Lec Cd,onco

COMMUNICABLE DISEASES Roberto M. Salvador Jr. R.N.,M.D. Infectious and Tropical Disease Specialist

Philippines top 10 leading causes of morbidity & mortality in the year 2007:            

Diarrhea Bronchitis Pneumonia Influenza Hypertension Tuberculosis Malaria Heart diseases Cancer Accidents Chronic obstructive pulmonary disease and other respiratory diseases Diabetes and Kidney diseases.

Host and Microbial Interaction INTRODUCTION Although most microorganisms live in harmony with the human body, some—called pathogens —can infect the body and cause disease. Infectious diseases range from mild illnesses, such as a cold, to fatal illnesses, such as AIDS. We occasionally come into contact with people or animals that are infected and thus expose ourselves to the pathogens of their diseases. In fact, our environment is such that everyday we live with some risk of exposure to diseases.

BLOOD/VECTOR BORNE DISEASES

Prevention 

Eradicate the source DOH CLEAN

C – chemically treated mosquito net L - larvae eating fish E – environmental sanitation A – anti-mosquito N – neem tree (oregano, eucalyptus)

Dengue Hemorrhagic Fever   

caused by dengue virus (Flaviridae) with 4 serotypes transmitted to a bite of female Aedes aegypti mosquito incubation period 2-7 days

Vectors: (day biting)  Aedes aegypti (breeds in water stored in houses)  Aedes albopictus  Culex fatigans

Clinical manifestations 

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

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4th – 7th day – Toxic or Hemorrhagic Stage – After the lyze of the fever, this is where the complication of dengue is expected to come out as manifested by abdominal pain, melena, indicating bleeding in the upper gastrointestinal tract, Unstable BP, narrow pulse pressure and shock.

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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 

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Grade I – Dengue fever, saddleback fever plus constitutional signs and symptoms plus positive tourniquet test Grade II – Stage I plus spontaneous bleeding, epistaxis, GI, cutaneous bleeding Grade III – Dengue Shock Syndrome, all of the following signs and symptoms plus evidence of circulatory failure Grade IV – Grade III plus irreversible shock and massive bleeding

Diagnostics Tourniquet test or Rumpel Leads Test – presumptive test for capillary fragility - keep cuff inflated for 6-10 mins (child), 1015 min (adults) - count the petechiae formation 1 sq inch (>20 petechiae/sq inch)

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Laboratory Procedures CBC  Bleeding Parameters  Serologic test 

 Dengue

blot, Dengue Igm

Other :  PT (Prothrombin Time)  APTT (Activated Partial Thromboplastin Time)  Bleeding time  Coagulation time Mgmt: symptomatic and supportive

Management Specific Therapy – none  Symptomatic/Supportive therapy 

 Intravenous

Fluids (IVF)  with hemoconcentration, 5-7 ml/kg/hr  with shock, 10-30ml/kg in <20mins

Use of Blood/Blood Products Platelet concentrate 1 unit/5-7kg Cryoprecipitate, 1unit/5kg FFP, 15ml/kg x 2-4hrs  given in patient in impending shock and unresponsive to isotonic or colloid transfusion.  Prolonged PT FWB 20cc/kg  active bleeding  check serum calcium PRBC 10cc/kg

Nursing Intervention       

Paracetamol (no aspirin) Giving of cytoprotectors Gastric Lavage trendelenburg position for shock Nasal packing with epinephrine No intramuscular injections manage anxiety of patient and family

Preventive measures Department of Health program for the control of Dengue Hemorrhagic Fever  S eek and destroy breeding places  S ay no to left and right defogging  S eek early consultation 

FILARIASIS

The disease often progresses to become chronic, debilitating and disfiguring disease since it’s symptoms are unnoticed or unfamiliar to health workers.  High rates in region 5(bicol), 8 (samar and leyte, II (davao) 

Filariasis   

Wuchereria bancrofti and Bulgaria malayi Transmitted to the bite of infected female mosquito (Aedes, Anopheles, Mansonia) The larvae are carried in the blood stream and lodged in lymphatic vessels and lymph glands where they mature in adult form

Two biological type  Nocturnal 

 microfilaria

circulate in peripheral blood at night (10pm – 2am)

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Diurnal  microfilaria

at daytime

circulate in greater concentration

Clinical Manifestations Acute stage  - filarial fever and lymphatic inflammation that occurs frequently as 10 times per year and usually abates spontaneously after 7 days  - Lymphadenitis (Inflammation of the lymph nodes)  - Lymphangitis (Inflammation of the lymph vessels)

Chronic Stage (10-15 years from the onset of the first attack)  - Hydrocele (Swelling of the scotum)  - Lymphedema (Temporary swelling of the upper and lower extremities)  - Elephantiasis (enlargement and thickening of the skin of the lower or upper extremities)

Laboratory Diagnosis 

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

Management Guidelines        

Specific Therapy Dietylcarbamazine (DEC) 6mg/KBW in divided doses for 12 consecutive days Ivermectine (Mectican) Supportive Therapy Paracetamol Antihistamine for allergic reaction due to DEC Vitamin B complex Elevation of infected limb, elastic stocking

DEC should be taken immediately after meals  It may cause loss of vision, night blindness, or tunnel vision with prolonged used.  Ivermectin is best taken as single dose with a full glass of water in an empty stomach.  Cannot be used in patient with asthma 

Preventive Measures Health teachings  Environmental Sanitation 

Leptospira interrogans  AKA Red water disease in cattle, Swineherd’s disease or Weil’s disease in humans 

Leptospirosis (Weil’s disease) 

a zoonotic systemic infection caused by Leptospires, that penetrate intact and abraded skin through exposure to water, wet soil contaminated with urine of infected animals.

Anicteric Type (without jaundice)  manifested by fever, conjunctival injection  signs of meningeal irritation Icteric Type (Weil Syndrome)  Hepatic and renal manifestation  Jaundice, hepatomegaly  Oliguria, anuria which progress to renal failure  Shock, coma, CHF  Convalescent Period

Diagnosis  

Clinical history and manifestation Culture  Blood:

during the 1st week  CSF: from the 5th to the 12th day  Urine: after the 1st week until convalescent period   

LAAT (Leptospira Agglutination Test) other laboratory BUN,CREA, liver enzymes

Treatment 

Specific  Penicillin

50000 units/kg/day  Tetracycline 20-40mg/kg/day

Non-specific  Supportive and symptomatic  Administration of fluids  Peritoneal dialysis for renal failure 

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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

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Plasmodium vivax   

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more widely distributed causes benign tertian malaria chills and fever every 48 hours in 3 days

Plasmodium falciparum   

common in the Philippines causes the most serious type of malaria because of high parasitic densities in blood. causes malignant tertian malaria

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Plasmodium malaria  

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much less frequent causes quartan malaria, fever and chills every 72 hrs in 4 days

Plasmodium ovale 

rarely seen.

Clinical Manifestation     

uncomplicated fever, chills, sweating every 24 – 36 hrs Complicated sporulation or segmentation and rupture of erythrocytes occurs in the brain and visceral organs. Cerebral malaria changes of sensorium, severe headache and vomiting  seizures 

Cold stage – 10-15 mins, chills, shakes  Hot stage – 4-6 hours, recurring high grade fever, severe headache, vomiting, abdominal pain, face is blue  Diaphoretic stage – excessive sweating 

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

Treatment:     

Determine the species of parasite Objectives of treatment Destroy all sexual forms of parasite to cure the clinical attack Destroy the excerythrocytes (EE) to prevent relapse Destroy gametocytes to prevent mosquito infections

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Treatment for P. falciparum  Chloroquine

tablet (150mg/base/tab) Day

1,2,3  Sulfadoxine/Pyrimethamine 500mg/25mg/tab, 3tabs single dose  Primaquine (15mg/tab) 3 tabs single dose 

Treatment for P. vivax  Chloroquine,

Day 1,2,3  Primaquine 1 tab OD for 14 days

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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 meningitidis, a gram negative diplococcus  transmitted through airborne or close contact  incubation is 1-3 days  natural reservoir is human nasopharynx 

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Clinical Manifestations  sudden

onset of high grade fever, rash and rapid deterioration of clinical condition within 24 hours

S/sx: 1. Meningococcemia – spiking fever, chills, arthralgia, sudden appearance of hemorrhagic rash 2. Fulminant Meningococcemia (Waterhouse Friederichsen) – septic shock; hypotension, tachycardia, enlarging petechial rash, adrenal insufficiency

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

Treatment: 

Antimicrobials Benzyl Penicillin 250-400000 u/kg/day  Chloramphenicol 100mg/kg/day 

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Symptomatic and supportive fever  seizures  hydration  respiratory function 

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Chemoprophylaxis Rifampicin 300-600mg q 12hrs x 4 doses  Ofloxacin 400mg single dose  Ceftriaxone 125-250mg IM single dose 

Nursing Intervention Provide strict isolation  Wearing of mask etc  Health teaching  Contact tracing  Prophylaxis  Meningococcal vaccine for high risk patients 

acute viral encephalomyelitis  incubation period is 4 days up to 19 years  risk of developing rabies, face bite 60%, upper extremities 15-40%, lower extremities 10%  100% fatal 

 pain

or numbness at the site of bite  fear of water  fear of air 4 STAGES

1. prodrome - fever, headache, paresthesia, 2. encephalitic – excessive motor activity, hypersensitivity to bright light, loud noise, hypersalivation, dilated pupils 3. brainstem dysfunction – dysphagia, hydrophobia, apnea 4. death

Rabies Virus The rabies virus is usually transmitted to humans by a bite from an infected dog, but the bite of any animal (wild or domestic) is suspect in an area where rabies is present. Symptoms of the disease appear after an incubation period of ten days to one year and include fever, breathing difficulties, and muscle spasms in the throat that make drinking painful. Death almost invariably occurs within three days to three weeks of the onset of symptoms. For this reason, the emphasis of treatment is on prevention. In the United States, veterinarians

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

Management  No treatment for clinical rabies  Prophylaxis

Postexposure prophylaxis Category I 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

1.Active 2.Passive

14 days

Active vaccine  Intradermal (0,3,7,30,90)  Intramuscular (0,3,7,14,28)  (0,7,21)

Passive Vaccine  a. ERIG wt in kg x .2 = cc to be injected im (ANST)  b. HRIG wt in Kg x .1333

Pre-exposure Prophylaxis  Intradermal/Intramuscular (0,7,21)

Infection control  Patient is isolated to prevent exposure of hospital personnel, watchers and visitors Preventive Measures  Education  Post-exposure and Pre-exposure Prophylaxis

TETANUS caused by Clostridium tetani, grows anaerobically  Tetanus spores are introduced into the wound contaminated with soil.  Incubation period 4-21 days 

Pathogenesis > a neurotoxin (tetanoplasmin) and hemolysin (tetanolysin) are produced 

Pathophysiology Clostridium tetani in puncture wound Tetanospasmin attack PNS and CNS GABA and Glycine inhibited Tetanic spasm

Clinical manifestation Difficulty of opening the mouth (trismus or lockjaw)  Risus sardonicus  Abdominal rigidity  Localized or generalized muscle spasm 

Criteria

Stage I

Stage II

Stage III

Incubation Period > 11 days

8-10 days

<7days

Trismus

mild

moderate

Severe

Muscle rigidity

mild

Pronounced

Severe, boardlike

Spasm

absent

Mild, short

Frequent, prolonged

absent

Present

Dyspnea, cyanosis absent

Treatment 1. Neutralize the toxin 2. Kill the microorganism 3. Prevent and control the spasm - muscle relaxants - Sedatives - Tranquilizers 4. Tracheostomy

Treatment: anti-toxin 

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Tetanus Anti-Toxin (TAT) Adult,children,infant 40,000 IU ½ IM,1/2 IV Neonatal Tetanus 20000 IU, 1/2IM, ½ IV TIG Neonates 1000 IU, IV drip or IM Adult, infant, children 3000 IU, IV drip or IM

Antimicrobial Therapy Penicillin !-3 mil units q 4hours Pedia 500000 – 2mil units q 4 hrs Neonatal 200000 units IV q 12hrs or q8hrs

Control of spasms  diazepam  chlorpromazine

Nursing care Patient should be in a quiet, darkened room, well ventilated.  Minimal/gentle handling of patient  Liquid diet via NGT  Prevent Injury 

Preventive Measures  Treatment of wounds  Tetanus toxoid

SCHISTOSOMIASIS caused by blood flukes, Schistosoma  has 3 species, S. haematobium, S. mansoni, S. japonicum  S. japonicum is endemic in the Philippines (Leyte, Samar, Sorsogon, Mindoro,Bohol)  Intermediate host, Oncomelania quadrasi 

cycle Eggs Escap e into Intesti nal lumen

Sex in portal vein

Adult in 2 days

(Miraci dia)

Oncol omela nia Quadr asi

Portal veins

Skin penetr ate

Sporo zyst Cercar ia

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Diagnosis:  Schistosoma  Rectal

eggs in stool

bipsy  Kato Katz  Ultrasound of HBT

Clinical Manifestation severe jaundice  edema  ascites  hepatosplenomegaly  S/S of portal hypertension 

Management Praziquantel 60mg/kg once dosing  Supportive and symptomatic 

Methods of Control Educate the public regarding the mode of transmission and methods of protection.  Proper disposal of feces and urine  Prevent exposure to contaminated water. To minimize penetration after accidental water exposure, towel dry and apply 70% alcohol. 

