been infected
and 25m have died
 About 40m live with HIV/AIDS – 38m
in developing countries and 28m in
Africa alone
 The spread is accelerating in India,
Russia, the Caribbean and China
 AIDS is stretching health care
systems beyond their limits
 There are 12m AIDS orphans –
they are estimated to rise to 40m
by 2010
 In Sub-Saharan Africa, 58% of
HIV/AIDS infected adults are
women. More than two-thirds of
newly infected teenagers are
female.
 Life expectancy has declined by
more than 10 years in South
Africa and Botswana – Swaziland
faces the risk of extinction
MOT:
 Sexual intercourse (oral, vaginal and anal)
 Exposure to contaminated blood, semen,
breast milk and other body fluids
 Blood Transfusion
 IV drug use
 Transplacental
 Needlestick injuries
HIGH RISK GROUP
 Homosexual or
bisexual
 Intravenous drug
users
 BT recipients before
1985
 Sexual contact with
HIV+
 Babies of mothers
who are HIV+
s/sx:
1. Acute viral illness (1 mo after initial
exposure) – fever, malaise,
lymphadenopathy
2. Clinical latency – 8 yrs w/ no sx; towards
end, bacterial and skin infections and
constitutonal sx – AIDS related complex;
CD4 counts 400-200
3. AIDS – 2 yrs; CD4 T lymphocyte < 200 w/
(+) ELISA or Western Blot and
opportunistic infections
How to Diagnose
 HIV+
2 consecutive positive ELISA and
1 positive Western Blot Test
 AIDS+
HIV+
CD4+ count below 500/ml
Exhibits one or more of the ff: (next slide)
 Full blown AIDS
CD4 is less than 200/ml
Exhibits one or more of the ff:
 Extreme fatigue
 Intermittent fever
 Night sweats
 Chills
 Lymphadenopathy
 Enlarged spleen
 Anorexia
 Weight loss
 Severe diarrhea
 Apathy and depression
 PTB
 Kaposis sarcoma
 Pneumocystis carinii
 AIDS dementia
Kaposis
Treatment
Anti-retroviral Therapy (ART) – ziduvirine
a. Prolong life
b. Reduce risk of opportunistic infection
c. Prolong incubation period
PREVENTION
A – ABSTINENCE
B – BE FAITHFUL
C – CONDOMS
D – DON’T USE DRUGS
Integrated Management of
Childhood Diseases

Dr. Salvador
 IMCI process can be used by doctors,
nurses and other health care personnel in
a primary health care facility like health
centers, clinics or OPD.

Dr. Salvador
Components of IMCI
 Upgrading the case management and
counseling skills of health care providers.
 Strengthening the health care system for
effective management of childhood illness
 Improving family and community practices
related to child health and nutrition.

Dr. Salvador
 Focused on the common childhood diseases.
1. Pneumonia
2. Measles
3. Malaria
4. Diarrhea
5. Malnutrition
6. Ear infection
7. Dengue

Dr. Salvador
IMCI case management
process
 Assess a child by checking first for danger signs,
examining the child, checking nutritional and
immunization status.
 Classify the child illness using the color coded triage
system
- (pink) urgent
- (yellow) OPD treatment
- (green) Home management

Dr. Salvador
 Identify the specific treatments for the
child. If the child needs urgent referral,
give essential treatment before the patient
is transferred.
 Provide practical treatment instructions
 Assess feeding problems
 Follow up care

Dr. Salvador
Dr. Salvador
Danger signs
 Not able to drink
 Vomiting
 Convulsions
 Abnormally sleepy

Dr. Salvador
Dr. Salvador
Parameters for assessing
dehydration
 Eyes – sunken, absent of tears, lack of laster
 Fontanelles
 Skin turgor
 Mouth
 Abnormally sleepy
 Level of thirst

Dr. Salvador
Dr. Salvador
Dr. Salvador
Dr. Salvador
Dr. Salvador
Dr. Salvador
Dr. Salvador
Dr. Salvador
Dr. Salvador
Dr. Salvador
Dr. Salvador
Dr. Salvador
Dr. Salvador
IMMUNOLOGY
What is immunity?
 “Protection” from infection, tumors,
etc.
 Innate immunity is always available
 Adaptive immunity distinguishes “self”
from “non-self” and involves immune
system “education”
 Responses that may result in host
tissue damage
Terms to define:
 Immunity-refers to the body’s specific protective response to an invading foreign
agent or organism
 Immunopathology - refers to study of diseases resulting from dysfunctions within
the immune system
 Antibody-a protein substance developed by the body in response to and
interacting with a specific antigen
 Antigen- substance that induced the production of antibody
 B-cells-cells that are important in producing circulating antibody
 Cytotoxic t-cells- lymphocytes that lyse cells
infected with virus ;also play
a role in graft rejection
 Helper t-cells- lymphocytes that attack foreign
invaders directly
 Immunoregulation - complex system of
checks and balances that regulates
or control immune responses
 Interferon- proteins formed when cells are
exposed to viral or foreign agents
 Lympokines - subs. Released by sensitized
lymphocytes when they
contact specific antigens
 Memory cells- cells that are responsible
recognizing antigens from
previous exposure and mounting
an immune response
 Natural killer cells- lymphocytes that
defends against microorganism and
malignant cells
 Stem cells- precursors of all blood cells,
reside primarily on bone marrow
 Suppressor T-cells-lympocytes that
decrease B cells activity to a level at
w/c the immune system
is compatible with life
Two types of immunity
 Innate immunity (not antigen-specific)
 Anatomical barriers
 Mechanical
 Biochemical
 Non-specific (eg. Low pH in stomach)
 Receptor-driven (eg. PAMP-recognition)
 Adaptive immunity (antigen-specific)
 Receptor-driven
 Pre-existingclones programmed to make a
specific immune response (humoral/cellular)
 Antigen

 A substance (antigen) that is capable of

reacting with the products of a specific
immune response, e.g., antibody or
specific sensitized T-lymphocytes.
 A “self” component may be considered an
antigen even though one does not
generally make immune responses
against those components.
Components of the
immune system
 platelets
Cells eosinophil
megakaryocyte
involved Pluripotent
T Lymphocyte

in neutrophil
hematopoietic
stem cell
B Lymphocyte
immunit
y common
basophil common lymphoid
myeloid progenit
progenito or
r plasma cell
mast cell
Natural
monocyte Killer cell

macrophage
 Where is that stuff?
Blood
Serum Leukocytes,
or Platelets and RBC
Plasma

Mononuclea Polymorphonucle
Serum Proteins
r Cells ar leukocytes (or
Granulocytes)

•Immunoglobulins •Lymphocytes •Neutrophils

•Complement (T cells, B •Eosinophils
•Clotting factors cells & NK •Basophils
•Many others cells)
•Monocytes
Lymphoid Organs
 Primary or central lymphoid organs
 bone marrow and thymus
 where lymphocytes are generated
 Secondary or peripheral lymphoid organs
 where adaptive immune responses are
initiated
Distribution of Lymphoid Tissues
Response to Initial
Infection
Course
of
Typical
Acute
Infectio
n
Innate Host Defense
Mechanisms

 Anatomic Factors
 Mechanical Factors
 Biochemical Factors
 Skin

 Stratified and cornified epithelium provides a

mechanical barrier
 Indigenous microbiota competes with
pathogens
 Acid pH inhibits growth of disease producing
bacteria
 Bactericidal long chain fatty acids in
sebaceous gland secretions
 Respiratory Tract
 Upper Respiratory Tract
 Nasal hairs induce turbulence
 Mucous secretions trap particles
 Mucous stream to the base of tongue where material is swallowed
 Nasal secretions contain antimicrobial substances
 Upper respiratory tract contains large resident flora
 Lower Respiratory Tract
 Particles trapped on mucous membranes of bronchi and bronchioles
 Beating action of cilia causes mucociliary stream to flow up into the
pharynx where it is swallowed
 90% of particles removed this way. Only smallest particles (<10µ in
diameter) reach alveoli
 Alveoli
 Alveolar macrophage rapidly phagocytize small particles
 Alimentary Tract
 General defense mechanisms
 Mucous secretions
 Integrity of of mucosal epithelium
 Peristaltic motions of the gut propel contents downward
 Secretory antibody and phagocytic cells
 Stomach
 Generally sterile due to low pH
 Small Intestine
 Upper portion contains few bacteria
 As distal end of ileum is reached flora increases
 Colon
 Enormous numbers of microorganisms
 50-60% of fecal dry weight is bacteria
 Genitourinary Tract
 Male
 No bacteria above urethrovesicular junction
 Frequent flushing action of urine
 Bactericidal substances from prostatic fluid
 pH of urine
 Bladder mucosal cells may be phagocytic
 Urinary sIgA

 Female (Vagina)
 Large microbial population (lactobacilli)
 Microorganisms produce low pH due to breakdown of glycogen
produced by mucosal cells
Receptors
 Almost all of biology occurs because
recognition
 Enzymatic action
 Interactions between cells
(cooperation/activation)
 Communication between cells
 Innate and adaptive immunity requires it
Characteristics of Adaptive
Immunity
 Immune response is highly specific for the antigen that
triggered it.
 Receptors on surface of immune cells have same specificity as the
antibody/effector activity that will be generated
 Exposure to antigen creates an immunologic “memory.”
 Due to clonal expansion and creation of a large pool of cells
committed to that antigen
 Subsequent exposure to the same antigen results in a rapid and
vigorous response
Natural Immunity
 Present at birth
 Provides a non specific response to any
foreign invader, regardless of the
invader’s composition.
 Basis is ability to distinguish between “self
and non-self”
Physical
 Skin and intact mucous membranes
 Cilia and coughing, sneezing

Chemical
 Acidic secretions, mucus, sweat, saliva and
tears
WBC
 Participate in both natural and acquired
 Fight invasion by foreign body or toxins

Neutrophils – 1st cell to arrived at the site of

inflammation
Eosinophils and basophils – increase in
stress and allergic reaction
Monocytes – “phagocytic cells”
Lymphocytes – major role in humoral and
cell mediated immune response
Acquired Immunity
 Develops as a result of prior exposure to
an antigen through immunization and by
contracting a disease
 Active acquired – immune defense are
developed by the person’s own body. Last
for lifetime
 Passive Acquired
- temporary immunity from another source
that has developed immunity through
previous disease or immunization
- used in emergencies to provide immunity
in disease when the risk is high
Response to Invasion
1. First line – Phagocytic immune response
- ability to ingest protein and dying cells
2. Humoral immune response
- begins with B lymphocytes which can transform to
antibodies
3. Cellular immune response
- involves T lymphocytes which can turn to
cytotoxic or killer T cells
Recognition Stage
 Body must first recognize invaders as
foreign body before it can react to them
 Using lymphnodes and lymphocytes for
surveillance
 Lymphocytes and monocytes helps each
other in detection
Proliferation Stage
 Circulating LN containing the antigenic
message returns to the nearest LN
 Once in the node, the sensitized
lymphocytes stimulates the T lymphocytes
differentiate into cytotoxic (killer) T cells
 B lymphocytes produce & release
antibodies
Response Stage
 B lymphocytes begins the humoral
response
 Migrate to LN that stimulate the residing
lymphocytes to become cells that attack
microbes directly (Killer cells)
Effector Stage
 Results in total destruction of the invading
microbes or complete neutralization of
toxin
 Interplay of antibodies (humoral immunity)
and action by the cytotoxic T cells (cellular
immunity)
Cellular and Humoral immune
response
Humoral Responses (B cells)
 Bacterial phagocytosis and lysis
 Anaphylaxis
 Allergic hay fever and asthma
 Immune complex disease
 Bacterial and viral infections
Cellular Responses (T cells)
 Transplant rejection
 Delayed hypersensitivity
 Graft Vs Host
 Tumor surveillance and destruction
 Viral, fungi, parasitic infection
Humoral Immune Response
 Characterized by production of antibodies
by the B lymphocytes in response to a
specific antigen
Antibodies
 Agglutinations – binds antigen facilitating
phagocytosis
 Opsonization – antigen-antibody is coated
with sticky substance promoting
phagocytosis
Types
IgG (75%)
 Appears in serum and tissues
 Assumes a major role in bloodborne and
tissue infections
 Activates the complement system
 Enhances phagocytosis
 Crosses placenta
IgA (15%)
 Appears in body fluids (blood,saliva, tears,
breat milk)
 Protects against respiratory, GIT and GUT
 Prevents absorption of antigens from food
 Passes to neonate in breast milk for
protection
IgM (10%)
 Appears mostly in intravascular serum
 First immunoglobulin produced in
response to bacterial or viral infection
 Activates complement systems
IgD (.2%)
 Appears in small amount in serum

