N107 LEC 12/04/06

PROF. RIDULME

INFLAMMATORY AND IMMUNE RESPONSES 1. unprotected vaginal, oral or anal intercourse

2. IV drug use with contaminated needles
I. Scope of Defense Mechanism 3. infected mother to fetus
A. Non-specific Defense Mechanism 4. health workers
1. External Non-specific Defense Mechanism 5. blood and blood product recipients
 Skin and mucous membrane 6. semen used for artificial insemination
 Specialized structures (nasal hairs,
eyelashes, tears) Stages and Manifestations
 Biochemical factors (pH, secretions, Stages Manifestations
lysozymes) Stage I Infectious mononucleosis-like or
Acute infections influenza-like symptoms
2. Internal Non-specific Defense Mechanism Stage II None
 Mononuclear phagocyte system Asymptomatic
(neutrophils, macrophages) Stage III Lymphadenopathy  1 cm,
Persistent generalized extrainguinal areas for more than 3
B. Specific Defense Mechanism lymphadenopathy mos.
1. Humoral Immune System (B cell) Stage IV
 Bacteria that produce acute infection Subgroup A Constitutional symptoms
 Bacterial exotoxins Subgroup B Neurologic disease
 Viruses that enter via blood stream Subgroup C Opportunistic infections (PCP
(poliomyelitis, hepatitis) pneumonia, histoplasmosis,
 Viruses that enter via mucosal tissues cryptococcosis, PTB, herpes
(enterovirus, cold virus, influenza) simplex)
Secondary cancer (Kaposi’s
2. Cell-mediated Immune System (T cell) Subgroup D sarcoma, cervical Ca, NHL)
 Chronic bacterial infection (syphilis, TB)
 Fungal infection
 Transplanted/transformed cells (cancer) Laboratory Diagnostics
1. Enzyme-linked immunoabsorbent assay (ELISA)
II. Manifestations of Inflammation 2. Western blot assay
A. Local Manifestations 3. CD4 count
1. redness (rubor) – d/t hyperemia 4. CD4/CD8 ratio
2. swelling (tumor) – caused by the fluid exudates 5. CBC
3. pain (dolor) – caused by pressure of fluid 6. Chest x-ray
exudates and chemical irritation of nerve endings 7. Sputum culture
4. loss of function (function laesa) – d/t swelling
and pain Medical Management
1. Protease inhibitors
B. Systemic Manifestations 2. Nucleoside reverse transcriptase inhibitors
1. fever 3. Non-nucleoside reverse transcriptase inhibitors
- d/t endogenous pyrogens 4. Antineoplastics
- part of defense mechanism; helps increase 5. Antibiotics
production of interferon 6. Antifungals
2. increased WBC 7. Antidiarrheals
3. increased erythrocyte sedimentation rate (ESR) – 8. Antidepressants
d/t increase in fibrogen 9. Appetite stimulants

Complications
1. Cancer (Kaposi’s sarcoma, cervical Ca, NHL)
HIV INFECTION AND AIDS 2. PCP pneumonia
 caused by human immunodeficiency virus (HIV), a 3. TB (M. avium, M. tuberculosis)
retrovirus 4. Fungal infection (candidiasis, histoplasmosis,
crytococcosis)
Pathogenesis 5. Protozoal infection (Toxoplasmosis)
 HIV attaches to the T4 helper cells 6. CMV (blindness)
 Virus replicates inside the T4 helper cells
 Depletion of T4 helper cells Nursing Process
 Opportunistic infections set in
Diagnosis
Risk factors 1. High risk for infection related to decreased immune
response

