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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, somecalled pathogenscan 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 (Flaviviridae) 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 manifestation

First 4 days Febrile or Invasive stage high grade fever, headache, body malaise, conjuctival injection, vomitting, epistaxis or gum bleeding, positive torniquet test.

4th 7th day Toxic or Hemorrhagic Stage After the lyze of the fever, this is were 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 torniquet 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 Leede Test presumptive test for capillary fragility - keep cuff inflated for 6-10 mins (child), 1015 min (adults) - count the petechiae formation 1 sq inch (>10-15 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 trendelenberg 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 its 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) circulate in greater concentration

Diurnal
microfilaria

at daytime

Clinical Manifestation
Acute stage - filarial fever and lymphatic inflammation tha occurs frequently as 10 times per year and usually abates spontaneously after 7 days - Lymphadenitis (Inflammation of the lymphnodes) - 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 en empty stomach. Cannot be used in patient with asthma

Preventive Measures
Health teachings Environmental Sanitation

Leptospira interogans AKA Red water disease in cattle, swineherds disease or weils disease in humans

Leptosiprosis (Weils 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, hepatomegally 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
Penicillin

50000 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

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, vomitting, 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 (4,4,2) Sulfadoxine/Pyrimethamine 500mg/25mg/tab, 3tab single dose Primaquine (15mg/tab) 3 tabs single dose

Treatment for P. Vivax


Choloroquine,

Day 1,2,3 (4,4,2) 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


quinine

plus doxycycline, or tetracycline and primaquine

Complications
severe

anemia cerebral malaria

- hypoglycemia

MENINGOCOCCEMIA
caused by Neisseria meningitides, a gram negative diplococcus transmitted through airborne or close contact incubation is 1-3 days natural reservoir is human nasopharynx

Clinical Manifestation
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 Friderichsen) septic shock; hypotension, tachycardia, enlarging petecchial rash, adrenal insufficiency

Laboratory Blood Culture Gram stain of peripheral smear, CSF and skin lesions CBC

Treatment:

antimicrobial

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 PPE Health teaching Contact tracing Prophylaxis Meninggococcal vaccine for high risk patient

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

Clinical Manifestation
pain or numbness fear of water fear of air

at the site of bite

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 recommend regular vaccination of domestic dogs.

Diagnosis FAT (fluorescent antibody test) Clinical history and signs and symptoms

Management No treatment for clinical rabies Prophylaxis

Postexposure prophylaxis
Category I Licking of intact skin Category II Abrasion, laceration, punctured wound on the lower extremities Category III Abrasion, laceration on upper extremities, head and neck Dog is killed, lost, died Observe the dog for 14 days
1.Active vaccine 2.Observe dog for

14 days

1.Active 2.Passive

Active vaccine (PDEV,PCEC,PVRV) 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 PPE Preventive Measures Education Post-exposure and Pre-exposure Prophylaxis

TETANUS
caused by Clostridium tetani, grows anaeronically 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 8-10 days moderate Pronounced Mild, short

Stage III <7days Severe Severe, boardlike Frequent, prolonged

Incubation Period > 11 days Trismus Muscle rigidity Spasm mild mild absent

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 IM,1/2 IV Neonatal Tetanus 20000 IU, 1/2IM, 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 IVP 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 (0,1,6,1,1)

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
Sex in portal vein
Eggs Escap e into Intesti nal lumen

Adult in 2 days

(Miraci dia)

Portal veins

Oncol omela nia Quadr asi

Skin penetr ate


Cercar ia

Sporo zyst

Diagnosis:
Schistosoma Rectal

eggs in stool

bipsy Kato Katz Ultrasound of HBT

Clinical Manifestation
severe jaundice edema ascites hepatosplenomegally S/S of portal hypertention

Management
Praziquantrel 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 Peyers patches of SI necrosis and

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 complication 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

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 promiscuous individuals Commercial sex workers Drug addicts

Possible Outcome
Most get well completely and develop life long immunity. 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 recepients 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 KlebsLoeffler 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, kedney, 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 loefflers 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) Diapgram 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 vomitting 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 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 worlds 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: Kochs 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 reactivated, Secondary TB 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

