N107 LEC 12/04/06PROF. RIDULME

INFLAMMATORY AND IMMUNE RESPONSES

I. Scope of Defense MechanismA. Non-specific Defense Mechanism

1. External Non-specific Defense Mechanism Skin and mucous membrane Specialized structures (nasal hairs,

eyelashes, tears) Biochemical factors (pH,

secretions, lysozymes)

2. Internal Non-specific Defense Mechanism Mononuclear phagocyte system

(neutrophils, macrophages)

B. Specific Defense Mechanism1. Humoral Immune System (B cell)

Bacteria that produce acute infection

Bacterial exotoxins Viruses that enter via blood stream

(poliomyelitis, hepatitis) Viruses that enter via mucosal

tissues (enterovirus, cold virus, influenza)

2. Cell-mediated Immune System (T cell) Chronic bacterial infection (syphilis,

TB) Fungal infection Transplanted/transformed cells

(cancer)

II. Manifestations of InflammationA. Local Manifestations

1. redness (rubor) – d/t hyperemia2. swelling (tumor) – caused by the fluid

exudates3. pain (dolor) – caused by pressure of

fluid exudates and chemical irritation of nerve endings

4. loss of function (function laesa) – d/t swelling and pain

B. Systemic Manifestations1. fever

- d/t endogenous pyrogens- part of defense mechanism; helps

increase production of interferon2. increased WBC3. increased erythrocyte sedimentation

rate (ESR) – d/t increase in fibrogen

HIV INFECTION AND AIDS

caused by human immunodeficiency virus (HIV), a retrovirus

Pathogenesis HIV attaches to the T4 helper cells Virus replicates inside the T4 helper cells Depletion of T4 helper cells Opportunistic infections set in

Risk factors1. unprotected vaginal, oral or anal intercourse2. IV drug use with contaminated needles3. infected mother to fetus4. health workers5. blood and blood product recipients6. semen used for artificial insemination

Stages and ManifestationsStages Manifestations

Stage IAcute infections

Infectious mononucleosis-like or influenza-like symptoms

Stage IIAsymptomatic

None

Stage IIIPersistent generalized lymphadenopathy

Lymphadenopathy 1 cm, extrainguinal areas for more than 3 mos.

Stage IVSubgroup ASubgroup BSubgroup C

Subgroup D

Constitutional symptomsNeurologic diseaseOpportunistic infections (PCP pneumonia, histoplasmosis, cryptococcosis, PTB, herpes simplex)Secondary cancer (Kaposi’s sarcoma, cervical Ca, NHL)

Laboratory Diagnostics1. Enzyme-linked immunoabsorbent assay (ELISA)2. Western blot assay3. CD4 count4. CD4/CD8 ratio5. CBC6. Chest x-ray7. Sputum culture

Medical Management1. Protease inhibitors2. Nucleoside reverse transcriptase inhibitors3. Non-nucleoside reverse transcriptase inhibitors4. Antineoplastics5. Antibiotics6. Antifungals7. Antidiarrheals8. Antidepressants9. Appetite stimulants

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Complications1. Cancer (Kaposi’s sarcoma, cervical Ca, NHL)2. PCP pneumonia3. TB (M. avium, M. tuberculosis)4. Fungal infection (candidiasis, histoplasmosis,

crytococcosis)5. Protozoal infection (Toxoplasmosis)6. CMV (blindness)

Nursing Process

Diagnosis1. High risk for infection related to decreased

immune response2. Altered nutrition: less than body requirements

r/t chewing/swallowing difficulties3. Coping, family: compromised r/t temporary

family disorganization and role changes4. Social isolation r/t inadequate personal

resources5. Fear r/t uncertainty of illness

Nursing Interventions1. Educate the client regarding the need for

repeat testing at 3, 6 and 12 mos. if risk factors are present even if the first diagnostic test is negative.

2. Use universal precautions when there is potential for contact with blood and body fluids known to transmit HIV.

3. Teach client regarding transmission of HIV and methods for safer sex with uninfected partners.

4. Identify factors that may interfere with nutrition (anorexia, nausea, vomiting, oral lesions, dysphagia).

5. Teach regarding self-administration of prescribed drugs, its side effects and compliance with drug therapy.

6. Encourage activity and rest periods.7. Administer supplemental oxygen as needed.8. Teach client to report signs of infection

immediately.9. Encourage use of constructive coping

mechanisms.10. Assist client with identification of support

systems.