The organism is pathogenic only in man  Spread chiefly by carriers, ingestion of infected foods  Endemic particularly in areas of low sanitation levels  Occurs more common in may to august 

MOT: oral fecal route S/sx: Rose spot (abdominal rashes), more than 7days Step ladder fever 40-41 deg, headache, abdominal pain, constipation (adults), mild diarrhea (children)

Pathophysiology Oral ingestion Bloodstream RES (lymph node, spleen, liver) Bloodstream Gallbladder Peyer’s patches of SI ulceration

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 complications a. Perforation – symptoms of sharp abdominal pain, abdominal rigidity and absent of bowel sounds. - prepare for intestinal decompression or surgical intervention b. Intestinal hemorrhage - withold food and give blood transfusion 

Nursing Interventions Environmental Sanitation  Food handlers sanitation permit  Supportive therapy  Assessment of complication (occuring on the 2nd to 3rd week of infection ) - typhoid psychosis, typhoid meningitis - typhoid ileitis 

Hepatitis Hepa A – fecal oral route  Hepa B – body fluids  Hepa C – non A non B, BT, body fluids  Hepa D – hypodermic, body fluids  Hepa E – fecal oral route, fatal and common among pregnant women  Hepa G – BT, parenteral 

Hepatitis A  

Infectious hepatitis, epidemic hepatitis Young people especially school children are most commonly affected.

Predisposing factors: - Poor sanitation, contaminated water supply, unsanitary preparation of food, malnutrition, disaster conditions

Incubation Period: 15-50 days Signs/Symptoms: - Influenza - Malaise and easy fatigability - Anorexia and abdominal discomfort - Nausea and vomiting - Fever, CLAD - jaundice

Dx: Anti HAV IgM – active infection Anti HAV IgG – old infection; no active disease Management: - Prophylaxis - Complete bed rest - Low fat diet but high sugar

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Ensure safe water for drinking Sanitary method in preparing handling and serving of food. Proper disposal of feces and urine. Washing hands before eating and after toilet use. Separate and proper cleaning of articles used by patient

Hepatitis B DNA, Hepa B virus  Serum hepa  Worldwide distribution  Main cause of liver cirrhosis and liver cancer 

IP: 2-5 months

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

High Risk group Newborns and infants of infected mothers  Health workers exposed to handling blood  Persons requiring frequent transfusions  Sexually promiscous individuals  Commercial sex workers  Drug addicts 

Possible Outcome Some become carriers of the virus and transmit disease to others.  Almost 90% of infected newborns become carriers 

Hepatitis C Post transfusion Hepatitis  Mode of transmission – percutaneous, BT  Predisposing factors – paramedical teams and blood recipients  Incubation period – 2weeks – 6 months 

Hepatitis D  

   

Dormant type Can be acquired only if with hepatitis B Hepatitis E If hepatitis E recurs at age 20-30, it can lead to cancer of the liver Enteric hepatitis Fecal-oral route

DX:  Elevated AST or SGPT (specific) and ALT or SGOT  Increased IgM during acute phase  (+) or REACTIVE HBsAg = INFECTED, may be acute, chronic or carrier  (+) HBeAg = highly infectious  ALT – 1st to increase in liver damage

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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 

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Mode of transmission is direct or indirect contact

Pathogenesis Pseudomembrane is formed by leukocytes, necrotic tissue and microorganism which is adherent to the tissues and leaves a raw bleeding when detached  Further development of toxins causing attack to the heart, kidney, liver and cranial nerve 

1. Nasal – invades nose by extension from

pharynx 2. Pharygeal - sorethroat causing dysphagia - Pseudomembrane in uvula, tonsils, soft palate - Bullneck – inflammation of cervical LN 3. Laryngeal - increasing hoarseness until aphonia - wheezing on expiration - dyspnea

Diagnosis Nose and throat swab using Loeffler’s medium  Schick test – determine susceptibility or immunity in diptheria  Maloney test – determines hypersensitivity to diptheria toxoid 

Complications   -

Toxic myocarditis – due to action of toxin in the heart muscles (1st 10-14 days) Neuritis caused by absorption of toxin in the nerve Palate paralysis (2nd week) Ocular palsy (5th week) Diaphragm paralysis (6-10wk causing GBS) Motor and skeletal muscle paralysis

Treatment Neutralize the toxins – antidiptheria serum  Kill the microorganism – penicillin  Prevent respiratory obstruction – tracheostomy, intubation 

Treatment Serum therapy (Diptheria antitoxin) - early administration aimed at neutralizing the toxin present in the general circulation  Antibiotics - Penicillin G 100000mg/kg.day - Erythromycin 40mg/kg 

Nursing Intervention Rest. - Patient should be confined to bed for at least 2 weeks - Prevent straining on defecation - vomiting is very exhausting, do not do procedures that may cause nausea

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Care for the nose and throat  Ice collar to reduce the pain of sorethroat  Soft and liquid diet 

Whooping Cough, 100 day fever Bordetella pertussis, B. parapertussis, B. bronchiseptica, gram (-) IP: 3-21 days MOT: airborne/droplet 

Signs and symptoms Invasion or catarrhal stage (7-14days) starts with ordinary cough  Spasmodic or paroxysmal - 5-10 spasms of explosive cough (no time to catch breath. A peculiar inspiratory crowing sound followed by prolonged expiration and a sudden noisy inspiration with a long high pitched “whoop” 



During attack the child becomes cyanotic and the eyes appear to bulge or popping out of the eyeball and tongue protrudes

Diagnosis WBC count 20000-50000  Culture with Bordet Gengou Agar 

Treatment Erythromycin shorten the period of communicability  Ampicillin if with allergy to erythromycin  Heperimmune pertusis gamma globulin in <2 years old (1.25ml IM)  Control of cough with sedatives 

Dx: WHO - >21 days cough + close contact w/ pertussis px + (+) culture OR rise in Ab to FHA or pertussis toxin * throat culture w/ Bordet gengou agar

Management CBR to conserve energy  Prevent aspiration  High calorie, bland diet  Omit milk and milk product because it increases the mucous  Refeeding of infants 20 min after vomiting  Milk should be given at room temperature 

complications Bronchopneumonia  Abdominal hernia  Severe malnutrition  TB, asthma  encephalitis 

Pre exposure prophylaxis for Diphtheria, Pertussis, Tetanus DPT- 0.5 ml IM 1 - 1 ½ months old 2 - after 4 weeks 3 - after 4 weeks 1st booster – 18 mos 2nd booster – 4-6 yo subsequent booster – every 10 yrs thereafter  Household contacts (+) primary immunization and (-) culture - booster dose (+) culture and (-) immunization – treated as a case of Diptheria 

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The world’s deadliest disease and remains as a major public health problem. Badly nourished, neglected and fatigued individuals are more prone Susceptibility is highest in children under 3 years AKA: Koch’s disease: Galloping consumption

Pulmonary Tuberculosis S/sx:  Wt loss  night sweats  low fever,  non productive to productive cough  anorexia,  Pleural effusion and hypoxemia  cervical lymphadenopathy

Pathophysiology Inhalation Local infiltration of neutrophils and macrohage Multiply and survive in macrophage Destroy bacteria present it to T helper cells in LN Sensitized T cells searches bacteria and release lymphokines Attract macrophages w/c attack bacteria

caseous necrosis bacteria dormant

Heal w/ fibrosis, calcification and granuloma; Primary If TB reactivated, Secondary TB

PPD – ID macrophages in skin take up Ag and deliver it to T cells T cells move to skin site, release lymphokines activate macrophages and in 48-72 hrs, skin becomes indurated - > 10 mm is (+)

Dx: Chest xray - cavitary lesion Sputum exam sputum culture

The National Tuberculosis Control Program Vision: A country where TB is no longer a public health problem. Mission: Ensure that TB DOTS services are available to the communities. Goal: To reduce the prevalence and mortality from TB by half by the year 2015

Targets: 1. To cure at least 85% of the sputum smear positive TB patient discovered. 2. Detect at least 70% of the estimated new sputum smear positive TB cases.

Category I

II

TB patient Intensive Maintainance New smear (+) New smear (-) 2HRZE 4 HR PTB with ext parenchymal Treatment Failure, 2HRZES/ 5 HRE Relapse, return 1HRZE after Default

III

IV

New Smear (-) PTB, with minimal CXR lesion

2HRZE

Chronic (still smear (+) after supervised treatment

MDRTB

4HRE

Mgmt:  short course – 6-9 months  long course – 9-12 months  DOTS- direct observe treatment short course  Case finding  Home meds (members of the family)  Referrals  Follow-up * 2 wks after medications – non communicable 3 successive (-) sputum - non communicable rifampicin - prophylactic

MDT side effects  r-orange urine  i-neuritis and hepatitis  p-hyperuricemia  e-impairment of vision  s-8th cranial nerve damage

Methods of Control Prompt treatment and diagnosis  BCG vaccination  Educate the public in mode of transmission and importance of early diagnosid  Improve social condition 

GIT

Amoebiasis Entamoeba histolytica, protozoa  IP: few days to months to years, usually 2- 4 weeks MOT: Ingestion of cysts from fecally contaminated sources (Oro- fecal route) oral and anal sexual practices  Extraintestinal amoebiasis- genitalia, spleen, liver, anal, lungs and meninges 

s/sx:  Blood streaked, watery mucoid diarrhea, foul smelling,  abdominal cramps  Pain on defecation (tenesmus)  Hyperactive bowel sounds

Diagnostic test Stool culture of 3 stool specimens  Sigmoidoscopy  Recto-sigmoidoscopy and coloscopy for intestinal amoebiasis 

Medical treatment Metronidazole – trichomonocide and amoebicide for intestinal and extra intestinal sites (monitor liver function test)  Diloxanide furoate – luminal amoebicide  Paromomycin – eradicate cyst of histolytica  Tinidazole – hepatic amebic abscess 

Bacillary Dysentery Shigellosis    

Shiga bacillus: dysenteriae (fatal), flexneri (Philippines), boydii, sonnei; gram (-) Shiga toxin destroys intestinal mucosa Humans are the only hosts Not part of normal intestinal flora

IP: 1-7 days MOT : oral fecal route

S/sx: fever, severe abdominal pain, diarrhea is watery to bloody with pus, tenesmus Dx: stool culture Mgmt: Oresol, Ampicillin, 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 Washerwoman’s skin, poor skin turgor Dx: stool culture mgmt: IV fluids, Tetracycline, Doxycycline, Erythromycin, Quinolones, Furazolidone and Sulfonamides (children)

Hookworm (Roundworm) Necator americanus, Ancylostoma duodenale  Leads to iron deficiency and hypochromic microcytic anemia  Gain entry via the skin 

Dx: microscopic exam (stool exam) Mgmt: Pyrantel Pamoate and Mebendazole  don’t give drug without (+) stool exam  members of the family must be examined and treated also