IgE (.004%)
 Allergic and hypersensitivity reactions
Inflammatory Mediators in Innate
Immunity
 Cytokines secreted by phagocytes in response to infection
include:
 IL-1
 activates vascular endothelium and lymphocytes
 Increases adhesiveness of leukocytes
 IL-6
 Induces B-cell terminal maturation into Ig-producing plasma cells
 IL-8
 Induces expression of b2 integrin adhesion molecules on neutrophils,
leading to neutrophil migration to infection site
 IL-12
 Activates NK cells and induces Th1-cell differentiation
 IL-18
 TNF-α
 Activates vascular endothelium and increases vascular permeability,
leading to accumulation of Ig and complement in infected tissues
Immune Cells and Innate Immunity

 Phagocytes
 Neutrophils
 Moncyte/macrophage
 Eosinophils (to a lesser extent)
 NK cells (large granular lymphocytes)
 Antibody-dependent cell-mediated cytotoxicity
(ADCC)
 Have two major functions
 Lysis of target cells
 Production of cytokines (IFN-γ and TNF-α )
 Act against intracellular pathogens
 Herpesviruses
 Leishmania
 Listeria monocytogenes
 Act against protozoa
 Toxoplasma
 Trypanasoma
Biological Consequences of
Antibody Affinity/Avidity
 Neutralization of toxins
 Complement activation
 Immune elimination of antigen
 Virus neutralization
 More intense immune complex disease in animals
 higher levels of circulating antigen-antibody complexes
 more intense localization of immune complexes on
basement membranes.
 more severe impairment of organ function
Complement activation
 A system of plasma proteins that interact with
 Antigen/antibodycomplexes
 Pathogen surface motifs (alternative and lectin pathways
 Activation of complement results in
 Chemo-attraction of inflammatory cells
 Peptide mediators of inflammation (anaphylatoxins)
 Increased blood vessel permeability
 Smooth muscle contraction
 Mast cell degranulation
 Opsonization of pathogens (enhances phagocytosis)
 Killing of pathogens (membrane attack complex)
Overview of the Complement
Cascade
Hypersensitivity Reactions
 Immune responses that result in tissue injury
Immune-mediated
hypersensitivity reactions
 Type I - Anaphylactic/Atopic
 Type II - Cytotoxic
 Type III - Toxic Complex
 Type IV - T-cell mediated
 Type V- Stimulatory
Immune-Mediated Hypersensitivities
Anaphylactic/Atopic
Hypersensitivity
(Type I )
 Atopy

 Describes the clinical features of individuals

who develop Type I hypersensitivity
 increased vascular permeability
 local edema
 itching

 Strong hereditary linkages

 Mediated by a serum factor termed "reagin"
 "Wheal and flare" reaction
Immediate and Late-Phase
Reactions

Wheal-and-flare reaction Late-phase reaction

(lasts up to 30 min post (develops approximately
injection) eight hours later and
persists several hours)
 IgE response is a local
event
site of allergen entry
local synthesis results in sensitization of
local mast cells
spillover of IgE enters circulation and
sensitizes mast cells and basophils
systemically
 IgE Levels in Disease

 Normal levels do not preclude atopy

 30% of random population allergic to at least one
common allergen
 Genetic background puts individual at risk
 family history indicates predisposition for atopy
 cannot predict specific reactions(s)
 higher level of IgE associated with increased risk of
atopy
Mast Cell
Activation/Degranulation
Antigen
IgE
Fc Receptor
 Contents of the Mast Cell Granules
Active agent Activity
Histamine Increases vascular permeability; elevates level
of cyclic AMP
Heparin Anticoagulation
Serotonin Increases vascular permeability
SRS-A Increases vascular permeability; causes
contraction of human bronchioles
Chymase Proteolysis
Hyaluronidase Increases vasuclar permeability
Eos. Chem. Factor Chemoattraction of eosinophils
Neut. Chem. Factor Chemoattraction of neutrophils
Platelet Agg. Factor Aggregates platelets
Risk of allergy: Family
50

40
percent of
children 30
with atopy
20

10

0
none one both
number of parents with history of allergy
 Hyposensitization
Allergen injections

Symptoms

IgG
Activity
Lymph. Trans.

IgE
Time
 Clinical Tests for Allergy

 Skin Tests
 Immediate Response (wheal & flare reaction; 20 min)
 increased vascular permeability
 local edema
 itching
 Late Reactions (5-24 hr)
 RAST (Radio Allergo Sorbent Test)
Cytotoxic Hypersensitivity (Type II)
Characteristics of Cytotoxic
Hypersensitivity
 Directed against cell surface or tissue antigen
 Characterized by complement cascade activation and
various effector cells
Complement
 Formation of membrane attack complex (lytic
enzymes)
 Activated C3 forms opsonin recognized by
phagocytes
 Formation of chemotactic factors
 Effector cells possess Fc and complement
receptors
 macrophages/monocytes
 neutrophils

 NK cells
Examples of Type II
Hypersensitivity
 Blood transfusion reactions
 Hemolytic disease of the newborn (Rh disease)
 Autoimmune hemolytic anemias
 Drug reactions
 Drug-induced loss of self-tolerance
 Hyperacute graft rejection
 Myasthenia gravis (acetylcholine receptor)
 Sensitivity to tissue antigens
Toxic Complex
Hypersensitivity (Type III)
Diseases associated with immune complexes
 Persistent infection
 microbial antigens
 deposition of immune complexes in kidneys
 Autoimmunity
 selfantigens
 deposition of immune complexes in kidneys,
joints, arteries and skin
 Extrinsic factors
 environmental antigens
 deposition of immune complexes in lungs
Inflammatory Mechanisms in Type
III
 Complement activation
anaphylatoxins
Chemotactic factors
 Neutrophils attracted
difficultto phagocytize tissue-trapped complexes
frustrated phagocytosis leads to tissue damage
Disease Models

 Serum sickness
 Arthus reaction
T-Cell Mediated Hypersensitivity
(Type IV / Delayed-Type)
Manifestations of T-Cell Mediated
Hypersensitivity
 Allergic reactions to bacteria, viruses and
fungi
 Contact dermatitis due to chemicals
 Rejection of tissue transplants
 General Characteristics of
DTH
 An exaggerated interaction between antigen and normal
CMI-mechanisms
 Requires prior priming to antigen
 Memory T-cells recognize antigen together with class II
MHC molecules on antigen-presenting cells
 Blast transformation and proliferation
 Stimulated T-cells release soluble factors (cytokines)
 Cytokines
 attractand activate macrophages and/or eosinophils
 help cytotoxic T-cells become killer cells, which cause tissue
damage
Types of Delayed
Hypersensitivity
Delayed Reaction maximal reaction time
Jones-Mote 24 hours
Contact 48-72 hours
tuberculin 48-72 hours
granulomatous at least 14 days
Contact Hypersensitivity
 Usually maximal at 48 hours
 Predominantly an epidermal reaction
 Langerhans cells are the antigen presenting cells
 a dendritic antigen presenting cell
 carry antigen to lymph nodes draining skin

 Associated with hapten-induced eczema

 nickel salts in jewellry
 picryl chloride
 acrylates
 p-Phenylene diamine in hair dyes
 chromates
 chemicals in rubber
 poison ivy (urushiol)
Poison Ivy
contact
dermatitis
Tuberculin Hypersensitivity

 Maximum at 48-72 hours

 Inflitration of lesion with mononuclear cells
 First described as a reaction to the lipoprotein antigen of tubercle
bacillus
 Responsible for lesions associated with bacterial allergy
 cavitation, caseation, general toxemia seen in TB
 May progress to granulomatous reaction in unresolved infection
Granulomatous
Hypersensitivity
 Clinically, the most important form of DTH, since it
causes many of the pathological effects in diseases which
involve T cell-mediated immunity
 Maximal at 14 days
 Continual release of cytokines
 Leads to accumulation of large numbers of macrophages
 Granulomas can also arise from persistence of
“indigestible” antigen such as talc (absence of
lymphocytes in lesion)
Epitheloid Cell Granuloma
Formation
 Large flattened cells with increased endoplasmic reticulum
 Multinucleate giant cells with little ER
 May see necrosis
 Damage due to killer T-cells recognizing antigen-coated
macrophages, cytokine-activated macrophages
 Attempt by the body to wall-off site of persistent infection
Examples of Microbial-Induced
DTH
Viruses (destructive skin rashes)
 smallpox
 measles
 herpes simplex
 Fungi
 candidiasis
 dematomycosis
 coccidioidomycosis
 histoplasmosis
 Parasites (against enzymes from the eggs lodged in liver)
 leishmaniasis
 schistosomiasis
 Type V Stimulatory Hypersensitivity

 Interaction of autoantibodies with cellular receptors

 Antibody binding mimics receptor-ligand interaction
 Examples
 thyroid stimulating antibody (mimics thyroid stimulating
hormone [TSH] of pituitary binds to thyroid cell receptor
 activation of B-cell by anti-immunoglobulin
Innate Hypersensitivity Reactions
 Toxic shock syndrome (S. aureus TSS toxin)
 hypotension, hypoxia, oliguria and microvascular abnormalities
 excessive release of TNF, IL-1, IL-6
 intravascular activation of complement
 Septicemia - Septic Shock
 primarily due to lipopolysaccharide
 Adult respiratory distress syndrome
 overwhelming accumulation of neutrophils in lung
 Platelet aggregation/adherence to macrophages by gram-positive bacteria
 Superantigens
 Gram positive enterotoxins
 react directly with T-cell receptors and induce massive cytokine release
Medical –Surgical
nursing
Auto-Immune disorders
Common Autoimmune disorders
 1. SLE
 2. Stevens-Johnson Syndrome
Systemic Lupus Erythematosus
 A chronic connective tissue disease
involving multiple organ systems
occurring most frequently in women

 A condition resulting from an auto-

antibody production, immune complex
formation AND TISSUE DAMAGE
Systemic Lupus Erythematosus
 Etiologic factors
 Auto-immune
 Genetic
 Viralfactors
 Hormonal factors
 Medications: HYDRALAZINE, INH,
Chlorpromazine
Systemic Lupus Erythematosus
 PATHOPHYSIOLOGY
 Dysfunctional Immune system produces
antibodies against the body cells
 The antibodies may attack multiple
organs:
 Skin
 Joints