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2. Altered nutrition: less than body requirements r/t Malar rash
chewing/swallowing difficulties Discoid rash
3. Coping, family: compromised r/t temporary family
disorganization and role changes Diagnostics
4. Social isolation r/t inadequate personal resources 1. Antinuclear antibody (ANA) test
5. Fear r/t uncertainty of illness 2. ESR
3. Serum complement
Nursing Interventions 4. CBC
1. Educate the client regarding the need for repeat testing at 3, 5. Urinalysis
6 and 12 mos. if risk factors are present even if the first 6. LE prep
diagnostic test is negative. 7. 12 lead ECG
2. Use universal precautions when there is potential for 8. Chest x-ray
contact with blood and body fluids known to transmit HIV.
3. Teach client regarding transmission of HIV and methods Medical Management
for safer sex with uninfected partners. 1. Anti-inflammatory drugs (NSAIDs, salicylates)
4. Identify factors that may interfere with nutrition (anorexia, 2. Antimalarial drugs
nausea, vomiting, oral lesions, dysphagia). 3. Corticosteroids
5. Teach regarding self-administration of prescribed drugs, its 4. Cytotoxic drugs
side effects and compliance with drug therapy. 5. Creams/emollients
6. Encourage activity and rest periods.
7. Administer supplemental oxygen as needed. Nursing Process
8. Teach client to report signs of infection immediately.
9. Encourage use of constructive coping mechanisms. Nursing Diagnosis
10. Assist client with identification of support systems. 1. Fluid volume excess r/t compromised regulatory
mechanism
SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) 2. High risk for infection r/t decreased immune response
 Autoimmune disease with no known cure or cause 3. Knowledge deficit r/t lack of exposure to information
 Characterized by periods of remissions and exacerbations 4. Self-esteem disturbance r/t change in body appearance
 F>M
Nursing Interventions
Pathogenesis 1. Facilitating learning by educating client on:
 Increase in autoantibody production as a result of a  Nature, course and treatment of disease
decreased or abnormal T suppressor cell function  Appropriate balance of rest and activity
 Avoidance of sun exposure (use of sunscreen,
sunglasses, wearing long-sleeved blouse, broad-
Clinical Manifestations brimmed hats)
Blood disorders (anemia, leukemia, lymphopenia,  Application of cosmetics and wigs
thrombocytopenia) 2. Administer medications as prescribed.
Renal disorders 3. Assist patient to gradually resume independence in ADL.
Arthritis 4. Monitor signs and symptoms of complications.
Immunologic disorder (anti-DNA antibody, (+) LE) 5. Keep skin lesions clean and dry.
Neurologic disorders 6. Encourage close follow-up care.
Serositis (pleuritis, pericarditis)
Oral ulcers
Antinuclear antibody
Photosensitivity
RHEUMATOID ARTHRITIS
 Chronic systemic, inflammatory disorder that affects Clinical Manifestations
primarily the peripheral joints, ligaments, tendons, muscles 1. Non-specific symptoms (fever, weight loss, fatigue)
and blood vessels 2. Bilateral and symmetrical swelling of joints
 Characterized by remissions and exacerbations 3. Morning stiffness
 Etiologic Factors: Immune factors, genetic and metabolic 4. Subcutaneous nodules
factors, infection 5. Limitation of movement of affected joint
6. Systemic manifestations (glaucoma, splenomegaly, aortic
Pathogenesis valve disease, etc.)
 Altered immune complexes that deposit in synovial fluid
causing inflammation and tissue injury and subsequent
joint destruction

Epidemiology
Rheumatoid 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.

Pathophysiology

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The 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

Environmental stimulus (antigen: an infectious organism)

Antigen-antibody response: production of normal immunoglobulins against the antigen

Genetic predisposition to Transformation of IgG and IgM

rheumatoid arthritis into rheumatoid factors (RF)

Formation of immune complexes in blood and synovial fluid

Inflammatory response

Activation of complement Increased blood flow and Continued immune response

system capillary permeability B lymphocytes stimulated
to produce more RF
T lymphocytes stimulated
Attraction of phagocytes to act against self-antigen
(neutrophils and macrophages)

Increased blood flow and

Release of lysosomal Increased outward capillary permeability
enzymes from phagocytes immigration of complement
and
Increased outward migration Increased blood flow and
Degradation of joint tissues of phagocytes capillary permeability

Attraction of more phagocytes

to ingest products of degradation

Chronic inflammatory joint disease

(rheumatoid arthritis)

Medical Management 1. Knowledge deficit (r/t arthritis) d/t lack of exposure of

1. Anti-inflammatory agents information
2. Corticosteroids 2. Self-care deficit r/t pain and musculoskeletal impairments
3. Disease Modifying Anti-rheumatic drugs (methotrexate, 3. Fatigue r/t chronic systemic disease
anti-malarials, sulfasalazine, gold) 4. Self-esteem disturbance d/t change in body appearance

Nursing Process
Nursing Interventions
Diagnosis 1. Assess/m
onitor
for:

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  Joints for pain, mobility, deformities and contractures 6. Encourage active ROM exercise.
 VS 7. Encourage use of cane, crutches or other assistive devices.
 Weight 8. Apply cold compress to acutely inflammed joints.
2. Administer medications as prescribed. 9. Apply heat via shower, bath or moist warm packs as
3. Encourage frequent rest periods. prescribed.
4. Splint acutely inflammed joints. 10. Provide emotional support and encouragement.
5. Encourage compliance with prescribed exercise program.