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) Autoimmune disease with no known cure or

cause Characterized by periods of remissions and

exacerbations F>M

Pathogenesis Increase in autoantibody production as a result

of a decreased or abnormal T suppressor cell function

Clinical Manifestations

Blood disorders (anemia, leukemia, lymphopenia, thrombocytopenia)

Renal disordersArthritisImmunologic disorder (anti-DNA antibody, (+) LE)Neurologic disordersSerositis (pleuritis, pericarditis)Oral ulcersAntinuclear antibodyPhotosensitivityMalar rashDiscoid rash

Diagnostics1. Antinuclear antibody (ANA) test2. ESR3. Serum complement4. CBC5. Urinalysis6. LE prep7. 12 lead ECG8. Chest x-ray

Medical Management1. Anti-inflammatory drugs (NSAIDs, salicylates)2. Antimalarial drugs3. Corticosteroids4. Cytotoxic drugs5. Creams/emollients

Nursing Process

Nursing Diagnosis1. Fluid volume excess r/t compromised

regulatory mechanism2. High risk for infection r/t decreased immune

response3. Knowledge deficit r/t lack of exposure to

information4. Self-esteem disturbance r/t change in body

appearance

Nursing Interventions1. Facilitating learning by educating client on:

Nature, course and treatment of disease Appropriate balance of rest and activity Avoidance of sun exposure (use of

sunscreen, sunglasses, wearing long-sleeved blouse, broad-brimmed hats)

Application of cosmetics and wigs2. Administer medications as prescribed.3. Assist patient to gradually resume

independence in ADL.4. Monitor signs and symptoms of complications.5. Keep skin lesions clean and dry.6. Encourage close follow-up care.

RHEUMATOID ARTHRITIS Chronic systemic, inflammatory disorder that

affects primarily the peripheral joints, ligaments, tendons, muscles and blood vessels

Characterized by remissions and exacerbations Etiologic Factors: Immune factors, genetic and

metabolic factors, infection

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Pathogenesis Altered immune complexes that deposit in

synovial fluid causing inflammation and tissue injury and subsequent joint destruction

Clinical Manifestations1. Non-specific symptoms (fever, weight loss,

fatigue)

2. Bilateral and symmetrical swelling of joints3. Morning stiffness4. Subcutaneous nodules5. Limitation of movement of affected joint6. Systemic manifestations (glaucoma,

splenomegaly, aortic valve disease, etc.)

EpidemiologyRheumatoid arthritis is more prevalent in women than men by a ratio of 2:1 or 3:1. It affects 1% to 3% of the population in the United States, with an estimated 200,000 cases diagnosed annually. Usually it appears during the productive years of life when career and family responsibilities are greatest.

PathophysiologyThe disease process within the joints (intraarticular) begins as an inflammation of the synovium with edema, vascular congestion, fibrin exudates, and cellular infiltrate. The inflammatory process is set off by some sort of irritation or damage to joint tissue. This is called a “triggering” event. White blood cells rush into the area, <hanggang dito lang talaga..>

Probable pathogenesis of rheumatoid arthritis

Medical Management1. Anti-inflammatory agents2. Corticosteroids3. Disease Modifying Anti-rheumatic drugs

(methotrexate, anti-malarials, sulfasalazine, gold)

Nursing Process

Diagnosis1. Knowledge deficit (r/t arthritis) d/t lack of

exposure of information2. Self-care deficit r/t pain and musculoskeletal

impairments3. Fatigue r/t chronic systemic disease

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Genetic predisposition torheumatoid arthritis

Environmental stimulus (antigen: an infectious

Antigen-antibody response: production of normal immunoglobulins against the

Transformation of IgG and IgMinto rheumatoid factors (RF)

Formation of immune complexes in blood and synovial fluid

Inflammatory response

Increased blood flow andcapillary permeability

Activation of complementsystem

Continued immune responseB lymphocytes stimulated

to produce more RFT lymphocytes stimulatedto act against self-antigenAttraction of phagocytes

(neutrophils and macrophages)