Paragonimiasis Chronic parasitic infection  Closely resembles PTB  Endemic areas: mindoro, camarines sur, norte, samar, sorsogon, leyte, albay, basilan 

Paragonimiasis AKA: Lung fluke disease  causative agent: Paragonimus westermani; Trematode  Eating raw or partially cooked fish or fresh water crabs 

Signs and symptoms Cough of long duration  Hemoptysis  Chest/back pain  PTB not responding to anti-koch’s meds 

Diagnosis - sputum examination – eggs in brown spots  Treatment 1. Praziquantel (Biltrizide) 2. Bithionol 

Ascariasis Common worldwide with greatest frequency in tropical countries.  Has an infection rate of 70-90% in rural areas  MOT: ingestion of embryonated egss (fecal-oral) 

Worms reach maturity 2 months after ingestion of eggs.  Adult worms live less than 10 months(18 months max.)  Female can produce up to 200000 eggs per day  Eggs may be viable in soils for months or years  Worms can reach 10-30cm in length 

MOT: ingestion of food contaminated by ascaris eggs larvae in large intestine penetrate wall lung where larvae grow and coughed up intestine larvae mature and passed out in feces

Initial symptom: loss of appetite  Worms in the stool  Fever  Wheezing  Vomiting  Abdominal distention  Diarhea  dehydration 

Medical Management 





Mebendazole (antihelmintic) effect occurs by blocking the glucose uptake of the organisms, reducing the energy until death Pyrantel pamoate: neuromuscular blocking effect which paralyze the helminth, allowing it to be expelled in the feces Piperazine citrate: paralyze muscles of parasite, this dislodges the parasites promoting their elimination

Nursing Intervention Environmental sanitation  Health teachings  Assessment of hydration status  Use of ORS  Proper waste disposal  Enteric precautions 

Complications Migration of the worm to different parts of the body Ears, mouth,nose  Loefflers Pneumonia  Energy protein malnutrition  Intestinal obstruction 

Tapeworm (Flatworms) 

Taenia saginata (cattle), Taenia solium (pigs)

MOT: fecal oral route (ingestion of food contaminated by the agent) s/sx: neurocysticercosis – seizures, hydrocephalus Dx: Stool Exam Mgmt: Praziquantel, Niclosamide

Nursing Intervention Promote hygiene  Environmental Sanitation  Proper waste and sewage disposal  Antihelmintic medications repeated after 2 weeks (entire family) 

PARALYTIC SHELLFISH POISONING 

A syndrome of characteristic symptoms predominantly neurologic which occurs within minutes or several hours after ingestion of poisonous shellfish

Single celled dinoflagellates (red planktons) become poisonous after heavy rain fall preceded by prolonged summer  Common in seas around manila bay, samar, bataan and zambales 



MOT = Ingestion of contaminated bi-valve shellfish



IP = within 30 minutes

CLINICAL MANIFESTATIONS: 

  

NUMBNESS OF THE FACE ESPECIALLY AROUND THE MOUTH VOMITING, DIZZINESS, HEADACHE TINGLING SENSATION, WEAKNESS RAPID PULSE, DIFFICULTY OF SPEECH ( DYSPHAGIA, RESPI PARALYSIS, DEATH.

MANAGEMENT AND CONTROL MEASURES:   



NO DEFINITE MEDICATIONS INDUCE VOMITING (EARLY INTERVENTION) DRINKING PURE COCONUT MILK (WEAKENS TOXIC EFFECT) DON’T GIVE DURING LATE STAGE IT MAY WORSEN THE CONDITION. NaHCO3 SOLUTION (25 GRAMS IN ½ GLASS OF WATER)



RESPIRATORY SUPPORT



AVOID USING VINEGAR IN COOKING SHELLFISH AFFECTED BY RED TIDE (15X virulence) TOXIN OF RED TIDE IS NOT TOTALLY DESTROYED IN COOKING. AVOID TAHONG, TALABA, HALAAN, KABIYA, ABANIKO. WHEN RED TIDE IS ON THE RISE.

 

Contact

Pediculosis 

Blood sucking lice/Pediculus humanus p. capitis-scalp p. palpebrarum-eyelids and eyelashes p. pubis-pubic hair p. corporis-body

MOT: skin contact, sharing of grooming implements s/sx: nits in hair/clothing, irritating maculopapular or urticarial rash Mgmt: disinfect implements, Lindane (Kwell) topical Permethrin (Nix) topical Dr. Salvador

Dr. Salvador

Dr. Salvador

Dr. Salvador

Scabies

  

Sarcoptes scabiei Pruritus (excreta of mites) Mites come-out from burrows to mate at night

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

Dr. Salvador

Dr. Salvador

Dx: biopsies/scrapings of lesions Mgmt: Permethrin (Nix) cream, crotamiton cream, Sulfur soap, antihistamines and calamine for pruritus, wash linens with hot water, single dose of Ivermectin, treat close contacts Dr. Salvador

Dx: biopsies/scrapings of lesions NURSING CARE a. Administer antihistamines or topical steroids to relieve itching. b. Apply topical antiscabies creams or lotion like lindane(kwell), Crotamiton (Eurax), permithrin

Dr. Salvador

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

Leprosy   

 

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

Dr. Salvador

Cardinal Sign  Presence

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

Dr. Salvador

Leprosy/Hansen’s disease * Lepromatous or malignant

- many microorganisms - open or infectious cases - negative lepromin test * Tuberculoid or benign - few organism - noninfectious - positive reaction to lepromin test Dr. Salvador

s/sx: • Early/Indeterminate – hypopigmented / hyperpigmented anesthetic macules/plaques •

Tuberculoid – solitary hypopigmened hypesthetic macule, neuritic pain, contractures of hand and foot, ulcers, eye involvement ie keratitis

•

Lepromatous – multiple lesions, Loss of lateral portion of eyebrows (madarosis), corugated skin (leonine facies), septal collapse (saddlenose) Dr. Salvador

Diagnosis Skin smear test  Skin lesion biopsy  Lepromin test 

Dr. Salvador

Mgmt:  MDT-RA 4073 (home meds)  Paucibacillary - 6-9 months 1. Dapsone 2. Rifampicin  Multibacillary- 12-24 months 1. Dapsone – mainstay; hemolysis, agranulocytosis 2. Clofazimine – reddish skin pimentation, intestinal toxicity 3. Rifampicin – bactericidal; renal and liver toxicity

Dr. Salvador

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

Dr. Salvador

Leprosy   

 

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

Cardinal Sign  Presence

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

Leprosy/Hansen’s disease * Lepromatous or malignant

- many microorganisms - open or infectious cases - negative lepromin test * Tuberculoid or benign - few organism - noninfectious - positive reaction to lepromin test

s/sx: • Early/Indeterminate – hypopigmented / hyperpigmented anesthetic macules/plaques •

Tuberculoid – solitary hypopigmened hypesthetic macule, neuritic pain, contractures of hand and foot, ulcers, eye involvement ie keratitis

•

Lepromatous – multiple lesions, Loss of lateral portion of eyebrows (madarosis), corugated skin (leonine facies), septal collapse (saddlenose)

Diagnosis Skin smear test  Skin lesion biopsy  Lepromin test 

Mgmt:  MDT-RA 4073 (home meds)  Paucibacillary - 6-9 months 1. Dapsone 2. Rifampicin  Multibacillary- 12-24 months 1. Dapsone – mainstay; hemolysis, agranulocytosis 2. Clofazimine – reddish skin pimentation, intestinal toxicity 3. Rifampicin – bactericidal; renal and liver toxicity

Acne Vulgaris      

Common, self limiting, multifactorial skin disease Over production of sebum, propionibacterium acnes, hormonal, Closed comedones – whiteheads Open comedones – blackheads Requires active treatment Intervention: don’t squeeze, prick or pick, Isotretinoin Accutane (avoid sunlight and vit A, may increase triglycerides), antibiotics

Dr. Salvador

Dr. Salvador

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

Dr. Salvador

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

Dr. Salvador

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

Dr. Salvador

Dr. Salvador

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

Dr. Salvador

Stage 1 -Skin

Stage 2

Stage 3

is intact -Top layer is missing -Reddened -Ulcer is area shallow, wih pink or red base - white or yellow eschar

-Deep

Stage 4

ulcer -Ulcer extends to extend to dermis and muscle and subcutaneou bones s areas - foul - white, gray smelling or yellow - brown or eschar black eschar - purulent - purulent discharge discharge

Dr. Salvador

Dr. Salvador

Risk Factors Malnutrition  Incontinence  Immobility  Skin shearing  Decreased sensory perception 

Dr. Salvador

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

Dr. Salvador

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

Dr. Salvador

ERUPTIVE FEVER

MEASLES Extremely contagious  Breastfed babies of mothers have 3 months immunity for measles  The most common complication is otitis media  The most serious complications are bronchopneumonia and encephalitis 

Measles, Rubeola, 7 Day Fever, Hard Red Measles    

RNA, Paramyxoviridae Active MMR and Measles vaccine Passive Measles immune globulin Lifetime Immunity

IP: 7-14 days MOT: droplets, airborne *Contagious 4 days before rash and 4 days after rash

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

- Koplik’s spots - Stimsons line  -

-

Eruptive stage Maculopapular rashes appears first on the hairline, forehead, post auricular area the spread to the extremities (cephalocaudal) Rashes are too hot to touch and dry High grade fever and increases steadily at the height of the rashes

 -

-

Stage of convalescence Rashes fade in the same manner leaving a dirty brownish pigmentation (desquamation) Black measles – severe form of measles with hemorrhagic rashes, epistaxis and melena

Rashes: maculopapaular, cephalocaudal (hairline and behind the ears to trunk and limbs), confluent, desquamation, pruritus

Complication Bronchopneumonia  Secondary infections  Encephalitis  Increase predisposition to TB 

 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 fetus of women in the 1st trimester 

s/sx: forscheimer’s (petechial lesion on buccal cavity or soft palate), - cervical lymphadenopathy, low grade fever - “ Oval, rose red papules about the size of pinhead Dx: clinical CX: rare; pneumonia, meningoencephalitis CX to pregnant women:  1st tri-congenital anomalies  2nd tri-abortion  3rd tri-pre mature delivery

Rashes: Maculopapular, Diffuse/not confluent, No desquamation, spreads from the face downwards



Chicken Pox, Varicella Herpes zoster virus (shingles),

varicella zoster virus(chicken pox)  Active : Varicella vaccine  Passive: VZIG, ZIG – given 72-96 hrs w/n exposure  Lifetime Immunity IP: 14-21 days MOT: Respiratory route * Contagious 1 day before rash and 6 days after first crop of vesicles S/sx: fever, malaise, headache

Rashes: Maculopapulovesicular (covered areas), Centrifugal, starts on face and trunk and spreads to entire body 

Leaves a pitted scar (pockmark)

CX furunculosis, erysipelas, meningoencephalitis 

Dormant: remain at the dorsal root ganglion and may recur as shingles (VZV)

Maxillary division of the trigeminal nerve

Mgmt: a. oral acyclovir b. Tepid water and wet compresses for pruritus c. Aluminum acetate soak for VZV d. Potassium Permanganate (ABO) a. Astringent effect b. Bactericidal effect c. Oxidizing effect (deodorize the rash)

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

Centripetal  contagious until all crusts disappeared Dx:  Paul’s test - instilling of vesicular fluid w/ small pox into the cornea; if keratitis develops, small pox Cx: same with chicken pox 

Emerging Diseases

Severe Acute Respiratory Syndrome

Coronavirus  Severe acute respiratory syndrome 

IP: 2-7 days Mortality rate – 5% only

1 Mainland

Visitor

2/15/03 3 Singapore 1 American Visitors Metropole Chinese Hotel Singapore Outbreak Hanoi Outbreak 2 Canadian Visitor Hongkong Outbreak Toronto, Canada Outbreak

A.C (Canada)

Narita, Japan

Philippines Pangasinan Tarlac Cordillera MetroManila San Lazaro Hospital (SARS UNIT)

Risk Factors:  history of recent travel to China, Hong Kong, singapore Taiwan, vietnam, canada. or close contact w/ ill persons with a hx of recent travel to such areas, OR  Is employed in an occupation at particular risk for SARS exposure, healthcare worker with direct patient contact or a worker in a laboratory that contains live SARS, OR  Is part of a cluster of cases of atypical pneumonia without an alternative diagnosis

Clinical Manifestations 

   

History of travel to SARS affected country or close contact with persons suspected of having SARS and within 14 days manifest the ff High grade fever (>38.0 c) Headache, body malaise, muscle pain Cough, sneezing, nasal congestion Difficulty of breathing after 2-7 days

 

SARS suspect Probable SARS

Diagnosis: Chest X-ray, CBC, Isolation of virus Mgt: Supportive Treat as Atypical Pneumonia Quarantine

AVIAN INFLUENZA

Serious consequences for ASIA

Avian Influenza….. Is an infectious disease of birds caused by Type A strains of the influenza virus  First identified in Italy more than 100 years ago  Occurs worldwide 

Infection causes a wide spectrum of symptoms in birds, ranging from mild illness to a highly contagious and rapidly fatal disease resulting in severe epidemics  “ highly pathogenic avian influenza” 

Pathogenesis







Avian influenza do not normally infect species other than birds and pigs First documented infection of humans with avian flu occurred in Hong Kong in 1997 Affected 18 humans, 6 died

Bird Flu 

Human cases of influenza A (H5N1) infection have been reported in Cambodia, China, Indonesia, Thailand, and Vietnam.