Comparison of Normal and Rheumatoid Joints

Rheumatoid Hands: Deformities and their

Structural Basis

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 <sori..malabo talaga e..>

Rheumatoid Arthritis

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

GENERAL
PRECAUTIONS live attenuated vaccine – MMR

Preventing Infection in the Community

1. Sanitation techniques Contraindications
2. Regulated health practices 1. previous anaphylaxis or anaphylactic-like reaction 7
3. Vaccination programs days after DPT vaccination
a. Passive immunization – temporary protection afforded 2. encephalopathy
by the acquisition of preformed antibodies 3. fever  40oC within 48 hours of vaccination
2 types: 4. seizure of shock-like manifestations 3 days after
a.1. Natural passive immunization immunization
a.2. Artificial passive immunization 5. live attenuated vaccines should not be given to
immunosuppressed patients
b. Active immunization – provides long term immunity 6. MMR contraindicated for pregnant women
by giving either a killed or a live attenuated vaccine,
thus stimulating either the humoral or cell mediated Preventing Infection in the Hospital Setting
immunity 1. Handwashing before and after each patient contact
Ex: killed vaccine – DPT

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2. Use sterile gloves when handling contaminated body fluids appearance
and secretions  Hypoxemia
3. Use aseptic technique when cleaning wounds Pleura Inflamma-tion  chest pain
4. Changing of infusion sets, catheters and solutions regularly of the pleura  pleural effusion
5. Handle all sharps and needles with care  dullness on percussion
6. Use of masks when taking care of patients with infections  decreased breath sounds
transmitted via airborne or droplet  decreased vocal fremitus
Respiratory Hypoventi-  decreased chest
RESPIRATORY INFECTIONS muscles lation expansion
 respiratory acidosis
I. Pneumonia: acute inflammation of lung tissue Lung Defense Bacteremia  Elevated WBC
System  tachypnea, fever
Classification of Pneumonia
Community Hospital Aspiration Laboratory and Diagnostics
Acquired Acquired Pneumonia 1. Complete Blood Count (CBC)
Pneumonia Pneumonia 2. Chest X-ray
Occur either in Also called Refers to 3. Blood culture
Charac- the community nosocomial pulmonary 4. Sputum Examination
teristics or 48 hours infection consequences
5. Arterial Blood Gas (ABG)
before Onset of resulting from the
hospitalization symptoms more entry of
than 48 hours endogenous or Nursing Process
after exogenous
hospitalization substances into the Nursing Diagnosis
lower airway 1. Ineffective airway clearance r/t copious tracheobronchial
Streptococcus P.aeruginosa, Streptococcus secretions
Etiologic pneumoniae, Staphylo-coccus pneumoniae, 2. Impaired gas exchange r/t alvelocapillary membrane
Factors H.influenza, pneumoniae, H.influenza,
changes
Mycoplasma Klebsiella Staphylo-coccus
pneumoniae pneumoniae, pneumoniae, 3. Risk for fluid volume deficit r/t fever and dyspnea
E.coli gastric contents 4. Altered nutrition: less than body requirements r/t increased
metabolic needs
Risk Factors
1. Conditions that produce mucus or bronchial obstruction Nursing Interventions
- smoking  Monitor for increased respiratory distress
- cancer, COPD  Administer oxygen therapy via nasal cannula
2. Immunosuppressed patients  Assist patient to cough effectively
3. Prolonged immobility  Suction airway using sterile technique
4. Depressed cough reflex (medication, debilitated state, weak  Assist with nebulizer therapy
respiratory muscles, decreased LOC)  Do chest physiotherapy
5. Alcohol intoxication  Administer antibiotics and bronchodilators as ordered
6. Respiratory therapy with improperly cleaned instruments  Ensure adequate fluid intake
7. Aging – may either be a primary problem or as a  Assist with ADL, pacing activities to prevent fatigue and
complication of a chronic disease respiratory distress
- clinical manifestations are usually atypical  If comatose, reposition patient q 2 h and do passive ROM q
4h
 Encourage deep breathing exercises q 2 h
Pathophysiology
 Offer small, frequent feedings with diet high in
Normal Patho- Clinical Manifestation carbohydrates and protein
Function physiology  Monitor for signs and symptoms of complications
Mucociliary Hypertrophy of Increased sputum (hypotensive shock, atelactasis, pleural effusion)
system mucous production and cough
membrane  anaerobic – foul smelling II. Pulmonary Tuberculosis
lining of the specimen  Caused by Mycobacterium tuberculosis
lungs resulting  Klebsiella – currant jelly  Spreads via airborne transmission (generally particles 1 to 5
in hypersec- color micrometers in diameter)
retion  Staphylococcus –
creamy yellow Risk Factors
 Pseudomonas – green 1. Close contact with someone who has active TB
 Viral – muco-purulent 2. Immunocompromised status
3. Substance abuse
 Localized or diffuse 4. Any person without adequate health care
Broncho-spasm wheezing; dyspnea 5. Pre-existing medical conditions
from increased 6. Living in overcrowded, substandard housing
secretions 7. Health care providers
Alveolo- Decreased  chest X-ray films:
capillary surface area for consolidated or
membrane gas exchange diffused/patchy