 Kidney

 Heart

 Brain
Systemic Lupus Erythematosus
 ASSESSMENT
 1. Constitutional symptoms-
headache, fatigue, fever, anorexia
 2. “Butterfly rashes” over the bridge
of nose and cheeks
 3. Photosensitivity
Systemic Lupus Erythematosus
 ASSESSMENT
 4. Renal involvement: failure,
proteinuria and hematuria
 5. CNS involvement: psychosis,
seizures and depression
 6. CVS: pericarditis
 7. Arthritis
Systemic Lupus Erythematosus
 LABORATORY TESTS
1. Elevated ESR, creatinine
2. CBC will show anemia,
thrombocytopenia
3. Positive ANA, LE
Systemic Lupus Erythematosus
 Medical Management
 1. Pharmacotherapy
 NSAIDs are given to manage arthritis
 Steroids are given to suppress
inflammation and the immune reaction
 Immunosuppressive drugs to suppress
immune response
Systemic Lupus Erythematosus
 Medical Management
 2. plasma exchange therapy
 To remove the circulating antibodies
Systemic Lupus Erythematosus
NURSING INTERVENTION
 1. Provide psychological support to
the patient and family
 2. Administer medications- steroids
and immunosuppressant
 3. Monitor for seizure development
 4. Monitor weight, VS
Systemic Lupus Erythematosus
NURSING INTERVENTION
 5. Avoid sun exposure
 6. Lifetime monitoring and lifestyle
changes
Toxic epidermal Necrolysis and
SJS
 Are potentially FATAL skin disorders
triggered by a reaction to a
medication or a viral infection that
results to skin changes
Toxic epidermal Necrolysis and
SJS
 Etiologic factors
1. medications:
 Sulfonamides, butazones, other
antibiotics and anti-seizure drugs
1. Viral infections
 AIDS
 Immunocompromised states
Toxic epidermal Necrolysis and
SJS
 Pathophysiology
 Thought to be auto-immune
Toxic epidermal Necrolysis and
SJS
 ASSESSEMENT FINDINGS
1. CONJUNCTIVAL BURINING AND
ITCHING- INITIALLY
2. Cutaneous tenderness
3. Fever
4. Cough
5. Sore throat, headache, malaise
Toxic epidermal Necrolysis and
SJS
 ASSESSEMENT FINDINGS
6. LARGE Flaccid bullae develop in
some areas
LARGE sheets of epidermis are shed
Fingernails, toenalis, eyebrows and
eyelashes are also shed
Toxic epidermal Necrolysis and
SJS
 ASSESSEMENT FINDINGS
6. The skin is painful with exudation
similar to burns- scalded skin
syndrome
Toxic epidermal Necrolysis and
SJS
 Diagnostic examination
1. Histologic studies of the skin
2. Immunoflourescent studies
Toxic epidermal Necrolysis and
SJS
 Medical management
1. Surgical debridement to remove the involved skin
2. IVF therapy to replace fluids
3. Culture of tissue samples
4. Intravenous Immunoglobulin administration
5. Systemic and topical antibiotics
Toxic epidermal Necrolysis and
SJS
 Nursing Interventions
1. Maintain skin integrity
 Use of circular turning frame
 Apply topical antibiotics
 Gently perform WARM compress
 Hydrotherapy in tub
 Oral hygiene
Toxic epidermal Necrolysis and
SJS
 Nursing Interventions
2. Provide Fluid Balance
 Monitor vital signs for hypovolemia
 Weigh daily
 Regulate IVF
 Provide Enteral and parenteral
feedings
Toxic epidermal Necrolysis and
SJS
 Nursing Interventions
3. Prevent Hypothermia
 Cotton blankets, heat lamps
 Provide skin care as quickly as
posible
Toxic epidermal Necrolysis and
SJS
 Nursing Interventions
4. Relieve the PAIN
 Administer prescribed analgesics
usually BEFORE performing painful
treatments
 Allay anxiety that may worsen pain
 Progressive muscle relaxation,
imagery may be suggested
Toxic epidermal Necrolysis and
SJS
 Nursing Interventions
5. Reduce anxiety
 Referral to appropriate resource
person
Toxic epidermal Necrolysis and
SJS
 Nursing Interventions
6. MANAGE complications
SEPSIS
 Maintain STRICT asepsis
 Wear sterile gloves
 Utilize a private room
 Protective garments shall be worn by visitors
Toxic epidermal Necrolysis and
SJS
 Nursing Interventions
6. MANAGE complications
Conjunctival Retraction, SCARS, corneal
lesions
 Keratoconjunctivitis- principal complication
 COOL , damp cloth over the eye to relieve
burning sensation
Toxic epidermal Necrolysis and
SJS
 Nursing Interventions
6. MANAGE complications
Conjunctival Retraction, SCARS, corneal
lesions
 Maintain cleanliness of the eye
 Administer eye drops and eye lubricants
 Use of eye patches
Oncology defined

 Branch of medicine that

deals with the study,
detection, treatment and
management of cancer and
neoplasia
 In the Philippines, cancer ranks third in leading
causes of morbidity and mortality after
communicable diseases and cardiovascular
diseases

 In the Philippines, 75% of all cancers occur

after age 50 years, and only about 3% occur
at age 14 years and below
 If the current low cancer prevention consciousness
persists, it is estimated that for every 1800 Filipinos,
one will develop cancer annually

 most Filipino cancer patients seek medical advice

only when symptomatic or at advanced stages: for
every two new cancer cases diagnosed annually,
one will die within the year
 The top cancer sites in the Philippines include
those cancers whose major causes are known
(where action can therefore be taken for primary
prevention), such as cancers of the lung/larynx
(anti-smoking campaign), liver (vaccination
against hepatitis B virus), cervix (safe sex) and
colon/rectum/stomach (healthy diet). Except for
the liver, the top Philippine cancer sites are also
the top cancers worldwide
Predisposing Factors
a. Age
Older individuals are more prone to Ca
b. Sex
women – breast, uterus, cervix cancer
Men – prostate, lung Ca
c. Urban Vs Rural
d. Geographic Distribution
e. Occupation
f. Hereditary
g. Stress
h. Precancerous lesions
- Pigmented moles, burn scars, benign
polyps, adenoma, fibrocystic disease
of the breast
i. Obesity
- Breast and colorectal Ca
Cancer Incidence
Women Men
Breast Prostate
Lung Lung
Colon and Rectum Colon and rectum
Uterine Urinary Bladder
Non-Hodgkin’s Non hodgkin
Lymphoma lymphoma
Carcinogenesis
 Initiation
- first step, chemicals, physical factors and
biologic agents, escape the normal
enzymatic mechanisms and alter the
genetic structure of the cellular DNA
- normally these alterations are reversed by
DNA repair mechanism or programmed
cellular suicide (apoptosis)
 Promotion
- Repeated exposure
- Causes expression of abnormal or
mutant genetic information
- Proto-oncogenes, “on switch”
- Ca suppressor genes, “turn off”
- P53 gene, a tumor suppressor gene
regulates whether cells repair or die
after DNA is damaged
 CARCINOGEN

INITIATION
DNA repair
Bind to DNA
Normal Cell

Permanent DNA damage Cell Death

Cell Proliferation
PROMOTION

NEOPLASTIC CELLS
 Progression
- Third step of cellular carcinogenesis
- The cellular changes formed during
initiation and promotion now exhibit
increased malignant behavior
Etiologic Factors
1. Viruses
 Oncogenic viruses
 Epstein Bar virus, burkitt’s lymphoma,
nasopharyngeal Ca, non-Hodgkin and hodgkin’s
lymphoma
 Herpes simplex Type II, cytomegalovirus and
HPV type 16,18,31,33, Cervix Ca
 HIV, kaposi sarcoma
 H. pylori, gastric Ca
2. Physical Agents
- Ultraviolent rays, especially in fair skinned
blue or green eyed people, skin Ca
- Radiation from x-ray or nuclear, leukemia,
multiple myeloma, Ca of lung, bone,
breast and thyroid

3. Hormones
Oral contraception or HRT, Inc. incidence of
hepatocellular, endometrial and breast Ca
4. Chemical Agents
- 75% related to environment
- Tobacco smoking, single most lethal
carcinogen, 30% of Ca deaths, lung, head
and neck esophagus, bladder panceas,
cervix ca
- chewing tobacco, ca of the oral cavity in
men younger than 40 years old
5. Industrial compounds
- Vinyl chloride (plastics, asbestos)
- Polycyclic aromatic hydrocarbons
(burning, auto and truck emission)
- Fertilizers and weed killers
- Dyes, (aniline dyes, hair dyes)
6. Dietary Factors
- Carcinogenic
fats, alcohol, salt cured or smoked
meats, high caloric content
- Proactive
high fiber, Cruciferous vegetables
( cabbage, broccoli, cauliflower, brussels,
sprouts) Carotenoids (carrots, tomatoes,
spinach, apricots, peaches, dark green
and yellow vegetables), vit E, C, zinc and
selenium
7. Genetics
- Oncogenes ( hidden/repressed genetic
code for Ca that exist in all individual
8. Age: Advancing age is a significant risk
factors
9. Immunologic Factors
a. Immunosuppressed individuals more
susceptible to cancer
What Do These Factors Have
In Common?
Fragments
Direct Damage & Deletions
To DNA
(e.g., radiation) CANCER

Chemical Base Mutations

Mutagens & Substitutions
(e.g., pollutants,
additives,drugs Membrane damage
and hormones) causing internal mutagens
Miscellaneous to form
Mutagens (dietary
fat and free radicals)
Immune response
 T lymphocytes, recognize tumor associated antigens,
possesses cytotoxic abilities
 Lymphokines, capable of killing and damaging Ca cells
 Macrophages, disrupt Ca cells

 B lymphocytes antibodies, defends the body against

malignant cells
 Natural killer cells, directly destroy Ca
American Ca Society recommendation

Site Gender Age Evaluation Frequency

Breast Female 20-39 CBE, Q 3 yrs

BSE Q month

>40 CBE Q year

BSE Q month

Mammogr Q year
am
Colon/rectum M/F >50y/o Fecal occult Q year
blood

and Flexible Q 5 years

sigmoidoscop
y

or Colonoscopy Q 10 years

or Double Q 5 years
conrast
barrium
enema
Prostate M >50 or < 50 if PSA and DRE Q year
high risk

Cervix F >18 or Pap smear Q year

younger if Pelvic exam
sexually
active

Cancer M/F >20-39 Other Ca Q 3 years

related check >40 types Q year
up
Characteristics of Ca
Characteristic Benign malignant
Cell characteristic Well differentiated Undifferentiated little
Resemble normal cells resemblance on normal
cells
Mode of growth Grows by expansion Grows at the periphery,
Not infiltrate the infiltrate and destroys
surrounding tissue the surrounding tissue

Rate of growth slow Variable, fast

Metastasis none Access to blood,

lymphatics and other
areas
 benign Malignant

General effects localized Anemia, weaness,

weight loss

Tissue destruction No tissue damage Extensive tissue

damage

Ability to cause death Does not usually cause Usually causes death
death
Metastasis
 Lymphatics
the most common mechanism
breast tumors, axillary, clavicular, and thoracic LN
 Hematogenous

disseminated through the blood stream

related to the vascularity of the tumor
 Angiogenesis – ability to induce the growth of new
capillaries from the host tissue to meet the nutrients and
oxygen
Classification and staging
a. Tissue of Origin
2. Carcinoma:
a. Squamous cell Ca – surface epithelium
b. Adenocarcinoma – glandular or
parenchymal
c. Sarcoma – connective tissue
d. Leukemia, Lymphoma
B. Staging – determines the size of the tumor and the existence of
metastasis

 TNM Classification
T – extent of primary tumor
N – absence or presence and extent of
regional lymph node metastasis
M – absence or presence of distance
metastasis
Primary Tumor (T)
TX – primary tumor cannot be assessed
TO – no evidence of primary tumor
Tis – carcinoma in situ
T1,2,3,4 – increasing size or local extent of
primary tumor

Regional lymph nodes (N)

NX – regional LN cannot be assessed
NO – no regional LN metastasis
N1,2,3 – increasing involvement of LN
 Distant Metastasis
MX – Distance metastasis cannot be
assessed
MO – No distant metastasis
M1 – distant metastasis
 Grading
- Classification of tumor cells
- Grade I – IV, define the type of tissue
which the tumor originated
 Normal T0, N0, M0
 Stage I T1, N0, M0
 Stage II T2, N1, M0
 Stage III T3, N2, M0
 Stage IV with metastasis
2. Histologic
a. Grade 1 - well differentiated
b. Grade 2 - Moderately differentiated more
abnormal
c. Grade 3 - Poorly differentiated, Very
abnormal
d. Grade 4 - Very immature, anaplastic
hard to even determine the tissue of
origin
Nomenclature of Neoplasia
Tumor is named according to:
1. Parenchyma, Organ or Cell
 Hepatoma- liver
 Osteoma- bone
 Myoma- muscle
Nomenclature of Neoplasia
Tumor is named according to:
2. Pattern and Structure, either GROSS or
MICROSCOPIC
 Fluid-filled CYST
 Glandular ADENO
 Finger-like PAPILLO
 Stalk POLYP
Nomenclature of Neoplasia
Tumor is named according to:
3. Embryonic origin
 Ectoderm ( usually gives rise to epithelium)
 Endoderm (usually gives rise to glands)
 Mesoderm (usually gives rise to Connective
tissues)
BENIGN TUMORS