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
I

TB patient

Intensive Maintainance
4 HR

New smear (+) New smear (-) 2HRZE PTB with ext parenchymal Treatment Failure, Relapse, return after Default

II

2HRZES/ 5 HRE 1HRZE

III

New Smear (-) PTB, with minimal CXR lesion


Chronic (still smear (+) after supervised treatment

2HRZE

4HRE

IV

MDRTB

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 Hystolitica, protozoa IP: few days to months to years, usually 2- 4 weeks MOT: Ingestion of cysts from fecally contaminated sources (Oral 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, TrimethoprimSulfamethoxazole, 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 Washerwomans 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 dont 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-kochs meds

Diagnosis - sputum examination eggs in brown spots Treatment 1. Praziquantrel (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 Pierazine 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 bivalve 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 (ATAXIA), DYSPHAGIA, RESPI PARALYSIS, DEATH.

MANAGEMENT AND CONTROL MEASURES:

NO DEFINITE MEDICATIONS INDUCE VOMITING (EARLY INTERVENTION) DRINKING PURE COCONUT MILK (WEAKENS TOXIC EFFECT) DONT GIVE DURING LATE STAGE IT MAY WORSEN THE CONDITION. NaHCO3 SOLUTION (25 GRAMS IN 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 lindasne(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 no hereditary Does not cross placenta

Dr. Salvador

Cardinal Sign
Presence

of Hansens bacilli in stained smear or dried biopsy material. Presence of localized areas of anesthesia

Dr. Salvador

Leprosy/Hansens 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 Hansens bacilli in stained smear or dried biopsy material. Presence of localized areas of anesthesia

Leprosy/Hansens 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: dont 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
-Skin

Stage 2
-Top

Stage 3
-Deep

Stage 4
-Ulcer

is

intact -Reddened area

layer is missing -Ulcer is shallow, wih pink or red base - white or yellow eschar

ulcer extends to dermis and subcutaneo us areas - white, gray or yellow eschar - purulent discharge

extend to muscle and bones - foul smelling - brown or black eschar - purulent 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

Clinical Manifestation
Pre eruptive stage - Patient is highly communicable - 4 characteristic features a. Coryza b. Conjunctivitis c. Photophobia d. Cough

- Kopliks spots - Stmsons 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


1. 2.

3.
4. 5.

6.

MANAGEMENT Supportive Hydration Proper nutrition Vitamin A Antibiotics 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 fetuse of women in the 1st trimester

s/sx: forschheimers (petecchial 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(chocken 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: Maculopapulovesicula r (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)

DNA, Pox virus Last case 1977 spreads from man-to-man only Active: Vaccinia pox virus IP: 1-3 weeks S/sx: Rashes: Maculopapulovesiculopustul ar

Small Pox, Variola

Centripetal contagious until all crusts disappeared Dx: Pauls 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 2/15/03 3 Singapore 1 American Visitors Metropole Chinese Hotel Singapore Outbreak Hanoi Outbreak 2 Canadian Visitor Hongkong Outbreak Toronto, Canada Outbreak

Visitor

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?

Its 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 persons 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

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

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 assymptomatic It is becoming increasingly resistant to penicillin

DX: gram stain and culture of cervical secretions on Thayer Martin VCN 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 FTA-ABS
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 twothirds 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 (AZT) a. Prolong life b. Reduce risk of opportunistic infection c. Prolong incubation period

PREVENTION
A ABSTINENCE B BE FAITHFUL C CONDOMS D DONT 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


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

Focused on the common childhood diseases. Pneumonia Measles Malaria Diarrhea Malnutrition Ear infection 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

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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 bodys 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

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 Mechanical Biochemical Non-specific (eg. Low pH in stomach) Receptor-driven (eg. PAMP-recognition)

barriers

Adaptive immunity (antigen-specific)


Receptor-driven Pre-existing

clones 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

Cells eosinophil megakaryocyte T Lymphocyte involved Pluripotent hematopoietic in neutrophil stem cell B Lymphocyte immunit y common
basophil mast cell monocyte macrophage common myeloid progenito r lymphoid progenit or plasma cell Natural Killer cell

platelets

Blood

Where is that stuff?