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 3 Active disease Anti-Koch’s medications
for 6 months
4 TB not clinically None
active
5 TB suspect Preventive chemotherapy
Pathophysiology with INH may be
instituted
Inhalation of mycobacterium
 Nursing Process
Multiplication of bacteria in lower airways
 Diagnosis
Transmission of bacteria to other parts 1. Ineffective airway clearance r/t increased and tenacious
(lymph nodes, kidneys, brain) sputum
 2. Knowledge deficit about treatment regimen and preventive
Immune system activated health measures
 3. Activity intolerance r/t fatigue and altered nutritional status
Formation of primary tubercle
 Nursing Interventions
Caseation necrosis 1. Increase fluid intake
 2. Do chest physiotherapy
Cavitation 3. Teach client to cover nose and mouth with disposable
tissues when sneezing, coughing and laughing to avoid
Classification of PTB transmission of particles
Class Description Medical Therapy 4. Advise patient on importance of adherence to medical
0 No TB exposure, not None therapy
infected 5. Educate patient on side effects of medications to report
1 (+) TB exposure Preventive chemotherapy immediately if symptoms occur
(-) infection 6. Encourage eating foods rich in carbohydrates and protein
2 (+) TB exposure, INH for 1 year
(+)infection, (<35 years old)
(-)disease
Clinical manifestations - RUQ pain
1. Anorexia - Murphy’s sign
2. Weight loss - Hepatomegaly
3. Fatigue - Elevated liver function test
4. Cough Circulating immune complexes - Arthralgia
5. Low-grade fever and complement system - Headache
6. Night sweats activation
Impaired bilirubin metabolism - Jaundice
Diagnostics - Dark-colored urine
1. History and PE - Clay-colored stools
2. Chest X-ray - Pruritus
3. Sputum smear and culture - Bleeding tendencies
4. Gastric aspirate - Increased total, conjugated
5. Tuberculin skin test and unconjugated bilirubin

Medical Management Diagnostics

A. First line drugs 1. History and PE
 INH and rifampicin for 6 months 2. Liver function test
 PZA, ethambutol/streptomycin for 2 months 3. Serologic exam
B. Second line drugs
Nursing Process
GASTROINTESTINAL INFECTIONS
Nursing Diagnosis
I. Viral Hepatitis 1. Activity intolerance r/t fatigue
2. Knowledge deficit: diagnostic test, manifestations,
Pathophysiology and Clinical Manifestations prophylaxis, treatment and prevention
Pathophysiology Clinical Manifestations 3. Altered nutrition: less than body requirements r/t increased
Necrosis and inflammation of - Fever metabolic needs and anorexia
hepatocytes - Chills 4. High risk for injury due to altered clotting prothrombin
- Nausea and vomiting time
- Anorexia