Release of lysosomalenzymes from phagocytes

Degradation of joint tissues

Attraction of more phagocytesto ingest products of degradation

Chronic inflammatory joint disease

Increased outward immigration of

complement andIncreased outward

migration of

Increased blood flow andcapillary permeability

Increased blood flow andcapillary permeability

4. Self-esteem disturbance d/t change in body appearance

Nursing Interventions1.Assess/

monitor for:Joints

for

pain, mobility, deformities and contractures VS Weight

2. Administer medications as prescribed.3. Encourage frequent rest periods.4. Splint acutely inflammed joints.

5. Encourage compliance with prescribed exercise program.

6. Encourage active ROM exercise.7. Encourage use of cane, crutches or other

assistive devices.8. Apply

cold

compress to acutely inflammed joints.9. Apply heat via shower, bath or moist warm

packs as prescribed.10. Provide emotional support and encouragement.

Comparison of Normal and Rheumatoid Joints

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Rheumatoid Hands: Deformities and their Structural Basis

<sori..malabo talaga e..>

Rheumatoid Arthritis

Health Care Workers’ Interventions Used to Break the Chain of Infection Transmission

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GENERAL PRECAUTIONS

Preventing Infection in the Community1. Sanitation techniques2. Regulated health practices3. Vaccination programs

a. Passive immunization – temporary protection afforded by the acquisition of preformed antibodies2 types:a.1.Natural passive immunizationa.2.Artificial passive immunization

b. Active immunization – provides long term immunity by giving either a killed or a live attenuated vaccine, thus stimulating either the humoral or cell mediated immunityEx: killed vaccine – DPT

live attenuated vaccine – MMR

Contraindications1. previous anaphylaxis or anaphylactic-like

reaction 7 days after DPT vaccination2. encephalopathy3. fever 40oC within 48 hours of vaccination4. seizure of shock-like manifestations 3 days

after immunization5. live attenuated vaccines should not be

given to immunosuppressed patients6. MMR contraindicated for pregnant women

Preventing Infection in the Hospital Setting1. Handwashing before and after each patient

contact

2. Use sterile gloves when handling contaminated body fluids and secretions

3. Use aseptic technique when cleaning wounds4. Changing of infusion sets, catheters and

solutions regularly5. Handle all sharps and needles with care6. Use of masks when taking care of patients with

infections transmitted via airborne or droplet

RESPIRATORY INFECTIONS

I. Pneumonia: acute inflammation of lung tissue

Classification of PneumoniaCommunity

Acquired Pneumonia

Hospital Acquired

Pneumonia

Aspiration Pneumonia

Charac-teristics

Occur either in the community or 48 hours before hospitalization

Also called nosocomial infectionOnset of symptoms more than 48 hours after hospitalization

Refers to pulmonary consequences resulting from the entry of endogenous or exogenous substances into the lower airway

Etiologic Factors

Streptococcus pneumoniae, H.influenza, Mycoplasma pneumoniae

P.aeruginosa, Staphylo-coccus pneumoniae, Klebsiella pneumoniae, E.coli

Streptococcus pneumoniae, H.influenza, Staphylo-coccus pneumoniae, gastric contents

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Risk Factors 1. Conditions that produce mucus or bronchial

obstruction- smoking- cancer, COPD

2. Immunosuppressed patients3. Prolonged immobility4. Depressed cough reflex (medication,

debilitated state, weak respiratory muscles, decreased LOC)

5. Alcohol intoxication6. Respiratory therapy with improperly cleaned

instruments7. Aging – may either be a primary problem or as

a complication of a chronic disease- clinical manifestations are usually atypical

PathophysiologyNormal

FunctionPatho-

physiologyClinical Manifestation

Mucociliary system

Hypertrophy of mucous membrane lining of the lungs resulting in hypersec-retion

Broncho-spasm from increased secretions

Increased sputum production and cough

anaerobic – foul smelling specimen

Klebsiella – currant jelly color

Staphylococcus – creamy yellow

Pseudomonas – green

Viral – muco-purulent

Localized or diffuse wheezing; dyspnea

Alveolo-capillary membrane

Decreased surface area for gas exchange

chest X-ray films: consolidated or diffused/patchy appearance

HypoxemiaPleura Inflamma-

tion of the pleura

chest pain pleural effusion dullness on

percussion decreased breath

sounds decreased vocal

fremitusRespiratory muscles

Hypoventi-lation

decreased chest expansion

respiratory acidosisLung Defense System

Bacteremia Elevated WBC tachypnea, fever

Laboratory and Diagnostics1. Complete Blood Count (CBC)2. Chest X-ray3. Blood culture4. Sputum Examination5. Arterial Blood Gas (ABG)