Serum or Plasma Leukocytes, Platelets and RBC

Serum Proteins

Mononuclea r Cells

Polymorphonucle ar leukocytes (or Granulocytes)

Immunoglobulins Complement Clotting factors Many others

Lymphocytes (T cells, B cells & NK cells) Monocytes

Neutrophils Eosinophils Basophils

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 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 (<10 in diameter) reach alveoli Alveolar macrophage rapidly phagocytize small particles

Lower Respiratory Tract


Alveoli

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 Generally sterile due to low pH Upper portion contains few bacteria As distal end of ilieum is reached flora increases Enormous numbers of microorganisms 50-60% of fecal dry weight is bacteria

Stomach

Small Intestine

Colon

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 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

Exposure to antigen creates an immunologic memory.


Natural Immunity
Present at birth Provides a non specific response to any foreign invader, regardless of the invaders 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 pagocytic 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 persons 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
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
1.

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


Induces expression of b2 integrin adhesion molecules on neutrophils, leading to neutrophil migration to infection site

IL-8

IL-12

Activates NK cells and induces Th1-cell differentiation

IL-18 TNF-a

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) Antibody-dependent cell-mediated cytotoxicity (ADCC) Have two major functions

NK cells (large granular lymphocytes)


Lysis of target cells Production of cytokines (IFN-g and TNF-a)

Act against intracellular pathogens


Herpesviruses Leishmania Listeria monocytogenes


Toxoplasma Trypanasoma

Act against protozoa

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/antibody complexes 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 (lasts up to 30 min post injection)

Late-phase reaction (develops approximately 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 Histamine Heparin Serotonin SRS-A Chymase Hyaluronidase Eos. Chem. Factor Neut. Chem. Factor Platelet Agg. Factor Activity Increases vascular permeability; elevates level of cyclic AMP Anticoagulation Increases vascular permeability Increases vascular permeability; causes contraction of human broncholes Proteolysis Increases vasuclar permeability Chemoattraction of eosinophils Chemoattraction of neutrophils Aggregates platelets

Risk of allergy: Family


50 40

percent of children with atopy

30 20 10 0

none

one

both

number of parents with history of allergy

Hyposensitization
Allergen injections

Symptoms

Activity

IgG 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 Sorbant 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
self

antigens 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
Chemotactic

activation
factors

anaphylatoxins

Neutrophils
difficult to

attracted
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
attract and

activate macrophages and/or eosinophils

Types of Delayed Hypersensitivity


Delayed Reaction reaction time Jones-Mote Contact tuberculin granulomatous days maximal
24 hours 48-72 hours 48-72 hours at least 14

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 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 cellmediated 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, cytokineactivated 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
primarily due to lipopolysaccharide overwhelming accumulation of neutrophils in lung

Septicemia - Septic Shock

Adult respiratory distress syndrome

Platelet aggregation/adherence to macrophages by grampositive 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 autoantibody production, immune complex formation AND TISSUE DAMAGE

Systemic Lupus Erythematosus

Etiologic factors
Auto-immune Genetic

Viral

factors 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 symptomsheadache, 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

1. 2.

3.

LABORATORY TESTS Elevated ESR, creatinine CBC will show anemia, thrombocytopenia 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

1.

Etiologic factors medications:

Sulfonamides, butazones, other antibiotics and anti-seizure drugs

2.

Viral infections

AIDS Immunocompromised states

Toxic epidermal Necrolysis and SJS

Pathophysiology

Thought to be auto-immune

Toxic epidermal Necrolysis and SJS

1.

2.
3. 4. 5.

ASSESSEMENT FINDINGS CONJUNCTIVAL BURINING AND ITCHING- INITIALLY Cutaneous tenderness Fever Cough 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

1. 2.

Diagnostic examination Histologic studies of the skin Immunoflourescent studies

Toxic epidermal Necrolysis and SJS

1.

2.
3. 4. 5.