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 Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E
Age group Older children and Young adults All age groups Young adults All age groups
young adults
Transmission Fecal-oral Percutaneous and Parenteral Same as Hepa B Fecal-oral
permucosal routes
Secretions that have Stools: 2 weeks Blood, semen, Blood Blood Feces
been found to before jaundice saliva,
contain infective nasopharyngeal
agent washings
Clinical onset abrupt insidious Insidious insidious Same as Hepa A
Diagnostic serologic IgM anti- HAV HbsAg, HbeAg, Anti-HCV Anti-HDV Anti-HVE
tests anti-HbeAg, anti-
HbcAg
Immunity IgG anti-HAV Anti-HBs No test available No test available No test available
Chronic carriers None 6%-10% 8% 80% Unknown
Subsequent chronic Absent 10% 20-70% Frequent Unknown
diseases
High-risk groups Staff and children at Drug addicts, fetus Persons receiving Same as for HBV Immigrants/travelers
day-care centers and of women with frequent blood from HEV epidemic
institutions infected mothers, transfusions areas
sexually active
people, health care
workers
Nursing Interventions 6. shock
1. Primary Prevention
 immunization to high-risk individuals Nursing Process
 administering immune globulins to those exposed to
Hepa A and B Diagnosis
 Thorough blood screening 1. Fluid volume deficit related to fluid lost through diarrhea
 Use of condoms during sexual activity 2. Knowledge deficit about the infection and the risk of
2. Secondary Prevention transmission to others
 proper handwashing by patient and staff
 contaminated needles and equipment should be Nursing Interventions
handled with great care 1. Assess degree of dehydration
 wearing of gloves when disposing infected stool and 2. Encourage patient to continue oral rehydration therapy
blood 3. Encourage mother to continue breastfeeding of infants
 proper cleansing, bagging and labeling of 4. Provide low residue, high calorie, high protein diet
contaminated items such as bed linens and bedpans 5. Educate patient on:
3. Intersperse rest periods in between activity to promote rest  Proper food handling and cooking
4. Encourage adequate fluid intake and promote a well-  Importance of handwashing
balanced diet  Importance of proper garbage and sewage disposal
5. Assess for signs of progressive disease and report 6. Monitor for signs and symptoms of complications
immediately to physician (bacteremia, shock)
6. Apply emollients and creams to reduce pruritus
7. Avoid activities that promote sweating and increased body LEPTOSPIROSIS
temperature  caused by spirochetes; clinical manifestations may range
8. Administer antihistamines as ordered from asymptomatic to fulminant
9. Advise patient not to scratch skin or if not tolerated, use a  mode of transmission: direct contact with infected urine,
soft cloth to rub skin blood or tissue
10. Monitor for signs of bleeding
11. Use of soft toothbrushes or swabs to avoid injury to gums Pathogenesis
and resultant bleeding  Leptospires enter the skin through abrasions or via mucous
12. Collect blood samples at one time to prevent bleeding membranes
 Leptospiremia develops
II. Infectious Diarrhea  Vasculitis develops causing:
 Transmitted through oral ingestion - Renal – interstitial nephritis and tubular necrosis
 Common organisms: E. coli, Salmonella typhi, Shigella (oliguria, proteinuria, hematuria, uremia)
species, Campylobacter, Giardia lamblia, Vibrio cholera - Liver – centrilobular necrosis (jaundice, increased
liver function tests, dark-colored urine, clay colored
Clinical Manifestations stool, hepatomegaly)
1. diarrhea - Lungs – pulmonary hemorrhage (hemoptysis, chest
2. fever pain, cough)
3. abdominal pain - Skeletal muscles – swelling and focal necrosis (calf
4. nausea and vomiting pain, rashes)
5. tachycardia