Nursing Process

Nursing Diagnosis1. Ineffective airway clearance r/t copious

tracheobronchial secretions2. Impaired gas exchange r/t alvelocapillary

membrane changes3. Risk for fluid volume deficit r/t fever and

dyspnea4. Altered nutrition: less than body requirements

r/t increased metabolic needs

Nursing Interventions Monitor for increased respiratory distress Administer oxygen therapy via nasal cannula Assist patient to cough effectively Suction airway using sterile technique Assist with nebulizer therapy Do chest physiotherapy Administer antibiotics and bronchodilators as

ordered Ensure adequate fluid intake Assist with ADL, pacing activities to prevent

fatigue and respiratory distress If comatose, reposition patient q 2 h and do

passive ROM q 4 h Encourage deep breathing exercises q 2 h Offer small, frequent feedings with diet high in

carbohydrates and protein Monitor for signs and symptoms of

complications (hypotensive shock, atelactasis, pleural effusion)

II. Pulmonary Tuberculosis Caused by Mycobacterium tuberculosis Spreads via airborne transmission (generally

particles 1 to 5 micrometers in diameter)

Risk Factors1. Close contact with someone who has active TB2. Immunocompromised status3. Substance abuse4. Any person without adequate health care5. Pre-existing medical conditions6. Living in overcrowded, substandard housing7. Health care providers

Pathophysiology

Inhalation of mycobacterium

Multiplication of bacteria in lower airways

Transmission of bacteria to other parts (lymph nodes, kidneys, brain)

Immune system activated

Formation of primary tubercle

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Caseation necrosis

Cavitation

Classification of PTBClass Description Medical Therapy

0 No TB exposure, not infected

None

1 (+) TB exposure(-) infection

Preventive chemotherapy

2 (+) TB exposure, (+)infection, (-)disease

INH for 1 year (<35 years old)

3 Active disease Anti-Koch’s medications for 6 months

4 TB not clinically active

None

5 TB suspect Preventive chemotherapy with INH may be instituted

Nursing Process

Diagnosis1. Ineffective airway clearance r/t increased and

tenacious sputum2. Knowledge deficit about treatment regimen

and preventive health measures3. Activity intolerance r/t fatigue and altered

nutritional status

Nursing Interventions1. Increase fluid intake2. Do chest physiotherapy3. Teach client to cover nose and mouth with

disposable tissues when sneezing, coughing and laughing to avoid transmission of particles

4. Advise patient on importance of adherence to medical therapy

5. Educate patient on side effects of medications to report immediately if symptoms occur

6. Encourage eating foods rich in carbohydrates and protein

Clinical manifestations1. Anorexia2. Weight loss3. Fatigue4. Cough5. Low-grade fever6. Night sweats

Diagnostics1. History and PE2. Chest X-ray3. Sputum smear and culture4. Gastric aspirate5. Tuberculin skin test

Medical ManagementA. First line drugs

INH and rifampicin for 6 months PZA, ethambutol/streptomycin for 2

monthsB. Second line drugs

GASTROINTESTINAL INFECTIONS

I. Viral Hepatitis

Pathophysiology and Clinical ManifestationsPathophysiology Clinical Manifestations

Necrosis and inflammation of hepatocytes

- Fever- Chills- Nausea and vomiting- Anorexia- RUQ pain

- Murphy’s sign- Hepatomegaly- Elevated liver function

testCirculating immune complexes and complement system activation

- Arthralgia- Headache

Impaired bilirubin metabolism

- Jaundice- Dark-colored urine- Clay-colored stools- Pruritus- Bleeding tendencies- Increased total,

conjugated and unconjugated bilirubin

Diagnostics1. History and PE2. Liver function test3. Serologic exam

Nursing Process

Nursing Diagnosis1. Activity intolerance r/t fatigue2. Knowledge deficit: diagnostic test,

manifestations, prophylaxis, treatment and prevention

3. Altered nutrition: less than body requirements r/t increased metabolic needs and anorexia

4. High risk for injury due to altered clotting prothrombin time

Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis EAge group Older children

and young adults

Young adults All age groups Young adults All age groups

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Transmission Fecal-oral Percutaneous and permucosal routes