Medical management Surgical debridement to remove the involved skin IVF therapy to replace fluids Culture of tissue samples Intravenous Immunoglobulin administration Systemic and topical antibiotics

Toxic epidermal Necrolysis and SJS

1.

Nursing Interventions 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
Breast

Men
Prostate

Lung
Colon and Rectum Uterine Non-Hodgkins Lymphoma

Lung
Colon and rectum Urinary Bladder Non hodgkin 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
Bind to DNA

DNA repair Normal Cell

Permanent DNA damage

Cell Death

PROMOTION

Cell Proliferation

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, burkitts lymphoma, nasopharyngeal Ca, non-Hodgkin and hodgkins 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, (analine 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?


Direct Damage To DNA (e.g., radiation) Chemical Mutagens (e.g., pollutants, additives,drugs and hormones) Fragments & Deletions CANCER Base Mutations & Substitutions Membrane damage causing internal mutagens Miscellaneous to form Mutagens (dietary fat and free radicals)

Immune response

T lymphocytes, recognize tumor associated antigens, possesses cytotoxix abilities Lymphokines, capable of killing and damaging Ca cells Macrophages, disrupt Ca cells IFN, antitumor properties B lymphocytes antibodies, defends the ody against malignant cells Natural killer cells, directly destroy Ca

American Ca Society recommendation


Evaluation Frequency CBE, BSE CBE BSE Q 3 yrs Q month Q year Q month

Site Breast

Gender Female

Age 20-39 >40

Mammo gram

Q year

Colon/rectu m

M/F

>50y/o

Fecal occult blood

Q year

and

Flexible Q 5 years sigmoidosco py Colonoscop y Double conrast barrium enema Q 10 years Q 5 years

or or

Prostate
Cervix

M
F

>50 or < 50 if high risk

PSA and DRE

Q year

>18 or younger if sexually active >20-39 >40

Pap smear Pelvic exam

Q year

Cancer related check up

M/F

Other Ca types

Q 3 years Q year

Characteristics of Ca
Characteristic
Cell characteristic

Benign
Well differentiated Resemble normal cells
Grows by expansion Not infiltrate the surrounding tissue slow

malignant
Undifferentiated little resemblance on normal cells
Grows at the periphery, infiltrate and destroys the surrounding tissue Variable, fast Access to blood, lymphatics and other areas

Mode of growth

Rate of growth Metastasis

none

benign General effects localized

Malignant Anemia, weaness, weight loss Extensive tissue damage Usually causes death

Tissue destruction

No tissue damage

Ability to cause death

Does not usually cause 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


Tissue of Origin 1. Carcinoma: a. Squamous cell Ca surface epithelium b. Adenocarcinoma glandular or parenchymal c. Sarcoma connective tissue d. Leukemia, Lymphoma
a.

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 Stage I Stage II Stage III Stage IV

T0, N0, M0 T1, N0, M0 T2, N1, M0 T3, N2, M0 with metastasis

2. Histologic
a.
b.

c.
d.

Grade 1 - well differentiated Grade 2 - Moderately differentiated more abnormal Grade 3 - Poorly differentiated, Very abnormal 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.

b.

Early detection and treatment are the cornerstones of cancer survival Educating the public about a healthy lifestyle and early detection

Health education
1.

2.

3. 4.

Reduce and avoid exposure to known carcinogens Eat a balanced diet of vegetables, fruits and whole grains, reducing fat and red smoked and cured meat. Limit alcohol beverages 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.

b.

c.

Depends on the location and type of biopsy May need to be NPO if sedation or contrast is used Inform the client about the procedure

Postprocedure
a.
b. c. d.

Control bleeding Monitor for infection Manage pain 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.
b. c.

d.

Assess for allergy if contrast is to be used NPO depending on the area being imaged, use of sedation or contrast Prepare patient for length of imaging, possible noise of machinery, need to remain still. Monitor the client for flushing, itching or nausea, indicating allergy to contrast.