 Suffix- “OMA” is used

 Adipose tissue- LipOMA
 Bone- osteOMA
 Muscle- myOMA
 Blood vessels- angiOMA
 Fibrous tissue- fibrOMA
MALIGNANT TUMOR

 Named according to embryonic cell origin

1. Ectodermal, Endodermal, Glandular,
Epithelial
 Use the suffix- “CARCINOMA”
 Pancreatic AdenoCarcinoma
 Squamos cell Carcinoma
MALIGNANT TUMOR

 Named according to embryonic cell origin

2. Mesodermal, connective tissue origin
 Use the suffix “SARCOMA
 FibroSarcoma
 Myosarcoma
 AngioSarcoma
“PASAWAY”

1. “OMA” but Malignant

 HepatOMA, lymphOMA, gliOMA,
melanOMA
2. THREE germ layers
 “TERATOMA”

3. Non-neoplastic but “OMA”

 Choristoma
 Hamatoma
Warning signs of Ca
 C – change in bowel or bladder habits
 A – sore that does not heal
 U – unusual bleeding or discharge
 U – unexplain sudden weight loss
 U – unexplained anemia
 T – thickening or lump
 I – indigestion or difficulty in swallowing
 O – obvious change in wart or mole
 N – nagging cough or hoarseness of voice
Screening
a. Early detection and treatment are the
cornerstones of cancer survival
b. Educating the public about a healthy
lifestyle and early detection
Health education
1. Reduce and avoid exposure to known
carcinogens
2. Eat a balanced diet of vegetables, fruits
and whole grains, reducing fat and red
smoked and cured meat.
3. Limit alcohol beverages
4. Exercise regularly
5. Reduce stress and encourage adequate
rest and relaxation
6. Follow screening recommendations
7. Know the seven warning signs
8. Seek medical attention
Diagnostic test
 Biopsy
- removal of tissue for histologic examination
- essential for choosing treatment
Types
a. FNAB
b. Incision
c. Excision
d. Punch
Preprocedure
a. Depends on the location and type of
biopsy
b. May need to be NPO if sedation or
contrast is used
c. Inform the client about the procedure
Postprocedure
a. Control bleeding
b. Monitor for infection
c. Manage pain
d. Inform the client how to obtain the results
B. Imaging
 X-ray, ultrasound, MRI, Ct scan
 Methods of obtaining information about the
presence, location and extend of tumor
 Method chosen is based on
1. ability to visualize tumor
2. Risk
3. Client comfort
4. Cost
Preprocedure
a. Assess for allergy if contrast is to be used
b. NPO depending on the area being imaged,
use of sedation or contrast
c. Prepare patient for length of imaging, possible
noise of machinery, need to remain still.
d. Monitor the client for flushing, itching or
nausea, indicating allergy to contrast.
Tumor Markers
CEA GI, lung, breast

Alpha feto Hepatocellular, gastric,

protein pancreatic, colon and lung
cancer
HCG Trophoblastic tumor, germ cell,
ovary
Acid Prostate cancer
phosphatase
CA 125 Ovarian cancer
Client Reaction during Diagnoses

 Client will use coping strategies to ↓ his anxiety level such

as:
 Denial-
 Rational inquiry-seek more information
 Affect Reversal-make light of the situation (laughing
etc.)
 Mutuality-share concerns and talk with other persons
 Suppression-conscious forgetting
 Displacement or redirection-do other things
Points to Remember

 Most client fear of death upon confirmation of

Cancer
 Clients usually ignored cardinal signs of Cancer
 Most often cancer is detected during routine exam
 Questions that need to be answered: Example (Is
the disease curable or not?)
Nursing Diagnosis
 Ineffective coping
 Anticipatory grieving
 Disturbed body image
 Fatigue
 Impaired elimination
 Hopelessness
 Impaired oral mucous membrane
 Nausea
 Impaired nutrition less than body
requirements
 acute pain
 Impaired skin integrity
Signs and symptoms of malignant neoplasia

 Proliferation of Ca cells
 Pressure
 Obstruction
 Pain ( late sign of Ca )
- Pressure on nerve endings
- Distention of organs/vessels
- Lack of O2 to tissue and organ
- Release of pain mediators
 Pleural effusion and ascites
 Ulceration and necrosis
- As tumor erodes BV and pressure on
tissue causes ischemia, tissue damage,
bleeding and infection
 Vascular thrombosis, Embolus,
Thrombophlebitis
 Tumors tends to produce abnormal
coagulation factors
 Paraneoplastic Syndrome
 Anemia
- Ca cells produces chemicals that interfere
with rbc production
- Iron uptake is greater in the tumor than
that deposited in the liver
- Blood loss from bleeding
 Hypercalcemia

- Increases and accelerates bone

breakdown and release of Calcium
 Anorexia – Cachexia Syndrome
- Final outcome of unrestrained Ca growth
- Ca deprived normal cells nutrition
- Protein depletion, serum albumin
decreases
- Tumors take up Na
- Act in the satiety center causing anorexia
- Taste sensation diminishes
 Take pain seriously, recognizing that only the
person in pain knows how it feels.
 Provide information and resources for pain
control.
 Communicate with genuineness, accurate
empathy, and nonpossessive warmth.
 Encourage sufferers to share their feelings and
network with other survivors.
 Respect culture norms and wishes of sufferers,
maximizing their control
 Encourage release of energy through joy-
producing activities.
 Monitor pain medications, effectiveness, and
adverse effects
Management of Cancer
 Cure
- eradication of malignant diseases
 Control

- prolonged survival and containment of cancer cell

growth
 Palliation

- relief of symptoms associated with the disease

Therapeutic Modalities for
Cancer
 Surgery
 Chemotherapy
 Radiation therapy
 Immunotherapy
 Bone Marrow Transplantation
Surgery
 The ideal and most frequently used
 Goals
a. Primary
b. Prophylactic
c. Palliative
d. reconstructive
 Removal of tissue for diagnosis, staging,
palliation or treatment of cancer.
 Most frequently used cancer therapy
 Most successful single therapy if cancer
has not spread
 Very often performed on an OPD or brief
stay basis
Diagnostic Surgery
 Biopsy
a. Excisional biopsy
- most frequently used for easily accessible
tumors of the skin, breast, ULGIT,URT
- provides the pathologist the cells and the entire
tissue
- decreases the chance of seeding the tumor
 Incisional Biopsy
- used if the tumor mass is too large to be
removed
- a wedge of tissue from the tumor is taken
 Needle Biopsy

- done on suspicious masses that are easily

accessible
- fast, inexpensive and easily performed
Surgery as primary treatment
 Remove the entire tumor or as much as is
feasible
1. Local excision
- if the mass is small
2. Wide or Radical Excision
- removal of the primary tumor, LN, adjacent and
surrounding tissue
- results in disfigurement and altered function
3. Salvage surgery
Prophylactic Surgery
- Removal of non-vital structures that are likely
to develop Ca
 Palliative Surgery

- when cure is not possible, the goal of

treatment is to make the patient as
comfortable as possible and to promote a
satisfying and productive life for as long as
possible
Radiation Therapy
 Used to control malignant disease when a tumor
cannot be removed surgically
 To relieve the symptoms of metastatic disease,
especially when the Ca spread to the brain, bone.
 A radiosensitive tumor is one that can be destroyed
by a dose of radiation that still allows for cell
regeneration in the normal tissue
Radiation Therapy
 Uses ionizing radiation to kill or limit the
growth of cancer cells. May be internal or
external
 Effect cannot be limited to cancer cells
only
 is a cancer treatment that uses high doses of
radiation to kill cancer cells and stop them from
spreading. At low doses, radiation is used as an
x-ray to see inside your body and take pictures,
such as x-rays of your teeth or broken bones.

 Radiation use in cancer treatment works in much

the same way, except that it is given at higher
doses.
 Radiation therapy is used to:

 Treat cancer. Radiation can be used to cure, stop,

or slow the growth of cancer.

 Reduce symptoms. When a cure is not possible,

radiation may be used to shrink cancer tumors in
order to reduce pressure. Radiation therapy used
in this way can treat problems such as pain, or it
can prevent problems such as blindness or loss of
bowel and bladder control.
 Cells are most vulnerable to radiation
during DNA synthesis and mitosis
 Most sensitive are those body tissue that
undergo frequent cell division. (BM,
Lymphatic, GIT, gonads)
 Tumors that are well oxygenated are more
sensitive to radiation
Radiosensitivity
 Highly sensitive
- ovaries, testes, bone marrow, blood,
intestines

 Low sensitivity
- muscle, brain, spinal cord
Types
a. Teletherapy (External Beam)
- x-rays are used to destroy cancerous cells at
the skin surface or deeper
b. Used more commonly
c. Client is not radioactive during treatment
d. Simulation – X-ray or Ct planning session to
identify the field which delivers maximum
radiation to the tumor and minimal to normal
tissue. Involves skin markings
e. Administered in fractions of the full dose, 5 days
a week for 4-6 weeks
b. Brachytherapy (Internal)
- used primarily in the head and neck,
gynecologic, prostate cancer
- delivers a high dose of radiation in a local
area using implants
- Client is radioactive only when implant is
in placed
- plan cares efficiently to minimize nurses,
exposure to implant, use shielding, wear a
film badge and maintain safe distance.
- Pregnant nurses should not care for
clients with implanted radiation
- Pickup dislodge implants with long forceps
placed in a special container.
- Body fluids of clients treated with systemic
radioactive iodine are radioactive; fluids of
client with implants are not
Radiation Dosage
 The lethal tumor dose is defined as the
dose that will eradicate 95% of the tumor
yet preserve normal tissue
Adverse Reaction
 Seen only in the organs in the radiation
field, except for systemic effects of
nausea, anorexia and fatigue
 Skin reactions are common and expected
with external beam
Toxicity
 Localized to the area being irradiated
 Alteration in oral mucosa, stomatitis, xerostomia,
change and loss of taste, decreased salivation
 Altered skin integrity, alopecia, erythema,
shedding, desquamation
 Thrombocytopenia
 Anemia
Radiation Safety

 Distance - the greater the distance the lesser the

exposure
 Time - the less time spent close to radiation the
less exposure (max of 30 min per shift)
 Shielding - use lead aprons and gloves
 Standards - kept as low as reasonably achievable
 Monitoring device - film badge (measure the whole
exposure of the nurse)
Side Effects
a. Skin: Itching, redness, burning,
sloughing
2. Keep skin free of foreign substance
3. Avoid use of medicated solutions
4. Avoid pressure, trauma, infection
5. Avoid exposure to heat, cold or sunlight
b. Anorexia, vomitting, nausea
1. Provide small, attractive feedings
2. Avoid extremes of temperatures
3. Administer antiemetics before meals
c. Diarrhea
 Encourage low residue, bland, high
protein foods
 Provide good perineal hygiene
 Monitor electrolytes, Na,K,Cl
d. Anemia. Leukopenia,
thrombocytopenia
 Isolate patient
 provide frequent rest period
 Encourage high protein diet
 Assess for bleeding
 Monitor lab results CBC, WBC, Plt
Chemotherapy
 Systemic treatment with chemicals which
destroy rapidly proliferating cells
 Used for cure in testicular, Hodgkin disease,
ALL, neuroblastoma, Wilms and Burkitt’s
lymphoma
 Used to control breast, nod-Hodgkin, small cell
lung and ovarian cancer
 Used palliative for relief of pain, obstruction and
to improve comfort
 What does chemotherapy do?

 Cure cancer - when chemotherapy destroys cancer

cells to the point that your doctor can no longer detect
them in your body and they will not grow back.

 Control cancer - when chemotherapy keeps cancer

from spreading, slows its growth, or destroys cancer
cells that have spread to other parts of your body.

 Ease cancer symptoms (also called palliative care) -

when chemotherapy shrinks tumors that are causing
pain or pressure.
Chemotherapy
Chemotherapy works by stopping or slowing the
growth of cancer cells, which grow and divide
quickly. But it can also harm healthy cells that
divide quickly, such as those that line your
mouth and intestines or cause your hair to grow.
Damage to healthy cells may cause side effects.
Often, side effects get better or go away after
chemotherapy is over.
 Sometimes, chemotherapy is used as the
only cancer treatment. But more often, you
will get chemotherapy along with surgery,
radiation therapy, or biological therapy.
Chemotherapy can:

 Make a tumor smaller before surgery or

radiation therapy. This is called
neo-adjuvant chemotherapy.
 Destroy cancer cells that may remain after surgery or
radiation therapy. This is called
adjuvant chemotherapy.