Parenteral Same as Hepa B Fecal-oral

Secretions that have been found to contain infective agent

Stools: 2 weeks before jaundice

Blood, semen, saliva, nasopharyngeal washings

Blood Blood Feces

Clinical onset abrupt insidious Insidious insidious Same as Hepa A Diagnostic serologic tests

IgM anti- HAV HbsAg, HbeAg, anti-HbeAg, anti-HbcAg

Anti-HCV Anti-HDV Anti-HVE

Immunity IgG anti-HAV Anti-HBs No test available No test available No test availableChronic carriers None 6%-10% 8% 80% UnknownSubsequent chronic diseases

Absent 10% 20-70% Frequent Unknown

High-risk groups Staff and children at day-care centers and institutions

Drug addicts, fetus of women with infected mothers, sexually active people, health care workers

Persons receiving frequent blood transfusions

Same as for HBV Immigrants/travelers from HEV epidemic areas

Nursing Interventions1. Primary Prevention

immunization to high-risk individuals administering immune globulins to those

exposed to Hepa A and B Thorough blood screening Use of condoms during sexual activity

2. Secondary Prevention proper handwashing by patient and staff contaminated needles and equipment

should be handled with great care wearing of gloves when disposing infected

stool and blood proper cleansing, bagging and labeling of

contaminated items such as bed linens and bedpans

3. Intersperse rest periods in between activity to promote rest

4. Encourage adequate fluid intake and promote a well-balanced diet

5. Assess for signs of progressive disease and report immediately to physician

6. Apply emollients and creams to reduce pruritus7. Avoid activities that promote sweating and

increased body temperature8. Administer antihistamines as ordered9. Advise patient not to scratch skin or if not

tolerated, use a soft cloth to rub skin10. Monitor for signs of bleeding11. Use of soft toothbrushes or swabs to avoid

injury to gums and resultant bleeding12. Collect blood samples at one time to prevent

bleeding

II. Infectious Diarrhea Transmitted through oral ingestion Common organisms: E. coli, Salmonella typhi, Shigella species, Campylobacter, Giardia lamblia, Vibrio cholera

Clinical Manifestations1. diarrhea

2. fever3. abdominal pain4. nausea and vomiting5. tachycardia6. shock

Nursing Process

Diagnosis1. Fluid volume deficit related to fluid lost through

diarrhea2. Knowledge deficit about the infection and the

risk of transmission to others

Nursing Interventions1. Assess degree of dehydration2. Encourage patient to continue oral rehydration

therapy3. Encourage mother to continue breastfeeding of

infants4. Provide low residue, high calorie, high protein

diet5. Educate patient on:

Proper food handling and cooking Importance of handwashing Importance of proper garbage and sewage

disposal6. Monitor for signs and symptoms of

complications (bacteremia, shock)

LEPTOSPIROSIS caused by spirochetes; clinical manifestations

may range from asymptomatic to fulminant mode of transmission: direct contact with

infected urine, blood or tissue

Pathogenesis Leptospires enter the skin through abrasions or

via mucous membranes Leptospiremia develops Vasculitis develops causing:

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- Renal – interstitial nephritis and tubular necrosis (oliguria, proteinuria, hematuria, uremia)

- Liver – centrilobular necrosis (jaundice, increased liver function tests, dark-colored urine, clay colored stool, hepatomegaly)

- Lungs – pulmonary hemorrhage (hemoptysis, chest pain, cough)

- Skeletal muscles – swelling and focal necrosis (calf pain, rashes)

Clinical Manifestations1. Influenza-like symptoms

fever retroorbital pain photophobia calf pain conjunctival suffusion lymphadenopathy mild jaundice hepatomegaly/ splenomegaly mental confusion maculopapular rashes

2. Weil’s syndrome jaundice renal dysfunction hemorrhagic diathesis

Laboratory Diagnostics1. isolation of leptospires2. microscopic agglutination test (MAT)3. urinalysis4. BUN, creatinine, electrolytes5. AST, ALT, bilirubin, alkaline phosphatase6. CBC7. Chest X-ray8. PT, PTT