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Clinical Manifestations Clinical Manifestations
1. Influenza-like symptoms 1. fever
 fever 2. myalgia
 retroorbital pain 3. retroorbital pain
 photophobia 4. back pain
 calf pain 5. lymphadenopathy
 conjunctival suffusion 6. petecchiae
 lymphadenopathy 7. bleeding diathesis
 mild jaundice 8. renal failure
 hepatomegaly/ splenomegaly 9. maculopapular rash
 mental confusion
 maculopapular rashes Diagnostics
2. Weil’s syndrome 1. IgM ELISA
 jaundice 2. Tourniquet test
 renal dysfunction 3. Serial CBC
 hemorrhagic diathesis
Nursing Process
Laboratory Diagnostics
1. isolation of leptospires Nursing Diagnosis
2. microscopic agglutination test (MAT) 1. Altered tissue perfusion r/t bleeding tendencies
3. urinalysis 2. Knowledge deficit about the disease and risk for spread of
4. BUN, creatinine, electrolytes infection or re-infection
5. AST, ALT, bilirubin, alkaline phosphatase 3. Potential for fluid volume deficit r/t bleeding
6. CBC
7. Chest X-ray Nursing Interventions
8. PT, PTT 1. Monitor VS regularly
2. Handle patient gently so as to prevent injury
Medical Management 3. Use soft-bristled toothbrush to prevent gum bleeding
1. Antibiotics 4. Encourage patient to increase fluid intake
2. Supportive treatment (dialysis, endotracheal intubation, 5. Avoid intramuscular injections as much as possible
blood transfusion) 6. Advise patient to avoid using NSAIDs or aspirin to prevent
GI bleeding
Nursing Process 7. Monitor for signs of complications (IC bleeding, viremia)
8. Provide high residue, high carbohydrate and high protein diet
Diagnosis 9. Advise patient to avoid Valsalva maneuver
1. High risk for injury r/t altered clotting mechanisms and 10. Advise patient on preventive measures
mental confusion  constantly remove waters in jars, vases and discarded
2. Altered body temperature: hyperthermia r/t inflammatory containers
processes of leptospirosis  apply anti-repellant on skin especially during the day
3. Fluid volume deficit r/t compromised regulatory time
mechanisms
RABIES
Nursing Interventions  acute viral illness of the CNS
1. Monitor for hemorrhagic manifestations; monitor PT and  transmitted via infected secretions, usually saliva or
PTT through transplantation of infected tissues
2. Assess level of consciousness and cognitive level  caused by the rabies virus
3. Provide safe environment (pad side rails, remove obstacles  mortality is almost 100%
in rooms, prevent falls)
4. Observe each stool for color, consistency, and amount Pathogenesis
5. Observe during blood transfusions
6. Administer Vit K as indicated Inoculation of virus in the epidermis onto mucous membrane
7. Encourage gentle blowing of nose 
8. Use small gauge needles for protection replication in striated muscle
9. Encourage oral fluid intake 
10. Monitor IV fluids, central venous lines or arterial ascends to the CNS
monitoring lines 
11. Assess for signs of dehydration dissemination to autonomic nerves
12. Monitor intake and output
13. Administer antibiotics as prescribed Stages and Clinical Manifestations
14. Apply cool sponges or icebag for elevated temperature Stages Clinical Manifestations
Prodromal  fever
DENGUE HEMORRHAGIC FEVER period  headache
caused by a Flaviviridae virus; transmitted by Aedes aegypti  malaise
mosquito  anorexia
 contains 4 subtypes  nausea and vomiting

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 Encephallic  confusion 5. Note any changes in behavior
phase  hallucinations 6. Provide a quiet environment
 combativeness 7. Provide long side rails and pad the rails
 muscle spasm 8. If comatose, monitor for signs and symptoms of
 meningismus complications
 seizures 9. If with fever, administer acetaminophen as prescribed
 opisthotonus 10. Keep skin clean and dry. Make sure that linens are not
 increased lacrimation crumpled.
 fever
 postural hypotension LEPROSY
 Chronic granulomatous infection that affects superficial
tissues
Tuberculoid Borderline Lepromatous  Involve cooler areas of the body (face, eyes, peripheral
Number of Single Several Many nerves, testes)
skin lesions  Caused by Mycobacterium leprae; grows slowly
Hair growth  Mode of transmission: direct human to human contact
on skin Absent Slightly Not affected
lesions decreased Types of Leprosy
Sensation in Glove and 1. enlarged peripheral nerves
lesions of the Completely Moderately stocking 2. leonine facies
extremities lost lost peripheral 3. thinning of lateral eyebrows
neuropathy 4. saddlenose deformity
Acid fast 5. hypesthesia followed by anesthesia
bacilli in skin None Several Innumerable 6. (-) sweating on site of lesion
scrapings 7. infertility
Lepromin Strongly No reaction No reaction 8. keratitis, blindness
skin test positive 9. muscle atrophy