 Help radiation therapy and biological therapy work

better.

 Destroy cancer cells that have come back (recurrent

cancer) or spread to other parts of your body (
metastatic cancer).
Cell Cycle
 Time required for one tissue cell to divide
and reproduce two identical daughter cells
1. Go – resting phase
2. G1 – RNA and protein synthesis occurs
3. S – DNA synthesis occurs
4. G2 – Premitotic phase
5. M – cell division occurs
 Chemotherapy may be given in many ways.
 Injection. The chemotherapy is given by a shot in a muscle in your arm, thigh,
or hip or right under the skin in the fatty part of your arm, leg, or belly.

 Intra-arterial (IA). The chemotherapy goes directly into the artery that is
feeding the cancer.

 Intraperitoneal (IP). The chemotherapy goes directly into the peritoneal cavity
(the area that contains organs such as your intestines, stomach, liver, and
ovaries).

 Intravenous (IV). The chemotherapy goes directly into a vein.

 Topically. The chemotherapy comes in a cream that you rub onto your skin.

 Orally. The chemotherapy comes in pills, capsules, or liquids that you swallow.
Antineolplastic agent
 Cell Cycle non-specific
1. Alkylating agents
- acts with DNA to hinder cell growth and division
- cisplatin, cyclophosphamide

2. Steroids and sex hormones

- alter the endocrine environment to make it less conducive
to growth of cancer cells.
3. Antitumor antibiotics
- interfere with DNA synthesis by binding
DNA. Prevent RNA synthesis
- Bleomycin, dactinomycin, doxorubicin,
mitomycin
- cardiac toxicity (daunorubicin,
doxorubicin)
 Cell Cycle Specific (S phase)
1. Antimetabolites
- foster cancer cell death by interfering with
cellular metabolic process
-5-flouroracil, methotrexate, cytarabine
- renal toxicity (methotrexate)
 Cell cycle specific (M phase)
1. Plant alkaloids
- makes the host body a less favorable
environment for the growth of cancer cells
- arrest metaphase by inhibiting mitotic
tubular formation. Inhibit DNA and RNA
synthesis
-vincristine, vinblastine
- Taxanes: Paclitaxel (bradycardia)
Chemotherapy
 Used to treat systemic diseases rather
than localized lesions that are amenable
to surgery and radiation
 Used in an attempt to destroy tumor cells
by interfering with cellular function and
reproduction
Chemotherapy
 Use of chemicals to destroy cancer cells
 Interferes DNA & RNA activities
associated with cell division
 Often used in combination with radiation
therapy
 Cytotoxic - is an agent capable of
destroying cells
 Cytotoxic drug - alkylating and
antimetabolites
 Can be combined with surgery or radiation
therapy
 Used to reduce the tumor size
preoperatively and to destroy the
remaining tumor cells preoperatively
 Eradication of 100% of tumor is nearly
impossible
 Goal is to eradicate enough of the tumor
so that the remaining tumor cells can be
destroyed by the immune system
Contraindication
 Infection
 Recent surgery
 Impaired renal or hepatic function
 Recent radiation therapy
 Pregnancy
 Bone marrow depression
 Extravasation –
cause tissue necrosis
and damage to
tendons, nerves and
blood vessels
Major side effects
a. GI System
1. Nausea and vomitting
- administer anti-emetics
- NPO 4-6 hrs before chemotherapy
- bland diet foods in small amounts after
treatment
 Diarrhea
 Stomatitis

- Good oral hygiene

- rinse with viscous lidocaine before meals
- rinse with plain water or hydrogen
peroxide after meals
- apply water soluble lubricants
- Suck popsicle to provide moisture
Hematologic (Myelosuppression)
1. Thrombocytopenia
- Avoid bumps or bruishing
- protect client from physical injury
- Avoid aspirin
- Avoid IM injections
- Assess for bleeding tendencies
b. Leukopenia
- use careful handwashing
- reverse isolation if WBC <1000
- assess for signs of respiratory infection
- Avoid crowds
c. Anemia
- Provide adequate rest periods
- monitor CBC
- Administer o2 PRN
 Integumentary System – Alopecia
- Explain hair loss is not permanent
- Support and encouragement

- Advise client to obtain wig

 Renal system

- may cause direct damage to kidneys by

excreting metabolites.
- encourage fluids and frequent voiding
- increased excretion of uric acid may
damage kidneys
- Administer allopurinol, Inc. OFI
 Reproductive System

1. Infertility and mutagenic damage to

chromosomes
2. Banking sperm
3. Use contraception
Side Effects from Radiation and Chemo
Therapy
 Neurologic/Sensory/Perceptual
 Meningeal irritation
 CN and peripheral neuropathy
 Cerebellar toxicity
 Ototoxicity
 Cardiac
 Pericardial Effusion
 Arrhythmias
 CHF
 Pulmonary
 Pleural Effusion
 Pneumonitis
 GIT
 Stomatitis
 Esophagitis
 Pharyngitis
 Taste alteration
 Anorexia
 Nausea and vomiting
 Constipation and diarrhea
 Weight loss
 GUT
 Nephrotoxicity
 Hemorrhagic cystitis
 Hyperuricemia
 Urine color changes
 Reproductive
 Loss of libido
 Impotence
 Amenorrhea
 Irregular menses
 Menopausal symptoms
 Azoospermia
 Sterility
 Gynecomastia
 Hepatic
 Hepatotoxicity
 Integumentary
 Alopecia
 Dermatitis and ulcers
 Hematopoietic
 ↓ bone marrow activity
 anemia, prone to infection and bleeding
tendency
 Metabolic
 TLS and Hyperkalemia
Perceived Change in Body Image

 Obvious reminder of disability

 need for prosthesis (breast, leg and
eye)
 need for hardware (wheel chair,
crutches)
 need for medication (CR therapy)
 extent of disability or limitation
Type of loss

 symbols of sexuality
 social acceptability (colostomy)
 ability to communicate (laryngectomy,
aphasia)
 anatomic changes (amputation)
Terminally Ill

 50% die from the disease

 time from diagnosis to death ranges from
weeks- years
 not all clients become terminally ill
 others die during initial treatment; others die
from complications of treatment
 Endpoint: no response to treatment and
progressions cannot be controlled
HOSPICE CARE
 standard of care for terminally ill cancer
clients
 symptom control
 pain management
 providing comfort and dignity
 24 hour – 7 day coverage
 services given are based on client’s need not
on its ability to pay
 One can suffer without physical pain and
one can have physical pain and not
necessarily suffer.
 The founder of the modern hospice
movement described suffering as “total
pain,” an experience of changing self-
perception, fear of physical distress and
dying, concerns about relationships,
changing self-perception, and memory of
other person’s suffering (
Ethical Issues

 caring can be just successful as

curing;
when curing is not an option
 care is exercised during the final stage
of life
Goals of Intervention

 to care without functional and

structural impairment
 if cure is not possible goals must
= prevent further metastasis
= relieve symptoms
= maintain high quality of life
Bone Marrow Transplant
 Used in the treatment of leukemia for
clients who have closely matched donors
and experiencing temporary remission
with chemotherapy
 Severe aplastic anemia, breast Ca, brain
Ca
Types
 Autologous
- own bone marrow, most common type
 Allogenic

- transplant from a genetically non-identical

donor
- sibbling most common type
procedure
1. Harvest – through multiple aspiration
from the iliac crest to retrieve sufficient
bone marrow for the transplant
- 500ml- 1000ml
2. Conditioning
- immunosuppressant therapy is given to
eradicate all malignant cells
3. Transplantation
a. administered through central line like BT
b. infused 30 min

4. Engraftment
a. transfused BM move to marrow forming
sites
b. occurs when WBC, erythrocytes, plt ct
begin to rise
c. takes 2-5 weeks
Complications:

1. Failure of engraftment.
2. Infection: higher risk 3-4 weeks
3. Pneumonia: principal cause of death
during first three months
4. Graft vs host disease – principal
complication
a. Acute – 1st 100 days post transplant
b. Chronic – 100-400 days
Nursing Care: Pretransplant
1. Provide protected environment
- strict reverse isolation
2. Monitor central lines frequency
3. Provide care receiving chemotherapy
Post transplant
1. Prevent infection
b. Maintain protective environment
c. Administer antibiotics
d. Check IV set ups q12hrs
2. Provide mouth care for stomatitis and
mucositis
3. Monitor carefully for bleeding
a. check for occult blood in emesis, stools
b. observe for easy bruising
c. Check platelet ct daily
d. replaced blood component
4. Maintain fluid and electrolyte balance
5. Provide client health teaching
Nursing Assessment

 Weight loss
 Frequent infection
 Skin problems
 Pain
 Hair Loss
 Fatigue
 Disturbance in body image/ depression
Managing effects of Cancer and
treatment
 Pain
1. Description
a. Whatever the client says it is, whenever the
client says it exists.
b. may be caused by treatment, cancer destruction
of tissue or pressure or pressure on nearby
structures and cancer progression
c. Bone metastasis are very common cause
Pain: Cancer and End of Life
 30% of clients experience pain at the time
of diagnosis.
 30% to 50% experience pain while
undergoing therapy.
 70% to 90% experience pain as cancer
advances and overcomes their defenses
 Cancer pain is complex, interactive, and
ever-changing. It comes from two general
sources: the cancer itself, and its various
treatments
 Cancer pain is more than a physical
symptom. It is a reminder of ones mortality
and a harbinger of death.
 It interferes with normal routines,
degrades the quality of life, and robs one
of rest, creativity, joy, and peace.
 Cancer pain adds stress and worry to its
sufferers and friends and family. For this
reason, healthcare professionals
 Nursing Interventions
a. Assess all clients for pain even if they do
not appear to be experiencing it.
b. Educate clients and families about
narcotic use
1. Correct use of narcotics results in
addiction in <1% of client
2. Narcotic dose may be increased with
increasing dose not have be reserved for
last resort use.
c. Instruct clients on nonpharmacologic
methods of pain management.
d. Administer pain medication as ordered,
utilizing a combination of non-narcotic and
narcotic analgesics
e. Oral route is preferred if possible
f. Meperidine (demerol) is seldom used to
treat cancer pain because it metabolizes
and accumulates during extended use.
 Myelosuppression
- reduced numbers of white and red blood
cells and platelets associated with cancer
or treatment
- Neutropenia <1000
- Thrombocytopenia < 100,000
- results in infection and bleeding
- the oral cavity is the primary site of
infection
 Assessment
Monitor for clinical manifestations of infection
1. Erythema, warmth, swelling at incision site
2. Fever
3. Shaking chills
4. Pain
5. Foul smelling duscharge
6. White oral plaque
7. Change in sensorium
 Monitor for clinical manifestation of
bleeding
1. Bruising and petechiae
2. Blood in the urine, stool and vomitus
3. Changes in mentation
4. Pain
5. Weak, rapid pulse, low blood pressure,
pale cool skin
Nursing intervention
a. Instruct practice of careful washing
b. Perform oral and perineum care
c. Place client in protective isolation
d. Administer antibiotics and antipyretics
e. Avoid unnecessary invasive procedures to
prevent bleeding or infection
f. Avoid shaving
g. Administer iced gastric lavage
Nursing Intervention

 MAINTAIN TISSUE INTEGRITY

 Handle skin gently
 Do NOT rub affected area
 Lotion may be applied
 Wash skin only with SOAP and Water
Nursing Intervention