Medical Management1. Antibiotics2. Supportive treatment (dialysis, endotracheal

intubation, blood transfusion)

Nursing Process

Diagnosis1. High risk for injury r/t altered clotting

mechanisms and mental confusion2. Altered body temperature: hyperthermia r/t

inflammatory processes of leptospirosis3. Fluid volume deficit r/t compromised regulatory

mechanisms

Nursing Interventions1. Monitor for hemorrhagic manifestations;

monitor PT and PTT2. Assess level of consciousness and cognitive

level3. Provide safe environment (pad side rails,

remove obstacles in rooms, prevent falls)4. Observe each stool for color, consistency, and

amount5. Observe during blood transfusions6. Administer Vit K as indicated7. Encourage gentle blowing of nose

8. Use small gauge needles for protection9. Encourage oral fluid intake10. Monitor IV fluids, central venous lines or

arterial monitoring lines11. Assess for signs of dehydration12. Monitor intake and output13. Administer antibiotics as prescribed14. Apply cool sponges or icebag for elevated

temperature

DENGUE HEMORRHAGIC FEVER caused by a Flaviviridae virus; transmitted by

Aedes aegypti mosquito contains 4 subtypes

Clinical Manifestations1. fever2. myalgia3. retroorbital pain4. back pain5. lymphadenopathy6. petecchiae7. bleeding diathesis8. renal failure9. maculopapular rash

Diagnostics1. IgM ELISA2. Tourniquet test3. Serial CBC

Nursing Process

Nursing Diagnosis1. Altered tissue perfusion r/t bleeding tendencies2. Knowledge deficit about the disease and risk for

spread of infection or re-infection3. Potential for fluid volume deficit r/t bleeding

Nursing Interventions1. Monitor VS regularly2. Handle patient gently so as to prevent injury3. Use soft-bristled toothbrush to prevent gum

bleeding4. Encourage patient to increase fluid intake5. Avoid intramuscular injections as much as

possible6. Advise patient to avoid using NSAIDs or aspirin

to prevent GI bleeding7. Monitor for signs of complications (IC bleeding,

viremia)8. Provide high residue, high carbohydrate and

high protein diet9. Advise patient to avoid Valsalva maneuver10. Advise patient on preventive measures

constantly remove waters in jars, vases and discarded containers

apply anti-repellant on skin especially during the day time

RABIES acute viral illness of the CNS transmitted via infected secretions, usually

saliva or through transplantation of infected tissues

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caused by the rabies virus mortality is almost 100%

Pathogenesis

Inoculation of virus in the epidermis onto mucous membrane

replication in striated muscle

ascends to the CNS

dissemination to autonomic nerves

Stages and Clinical ManifestationsStages Clinical Manifestations

Prodromal period

fever headache malaise anorexia nausea and vomiting

Encephallic phase

confusion hallucinations combativeness muscle spasm meningismus seizures opisthotonus increased lacrimation fever postural hypotension

Brainstem dysfunction

diplopia facial palsies difficulty with

deglutition hydrophobia coma apnea

Death Death

Diagnostics1. History and PE2. Viral culture

3. Histologic and microscopic examination of Negri bodies in postmortem brain

Medical Management1. Post-exposure prophylaxis

a. Local wound therapy – mechanical and chemical cleansing of infected site

b. Passive immunization – Human rabies immune globulin (HRIG)

2. Active immunization – give 5 doses of antirabies vaccine within 28 days

Nursing Process

Diagnosis1. Potential for injury related to seizures2. Ineffective breathing pattern related to

neuromuscular impairment3. Impaired swallowing related to neuromuscular

impairment

Nursing Interventions1. Monitor VS regularly2. Assess for signs of respiratory distress. Closely

monitor for breath sounds, rate and character of respiration.

3. Have a plastic airway readily available on bedside.

4. Have suction and oxygen available at bedside5. Note any changes in behavior6. Provide a quiet environment7. Provide long side rails and pad the rails8. If comatose, monitor for signs and symptoms

of complications9. If with fever, administer acetaminophen as

prescribed10. Keep skin clean and dry. Make sure that linens

are not crumpled.