Clinical manifestations 

Patients develop fever, sore throat, cough, in fatal cases, severe respiratory distress may result secondary to pneumonia

A constantly mutating virus 

All type A influenza virus, including those that regularly cause seasonal epidemics of influenza in humans are genetically labile and well adapted to elude host defenses



So far bird flu is mainly transmitted between birds, but experts fear the H5N1 virus could be devastating to humans if it genetically mutates and develops the capacity to be transmitted from human to human.



Novel influenza A (H1N1) is a new flu virus of swine origin that was first detected in April, 2009.



Reassortment of 4 viruses from pigs, humans and birds



The virus is infecting people and is spreading from person-to-person, and has sparked a growing outbreak of illness in the United States with an increasing number of cases being reported internationally as well.

Dr. Salvador

Why is this new H1N1 virus sometimes called “swine flu”? 



This virus was originally referred to as “swine flu” because laboratory testing showed that many of the genes in this new virus were very similar to influenza viruses that normally occur in pigs in North America. But further study has shown that this new virus is very different from what normally circulates in North American pigs. It has two genes from flu viruses that normally circulate in pigs in Europe and Asia and avian genes and human genes. Scientists call this a “quadruple reassortant” virus.



How does this new H1N1 virus spread? Spread of this H1N1 virus is thought to be happening in the same way that seasonal flu spreads. Flu viruses are spread mainly from person to person through coughing or sneezing by people with influenza. Sometimes people may become infected by touching something with flu viruses on it and then touching their mouth or nose.

How severe is illness associated with this new H1N1 virus? 



It’s not known at this time how severe this virus will be in the general population. In seasonal flu, there are certain people that are at higher risk of serious flu-related complications. This includes people 65 years and older, children younger than five years old, pregnant women, and people of any age with chronic medical conditions.

WHO Pandemic Levels Here is a quick look at the WHO's pandemic alert phases: Phase 1: A virus in animals has caused no known infections in humans. Phase 2: An animal flu virus has caused infection in humans. Phase 3: Sporadic cases or small clusters of disease occur in humans. Human-to-human transmission, if any, is insufficient to cause community-level outbreaks.

Phase 4: The risk for a pandemic is greatly increased but not certain. The disease-causing virus is able to cause community-level outbreaks. Phase 5: Still not a pandemic, but spread of disease between humans is occurring in more than one country of one WHO region. Phase 6: This is the pandemic level. Community-level outbreaks are in at least one additional country in a different WHO region from phase 5. A global pandemic is under way.

“In response to the intensifying

outbreak, the World Health Organization raised the worldwide pandemic alert level to Phase 5” A phase 5 alert means there is sustained human to human spread in at least two countries. It also signals that efforts to produce a vaccine will be ramped up.

Case Definitions for H1N1 Clinical case description:  Acute febrile illness (fever >38C) 1. Suspected case – individual with influenze like illness who has close contact with an ill confirmed case of influenza virus infection OR a person with influenza like illness with recent history of contact with an animal with confirmed or suspected H1N1 virus OR a person with influenza like illness who has traveled to an area where there are confirmed cases of H1N! Within 7 days of onset of illness



Close contact - within 6 feet for an ill person who is confirmed case of swine influenza



Probable Case – an individual with an influenza test that is positive for influenza A, but non subtypable by reagents used to detect seasonal influenza virus An individual with a clinically compatible illness or who died of an unexplained acute respiratory illness who is considered to be an epidemiologically linked to a probable or confirmed case



Confirmed case – an individual with laboratory confirmed H1N1 virus by 1 or more of the ff: a. real time TR-PCR b. Viral culture c. Four-fold rise in influenza A (H1N1) specific antibodies

Signs and Symptoms Fever and chills  cough  sore throat  Nasal congestion  Myalgia  Pneumonia  Respiratory failure 

For interview of an ill, suspected or confirmed case; a. keep distance of at least 6 feet from the ill person b. Personal protective equipment: fit tested N95 respirator 

For collecting respiratory specimens a. Personal protective equipment b. When completed place all PPE in biohazard bag for appropriate disposal c. Wash hands thoroughly with soap and water or alcohol based gel 



How long can influenza virus remain viable on objects (such as books and doorknobs)? Studies have shown that influenza virus can survive on environmental surfaces and can infect a person for up to 2-8 hours after being deposited on the surface

Treatment: 

If you get sick, antiviral drugs can make your illness milder and make you feel better faster. They may also prevent serious influenza complications. For treatment, antiviral drugs work best if started as soon after getting sick as possible, and might not work if started more than 48 hours after illness starts.

Prevention: 

Influenza antiviral drugs also can be used to prevent influenza when they are given to a person who is not ill, but who has been or may be near a person with swine influenza. When used to prevent the flu, antiviral drugs are about 70% to 90% effective. When used for prevention, the number of days that they should be used will vary depending on a person’s particular situation.

Recommendation for Prophylaxis Priority groups to receive antiviral agents for prophylaxis are those who have potential contact with droplets from a patient without having an adequate PPE - Health worker - First responders - Workers providing essential services  Other people like household contacts of probable or confirmed case 

Anti-viral treatment should be given to:  Confirmed case  Probable case  Suspected case at high risk of severe disease

Antiviral treatment Oseltamavir (Tamiflu) 75mg/cap or 12mg/ml - <15kg 30mg BID for 5 days - >15-23kg 45mg BID - >23-40kg 60mg BID - >40kg 75mg BID



For prophylaxis 1 cap OD x 10 days

Zanamavir (relenza) - alternate drug in patient >7 years old - 2 inhalations BID for 5 days



Discharge Guidelines 7 days after the resolution of fever  Children can shed virus for 21 days after onset of illness  Family should be educated on personal hygiene and infection control measures. 

Infection control 

Main route of human to human transmission is via respiratory droplets which are expelled by speaking, sneezing or coughing

Public health measures Suspension of public events  limitation of movement from one area  Suspension of travel to a country with outbreaks of influenza  Closure or limitation of people in public places or establishments  Cancellation of mass gatherings 

Personal Protective Equipment Health care personnel Key elements 1. Use of medical or surgical gloves 2. Emphasize hand hygiene and provide hand hygiene facilities and supplies 

General public Promote physical distance (1 meter)  Avoid crowded situations  Refrain from touching mouth and nose  Perform hand hygiene frequently  Improve airflow in living space  People who have contact with influenza cases shall stay in their homes 

Guidelines in use of mask Place mask carefully to cover the mouth and nose and tie securely to minimize gaps between the face and the mask  While in use, avoid touching the mask  Replaced the mask with new clean, dry mask as soon it become damp/humid  Discard single use of mask 



Can H1N1 influenza virus be spread at recreational water venues outside of the water? Yes, recreational water venues are no different than any other group setting. The spread of this novel H1N1 flu is thought to be happening in the same way that seasonal flu spreads. Flu viruses are spread mainly from person to person through coughing or sneezing of people with influenza. Sometimes people may become infected by touching something with flu viruses on it and then touching their mouth or nose.



What can I do to protect myself from getting sick? There is no vaccine available right now to protect against this new H1N1 virus. There are everyday actions that can help prevent the spread of germs that cause respiratory illnesses like influenza.

Take these everyday steps to protect your health:  

  

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

What is the best technique for washing my hands to avoid getting the flu? Washing your hands often will help protect you from germs. Wash with soap and water or clean with alcoholbased hand cleaner. CDC recommends that when you wash your hands -- with soap and warm water -- that you wash for 15 to 20 seconds. When soap and water are not available, alcohol-based disposable hand wipes or gel sanitizers may be used. You can find them in most supermarkets and drugstores. If using gel, rub your hands until the gel is dry. The gel doesn't need water to work; the alcohol in it kills the germs on your hands.

What should I do if I get sick? 





If you live in areas where people have been identified with new H1N1 flu and become ill with influenza-like symptoms, including fever, body aches, runny or stuffy nose, sore throat, nausea, or vomiting or diarrhea, you should stay home and avoid contact with other people, except to seek medical care. If you have severe illness or you are at high risk for flu complications, contact your health care provider or seek medical care. Your health care provider will determine whether flu testing or treatment is needed If you become ill and experience any of the following warning signs, seek emergency medical care

       

In children emergency warning signs that need urgent medical attention include: Fast breathing or trouble breathing Bluish or gray skin color Not drinking enough fluids Severe or persistent vomiting Not waking up or not interacting Being so irritable that the child does not want to be held Flu-like symptoms improve but then return with fever and worse cough

In adults, emergency warning signs that need urgent medical attention include:  Difficulty breathing or shortness of breath  Pain or pressure in the chest or abdomen  Sudden dizziness  Confusion  Severe or persistent vomiting  Flu-like symptoms improve but then return with fever and worse cough 

Health alert Notice For travellers  Monitor health for 10 days  If become ill with fever accompanied by cough, sore throat, nasal congestion or DOB consult a physician 

Gonorrhea, Morning drop, Clap, Jack Neisseria gonorrheae, gram (+) IP: 3-7 days S/sx: Females: usually asymptomatic or minimal urethral discharge w/ lower abdominal pain - sterility or ectopic pregnancy Male: Mucopurulent discharge, Painful urination - decreased sperm count 

Clinical problems The most common reportable communicable disease  Has a short incubation period which permits rapid spread and a high percentage of females are asymptomatic  It is becoming increasingly resistant to penicillin 

DX: gram stain and culture of cervical secretions on Thayer Martin medium

Mgmt: single dose only  Ceftriaxone (Rocephin) 125 mg IM  Ofloxacin (Floxin) 400 mg orally  treat concurrently with Doxycycline or Azithromycin for 50% infected w/ Clamydia CX: PID, ectopic pregnancy and infertility, peritonitis, perihepatitis, Ophthalmia neonatorum, sepsis and arthritis

Syphilis 

Treponema pallidum, spirochete “ Beautiful” fast moving but delicate spiral thread



IP: 10-90 days



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

Chancre of the anus Chancre of the fingers

Chancre of the lip

Chancre of the labia Chancre on the labia minora



Secondary – systemic; generalized macular papular rash including palms and soles and painless wartlike lesions in vulva or scrotum (condylomata lata) and lymphadenopathy



Tertiary – (6-40 years) neurosyphilis/permanent damage (insanity); gumma (necrotic granulomatous lesions), aortic aneurysm

DX: Dark-field examination of lesion- 1st and 2nd stage Non specific VDRL and RPR

Mgmt  Primary and secondary - Pen G  Tertiary - IV Pen G

The most common STD in the US  Transmission is thru vaginal or rectal intercourse, or oral- genital contact with infected person. 