 MANAGEMENT OF STOMATITIS
 Use soft-bristled toothbrush
 Oral rinses with saline gargles/ tap water
 Avoid ALCOHOL-based rinses
Nursing Intervention
 MANAGEMENT OF ALOPECIA
Alopecia begins within 2 weeks of therapy
 Regrowth within 8 weeks of termination
 Encourage to acquire wig before hair loss
occurs
 Encourage use of attractive scarves and hats
 Provide information that hair loss is temporary
BUT anticipate change in texture and color
Nursing Intervention
 PROMOTE NUTRITION
 Serve food in ways to make it appealing
 Consider patient’s preferences
 Provide small frequent meals
 Avoids giving fluids while eating
 Oral hygiene PRIOR to mealtime
 Vitamin supplements
Nursing Intervention
 RELIEVE PAIN
 Mild pain- NSAIDS
Moderate pain- Weak opiods
 Severe pain- Morphine
 Administer analgesics round the clock
with additional dose for breakthrough pain
Nursing Intervention
 DECREASE FATIGUE
 Plan daily activities to allow alternating
rest periods
 Light exercise is encouraged
 Small frequent meals
Nursing Intervention
 IMPROVE BODY IMAGE
 Therapeutic communication is essential
 Encourage independence in self-care
and decision making
 Offer cosmetic material like make-up
and wigs
Nursing Intervention
 ASSIST IN THE GRIEVING PROCESS
 Some cancers are curable
 Grieving can be due to loss of health, income,
sexuality, and body image
 Answer and clarify information about cancer and
treatment options
 Identify resource people
 Refer to support groups
Nursing Intervention
 MANAGE COMPLICATION: INFECTION
 Fever is the most important sign (38.3)
 Administer prescribed antibiotics X 2weeks
 Maintain aseptic technique
 Avoid exposure to crowds
 Avoid giving fresh fruits and veggie
 Handwashing
 Avoid frequent invasive procedures
Nursing Intervention
 MANAGE COMPLICATION: Septic
shock
 Monitor VS, BP, temp
 Administer IV antibiotics
 Administer supplemental O2
Nursing Intervention
 MANAGE COMPLICATION: Bleeding
 Thrombocytopenia (<100,000) is the
most common cause
 <20, 000 spontaneous bleeding
 Use soft toothbrush
 Use electric razor
 Avoid frequent IM, IV, rectal and
catheterization
 Soft foods and stool softeners
Colon cancer
 Adenocarcinoma is the most common type
 Metastasis is common to the liver
 2nd most common site for cancer in men
and women
 Ages >50-60
 May be caused by diverticulitis, chronic
ulcerative colitis, familial polyposis
Cancer sites
 Sigmoid colon – 33%
 Rectum – 27%
 Ascending Colon – 22%
 Transverse colon – 11%
 Descending colon 6%
Metastatic sites
1. Liver the most common site
2. Peritoneal surface
3. Spread via lymphatics to lung, bone and
brain
COLON CANCER
 Risk factors
 1. Increasing age
 2. Family history
 3. Previous colon CA or polyps
 4. History of IBD
 5. High fat, High protein, LOW
fiber
 6. Breast Ca and Genital Ca
COLON CANCER

 Sigmoid colon is the most common site

 Predominantly adenocarcinoma
 If early 90% survival
 34 % diagnosed early
 66% late diagnosis
COLON CANCER

 PATHOPHYSIOLOGY
 Benign neoplasm DNA alteration
malignant transformation malignant
neoplasm  cancer growth and invasion
 metastasis (liver)
COLON CANCER

 ASSESSMENT FINDINGS
1. Change in bowel habits- Most common
 2. Blood in the stool
 3. Anemia
 4. Anorexia and weight loss
 5. Fatigue
 6. Rectal lesions- tenesmus, alternating D and C
 Right sided lesions
- dull abdominal pain, melena
Left sided lesions
- signs of obstruction and bright red stool
Rectal lesion
- tenesmus, rectal pain. Incomplete BM.,
bloody stool, constipation
Colon cancer

 Diagnostic findings
 1. Fecal occult blood
 2. Sigmoidoscopy and colonoscopy
 3. BIOPSY
 4. CEA- carcino-embryonic antigen
Colon cancer

 Complications of colorectal CA
 1. Obstruction
 2. Hemorrhage
 3. Peritonitis
 4. Sepsis
Colon cancer

 MEDICAL MANAGEMENT
 1. Chemotherapy- 5-FU
 2. Radiation therapy
Colon cancer

 SURGICAL MANAGEMENT
 Surgery is the primary treatment
 Based on location and tumor size
 Resection, anastomosis, and colostomy
(temporary or permanent)
 Right hemicolectomy – primary surgery for
cancer of the ascending colon
- removal of the terminal ileum, cecum, right
transverse colon
 Left hemicolectomy – primary surgery for
cancer of descending and sigmoid colon
- removal of the distal transverse,
descending and sigmoid colon
Colostomy
a. Single barrel – proximal colon is brought to
the surface forming one stoma’
b. Double barrel – two stomas, proximal
excretes stool, distal secretes mucus
c. Stool formation depends on
1. Ascending – loose, liquid
2. Transverse – semisolid
3. descending – soft, formed stool
 Sexual dysfunction affects 15 – 1005
depending on the client age, surgical
technique
Colon cancer

NURSING INTERVENTION
Pre-Operative care
 1. Provide HIGH protein, HIGH calorie and LOW
residue diet
 2.Provide information about post-op care and
stoma care
 3. Administer antibiotics 3-5 day prior
Colon cancer

NURSING INTERVENTION
Pre-Operative care
 4. Enema or colonic irrigation the evening
and the morning of surgery
 5. NGT is inserted to prevent distention
 6. Monitor UO, F and E, Abdomen PE
Colon cancer

NURSING INTERVENTION
Post-Operative care
 1. Monitor for complications
a. Leakage from the site
b. prolapse of stoma
c. Infection
d. Bowel obstruction
 2. Assess the abdomen for return of peristalsis
Colostomy Care
 Prevent skin breakdown
- cleans skin around stoma with mild soap,
water and padding motion
- assess skin regularly for irritation
- avoid use of adhesive on irritated skin
 Control odor
- change pouch
- empty bag frequently and provide
ventilation, use deodorizer
- Avoid gas producing foods
 Promote adequate stomal drainage

- assess stoma for color and intactness

- mucoid/serosanguinous drainage 1st 24hrs
- assess for flatus
 Irrigate colostomy as needed
- position client on toilet or high fowlers
- fill irrigation bag with water (500-1000ml)
- Remove old pouch and clean skin
- lubricate catheter and insert to stoma
- allow fecal contents to drain
 Provide adequate nutrition
 2500ml liquids/day
Health teaching when discharge
a. change in odor, consistency and color of
stool
b. bleeding from stoma
c. persistent constipation and diarrhea
d. persistent leakage around the stoma
e. skin irritation
Colon cancer

 NURSING INTERVENTION:
COLOSTOMY CARE
 Colostomy begins to function 3-6 days
after surgery
 The drainage maybe soft/mushy or semi-
solid depending on the site
Colon cancer

 NURSING INTERVENTION:
COLOSTOMY CARE
 BEST time to do skin care is after shower
 Apply tape to the sides of the pouch
before shower
 Assume a sitting or standing position in
changing the pouch
Colon cancer

 NURSING INTERVENTION:
COLOSTOMY CARE
 Instruct to GENTLY push the skin down
and the pouch pulling UP
 Wash the peri-stomal area with soap and
water
 Cover the stoma while washing the peri-
stomal area
Colon cancer

 NURSING INTERVENTION:
COLOSTOMY CARE
 Lightly pat dry the area and NEVER rub
 Lightly dust the peri-stomal area with
nystatin powder
Colon cancer

 NURSING INTERVENTION:
COLOSTOMY CARE
 Empty the pouch or change the pouch
when
 1/3to ¼ full (Brunner)
 ½ to 1/3 full (Kozier)
Breast Cancer

 The most common cancer in FEMALES

 Numerous etiologies implicated
Breast Cancer

RISK FACTORS
 1. Genetics- BRCA1 And BRCA 2
 2. Increasing age ( > 50yo)
 3. Family History of breast cancer
 4. Early menarche and late menopause
 5. Nulliparity
 6. Late age at pregnancy
Breast Cancer

RISK FACTORS
 7. Obesity
 8. Hormonal replacement
 9. Alcohol
 10. Exposure to radiation
Breast Cancer

PROTECTIVE FACTORS
 1. Exercise
 2. Breast feeding
 3. Pregnancy before 30 yo
 BREAST
EXAMINATION
 CLINICAL BREAST
EXAMINATION
SELF BREAST
EXAMINATION
 Stages I and 2 are 70-90% curable
 Invasive or infiltrating, capable of
metastasis
a. Ductal – 70%
b. Lobular – 10 % higher incidence of
contralateral breast cancer
Breast Cancer

ASSESSMENT FINDINGS
 1. MASS- the most common location is the upper outer
quadrant
 2. Mass is NON-tender. Fixed, hard with irregular borders
 3. Skin dimpling
 4. Nipple retraction
 5. Peau d’ orange
Breast Cancer

 LABORATORY FINDINGS
 1. Biopsy procedures
 2. Mammography
 3. Tumor marker CA 2729
Breast Cancer

 Breast cancer Staging

 TNM staging
 I - < 2cm
 II - 2 to 5 cm, (+) LN
 III - > 5 cm, (+) LN
 IV- metastasis
Metastatic sites
 Bone
 Liver
 Lung
 Brain
Treatment
 Surgical management is the primary
treatment for breast cancer
 Breast conservation (lumpectomy,
segmental resection)
- removal of the cancer with margin of
healthy tissue
- If followed by radiation therapy has
equivalent 5 year survival to mastectomy
1. Simple – removal of all breast, nipple
and skin
2. Modified radical – axillary lymphnodes
are removed
3. Radical mastectomy – pectoral muscles
are removed
Medical therapy
 External beam radiation therapy 3 weeks
after surgery. Most commonly used
 Chemotherapy
 Tamoxifen therapy
Breast Cancer

NURSING INTERVENTION : PRE-OP

 1. Explain breast cancer and treatment options
 2. Reduce fear and anxiety and improve
coping abilities
 3. Promote decision making abilities
 4. Provide routine pre-op care:
 Consent, NPO, Meds, Teaching about
breathing exercise
Breast Cancer
NURSING
INTERVENTION :
Post-OP
1. Position patient:
 Supine
 Affected extremity
elevated to reduce
edema
Breast Cancer

NURSING INTERVENTION : Post-OP

2. Relieve pain and discomfort
 Moderate elevation of extremity
 IM/IV injection of pain meds
 Warm shower on 2nd day post-op
Breast Cancer

NURSING INTERVENTION : Post-OP

3. Maintain skin integrity
 Immediate post-op: snug dressing with drainage
 Maintain patency of drain (JP)
 Monitor for hematoma w/in 12H and apply
bandage and ice, refer to surgeon
Breast Cancer

NURSING INTERVENTION : Post-OP

3. Maintain skin integrity
 Drainage is removed when the
discharge is less than 30 ml in 24 H
 Lotions, Creams are applied ONLY
when the incision is healed in 4-6 weeks
Breast Cancer
NURSING INTERVENTION : Post-OP
Promote activity
 Support operative site when moving
 Hand, shoulder exercise done on
2ndday
 Post-op mastectomy exercise 20
mins TID
 NO BP or IV procedure on operative
site
Breast Cancer

NURSING INTERVENTION : Post-OP

Promote activity
 Heavy lifting is avoided
 Elevate the arm at the level of the
heart
 On a pillow for 45 minutes TID to
relieve transient edema
Breast Cancer

NURSING INTERVENTION : Post-OP

MANAGE COMPLICATIONS
 Lymphedema
 10-20% of patients
 Elevate arms, elbow above shoulder and
hand above elbow
 Hand exercise while elevated
 Refer to surgeon and physical therapist
Breast Cancer

NURSING INTERVENTION : Post-OP

MANAGE COMPLICATIONS
 Hematoma
 Notify the surgeon
 Apply bandage wrap (Ace wrap) and
ICE pack
Breast Cancer

NURSING INTERVENTION : Post-OP

TEACH FOLLOW-UP care
 Regular check-up
 Monthly BSE on the other breast
 Annual mammography
Lung Ca
 The number 1 cancer killer
in men and women
 6th to 7th decade of life
 70% involvement of
lymphnodes
 85% caused by inhalation
of carcinogenic chemicals
Pathophysiology
 Arise from a single transformed epithelial cell
in the tracheobronchial airways.
a. Adenocarcinoma - most prevalent carcinoma
of the lung for men and women, peripherally
located and often metastasized
b. Squamous cell Ca – centrally located and
arises in the segmental and subsegmental
bronchi
 Large cell Ca – fast growing tumor that
arise peripherally
 Bronchioalveolar – slower growing and
arises at the alveoli
Classification and staging

 Non small cell Ca – 70-75%

a. Adenocarcinoma
- most common (40%)
- slowest growing, metastasize early
b. Squamous cell – 30%
c. Large cell – rarest
- has the worst prognosis
Small cell (25%)
a. Oat cell (90%)
- very aggressive and
metastasize at
diagnosis.
 5 year survival rate is 48% if detected
early and localize (rare)
 Overall 5 year survival rate is 15%
Risk factors
 Tobacco smoking
- single most important preventable cause
of death
- 10x more common than in non-smoker
- passive smoke exposure increases the
risk to 35%
 Environmental and occupational exposure
- arsenic, asbestos, mustard gas, oil,
radiation
 .genetics
 Diet
Clinical manifestation
 Develops insidiously and is asymptomatic
until late in the course
 s/sx depends on the location and size of
the tumor, degree of obstruction and
metastasis
 Cough or chronic cough
- dry, persistent without sputum production
 Wheezing
 Hemoptysis or blood tinged sputum
 Chest and shoulder pain
Common sites of metastasis
 LN
 Bone
 Brain
 Contralateral lung
 Adrenal glands
 Liver
 Screening test: No screening program
currently exist.