LEPROSY Chronic granulomatous infection that affects

superficial tissues Involve cooler areas of the body (face, eyes,

peripheral nerves, testes) Caused by Mycobacterium leprae; grows slowly Mode of transmission: direct human to human

contact

Types of Leprosy1. enlarged peripheral nerves2. leonine facies3. thinning of lateral eyebrows4. saddlenose deformity5. hypesthesia followed by anesthesia6. (-) sweating on site of lesion7. infertility8. keratitis, blindness9. muscle atrophy

Complications1. secondary infections2. trauma3. contractures

Laboratory Diagnostics

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Tuberculoid

Borderline Lepromatous

Number of skin lesions

Single Several Many

Hair growth on skin lesions

Absent Slightly decreased

Not affected

Sensation in lesions of the extremities

Completely lost

Moderately lost

Glove and stocking

peripheral neuropathy

Acid fast bacilli in skin scrapings

None Several Innumerable

Lepromin skin test

Strongly positive

No reaction No reaction

1. Skin scrapings2. Skin biopsy3. Lepromin test

Medical Management1. Dapsone for 24 months2. Rifampicin for 6 months3. Clofazimine

Nursing Process

Diagnosis1. Potential for injury related to decreased tactile

sensation2. Fear related to stigmatization and to prognosis

and complications3. Knowledge deficit about the infection and the

risk of transmission to others

Nursing Interventions1. Advise patient to regularly inspect skin for

redness, abrasions or any signs of infection and trauma

2. Always keep fingernails short and clean3. Encourage both active and passive ROM

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4. Facilitating learning by educating client on nature, course and treatment and possible complications of disease

5. Advise patient on importance of compliance to medications

6. Promote positive coping strategies of patient

Nursing Process

Diagnosis1. Knowledge deficit about the disease and risk

for spread of infection or re-infection2. Non-compliance with treatment

3. Fear related to stigmatization and to prognosis and complications

Nursing Interventions1. Educate client regarding:

Risk factors Use of condoms or practice safe sex Possible complications (ectopic pregnancy,

infertility, neurosyphilis, gonococcal arthritis, aortitis)

Medications and their side effects2. Administer antibiotics as ordered

SEXUALLY TRANSMITTED DISEASES

Syphilis Gonorrhea Chlamydia trachomatis

Herpes Simplex Type

2

Condyloma Acuminata

Signs and Symptoms

1° syphilis – chancre2° syphilis – hematogenous spread Rashes Condyloma lata Fever, malaise Lymphadenopathy

Weight loss3° syphilis Gumma Aortitis Neurosyphilis

Increased vaginal secretions

Increased vaginal pruritus

Penile discharge

Dysuria

Dyspareunia Increased vaginal pruritus

Increased vaginal secretions

Infertility Dysuria

Vesicular eruptions on the penile shaft, vagina, vulva or cervix

Wart-like cauliflower-like lesions on the penis and vulva

Diagnostics VDRL/RPR Gram stain Culture Viral culture CultureMedical Management

Benzanthine Penicillin

Doxycycline

CeftriaxoneDoxycycline

DoxycyclineAzythromycin

Acyclovir CryotherapyElectrosurgery

Podophyllin

Gumma Herpes Simplex Type 2 Condyloma LataSyphilis

PENICILLIN FAMILY ANTIBIOTICS

Name Mechanism of Action

Pharmacokinetics Adverse Effects Therapeutic Effects

Pen GAqueous crystalline Pen GBenzathine Pen GProcaine Pen G

Inhibits bacterial cell wall synthesis

Cannot survive passage through stomach Crystalline Pen G IV

Procaine and Benzathine Pen G IM

Allergy Superinfections (Clostridium difficile)

Streptococci pneumoniae

Group A Beta-hemolytic strep

Neisseria gonorrhea

Treponema pallidum

Pen V Same oral Same

Amino penicillinsAmoxicillinAmpicillin

Same Ampicillin – IV/oral

Amoxicillin - oral

Same Broader gram (-) coverage than above penicillins

SamePenicillinase resistant penicillins (IV)

MethicillinNafcillin

Same IV Same

Skin and other infections caused by Staphylococcus aureus

Penicillinase resistant penicillins (PO)

CloxacillinDicloxacillinNafcillin

Same Oral Same

Combination of penicillin with beta-lactamase inhibitors

Amoxillin + clavulanate (Augmentin)

Ampicillin + sulbactam (Unasyn)