Signs and symptoms Usually asymptomatic  Gray-white discharge with burning or itchiness at the urethral opening  Lymphogranuloma venereum, enlarged unilateral lymphnodes 

Chlamydia   

Gram stain Antigen detection test on cervical smear Urinalysis

Mgmt:  Doxycycline or Azithromycin CX:  PID  Ectopic pregnancy  Fetus transmittal (vaginal birth)

Herpes Genitalis HSV 2 S/sx: Painful sexual intercourse, Painful vesicles (cervix, vagina, perineum, glans penis) Dx:  Viral culture  Pap smear (shows cellular changes)  Tzanck smear (scraping of ulcer for staining) 

Mgmt: Anti viral - acyclovir (zovirax) CX:  Meningitis  Neonatal infection (vaginal birth)

Genital Warts, Condyloma Acuminatum 

HPV type 6 & 11, papilloma virus

S/sx: Single or multiple soft, fleshy painless growth of the vulva, vagina, cervix, urethra, or anal area, Vaginal bleeding, discharge, odor and dyspareunia DX:  Pap smear-shows cellular changes (koilocytosis)  Acetic acid swabbing (will whiten lesion)

Cauliflower or hyperkeratotic papular lesions  Treatment - liquid nitrogen - podophylin resin 

Mgmt: Laser treatment is more effective CX:  Neoplasia  Neonatal laryngeal papillomatosis (vaginal birth)

Candidiasis, Moniliasis 

Candida Albicans, Yeast or fungus

S/sx: Cheesy white discharge, \Extreme itchiness DX:  KOH (wet smear indicate positive result) Mgmt:  Imidazole, Monistat, Diflucan CX:  Oral thrush to baby (vaginal birth)

HIV and AIDS 

Retrovirus (HIV1 & HIV2)



Attacks and kills CD4+ lymphocytes (T-helper)



Capable of replicating in the lymphocytes undetected by the immune system



Immunity declines and opportunistic microbes set in No known cure



HIV/AIDS Reverses Development and Poses Serious Threat to Future Generations  

 

Since 1980s, 60m have been infected and 25m have died About 40m live with HIV/AIDS – 38m in developing countries and 28m in Africa alone The spread is accelerating in India, Russia, the Caribbean and China AIDS is stretching health care systems beyond their limits







There are 12m AIDS orphans – they are estimated to rise to 40m by 2010 In Sub-Saharan Africa, 58% of HIV/AIDS infected adults are women. More than two-thirds of newly infected teenagers are female. Life expectancy has declined by more than 10 years in South Africa and Botswana – Swaziland faces the risk of extinction

MOT:  Sexual intercourse (oral, vaginal and anal)  Exposure to contaminated blood, semen, breast milk and other body fluids  Blood Transfusion  IV drug use  Transplacental  Needlestick injuries

HIGH RISK GROUP  Homosexual or bisexual  Intravenous drug users  BT recipients before 1985  Sexual contact with HIV+  Babies of mothers who are HIV+

s/sx: 1. Acute viral illness (1 mo after initial exposure) – fever, malaise, lymphadenopathy 2. Clinical latency – 8 yrs w/ no sx; towards end, bacterial and skin infections and constitutonal sx – AIDS related complex; CD4 counts 400-200 3. AIDS – 2 yrs; CD4 T lymphocyte < 200 w/ (+) ELISA or Western Blot and opportunistic infections

How to Diagnose 





HIV+ 2 consecutive positive ELISA and 1 positive Western Blot Test AIDS+ HIV+ CD4+ count below 500/ml Exhibits one or more of the ff: (next slide) Full blown AIDS CD4 is less than 200/ml

Exhibits one or more of the ff:              

Extreme fatigue Intermittent fever Night sweats Chills Lymphadenopathy Enlarged spleen Anorexia Weight loss Severe diarrhea Apathy and depression PTB Kaposis sarcoma Pneumocystis carinii AIDS dementia

Kaposis

Treatment Anti-retroviral Therapy (ART) – ziduvirine a. Prolong life b. Reduce risk of opportunistic infection c. Prolong incubation period



PREVENTION A – ABSTINENCE B – BE FAITHFUL C – CONDOMS D – DON’T USE DRUGS

Integrated Management of Childhood Diseases

Dr. Salvador



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

Dr. Salvador

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

Dr. Salvador

 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

Dr. Salvador

Dr. Salvador

Dr. Salvador

Dr. Salvador

Dr. Salvador

Dr. Salvador

Dr. Salvador

Dr. Salvador

Dr. Salvador

Dr. Salvador

Dr. Salvador

Dr. Salvador

IMMUNOLOGY

What is immunity? “Protection” from infection, tumors, etc.  Innate immunity is always available  Adaptive immunity distinguishes “self” from “non-self” and involves immune system “education”  Responses that may result in host tissue damage 

Terms to define: 





 

Immunity-refers to the body’s specific protective response to an invading foreign agent or organism Immunopathology - refers to study of diseases resulting from dysfunctions within the immune system Antibody-a protein substance developed by the body in response to and interacting with a specific antigen Antigen- substance that induced the production of antibody B-cells-cells that are important in producing circulating antibody

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

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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

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



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Memory cells- cells that are responsible recognizing antigens from previous exposure and mounting an immune response Natural killer cells- lymphocytes that defends against microorganism and malignant cells Stem cells- precursors of all blood cells, reside primarily on bone marrow Suppressor T-cells-lympocytes that decrease B cells activity to a level at w/c the immune system is compatible with life

Two types of immunity 

Innate immunity (not antigen-specific)  Anatomical

barriers

 Mechanical  Biochemical  



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

Adaptive immunity (antigen-specific)  Receptor-driven  Pre-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

platelets

Cells eosinophil megakaryocyte T Lymphocyte involved Pluripotent hematopoietic in neutrophil stem cell B Lymphocyte immunit y common basophil

mast cell

common myeloid progenito r

lymphoid progenit or plasma cell Natural Killer cell

monocyte macrophage

Blood

Serum Proteins

•Immunoglobulins •Complement •Clotting factors •Many others

Where is that stuff? Serum or Plasma

Leukocytes, Platelets and RBC

Mononuclea r Cells

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

Polymorphonucle ar leukocytes (or Granulocytes) •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     



Lower 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 (<10µ in diameter) reach alveoli

Alveoli 

Alveolar macrophage rapidly phagocytize small particles

Alimentary Tract 

General defense mechanisms    



Stomach 



Generally sterile due to low pH

Small Intestine  



Mucous secretions Integrity of of mucosal epithelium Peristaltic motions of the gut propel contents downward Secretory antibody and phagocytic cells

Upper portion contains few bacteria As distal end of ileum is reached flora increases

Colon  

Enormous numbers of microorganisms 50-60% of fecal dry weight is bacteria

Genitourinary Tract 

Male  No

bacteria above urethrovesicular junction  Frequent flushing action of urine  Bactericidal substances from prostatic fluid  pH of urine  Bladder mucosal cells may be phagocytic  Urinary sIgA 

Female (Vagina)  Large

microbial population (lactobacilli)  Microorganisms produce low pH due to breakdown of glycogen produced by mucosal cells

Receptors 

Almost all of biology occurs because recognition  Enzymatic

action  Interactions between cells (cooperation/activation)  Communication between cells 

Innate and adaptive immunity requires it

Characteristics of Adaptive Immunity 

Immune response is highly specific for the antigen that triggered it. 



Receptors on surface of immune cells have same specificity as the antibody/effector activity that will be generated

Exposure to antigen creates an immunologic “memory.”  

Due to clonal expansion and creation of a large pool of cells committed to that antigen Subsequent exposure to the same antigen results in a rapid and vigorous response

Natural Immunity Present at birth  Provides a non specific response to any foreign invader, regardless of the invader’s composition.  Basis is ability to distinguish between “self and non-self” 

Physical  Skin and intact mucous membranes  Cilia and coughing, sneezing Chemical  Acidic secretions, mucus, sweat, saliva and tears

WBC  Participate in both natural and acquired  Fight invasion by foreign body or toxins Neutrophils – 1st cell to arrived at the site of inflammation Eosinophils and basophils – increase in stress and allergic reaction Monocytes – “phagocytic cells” Lymphocytes – major role in humoral and cell mediated immune response

Acquired Immunity Develops as a result of prior exposure to an antigen through immunization and by contracting a disease  Active acquired – immune defense are developed by the person’s own body. Last for lifetime 

Passive Acquired - temporary immunity from another source that has developed immunity through previous disease or immunization - used in emergencies to provide immunity in disease when the risk is high



Response to Invasion 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  



IL-6 





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

IL-12 



Induces B-cell terminal maturation into Ig-producing plasma cells

IL-8 



activates vascular endothelium and lymphocytes Increases adhesiveness of leukocytes

Activates NK cells and induces Th1-cell differentiation

IL-18 TNF-α 

Activates vascular endothelium and increases vascular permeability, leading to accumulation of Ig and complement in infected tissues

Immune Cells and Innate Immunity 

Phagocytes   



Neutrophils Moncyte/macrophage Eosinophils (to a lesser extent)

NK cells (large granular lymphocytes)  

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



Act against intracellular pathogens   



Lysis of target cells Production of cytokines (IFN-γ and TNF-α ) Herpesviruses Leishmania Listeria monocytogenes

Act against protozoa  

Toxoplasma Trypanasoma

Biological Consequences of Antibody Affinity/Avidity     

Neutralization of toxins Complement activation Immune elimination of antigen Virus neutralization More intense immune complex disease in animals  higher levels of circulating antigen-antibody complexes  more intense localization of immune complexes on basement membranes.  more severe impairment of organ function

Complement activation 

A system of plasma proteins that interact with  Antigen/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 bronchioles 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

IgG

Activity

Lymph. Trans. IgE Time

Clinical Tests for Allergy 

Skin Tests  Immediate

Response (wheal & flare reaction; 20 min)  increased vascular permeability  local edema  itching  Late Reactions (5-24 hr) 

RAST (Radio Allergo Sorbent Test)

Cytotoxic Hypersensitivity (Type II)

Characteristics of Cytotoxic Hypersensitivity Directed against cell surface or tissue antigen  Characterized by complement cascade activation and various effector cells 

Complement 





Formation of membrane attack complex (lytic enzymes) Activated C3 forms opsonin recognized by phagocytes Formation of chemotactic factors  Effector cells possess Fc and complement receptors macrophages/monocytes  neutrophils  NK cells 

Examples of Type II Hypersensitivity        

Blood transfusion reactions Hemolytic disease of the newborn (Rh disease) Autoimmune hemolytic anemias Drug reactions Drug-induced loss of self-tolerance Hyperacute graft rejection Myasthenia gravis (acetylcholine receptor) Sensitivity to tissue antigens

Toxic Complex Hypersensitivity (Type III)

Diseases associated with immune complexes 

Persistent infection  microbial

antigens  deposition of immune complexes in kidneys 

Autoimmunity  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

activation

anaphylatoxins Chemotactic

 Neutrophils difficult

factors

attracted

to 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  help cytotoxic T-cells become killer cells, which cause tissue damage

Types of Delayed Hypersensitivity Delayed Reaction Jones-Mote Contact tuberculin granulomatous

maximal reaction time 24 hours 48-72 hours 48-72 hours at least 14 days

Contact Hypersensitivity   

Usually maximal at 48 hours Predominantly an epidermal reaction Langerhans cells are the antigen presenting cells 

a dendritic antigen presenting cell  carry antigen to lymph nodes draining skin 

Associated with hapten-induced eczema       

nickel salts in jewellry picryl chloride acrylates p-Phenylene diamine in hair dyes chromates chemicals in rubber poison ivy (urushiol)

Poison Ivy contact dermatitis

Tuberculin Hypersensitivity   



Maximum at 48-72 hours Inflitration of lesion with mononuclear cells First described as a reaction to the lipoprotein antigen of tubercle bacillus Responsible for lesions associated with bacterial allergy  cavitation,



caseation, general toxemia seen in TB

May progress to granulomatous reaction in unresolved infection

Granulomatous Hypersensitivity 

   

Clinically, the most important form of DTH, since it causes many of the pathological effects in diseases which involve T cell-mediated immunity Maximal at 14 days Continual release of cytokines Leads to accumulation of large numbers of macrophages Granulomas can also arise from persistence of “indigestible” antigen such as talc (absence of lymphocytes in lesion)

Epitheloid Cell Granuloma Formation Large flattened cells with increased endoplasmic reticulum  Multinucleate giant cells with little ER  May see necrosis  Damage due to killer T-cells recognizing antigen-coated macrophages, cytokine-activated macrophages  Attempt by the body to wall-off site of persistent infection 

Examples of Microbial-Induced DTH Viruses (destructive skin rashes)   



Fungi    



smallpox measles herpes simplex 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)   



Septicemia - Septic Shock 





primarily due to lipopolysaccharide

Adult respiratory distress syndrome 



hypotension, hypoxia, oliguria and microvascular abnormalities excessive release of TNF, IL-1, IL-6 intravascular activation of complement

overwhelming accumulation of neutrophils in lung

Platelet aggregation/adherence to macrophages by gram-positive bacteria Superantigens  

Gram positive enterotoxins react directly with T-cell receptors and induce massive cytokine release

Medical –Surgical nursing Auto-Immune disorders

Common Autoimmune disorders  1.