Assessment:
a. Clients are very rarely symptomatic at
the time of diagnosis.
b. Persistent cough and dyspnea
c. Recurrent bronchitis and pneumonia
d. Blood streaked sputum
e. Chest pain
Diagnostics

 Chest xray (solitary peripheral nodule,

coin lesion)
 Ct scan of the chest
 Fiberoptic bronchoscopy
 Fine needle biopsy under ct scan
Surgical Management

 Dependent on whether the tumor is resectable

 May be cure for non small cell if no metastasis
occurred and lung function is sufficient on
removal of all or part of the lungs (50%)
 Lobectomy – removal of lobe (common)
 Pneumonectomy – removal of the lung
 Segmentectomy – partial removal of the lung
lobe
Adjuvant therapy
 Chemotherapy is the primary treatment for
small cell
 Radiation is standard post op for
advanced non-small cell
 Radiation therapy – for localized
intrathoracic lung ca and palliation for
hemoptysis, obstruction dysphagia and
pain
 Chemotherapy
 Immunotherapy
Nursing Intervention
 Assess for signs of superior vena cava syndrome
 Postlobectomy, manage chest tube
 Assess respiration and for presence of
pneumothorax or atelectasis
 Position properly post-op

1. Lobectomy – avoid prolonged lying on the

operative site
2. Pneumonectomy – position on the back or
operative side only
 Instruct the client on deep breathing,
coughing and ambulation
 Pain management to promote deep
breathing
 Refer client to smoking cessation
Prostate Cancer
 a slow growing malignancy of the
prostate gland
 Usually an adenocarcinoma
 This usualy spread via blood stream to
the vertebrae
 2nd most common cause of cancer
deaths
 190000 new cases each year and 30,000
deaths annually
 Over 80% are diagnosed in early stages.
Allowing an almost 100% 5 year survival
rate.
 Overall for all stages survival is 96%
Prostate Cancer
 Predisposing factor
 Age
 Strong family history
 High fat diet may play a role
 Having a vasectomy may play a role
Prostate Cancer
 Assessment Findings
1. DRE: hard, pea-sized nodules on the
anterior rectum
2. Hematuria
3. Urinary obstruction
4. Pain on the perineum radiating to the
leg
Prostate Cancer
 Diagnostic tests
1. DRE
2. Prostate specific antigen (PSA)
3. Elevated SERUM ACID PHOSPHATASE
indicates SPREAD or Metastasis
Surgical Management
 Radical prostatectomy – removal of
prostate, capsule, ejaculatory ducts,
seminal vesicles plus lymphnodes
 Watchful waiting without intervention may
be appropriate in men over 70 years of
age with small, early stage cancers
Prostate Cancer
Medical and surgical management
1. Prostatectomy
2. TURP
3. Chemotherapy: hormonal therapy to
slow the rate of tumor growth
4. Radiation therapy
Prostate Cancer
Nursing Interventions
1. Prepare patient for chemotherapy
2. Prepare for surgery
Prostate Cancer
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
4. Provide for bladder retraining after foley
catheter removal
a. Perineal exercises
b. restrict caffeine
c. limit fluid intake at night
5. Education
a. Avoid lifting, straining, and prolonged
travel
b. possible impotence
Bladder Cancer
 Transitional cell carcinoma – most
common (90-95%)
 Approximately 54300 new cases and
12400 deaths
 No screening for early detection
Risk factors
 Smoking
 Occupational
exposures
 Caucasian males >50
years old
Asessment
 Gross, painless hematuria
 Dysuria
 Urinary frequency
 Urgency
 Urinary hesitancy
 Suprapubic, rectum, back pain
Diagnostic
 Urinary cytology – late morning or early afternoon
 Bladder washing more reliable
 Flow cytometry – examine DNA content of urine
cells
 IVP – evaluate upper urinary tracts
 Cystoscopy – tumor visualization and biopsy
 CT scan, transurethral ultrasound, MRI
 Tumor marker – p53 and epidermal growth factor
in late stage
Surgical management
 Transurethral resection and fulguration
(Destruction of surrounding tissue with
electricity) most common for low grade Ca
 Radical cystectomy (bladder, prostate,
seminal vesicles, urethra, ovary, FT are
removed) for high grade tumors
Adjuvant therapy
 Radiation therapy – used in invasive
cancer
 Chemotherapy – cisplatin, methotrexate,
vincristine
Nursing interventions
 Instruct on preop low residue and clear liquid
diet
 Assess for urinary stoma and teach
maintainance of ileal conduit and appliance
 Assess urinary output (should produce urine
immediately) for infection and signs of peritonitis
 Discuss possible sexual dysfunction
Kidney Cancer
 Renal cell , most
common 85%
 Poor prognostic
indicators
a. LN involvement
b. invasion of renal
capsule
c. metastasis
Risk factors
 Male gender
 Hispanic
 Over 55 years old
 Cigarette smoking
 Occupational exposure, asbestos, lead
 Heavy use of aspirin
Metastatic sites
 Spread through venous and lymphatic
route to lungs, bone and liver
 Direct extension of the renal vein
 5 year survival is less than 10% for stage
4
 30-50% are diagnosed late with
metastasis
assessment
 Gross hematuria
 Dull aching pain
 Abdominal mass

Diagnostics
- MRI, CT, IVP
Surgical management
 Radical nephrectomy
and renal hilar LN
dissection
 Radiation
 Chemotherapy,
cisplatin, vinblastine,
methotrexate
Nursing intervention
 Atelectasis and pneumonia prevention
(nephrectomy close to diaphragm)
 Assess for signs of hemorrhage
 Monitor urine output and renal function of
remaining kidney
 Pain management
 Assessment and prevention of paralytic ileus
Skin cancer
 Malignant lesion of the skin, which may or may
not metastasized

Types
a. Basal cell – most common type arising from the
basal cells contained in the epidermis
b. Squamous Cell – 2nd most common type in
whites.tumor of the keratinocytes
Metastasized to the LN and fatal
c. Malignant melanoma – can metastasized
to the brain, lung, bone, skin. Fatal
SKIN CANCER
 Causes: UV light exposure, chronic
irritation and friction
 Dx: skin biopsy
 S/sx: change in color, size, shape of lesion
 Monitor lesions that do not
heal
 Removed moles or lesions
that are subject to chronic
irritations
 Avoid contact with chemical
irritants
 Use sun screen lotions and
clothing
 Avoid sun exposure
between 11am-3pm
Contact Dermatitis
 Inflammatory response after contact with a
specific antigen
Assessment:
a. Pruritus and burning
b. Edema
c. Erythema at the point of contact
d. Signs of infection
e. Vesicles with drainage
Gastric Cancer
 Approximately 22000 cancers and 13,000
deaths per year
 African americans, japanese, chinese and
US have higher incidence
 95% are adenocarcinomas
 Prognosis is poor, 5 year survival rate is 5-
15 %
Risk factors
 Male > 40 years of age
 Low socioeconomic status
 Poor nutritional health habits and vitamin A deficiency
 Family history
 Previous gastric resection
 Pernicious anemia
 H. pylori infection
 Gastric atrophy and chronic gastritis
 Rubber workers and coal miners
Metastatic sites
 Direct extension to the pancreas, liver,
esophagus.
 Intraperitoneal dissemination to ovary
 Nodal spread to the neck
 Bloodstream metastasis to the lung,
adrenal, liver, bone and peritoneal cavity
Screening
 Among high risk
person’s only
 Barium x-ray or
endoscopy
Assessment

 Early manifestations are non-specific

 Upper epigastrium, retrosternal pain
 Uneasy sense of fullness after meals
 Loss of appetite
 Nausea and vomiting
 Weakness
 Fatigue
 anemia
Diagnostic procedure
 EGD
 Biopsy
 Endoscopic ultrasound
 Double contrast upper GI series
 CT scan
Surgical management
 Only treatment that is
potentially curative
 Total gastrectomy
 Radical subtotal
gastrectomy
a. Billroth I
b. Billroth II
 Proximal subtotal
gastrectomy
 Paliation of symptoms
Adjuvant therapy
 External beam radiation for control of
unresectable tumors, palliation and
increased survival.
 Chemotherapy has little impact – 5 FU,
doxorubicin, mitomycin
Nursing Intervention
 Goal is control of clinical manifestation
and supporting optimal functioning
 Assess the nutritional status

- small frequent feeding low carbohydrate,

high fat, high protein.
- restrict fluids 30 minutes after meals
reducing risk of dumping syndrome
Postoperative
 Respiratory status: reflux aspiration
 Infection
 Pain – potential anastomotic leak obstruction
 Bezoar (food clumping) formation causing gastric
outlet obstruction
 Bleeding
 Dumping syndrome
 anemia
Cancer of the esophagus
 >3x more common in men
 Occurs in the fifth decade of life
 Chronic irritation, ingestion of alcohol and
tobacco use
 GERD and Barret’s Esophagus
 Usually squamous cell epidermoid type
Clinical manifestation
 Dyspahgia
 Mass in the throat
 Regurgitation of undigested foods
 Foul breath and hiccups
Head and neck cancers
 71,000 new cases and 19,000 deaths
 40% are found in the oral cavity but may be found in the
larynx, oropharynx, nasal cavity and salivary glands
 95% are squamous cell carcinoma
 5 year survival for early stage is 95% and late stage
less than 50%
 Most will present with advanced disease due to
substance abuse
Risk factors
 Male over 50 years old
 Tobacco use (major cause)
 Heavy alcohol use (combine with tobacco
95%)
 Poor oral hygiene
Metastatic sites
 Neck lymph nodes (common)
 Local and regional spread within the head
and neck
 Distance metastasis is rare
Screening
 No screening guidelines exists
 High risk clients should have through head
and neck examinations and referral to
smoking and alcohol cessation programs
Assessment
 Depends on the location
 Throat pain
 Persistent hoarseness
 Painless mass
 Pain
 White or red spots in the oral cavity
 Nasal stuffiness
Diagnostic studies
 Thorough physical examination of neck
and oral cavity
 Fiberoptic nasopharyngoscopy
 Direct laryngoscopy
 X-rays, barrium swallow MRI, CT
 biopsy
Surgical management

 Surgery and radiation is the primary

treatment
 Reconstructive surgery may be needed
 Radiation and chemotherapy may be used
to debulk unresectable tumors
Adjuvant therapy
 Radiation is the primary treatment for
nasopharynx tumors
 Brachytherapy in oral cavity
 Chemotherapy is used for:
a. Recurrent and metastatic tumors
b. Making tumor more sensitive to radiation
Nursing interventions
 Primary role is assisting clients in coping with
issues of dysfunction, losses and body image
changes
 Monitor for delirium tremens in client with alcohol
abuse
 Airway management
a. tracheostomy
b. humidity
c. suctioning
d. stoma care
 Provide oral care with saline or peroxide
solution. (avoid mouthwashes that are
drying to mucosa)
 Assess ability to swallow and ensure
safety when eating
Central Nervous System cancers