Brainstem  diplopia Complications

dysfunction  facial palsies 1. secondary infections
 difficulty with deglutition 2. trauma
 hydrophobia 3. contractures
 coma
 apnea Laboratory Diagnostics
Death  Death 1. Skin scrapings
2. Skin biopsy
Diagnostics 3. Lepromin test
1. History and PE
2. Viral culture Medical Management
3. Histologic and microscopic examination of Negri bodies in 1. Dapsone for 24 months
postmortem brain 2. Rifampicin for 6 months
3. Clofazimine
Medical Management
1. Post-exposure prophylaxis Nursing Process
a. Local wound therapy – mechanical and chemical
cleansing of infected site Diagnosis
b. Passive immunization – Human rabies immune 1. Potential for injury related to decreased tactile sensation
globulin (HRIG) 2. Fear related to stigmatization and to prognosis and
2. Active immunization – give 5 doses of antirabies vaccine complications
within 28 days 3. Knowledge deficit about the infection and the risk of
transmission to others
Nursing Process
Nursing Interventions
Diagnosis 1. Advise patient to regularly inspect skin for redness,
1. Potential for injury related to seizures abrasions or any signs of infection and trauma
2. Ineffective breathing pattern related to neuromuscular 2. Always keep fingernails short and clean
impairment 3. Encourage both active and passive ROM
3. Impaired swallowing related to neuromuscular impairment

Nursing Interventions
1. Monitor VS regularly
2. 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 bedside

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4. Facilitating learning by educating client on nature, course 3. Fear related to stigmatization and to prognosis and
and treatment and possible complications of disease complications
5. Advise patient on importance of compliance to medications
6. Promote positive coping strategies of patient Nursing Interventions
1. Educate client regarding:
Nursing Process  Risk factors
 Use of condoms or practice safe sex
Diagnosis  Possible complications (ectopic pregnancy, infertility,
1. Knowledge deficit about the disease and risk for spread of neurosyphilis, gonococcal arthritis, aortitis)
infection or re-infection  Medications and their side effects
2. Non-compliance with treatment 2. Administer antibiotics as ordered

SEXUALLY TRANSMITTED DISEASES

Syphilis Gonorrhea Chlamydia Herpes Simplex Condyloma

trachomatis Type 2 Acuminata
Signs and 1° syphilis – chancre  Increased  Dyspareunia  Vesicular  Wart-like
Symptoms 2° syphilis – vaginal  Increased eruptions on the cauliflower-like
hematogenous spread secretions vaginal pruritus penile shaft, lesions on the
 Rashes  Increased  Increased vagina, vulva or penis and vulva
 Condyloma lata vaginal pruritus vaginal cervix
 Fever, malaise  Penile secretions
 Lymphadenopathy discharge  Infertility
 Weight loss  Dysuria  Dysuria
3° syphilis
 Gumma
 Aortitis
 Neurosyphilis
Diagnostics VDRL/RPR Gram stain Culture Viral culture Culture
Medical Benzanthine Ceftriaxone Doxycycline Acyclovir Cryotherapy
Management Penicillin Doxycycline Azythromycin Electrosurgery
Doxycycline Podophyllin

Gumma Herpes Simplex Type 2 Condyloma Lata Syphilis

PENICILLIN FAMILY ANTIBIOTICS

Name Mechanism of Action Pharmacokinetics Adverse Effects Therapeutic Effects

Pen G Cannot survive passage  Allergy  Streptococci
Aqueous crystalline Pen Inhibits bacterial cell through stomach  Superinfections pneumoniae
G wall synthesis  Crystalline Pen G IV (Clostridium difficile)  Group A Beta-
Benzathine Pen G  Procaine and hemolytic strep
Procaine Pen G Benzathine Pen G IM  Neisseria gonorrhea
 Treponema pallidum
Pen V Same oral Same
Amino penicillins  Ampicillin –  Broader gram (-)
Amoxicillin Same IV/oral Same coverage than above
Ampicillin  Amoxicillin - oral penicillins
 Same
Penicillinase resistant  Skin and other
penicillins (IV) infections caused by
Methicillin Same IV Same Staphylococcus aureus
Nafcillin
Oxacillin
Penicillinase resistant
penicillins (PO)
Cloxacillin Same Oral Same
Dicloxacillin
Nafcillin
Oxacillin
Combination of  Augmentin – oral  Covers both gram
penicillin with beta-  Unasyn - IV (-) and (+) bacteria
lactamase inhibitors Same Same  Anaerobic bacteria
 Amoxillin +  Pseudomonas
clavulanate
(Augmentin)
 Ampicillin +
sulbactam (Unasyn)
Anti-pseudomonal  IV  Anaerobic coverage
penicillins Same Same
Ticarcillin
Carbenicillin
Piperacillin