Same

Augmentin – oral

Unasyn - IV Same

Covers both gram (-) and (+) bacteria

Anaerobic bacteria

Pseudomonas

Anti-pseudomonal penicillins

TicarcillinCarbenicillinPiperacillin

Same IV

Same Anaerobic coverage

BETA-LACTAMASE INHIBITORS

I. Cephalosporins1st generation

CephalexinCefazolinCephradineCephalothin

Competitive inhibitor of the transpeptidase enzyme; inhibits bacterial wall synthesis

Oral Cephalexin

IV Cephalothin Cefazolin

Cephadrine – oral/IVRenal excretion

Allergic reaction Superimposed infections

Gram (+) coverage

2nd generationCefaclorCefoxitinCefuroximeCefamandole

Same

Oral Cefaclor

Oral/IV Cefuroxime

The rest is IV

Same as aboveCefamandole:

Interferes with Vit K dependent clotting factors

Interferes with metabolism of alcohol

Gram (-) and (+) bacteria

3rd generationCeftriaxoneCeftazidimeCefiximeCefoperazone

SameOral Cefixime

The rest is IVSame as above

Gram (-) bacteriaCeftriaxone – good penetration in the CSF

4th generationCefepime Same IV Same

Gram (-) Pseudomonas aeruginosa

II. Carbapenems Imipenem Meropenem

Inhibits bacterial cell wall synthesis

IV or IM Renal excretion

Nausea & vomiting

Gram (-) & (+) Anaerobes

Allergy seizures

III. MonobactamsAztreonam Inhibits bacterial

wall synthesis IV or IM Renal excretion

No allergic cross-reactivity with penicillins

Gram (-) organisms

ANTI-RIBOSOMAL ANTIBIOTICS

Name MOA Pharmacokinetics Adverse Effects Therapeutic UseChloramphenicol Binds to 50S

ribosomal sub-unit and inhibits

protein synthesis

Oral or IV Metabolized by the liver

Excreted via kidney

Bone marrow depression

Gray baby syndrome (cyanosis, vomiting, green stools & vasomotor collapse)

Bacterial meningitis in infants

Ricketsial infection in children & pregnant women

Clindamycin Same Oral or IV Excreted from bile and urine

Pseudomembranous colitis

Anaerobes (peritonitis, PID)

Gram (+) organisms if allergic to penicillins and cephalosporins

Toxoplasma gondii

Erythromycin Same Oral or IV Concentrated in the liver

Reversible cholestatic hepatitis

Epigastric distress Transient reversible deafness with very high doses

Candida vaginits

Chlamydia trachomatis

Bordatella pertussis

Mycoplasma pneumoniae

Corynebacterium diphtheriae

Strep & Staph infection for allergic to penicillin

TetracyclineDoxycycline

Binds to 30S ribosomal sub-unit

and inhibits protein synthesis

Food and milk impairs oral absorption

Excretion Urine- tetracycline

Stool- doxycycline

GI irritation Renal and hepatic toxicity

Fanconis syndrome Teratogenic

Chlamydia trachomatis

Mycoplasma pneumoniae

Entamoeba histolytics

Treponema pallidum

Aminoglycosides Same as above IV or IM Diffuses inflamed meninges

Synergistic with penicillin

Nephrotoxic Ototoxic

Gram (-) enteric organisms

Mycobacterium tuberculosis

Spectinomycin Same as above IM Neisseria gonorrhea

MISCELLANEOUS ANTIBIOTICS

Name MOA Pharmacokinetics Adverse Effects Therapeutic Effects

FluoroquinonesCiprofloxacin

Inhibits DNA gyrase Oral or IV Excellent tissue

GI symptoms Damage to

Hospital-acquired infections

LevofloxacinOfloxacinSparfloxacin

penetration Renal excretion

cartilage CNS symptoms

Chronic infections

Diarrhea caused by enteric organisms

Vancomycin Inhibits cell wall synthesis

IV Red man syndrome if infused rapidly

MRSA Enterococcus

Trimethoprim/ Sulfamethoxazole

Inhibits tetrahydrofolate synthesis

Oral or IV GI upset Skin rashes Bone marrow suppression

Not used in 1st trimester – increased fetal bilirubin

Macrocytic anemia

GUT infections Pneumocystis carinii