 17,000 primary brain tumors

 >100,000 metastatic
 Progmosis depends on type and location
but generally poor
 Risk factor very little known
metastasis
 Distance metastasis is rare
 Possibly lung or bone may occur
 Spinal tumor usually do not metastasize

 No screening programs exist

assessment
 Vary greatly depending on the location, may be related
to the displacement of the brain, increase ICP, spinal
cord compression
 Change in LOC
 Headache
 Pupil changes or papilledema
 Motor or sensory deficits
 Weakness (spinal cord tumors)
 Vomiting
 Seizures
 Vital sign changes
 Pain – most common clinical manifestation
in spinal cord tumors
 Bowel or bladder dystfunction
diagnostics
 CT, MRI
 Position emission tomography
 Cerebral angiography
 Lumbar puncture
Surgical management
 Initial treatment for most brain and spinal cord tumors
 Goal is to remove all or as much as possible of the
tumor
 Biopsy used for diagnosis or surgical treatment

1. CT or MRI guided needle biopsy through burr hole

2. Open biopsy via craniotomy
3. Stereotactic biopsy – tumor located with three
dimensional coordinates biopsied or removed – most
common
Adjuvant therapy
a. Radiation therapy
- Standard treatment for metastatic tumors
- Used when primary tumors cannot be resected
b. Chemotherapy
- Use is limited by the blood brain barrier
- Not curative but may contribute to survival rated
- Plays little role in spinal cord tumors
- Ommaya reservoir used to deliver chemotherapy
into CSF (preferred method)
Nursing Interventions
 Will depend on the location
 Neurologic assessment for LOC, seizures, infection,
hemorrhage, cerebral edema, ICP increase
 Administer drug to treat cerebral edema
 Administer analgesia and teach relaxation techniques
Cervical Cancer
 13,000 new cancers
and 4000 deaths
 Very treatable and
curable
 80-90% are
squamous carcinoma
Risk factors
 Sexual intercourse before age 17, multiple
partners
 Sexual partner who has multiple partners
 Cigarette smoking
 Human papilloma virus
 Lower socioeconomic status
Metastatic sites
 Abdomen and pelvis
 Lung
 Liver
 Bone
Screening

 Pap’s smear
beginning at age 18
or sexually active
assessment
 Asymptomatic in the early stage
 Watery vaginal discharge
 Late manifestation, postcoital, heavy or
intermenstrual bleeding.
diagnostics
 Colposcopy – application of acetic acid
followed by magnified examination of the
pelvis
 Biopsy
 Endocervical curettage
 Cone biopsy
Management
 Total abdominal hysterectomy and
lymphadenectomy
 Depends on the stage and desire for child
bearing
 Radiation therapy
 Chemotherapy for advanced disease
 Laser therapy
- used when all boundaries of the lesion are
visible during colposcopic examination.
- minimal bleeding is associated with the
procedure.
- slight vaginal discharge is expected following
the procedure and healing occurs in 6 to 12
weeks.
Conization

- a cone shaped area of the cervix is removed

- performed in women who desire further childbearing.
- long term follow up care is needed, as new lesions can
develop
- the risk of procedure includes hemorrhage, uterine
perforation, incompetent cervix and preterm labor in
future pregnancies.
Hysterectomy
- For microinvasive cancer if childbearing is not
desired.
- A vaginal approach is most commonly
performed.
- A radical hysterectomy and bilateral
lymphnode dissection may be performed for
cancer that has spread beyond the cervix but
not to the pelvic wall.
Nursing intervention
 Assess for changes in bowel and bladder pattern
 Bladder training
 If laser surgery for early diseases is used,
instruct to avoid douching, tampoons and sexual
activity for 2-4 weeks
 Assess for sexual dysfunction, surgical
shortening of vagina, vaginal dryness
Endometrial Cancer
 Highest incidence for caucasians
 90% are adenocarcinoma
 5 year survival is 96% for early stage and
26% for late
Risk factors
 Female over 50
 High cumulative exposure to endogenous and
exogenous estrogen
 Nulliparity
 Family hx of breast or ovarian cancer
 Infertility
 Diabetes
 Hypertention
 obesity
Assessment
 Abnormal vaginal bleeding
 Pain in later stage

Diagnostics
a. Pelvic examination
b. Pap smear
c. Endometrial biopsy 90% effective
d. D and C
Management
 Used for staging
 TAHBSO and peritoneal washing, omentectomy
 Adjuvant therapy is not required in early stage
 Intravaginal radiation for early stage low grade tumors
 Pelvic external beam for high grade
 Hormonal therapy (progestins) and chemotherapy for
advanced disease
Nursing intervention
 Encourage and instruct the importance of
regular pelvic examination
 Pain management
 Prevention of postsurgical venous stasis
1. encourage turning and ambulation
2. antiembolic stockings
 Instruct signs of recurrence like vaginal
bleeding, pelvic pain and constipation
Ovarian Cancer
 Second most common gynecologic cancer
after uterine
 Most common cause of gynecologic
cancer death
 Industrial countries have higher incidence
 5 year survival is 30-35%
 60-70% are diagnosed at stage III
Risk Factors
 Women mid 50-70 (peak 55-59)
 Higher education and socioeconomic status
 History of breast and endometrial cancer
 No pregnancy, infertility, Non use of OCP
 Mutation of BRCA 1 or 2
 Hereditary non polyposis cancer
Assessment
 No early clinical
examination
 Abdominal discomfort
or enlargement
 Indigestion and
flatulence that persist
without explanation
Diagnostics
 Pelvic examination
 Ultrasound and Ct scan
 CA 125
 Barium enema, cystoscopy IVP
Surgical management
 Peritoneal washing to
find cancer cells in
fluid
 TAHBSO – primary
treatment
 Chemotherapy
 Radiation therapy
Testicular cancer
 Most common cancer of men between 15-
35 years of age.
 Aggressive and spreads quickly although
highly curable if early detected
 93% seminomatous histologic type, which
are slow grower
Risk factors
 Male 20-30 years old
 Family or personal
history
 History of
undescended testes
 infertility
Assessment
 Small, hard scrotal mass
 Scrotal pain, swelling, pulling sensation
 Low back pain
 Cough, hemoptysis
 gynecomastia
PHYSICAL EXAMINATION OF THE
GENITALS
1. Establish a
therapeutic
relationship to
facilitate successful
physical examination
1. Explain each step
carefully
 Increased patient
comfort while doing
the exam
 maintain eye contact
 proceed in an
unhurried manner
 involved the person
in the examination
 Position the patient for
the procedure
 standing while the
examiner sits on the stool
 lying on his side with legs
spread slightly
 Notice hair distribution
 Observe skin for lesion,
swelling or discoloration
 Inspect and palpate the
length and all sides of
the penis
 look for lesions,
discharge, atrophy or
inflammation
 check if circumcised or
uncircumcised
 observe the urethral
meatus for displacement
or discharge
 Inspect the scrotum first
and then the testicles
 look for the skin of the
scrotum, signs of swelling,
nodules and lesions
 left testis normally hangs
lower than the right
 palpate each testis with
your thumb and two fingers
 testis are 4-6cm long, firm
ovoid in shape, smooth
and sensitive
 Scrotal
transillumination
 in a dark room, place a
strong, lighted flashlight
next to the scrotum
 normally light passes
through the scrotum
 if with tumor, does not
transluminate
 if with hydrocele it will
shine red
Self Examination
  self examination can detect testicular cancer
while it is treatable
 Explain the procedure carefully and provide
opportunities to ask questions and express
concerns
 If possible, give literature
 Develop a habit of doing self examination once a
month
 Use a mirror to check for inaccessible places
 Look for any changes from normal to abnormal
findings
 Best time to do testicular self examination is
after a shower when you are warm, making the
scrotum relaxed and easier to examine
Technique in testicular self examination

 hold the scrotum in

the palms of your
hands and examine
each testicle with a
thumb and fingers of
both hands
 roll the testicles
between your thumb
and fingers
 Do not hesitate to
seek professional
assessment and
advice if anything
unusual. It is better to
learn that everything
is OK than to wait
long
Diagnostic test
 Bimanual scrotal palpation
 Ultrasound
 AFP and BHCG
 Chest x-ray
management
 Transinguinal orchiectomy and
retroperitoneal LN dissection
 Nerve sparing techniques to preserve
fertility
 Cisplatin based prior to chemotherapy
primary treatment for men with advanced
disease
Nursing Intervention
 Instruct about testicular examination
 Offer sperm banking prior to treatment
 Postoperative (inguinal orchiectomy)

- OPD procedure
- pain management ice to scrotal area
- wear supporting, avoid heavy lifting for 4-6 weeks
and avoid standing for long periods
- Fertility may be lost but orgasm remains
Hodgkin’s disease
 Malignancy of the immune system
 Usually in the involved LN, tonsils, spleen
and bone marrow
 Characterized by presence of reed-
sternberg cells in the nodes
Assessment
 Fever, malaise, fatique, weakness
 Night sweats, loss of appetite
 Persistence non-productive cough
 Anemia, thrombocytopenia
 (+) biopsy of cervical
 (+) Ct Scan of the liver and spleen
Diagnostic test
 Predisposing factors
a. Prior radiation therapy
b. Prior chemotherapy
c. Genetics
d. Family history
 Physical exam
a. Lymphadenopathy
b. Hepatosplenomegally
Tumor evaluation
 Chest xray
 CT of neck, chest, abdomen
 Tumor biopsy
 Bilateral bone marrow biopsy
 Bone scan
Management
 Radiation
 chemotherapy
leukemia
 Malignancy that involves the blood forming
tissues on the bone marrow, spleen,
lymphnodes
 ALL – abnormal proliferation of immature
lymphoblast
 AML

- proliferation of immature myeloblast

- Predisposing factors, down syndrome,
chemotherapy (alkylating agents)
- Peak age 2-5 years old
Assessment
 Symptomatic anemia
- pallor, fatigue
 Thrombocytopenia

- petechiae, bleeding
 Neutropenia

- fever, infection
 Enlarged LN
 Hepatosplenomegally
 Bone pain
 Neurological symptoms

- invrease ICP
Tumor evaluation
Bone marrow aspiration and biopsy
1. greater than 25% blast indicate leukemia
2. Chest xray to check for mediastinal mass
Management of ALL
 Sanctuary chemotherapy
- CNS prophylaxis
- Inthratecal methotrexate
 Systemic chemotherapy (2 phases)

- 3 drug: Vincristine, Prednisone, L-

asparginase
- 4 drug: + daunorubicin
Oncological emergency
 Sepsis and DIC
- maintain strict asepsis techniques
- administer IV antibiotics
- Administer blood products
Oncologic Emergencies
 Superior Vena Cava Syndrome
- compression or invasion of the SVC by
tumor, enlarged lymph nodes that obstruct
venous circulation or drainage of the head,
neck, arms and thorax
- associated with lung Ca
- may lead to cerebral anoxia, laryngeal
edema, bronchial obstruction and death
Clinical manifestation
 Progressive shortness of breath, swelling
of face, cough
 Edema of the neck, arms, hands reported
sensation of tightness and dysphagia
 Increased intracranial pressure
 Dilated jugular veins
Management
 Radiation therapy to shrink tumor size and
relieve symptoms
 Chemotherapy for radiation resistant
tumor
 Surgery to redirect blood flow
 Supportive measures
Spinal cord compression
 Potentially leading to permanent
neurologic impairment
 Metastatic cancer (breast, lung, kidney,
prostate, lymphoma)
Clinical manifestation
 Local inflammation, edema, venous stasis
 Pain exacerbated by movements,
coughing, sneezing, Valsalva maneuver
 Bladder and bowel dysfunction above S2,
overflow incontinence, S3-5, bowel
incontinence
 Spinal cord compression
 SIADH
 Hypercalemia
 SVC syndrome
 Tumor lysis tumor