SLE  2. Stevens-Johnson Syndrome

Systemic Lupus Erythematosus 

A chronic connective tissue disease involving multiple organ systems occurring most frequently in women



A condition resulting from an 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: 

1.

Sulfonamides, butazones, other antibiotics and anti-seizure drugs

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

Men

Breast

Prostate

Lung

Lung

Colon and Rectum

Colon and rectum

Uterine

Urinary Bladder

Non-Hodgkin’s Lymphoma

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 DNA repair Bind to DNA

Permanent DNA damage

PROMOTION

Cell Proliferation

NEOPLASTIC CELLS

Normal Cell

Cell Death

 -

Progression Third step of cellular carcinogenesis The cellular changes formed during initiation and promotion now exhibit increased malignant behavior

Etiologic Factors 1.  

  

Viruses Oncogenic viruses Epstein Bar virus, burkitt’s lymphoma, nasopharyngeal Ca, non-Hodgkin and hodgkin’s lymphoma Herpes simplex Type II, cytomegalovirus and HPV type 16,18,31,33, Cervix Ca HIV, kaposi sarcoma H. pylori, gastric Ca

2. Physical Agents - Ultraviolent rays, especially in fair skinned blue or green eyed people, skin Ca - Radiation from x-ray or nuclear, leukemia, multiple myeloma, Ca of lung, bone, breast and thyroid 3. Hormones Oral contraception or HRT, Inc. incidence of hepatocellular, endometrial and breast Ca

4. Chemical Agents - 75% related to environment - Tobacco smoking, single most lethal carcinogen, 30% of Ca deaths, lung, head and neck esophagus, bladder panceas, cervix ca - chewing tobacco, ca of the oral cavity in men younger than 40 years old

5. Industrial compounds - Vinyl chloride (plastics, asbestos) - Polycyclic aromatic hydrocarbons (burning, auto and truck emission) - Fertilizers and weed killers - Dyes, (aniline dyes, hair dyes)

6. Dietary Factors - Carcinogenic fats, alcohol, salt cured or smoked meats, high caloric content - Proactive high fiber, Cruciferous vegetables ( cabbage, broccoli, cauliflower, brussels, sprouts) Carotenoids (carrots, tomatoes, spinach, apricots, peaches, dark green and yellow vegetables), vit E, C, zinc and selenium

7. Genetics - Oncogenes ( hidden/repressed genetic code for Ca that exist in all individual 8. Age: Advancing age is a significant risk factors 9. Immunologic Factors a. Immunosuppressed individuals more susceptible to cancer

What Do These Factors Have In Common? 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 cytotoxic abilities Lymphokines, capable of killing and damaging Ca cells Macrophages, disrupt Ca cells B lymphocytes antibodies, defends the body against malignant cells Natural killer cells, directly destroy Ca

American Ca Society recommendation Site

Gender

Breast

Female

Age

Evaluation Frequency

20-39

CBE, BSE

Q 3 yrs Q month

>40

CBE BSE

Q year Q month

Mammogr Q year am

Colon/rectum

M/F

>50y/o

Fecal occult blood

and

Q year

Flexible Q 5 years sigmoidoscop y

or

Colonoscopy Q 10 years

or

Double conrast barrium enema

Q 5 years

Prostate

M

>50 or < 50 if PSA and DRE Q year high risk

Cervix

F

>18 or younger if sexually active

Pap smear Pelvic exam

Q year

Cancer related check up

M/F

>20-39 >40

Other Ca types

Q 3 years Q year

Characteristics of Ca Characteristic

Benign

malignant

Cell characteristic

Well differentiated Undifferentiated little Resemble normal cells resemblance on normal cells

Mode of growth

Grows by expansion Not infiltrate the surrounding tissue

Grows at the periphery, infiltrate and destroys the surrounding tissue

Rate of growth

slow

Variable, fast

Metastasis

none

Access to blood, lymphatics and other areas

benign

Malignant

General effects

localized

Anemia, weaness, weight loss

Tissue destruction

No tissue damage

Extensive tissue damage

Ability to cause death

Does not usually cause Usually causes death death

Metastasis Lymphatics the most common mechanism breast tumors, axillary, clavicular, and thoracic LN  Hematogenous disseminated through the blood stream related to the vascularity of the tumor  Angiogenesis – ability to induce the growth of new capillaries from the host tissue to meet the nutrients and oxygen 

Classification and staging Tissue of Origin 2. 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

Hepatocellular, gastric, pancreatic, colon and lung cancer

HCG

Trophoblastic tumor, germ cell, ovary

Acid phosphatase

Prostate cancer

CA 125

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 thrombosis, Embolus, Thrombophlebitis  Tumors tends to produce abnormal coagulation factors 

Paraneoplastic Syndrome  Anemia - Ca cells produces chemicals that interfere with rbc production - Iron uptake is greater in the tumor than that deposited in the liver - Blood loss from bleeding  Hypercalcemia - Increases and accelerates bone breakdown and release of Calcium 

 -

Anorexia – Cachexia Syndrome Final outcome of unrestrained Ca growth Ca deprived normal cells nutrition Protein depletion, serum albumin decreases Tumors take up Na Act in the satiety center causing anorexia Taste sensation diminishes

      

Take pain seriously, recognizing that only the person in pain knows how it feels. Provide information and resources for pain control. Communicate with genuineness, accurate empathy, and nonpossessive warmth. Encourage sufferers to share their feelings and network with other survivors. Respect culture norms and wishes of sufferers, maximizing their control Encourage release of energy through 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,URT - provides the pathologist the cells and the entire tissue - decreases the chance of seeding the tumor 

Incisional Biopsy - used if the tumor mass is too large to be removed - a wedge of tissue from the tumor is taken  Needle Biopsy - done on suspicious masses that are easily accessible - fast, inexpensive and easily performed 

Surgery as primary treatment Remove the entire tumor or as much as is feasible 1. Local excision - if the mass is small 2. Wide or Radical Excision - removal of the primary tumor, LN, adjacent and surrounding tissue - results in disfigurement and altered function 3. Salvage surgery 

Prophylactic Surgery - Removal of non-vital structures that are likely to develop Ca  Palliative Surgery - when cure is not possible, the goal of treatment is to make the patient as comfortable as possible and to promote a satisfying and productive life for as long as possible

Radiation Therapy Used to control malignant disease when a tumor cannot be removed surgically  To relieve the symptoms of metastatic disease, especially when the Ca spread to the brain, bone.  A radiosensitive tumor is one that can be destroyed by a dose of radiation that still allows for cell regeneration in the normal tissue 

Radiation Therapy Uses ionizing radiation to kill or limit the growth of cancer cells. May be internal or external  Effect cannot be limited to cancer cells only 



is a cancer treatment that uses high doses of radiation to kill cancer cells and stop them from spreading. At low doses, radiation is used as an x-ray to see inside your body and take pictures, such as x-rays of your teeth or broken bones.



Radiation use in cancer treatment works in much the same way, except that it is given at higher doses.



Radiation therapy is used to:



Treat cancer. Radiation can be used to cure, stop, or slow the growth of cancer.



Reduce symptoms. When a cure is not possible, radiation may be used to shrink cancer tumors in order to reduce pressure. Radiation therapy used in this way can treat problems such as pain, or it can prevent problems such as blindness or loss of bowel and bladder control.

Cells are most vulnerable to radiation during DNA synthesis and mitosis  Most sensitive are those body tissue that undergo frequent cell division. (BM, Lymphatic, GIT, gonads)  Tumors that are well oxygenated are more sensitive to radiation 

Radiosensitivity Highly sensitive - ovaries, testes, bone marrow, blood, intestines



Low sensitivity - muscle, brain, spinal cord



Types a. Teletherapy (External Beam) - x-rays are used to destroy cancerous cells at the skin surface or deeper b. Used more commonly c. Client is not radioactive during treatment d. Simulation – X-ray or Ct planning session to identify the field which delivers maximum radiation to the tumor and minimal to normal tissue. Involves skin markings e. Administered in fractions of the full dose, 5 days a week for 4-6 weeks

b. Brachytherapy (Internal) - used primarily in the head and neck, gynecologic, prostate cancer - delivers a high dose of radiation in a local area using implants - Client is radioactive only when implant is in placed - plan cares efficiently to minimize nurses, exposure to implant, use shielding, wear a film badge and maintain safe distance.

-

Pregnant nurses should not care for clients with implanted radiation Pickup dislodge implants with long forceps placed in a special container. Body fluids of clients treated with systemic radioactive iodine are radioactive; fluids of client with implants are not

Radiation Dosage 

The lethal tumor dose is defined as the dose that will eradicate 95% of the tumor yet preserve normal tissue

Adverse Reaction Seen only in the organs in the radiation field, except for systemic effects of nausea, anorexia and fatigue  Skin reactions are common and expected with external beam 

Toxicity Localized to the area being irradiated  Alteration in oral mucosa, stomatitis, xerostomia, change and loss of taste, decreased salivation  Altered skin integrity, alopecia, erythema, shedding, desquamation  Thrombocytopenia  Anemia 

Radiation Safety Distance - the greater the distance the lesser the exposure  Time - the less time spent close to radiation the less exposure (max of 30 min per shift)  Shielding - use lead aprons and gloves  Standards - kept as low as reasonably achievable  Monitoring device - film badge (measure the whole exposure of the nurse) 

Side Effects a. 2. 3. 4. 5.

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 hygiene  Monitor electrolytes, Na,K,Cl 

d. Anemia. Leukopenia, thrombocytopenia Isolate patient  provide frequent rest period  Encourage high protein diet  Assess for bleeding  Monitor lab results CBC, WBC, Plt 

Chemotherapy Systemic treatment with chemicals which destroy rapidly proliferating cells  Used for cure in testicular, Hodgkin disease, ALL, neuroblastoma, Wilms and Burkitt’s lymphoma  Used to control breast, nod-Hodgkin, small cell lung and ovarian cancer  Used palliative for relief of pain, obstruction and to improve comfort 



What does chemotherapy do?



Cure cancer - when chemotherapy destroys cancer cells to the point that your doctor can no longer detect them in your body and they will not grow back.



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



Ease cancer symptoms (also called palliative care) when chemotherapy shrinks tumors that are causing pain or pressure.

Chemotherapy Chemotherapy works by stopping or slowing the growth of cancer cells, which grow and divide quickly. But it can also harm healthy cells that divide quickly, such as those that line your mouth and intestines or cause your hair to grow. Damage to healthy cells may cause side effects. Often, side effects get better or go away after chemotherapy is over.



Sometimes, chemotherapy is used as the only cancer treatment. But more often, you will get chemotherapy along with surgery, radiation therapy, or biological therapy. Chemotherapy can:



Make a tumor smaller before surgery or radiation therapy. This is called neo-adjuvant chemotherapy.



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



Help radiation therapy and biological therapy work better.



Destroy cancer cells that have come back (recurrent cancer) or spread to other parts of your body ( metastatic cancer).

Cell Cycle 

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 GI System 1. Nausea and vomitting - administer anti-emetics - NPO 4-6 hrs before chemotherapy - bland diet foods in small amounts after treatment

a.