Tumor Markers
CEA GI, lung, breast

Alpha feto protein HCG


Acid phosphatase CA 125

Hepatocellular, gastric, pancreatic, colon and lung cancer Trophoblastic tumor, germ cell, ovary Prostate cancer
Ovarian cancer

Client Reaction during Diagnoses

Client will use coping strategies to his anxiety level such as: DenialRational 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 throbosis, 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 acce;erates 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 joyproducing 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

a. b. c.

d.

The ideal and most frequently used Goals Primary Prophylactic Palliative 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,URTI - 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 Cells most sensitive during M and G2 phase

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 implaint 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

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

Side Effects
a.
1. 2. 3. 4.

Skin: Itching, redness, burning, sloughing Keep skin free of foreign substance Avoid use of medicated solutions Avoid pressure, trauma, infection Avoid exposure to heat, cold or sunlight

b. Anorexia, vomitting, nausea


1.
2. 3.

Provide small, attractive feedings Avoid extremes of temperatures Administer antiemetics before meals

c. Diarrhea
Encourage low residue, bland, high protein foods Provide good perineal hygine 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 Burkitts 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 neoadjuvant 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

1.
2. 3. 4. 5.

Time required for one tissue cell to divide and reproduce two identical daughter cells Go resting phase G1 RNA and protein synthesis occurs S DNA synthesis occurs G2 Premitotic phase 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 PRM

Integumentary System Alopecia - Explain hair loss is not permanent - Support and encouragement - Scalp tournique or scalp hypothermia to minimize hairloss - 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 clients 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 selfperception, fear of physical distress and dying, concerns about relationships, changing self-perception, and memory of other persons 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
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
1.

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:
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
1.

Nursing Care: Pretransplant


Provide protected environment - strict reverse isolation 2. Monitor central lines frequency 3. Provide care receiving chemotherapy
1.

Post transplant
Prevent infection a. Maintain protective environment b. Administer antibiotics c. Check IV set ups q12hrs 2. Provide mouth care for stomatitis and mucositis
1.

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

1. 2. 3. 4. 5.

Monitor for clinical manifestation of bleeding Bruising and petechiae Blood in the urine, stool and vomitus Changes in mentation Pain Weak, rapid pulse, low blood pressure, pale cool skin

Nursing intervention
a.
b. c.

d.
e. f. g.

Instruct practice of careful washing Perform oral and perineum care Place client in protective isolation Administer antibiotics and antipyretics Avoid unnecessary invasive procedures to prevent bleeding or infection Avoid shaving 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 patients preferences Provide small frequent meals Avoids giving fluids while eating

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.
2. 3.

Liver the most common site Peritoneal surface 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

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
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
a.

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 semisolid 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 peristomal 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

1/3

to full (Brunner) 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.

2.

3.

Simple removal of all breast, nipple and skin Modified radical axillary lymphnodes are removed 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

a.

b.

Arise from a single transformed epithelial cell in the tracheobronchial airways. Adenocarcinoma - most prevalent carcinoma of the lung for men and women, peripherally located and often metastasized 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 assymptomatic 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 hemprtysis, 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

1.

2. 3. 4.

Assessment Findings DRE: hard, pea-sized nodules on the anterior rectum Hematuria Urinary obstruction Pain on the perineum radiating to the leg

Prostate Cancer
Diagnostic tests 1. DRE 2. Prostatic 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 nigth 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 exdamine 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, overy, 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

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 515 %

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 persons only Barrium 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 Barrets Esophagus Usually squamous cell epidermoid type

Clinical manifestation
Dyspahgia Mass in the throat Regurgitation of undigested foods Foul breath and hiccups

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
CT or MRI guided needle biopsy through burr hole Open biopsy via craniotomy Stereotactic biopsy tumor located with three dimensional coordinates bipsied or removed most common

1. 2. 3.

Adjuvant therapy
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)
a.

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

Paps smear beginning at age 18 or sexually active

assessment
Assymptomatic 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 Barrium 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 1535 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 hydrocelle 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

Hodgkins disease
Malignancy of the immune system Usually in the involved LN, tonsils, spleen and bone marrow Characterized by presence of reedsternberg 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

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 sindrome Tumor lysis tumor