BETA-LACTAMASE INHIBITORS

I. Cephalosporins
1st generation Competitive inhibitor of Oral  Allergic reaction  Gram (+) coverage
Cephalexin the transpeptidase  Cephalexin  Superimposed
Cefazolin enzyme; inhibits IV infections
Cephradine bacterial wall synthesis  Cephalothin
Cephalothin  Cefazolin
Cephadrine – oral/IV
Renal excretion
2nd generation Oral Same as above Gram (-) and (+) bacteria
Cefaclor  Cefaclor Cefamandole:
Cefoxitin Same Oral/IV  Interferes with Vit
Cefuroxime  Cefuroxime K dependent clotting
Cefamandole The rest is IV factors
 Interferes with
metabolism of
alcohol
3rd generation Gram (-) bacteria
Ceftriaxone Oral Ceftriaxone – good
Ceftazidime Same  Cefixime Same as above penetration in the CSF
Cefixime The rest is IV
Cefoperazone
4th generation Gram (-) Pseudomonas
Cefepime Same IV Same aeruginosa

II. Carbapenems
 Imipenem Inhibits bacterial cell  IV or IM  Nausea & vomiting  Gram (-) & (+)
 Meropenem wall synthesis  Renal excretion  Allergy  Anaerobes
 seizures

III. Monobactams
Aztreonam Inhibits bacterial  IV or IM No allergic cross- Gram (-) organisms
wall synthesis  Renal excretion reactivity with
penicillins

ANTI-RIBOSOMAL ANTIBIOTICS
 Name MOA Pharmacokinetics Adverse Effects Therapeutic Use
Chloramphenicol Binds to 50S ribosomal  Oral or IV  Bone marrow depression  Bacterial meningitis
sub-unit and inhibits  Metabolized by the  Gray baby syndrome in infants
protein synthesis liver (cyanosis, vomiting, green  Ricketsial infection in
 Excreted via stools & vasomotor children & pregnant
kidney collapse) women
Clindamycin Same  Oral or IV  Pseudomembranous  Anaerobes
 Excreted from bile colitis (peritonitis, PID)
and urine  Gram (+) organisms
if allergic to penicillins
and cephalosporins
 Toxoplasma gondii
Erythromycin Same  Oral or IV  Reversible cholestatic  Chlamydia
 Concentrated in the hepatitis trachomatis
liver  Epigastric distress  Bordatella pertussis
 Transient reversible  Mycoplasma
deafness with very high pneumoniae
doses  Corynebacterium
 Candida vaginits diphtheriae
 Strep & Staph
infection for allergic to
penicillin
Tetracycline Binds to 30S ribosomal  Food and milk  GI irritation  Chlamydia
Doxycycline sub-unit and inhibits impairs oral  Renal and hepatic trachomatis
protein synthesis absorption toxicity  Mycoplasma
Excretion  Fanconis syndrome pneumoniae
 Urine- tetracycline  Teratogenic  Entamoeba
 Stool- doxycycline histolytics
 Treponema pallidum
Aminoglycosides Same as above  IV or IM  Nephrotoxic  Gram (-) enteric
 Diffuses inflamed  Ototoxic organisms
meninges  Mycobacterium
 Synergistic with tuberculosis
penicillin
Spectinomycin Same as above IM Neisseria gonorrhea

MISCELLANEOUS ANTIBIOTICS

Name MOA Pharmacokinetics Adverse Effects Therapeutic Effects

Fluoroquinones Inhibits DNA gyrase  Oral or IV  GI symptoms  Hospital-acquired
Ciprofloxacin  Excellent tissue  Damage to cartilage infections
Levofloxacin penetration  CNS symptoms  Chronic infections
Ofloxacin  Renal excretion  Diarrhea caused by
Sparfloxacin enteric organisms
Vancomycin Inhibits cell wall IV Red man syndrome if  MRSA
synthesis infused rapidly  Enterococcus
Trimethoprim/ Inhibits tetrahydrofolate  GI upset  GUT infections
Sulfamethoxazole synthesis Oral or IV  Skin rashes  Pneumocystis carinii
 Bone marrow
suppression
 Not used in 1st
trimester – increased
fetal bilirubin
 Macrocytic anemia