Diarrhea  Stomatitis - Good oral hygiene - rinse with viscous lidocaine before meals - rinse with plain water or hydrogen peroxide after meals - apply water soluble lubricants - Suck popsicle to provide moisture 

Hematologic (Myelosuppression) 1. Thrombocytopenia - Avoid bumps or bruishing - protect client from physical injury - Avoid aspirin - Avoid IM injections - Assess for bleeding tendencies



b. Leukopenia - use careful handwashing - reverse isolation if WBC <1000 - assess for signs of respiratory infection - Avoid crowds c. Anemia - Provide adequate rest periods - monitor CBC - Administer o2 PRN

Integumentary System – Alopecia - Explain hair loss is not permanent - Support and encouragement



- Advise client to obtain wig  Renal system - may cause direct damage to kidneys by excreting metabolites. - encourage fluids and frequent voiding

- increased excretion of uric acid may damage kidneys - Administer allopurinol, Inc. OFI  Reproductive System 1. Infertility and mutagenic damage to chromosomes 2. Banking sperm 3. Use contraception

Side Effects from Radiation and Chemo Therapy            

Neurologic/Sensory/Perceptual Meningeal irritation CN and peripheral neuropathy Cerebellar toxicity Ototoxicity Cardiac Pericardial Effusion Arrhythmias CHF Pulmonary Pleural Effusion Pneumonitis

GIT  Stomatitis  Esophagitis  Pharyngitis  Taste alteration  Anorexia  Nausea and vomiting  Constipation and diarrhea  Weight loss 

GUT  Nephrotoxicity  Hemorrhagic cystitis  Hyperuricemia  Urine color changes 

Reproductive  Loss of libido  Impotence  Amenorrhea  Irregular menses  Menopausal symptoms  Azoospermia  Sterility  Gynecomastia 

       

 

Hepatic Hepatotoxicity Integumentary Alopecia Dermatitis and ulcers Hematopoietic ↓ bone marrow activity anemia, prone to infection and bleeding tendency Metabolic TLS and Hyperkalemia

Perceived Change in Body Image Obvious reminder of disability  need for prosthesis (breast, leg and eye)  need for hardware (wheel chair, crutches)  need for medication (CR therapy)  extent of disability or limitation 

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

Terminally Ill 50% die from the disease  time from diagnosis to death ranges from weeks- years  not all clients become terminally ill  others die during initial treatment; others die from complications of treatment  Endpoint: no response to treatment and progressions cannot be controlled 

HOSPICE CARE standard of care for terminally ill cancer clients  symptom control  pain management  providing comfort and dignity  24 hour – 7 day coverage  services given are based on client’s need not on its ability to pay 

One can suffer without physical pain and one can have physical pain and not necessarily suffer.  The founder of the modern hospice movement described suffering as “total pain,” an experience of changing selfperception, fear of physical distress and dying, concerns about relationships, changing self-perception, and memory of other person’s suffering ( 

Ethical Issues caring can be just successful as curing; when curing is not an option  care is exercised during the final stage of life 

Goals of Intervention to care without functional and structural impairment  if cure is not possible goals must = prevent further metastasis = relieve symptoms = maintain high quality of life 

Bone Marrow Transplant Used in the treatment of leukemia for clients who have closely matched donors and experiencing temporary remission with chemotherapy  Severe aplastic anemia, breast Ca, brain Ca 

Types Autologous - own bone marrow, most common type  Allogenic - transplant from a genetically non-identical donor - sibbling most common type 

procedure 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 b. Maintain protective environment c. Administer antibiotics d. 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 patient’s preferences Provide small frequent meals Avoids giving fluids while eating Oral hygiene PRIOR to mealtime Vitamin supplements

Nursing Intervention RELIEVE PAIN  Mild pain- NSAIDS Moderate pain- Weak opiods  Severe pain- Morphine  Administer analgesics round the clock with additional dose for breakthrough pain 

Nursing Intervention DECREASE FATIGUE  Plan daily activities to allow alternating rest periods  Light exercise is encouraged  Small frequent meals 

Nursing Intervention IMPROVE BODY IMAGE  Therapeutic communication is essential  Encourage independence in self-care and decision making  Offer cosmetic material like make-up and wigs 

Nursing Intervention ASSIST IN THE GRIEVING PROCESS  Some cancers are curable  Grieving can be due to loss of health, income, sexuality, and body image  Answer and clarify information about cancer and treatment options  Identify resource people  Refer to support groups 

Nursing Intervention        

MANAGE COMPLICATION: INFECTION Fever is the most important sign (38.3) Administer prescribed antibiotics X 2weeks Maintain aseptic technique Avoid exposure to crowds Avoid giving fresh fruits and veggie Handwashing Avoid frequent invasive procedures

Nursing Intervention MANAGE COMPLICATION: Septic shock  Monitor VS, BP, temp  Administer IV antibiotics  Administer supplemental O2 

Nursing Intervention MANAGE COMPLICATION: Bleeding  Thrombocytopenia (<100,000) is the most common cause  <20, 000 spontaneous bleeding  Use soft toothbrush  Use electric razor  Avoid frequent IM, IV, rectal and catheterization  Soft foods and stool softeners 

Colon cancer

Adenocarcinoma is the most common type  Metastasis is common to the liver  2nd most common site for cancer in men and women  Ages >50-60  May be caused by diverticulitis, chronic ulcerative colitis, familial polyposis 

Cancer sites Sigmoid colon – 33%  Rectum – 27%  Ascending Colon – 22%  Transverse colon – 11%  Descending colon 6% 

Metastatic sites 1. 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 PATHOPHYSIOLOGY  Benign neoplasm DNA alteration malignant transformation malignant neoplasm  cancer growth and invasion  metastasis (liver) 

COLON CANCER 

    

ASSESSMENT FINDINGS 1. Change in bowel habits- Most common 2. Blood in the stool 3. Anemia 4. Anorexia and weight loss 5. Fatigue 6. Rectal lesions- tenesmus, alternating D and C

Right sided lesions - dull abdominal pain, melena Left sided lesions - signs of obstruction and bright red stool Rectal lesion - tenesmus, rectal pain. Incomplete BM., bloody stool, constipation 

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

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

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

Colon cancer SURGICAL MANAGEMENT  Surgery is the primary treatment  Based on location and tumor size  Resection, anastomosis, and colostomy (temporary or permanent) 

Right hemicolectomy – primary surgery for cancer of the ascending colon - removal of the terminal ileum, cecum, right transverse colon



Left hemicolectomy – primary surgery for cancer of descending and sigmoid colon - removal of the distal transverse, descending and sigmoid colon



Colostomy 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 ¼ full (Brunner)  ½ to 1/3 full (Kozier)

Breast Cancer The most common cancer in FEMALES  Numerous etiologies implicated 

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

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

Breast Cancer PROTECTIVE FACTORS  1. Exercise  2. Breast feeding  3. Pregnancy before 30 yo

BREAST EXAMINATION



CLINICAL BREAST EXAMINATION

SELF BREAST EXAMINATION

Stages I and 2 are 70-90% curable  Invasive or infiltrating, capable of metastasis a. Ductal – 70% b. Lobular – 10 % higher incidence of contralateral breast cancer 

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

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

Breast Cancer Breast cancer Staging  TNM staging  I - < 2cm  II - 2 to 5 cm, (+) LN  III - > 5 cm, (+) LN  IV- metastasis 

Metastatic sites Bone  Liver  Lung  Brain 

Treatment Surgical management is the primary treatment for breast cancer  Breast conservation (lumpectomy, segmental resection) - removal of the cancer with margin of healthy tissue - If followed by radiation therapy has equivalent 5 year survival to mastectomy 

1. 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 asymptomatic until late in the course  s/sx depends on the location and size of the tumor, degree of obstruction and metastasis 

Cough or chronic cough - dry, persistent without sputum production  Wheezing  Hemoptysis or blood tinged sputum  Chest and shoulder pain 

Common sites of metastasis LN  Bone  Brain  Contralateral lung  Adrenal glands  Liver 



Screening test: No screening program currently exist.

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

Diagnostics Chest xray (solitary peripheral nodule, coin lesion)  Ct scan of the chest  Fiberoptic bronchoscopy  Fine needle biopsy under ct scan 

Surgical Management  

  

Dependent on whether the tumor is resectable May be cure for non small cell if no metastasis occurred and lung function is sufficient on removal of all or part of the lungs (50%) Lobectomy – removal of lobe (common) Pneumonectomy – removal of the lung Segmentectomy – partial removal of the lung lobe

Adjuvant therapy Chemotherapy is the primary treatment for small cell  Radiation is standard post op for advanced non-small cell 

Radiation therapy – for localized intrathoracic lung ca and palliation for hemoptysis, obstruction dysphagia and pain  Chemotherapy  Immunotherapy 

Nursing Intervention Assess for signs of superior vena cava syndrome  Postlobectomy, manage chest tube  Assess respiration and for presence of pneumothorax or atelectasis  Position properly post-op 1. Lobectomy – avoid prolonged lying on the operative site 2. Pneumonectomy – position on the back or operative side only 

Instruct the client on deep breathing, coughing and ambulation  Pain management to promote deep breathing  Refer client to smoking cessation 

Prostate Cancer a slow growing malignancy of the prostate gland  Usually an adenocarcinoma  This usualy spread via blood stream to the vertebrae  2nd most common cause of cancer deaths 

190000 new cases each year and 30,000 deaths annually  Over 80% are diagnosed in early stages. Allowing an almost 100% 5 year survival rate.  Overall for all stages survival is 96% 

Prostate Cancer 

Predisposing factor  Age  Strong

family history  High fat diet may play a role  Having a vasectomy may play a role

Prostate Cancer  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. Prostate specific antigen (PSA) 3. Elevated SERUM ACID PHOSPHATASE indicates SPREAD or Metastasis 

Surgical Management Radical prostatectomy – removal of prostate, capsule, ejaculatory ducts, seminal vesicles plus lymphnodes  Watchful waiting without intervention may be appropriate in men over 70 years of age with small, early stage cancers 

Prostate Cancer Medical and surgical management 1. Prostatectomy 2. TURP 3. Chemotherapy: hormonal therapy to slow the rate of tumor growth 4. Radiation therapy

Prostate Cancer Nursing Interventions 1. Prepare patient for chemotherapy 2. Prepare for surgery

Prostate Cancer Nursing Interventions: Post-prostatectomy 1. Maintain continuous bladder irrigation. Note that drainage is pink tinged w/in 24 hours 2. Monitor urine for the presence of blood clots and hemorrhage 3. Ambulate the patient as soon as urine begins to clear in color

4. Provide for bladder retraining after foley catheter removal a. Perineal exercises b. restrict caffeine c. limit fluid intake at night 5. Education a. Avoid lifting, straining, and prolonged travel b. possible impotence

Bladder Cancer Transitional cell carcinoma – most common (90-95%)  Approximately 54300 new cases and 12400 deaths  No screening for early detection 

Risk factors  



Smoking Occupational exposures Caucasian males >50 years old

Asessment Gross, painless hematuria  Dysuria  Urinary frequency  Urgency  Urinary hesitancy  Suprapubic, rectum, back pain 

Diagnostic       

Urinary cytology – late morning or early afternoon Bladder washing more reliable Flow cytometry – examine DNA content of urine cells IVP – evaluate upper urinary tracts Cystoscopy – tumor visualization and biopsy CT scan, transurethral ultrasound, MRI Tumor marker – p53 and epidermal growth factor in late stage

Surgical management Transurethral resection and fulguration (Destruction of surrounding tissue with electricity) most common for low grade Ca  Radical cystectomy (bladder, prostate, seminal vesicles, urethra, ovary, FT are removed) for high grade tumors 

Adjuvant therapy Radiation therapy – used in invasive cancer  Chemotherapy – cisplatin, methotrexate, vincristine 

Nursing interventions 







Instruct on preop low residue and clear liquid diet Assess for urinary stoma and teach maintainance of ileal conduit and appliance Assess urinary output (should produce urine immediately) for infection and signs of peritonitis Discuss possible sexual dysfunction

Kidney Cancer Renal cell , most common 85%  Poor prognostic indicators a. LN involvement b. invasion of renal capsule c. metastasis 

Risk factors Male gender  Hispanic  Over 55 years old  Cigarette smoking  Occupational exposure, asbestos, lead  Heavy use of aspirin 

Metastatic sites Spread through venous and lymphatic route to lungs, bone and liver  Direct extension of the renal vein  5 year survival is less than 10% for stage 4  30-50% are diagnosed late with metastasis 

assessment   

Gross hematuria Dull aching pain Abdominal mass

Diagnostics - MRI, CT, IVP

Surgical management 

 

Radical nephrectomy and renal hilar LN dissection Radiation Chemotherapy, cisplatin, vinblastine, methotrexate

Nursing intervention Atelectasis and pneumonia prevention (nephrectomy close to diaphragm)  Assess for signs of hemorrhage  Monitor urine output and renal function of remaining kidney  Pain management  Assessment and prevention of paralytic ileus 

Skin cancer



Malignant lesion of the skin, which may or may not metastasized

Types a. Basal cell – most common type arising from the basal cells contained in the epidermis

b. Squamous Cell – 2nd most common type in whites.tumor of the keratinocytes Metastasized to the LN and fatal c. Malignant melanoma – can metastasized to the brain, lung, bone, skin. Fatal

SKIN CANCER Causes: UV light exposure, chronic irritation and friction  Dx: skin biopsy  S/sx: change in color, size, shape of lesion 

 

  

Monitor lesions that do not heal Removed moles or lesions that are subject to chronic irritations Avoid contact with chemical irritants Use sun screen lotions and clothing Avoid sun exposure between 11am-3pm

Contact Dermatitis Inflammatory response after contact with a specific antigen Assessment: a. Pruritus and burning b. Edema c. Erythema at the point of contact d. Signs of infection e. Vesicles with drainage 

Gastric Cancer Approximately 22000 cancers and 13,000 deaths per year  African americans, japanese, chinese and US have higher incidence  95% are adenocarcinomas  Prognosis is poor, 5 year survival rate is 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 person’s only Barium x-ray or endoscopy

Assessment        

Early manifestations are non-specific Upper epigastrium, retrosternal pain Uneasy sense of fullness after meals Loss of appetite Nausea and vomiting Weakness Fatigue anemia

Diagnostic procedure EGD  Biopsy  Endoscopic ultrasound  Double contrast upper GI series  CT scan 

Surgical management Only treatment that is potentially curative  Total gastrectomy  Radical subtotal gastrectomy a. Billroth I b. Billroth II  Proximal subtotal gastrectomy  Paliation of symptoms 

Adjuvant therapy External beam radiation for control of unresectable tumors, palliation and increased survival.  Chemotherapy has little impact – 5 FU, doxorubicin, mitomycin 

Nursing Intervention Goal is control of clinical manifestation and supporting optimal functioning  Assess the nutritional status - small frequent feeding low carbohydrate, high fat, high protein. - restrict fluids 30 minutes after meals reducing risk of dumping syndrome 

Postoperative    

  

Respiratory status: reflux aspiration Infection Pain – potential anastomotic leak obstruction Bezoar (food clumping) formation causing gastric outlet obstruction Bleeding Dumping syndrome anemia

Cancer of the esophagus >3x more common in men  Occurs in the fifth decade of life  Chronic irritation, ingestion of alcohol and tobacco use  GERD and Barret’s Esophagus  Usually squamous cell epidermoid type 

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

Head and neck cancers     

71,000 new cases and 19,000 deaths 40% are found in the oral cavity but may be found in the larynx, oropharynx, nasal cavity and salivary glands 95% are squamous cell carcinoma 5 year survival for early stage is 95% and late stage less than 50% Most will present with advanced disease due to substance abuse

Risk factors Male over 50 years old  Tobacco use (major cause)  Heavy alcohol use (combine with tobacco 95%)  Poor oral hygiene 

Metastatic sites Neck lymph nodes (common)  Local and regional spread within the head and neck  Distance metastasis is rare 

Screening No screening guidelines exists  High risk clients should have through head and neck examinations and referral to smoking and alcohol cessation programs 

Assessment Depends on the location  Throat pain  Persistent hoarseness  Painless mass  Pain  White or red spots in the oral cavity  Nasal stuffiness 

Diagnostic studies Thorough physical examination of neck and oral cavity  Fiberoptic nasopharyngoscopy  Direct laryngoscopy  X-rays, barrium swallow MRI, CT  biopsy 

Surgical management Surgery and radiation is the primary treatment  Reconstructive surgery may be needed  Radiation and chemotherapy may be used to debulk unresectable tumors 

Adjuvant therapy 

  a. b.

Radiation is the primary treatment for nasopharynx tumors Brachytherapy in oral cavity Chemotherapy is used for: Recurrent and metastatic tumors Making tumor more sensitive to radiation

Nursing interventions Primary role is assisting clients in coping with issues of dysfunction, losses and body image changes  Monitor for delirium tremens in client with alcohol abuse  Airway management a. tracheostomy b. humidity c. suctioning d. stoma care 

Provide oral care with saline or peroxide solution. (avoid mouthwashes that are drying to mucosa)  Assess ability to swallow and ensure safety when eating 

Central Nervous System cancers 17,000 primary brain tumors  >100,000 metastatic  Progmosis depends on type and location but generally poor  Risk factor very little known 

metastasis Distance metastasis is rare  Possibly lung or bone may occur  Spinal tumor usually do not metastasize 



No screening programs exist

assessment 

    

Vary greatly depending on the location, may be related to the displacement of the brain, increase ICP, spinal cord compression Change in LOC Headache Pupil changes or papilledema Motor or sensory deficits Weakness (spinal cord tumors)

Vomiting  Seizures  Vital sign changes  Pain – most common clinical manifestation in spinal cord tumors  Bowel or bladder dystfunction 

diagnostics CT, MRI  Position emission tomography  Cerebral angiography  Lumbar puncture 

Surgical management   

1. 2. 3.

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 biopsied or removed – most common

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 

Pap’s smear beginning at age 18 or sexually active

assessment Asymptomatic in the early stage  Watery vaginal discharge  Late manifestation, postcoital, heavy or intermenstrual bleeding. 

diagnostics Colposcopy – application of acetic acid followed by magnified examination of the pelvis  Biopsy  Endocervical curettage  Cone biopsy 

Management Total abdominal hysterectomy and lymphadenectomy  Depends on the stage and desire for child bearing  Radiation therapy  Chemotherapy for advanced disease 

Laser therapy - used when all boundaries of the lesion are visible during colposcopic examination. - minimal bleeding is associated with the procedure. - slight vaginal discharge is expected following the procedure and healing occurs in 6 to 12 weeks.



Conization - a cone shaped area of the cervix is removed - performed in women who desire further childbearing. - long term follow up care is needed, as new lesions can develop - the risk of procedure includes hemorrhage, uterine perforation, incompetent cervix and preterm labor in future pregnancies.

Hysterectomy -

For microinvasive cancer if childbearing is not desired. A vaginal approach is most commonly performed. A radical hysterectomy and bilateral lymphnode dissection may be performed for cancer that has spread beyond the cervix but not to the pelvic wall.

Nursing intervention Assess for changes in bowel and bladder pattern  Bladder training  If laser surgery for early diseases is used, instruct to avoid douching, tampoons and sexual activity for 2-4 weeks  Assess for sexual dysfunction, surgical shortening of vagina, vaginal dryness 

Endometrial Cancer Highest incidence for caucasians  90% are adenocarcinoma  5 year survival is 96% for early stage and 26% for late 

Risk factors        

Female over 50 High cumulative exposure to endogenous and exogenous estrogen Nulliparity Family hx of breast or ovarian cancer Infertility Diabetes Hypertention obesity

Assessment  

Abnormal vaginal bleeding Pain in later stage

Diagnostics a. Pelvic examination b. Pap smear c. Endometrial biopsy 90% effective d. D and C

Management      

Used for staging TAHBSO and peritoneal washing, omentectomy Adjuvant therapy is not required in early stage Intravaginal radiation for early stage low grade tumors Pelvic external beam for high grade Hormonal therapy (progestins) and chemotherapy for advanced disease

Nursing intervention Encourage and instruct the importance of regular pelvic examination  Pain management  Prevention of postsurgical venous stasis 1. encourage turning and ambulation 2. antiembolic stockings  Instruct signs of recurrence like vaginal bleeding, pelvic pain and constipation 

Ovarian Cancer Second most common gynecologic cancer after uterine  Most common cause of gynecologic cancer death  Industrial countries have higher incidence  5 year survival is 30-35%  60-70% are diagnosed at stage III 

Risk Factors Women mid 50-70 (peak 55-59)  Higher education and socioeconomic status  History of breast and endometrial cancer  No pregnancy, infertility, Non use of OCP  Mutation of BRCA 1 or 2  Hereditary non polyposis cancer 

Assessment 

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No early clinical examination Abdominal discomfort or enlargement Indigestion and flatulence that persist without explanation

Diagnostics Pelvic examination  Ultrasound and Ct scan  CA 125  Barium enema, cystoscopy IVP 

Surgical management 

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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  

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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

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Increased patient comfort while doing the exam  

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maintain eye contact proceed in an unhurried manner

involved the person in the examination

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Position the patient for the procedure 

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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

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Inspect and palpate the length and all sides of the penis 

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look for lesions, discharge, atrophy or inflammation check if circumcised or uncircumcised observe the urethral meatus for displacement or discharge

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Inspect the scrotum first and then the testicles 

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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

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Scrotal transillumination 

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in a dark room, place a strong, lighted flashlight next to the scrotum normally light passes through the scrotum if with tumor, does not transluminate if with hydrocele it will shine red

Self Examination

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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

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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 

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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

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Do not hesitate to seek professional assessment and advice if anything unusual. It is better to learn that everything is OK than to wait long

Diagnostic test Bimanual scrotal palpation  Ultrasound  AFP and BHCG  Chest x-ray 

management Transinguinal orchiectomy and retroperitoneal LN dissection  Nerve sparing techniques to preserve fertility  Cisplatin based prior to chemotherapy primary treatment for men with advanced disease 

Nursing Intervention Instruct about testicular examination  Offer sperm banking prior to treatment  Postoperative (inguinal orchiectomy) - OPD procedure - pain management ice to scrotal area - wear supporting, avoid heavy lifting for 4-6 weeks and avoid standing for long periods - Fertility may be lost but orgasm remains 

Hodgkin’s disease Malignancy of the immune system  Usually in the involved LN, tonsils, spleen and bone marrow  Characterized by presence of 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 

leukemia 

Malignancy that involves the blood forming tissues on the bone marrow, spleen, lymphnodes

ALL – abnormal proliferation of immature lymphoblast  AML - proliferation of immature myeloblast - Predisposing factors, down syndrome, chemotherapy (alkylating agents) - Peak age 2-5 years old 

Assessment Symptomatic anemia - pallor, fatigue  Thrombocytopenia - petechiae, bleeding  Neutropenia - fever, infection 

Enlarged LN  Hepatosplenomegally  Bone pain  Neurological symptoms - invrease ICP 

Tumor evaluation Bone marrow aspiration and biopsy 1. greater than 25% blast indicate leukemia 2. Chest xray to check for mediastinal mass

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Management of ALL Sanctuary chemotherapy - CNS prophylaxis - Inthratecal methotrexate  Systemic chemotherapy (2 phases) - 3 drug: Vincristine, Prednisone, Lasparginase - 4 drug: + daunorubicin 

Oncological emergency Sepsis and DIC - maintain strict asepsis techniques - administer IV antibiotics - Administer blood products

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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

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Clinical manifestation Progressive shortness of breath, swelling of face, cough  Edema of the neck, arms, hands reported sensation of tightness and dysphagia  Increased intracranial pressure  Dilated jugular veins 

Management Radiation therapy to shrink tumor size and relieve symptoms  Chemotherapy for radiation resistant tumor  Surgery to redirect blood flow  Supportive measures 

Spinal cord compression Potentially leading to permanent neurologic impairment  Metastatic cancer (breast, lung, kidney, prostate, lymphoma) 

Clinical manifestation Local inflammation, edema, venous stasis  Pain exacerbated by movements, coughing, sneezing, Valsalva maneuver  Bladder and bowel dysfunction above S2, overflow incontinence, S3-5, bowel incontinence 

Spinal cord compression  SIADH  Hypercalemia  SVC syndrome  Tumor lysis tumor 