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N107 LEC 12/04/06

PROF. RIDULME

INFLAMMATORY AND IMMUNE RESPONSES  caused by human immunodeficiency virus


(HIV), a retrovirus
I. Scope of Defense Mechanism
A. Non-specific Defense Mechanism Pathogenesis
1. External Non-specific Defense  HIV attaches to the T4 helper cells
Mechanism
 Virus replicates inside the T4 helper cells
 Skin and mucous membrane
 Depletion of T4 helper cells
 Specialized structures (nasal hairs,
 Opportunistic infections set in
eyelashes, tears)
 Biochemical factors (pH,
Risk factors
secretions, lysozymes)
1. unprotected vaginal, oral or anal intercourse
2. IV drug use with contaminated needles
2. Internal Non-specific Defense
3. infected mother to fetus
Mechanism
4. health workers
 Mononuclear phagocyte system 5. blood and blood product recipients
(neutrophils, macrophages) 6. semen used for artificial insemination
B. Specific Defense Mechanism Stages and Manifestations
1. Humoral Immune System (B cell)
Stages Manifestations
 Bacteria that produce acute Stage I Infectious mononucleosis-
infection Acute infections like or influenza-like
 Bacterial exotoxins symptoms
 Viruses that enter via blood stream Stage II None
(poliomyelitis, hepatitis) Asymptomatic
 Viruses that enter via mucosal Stage III Lymphadenopathy ≥ 1 cm,
tissues (enterovirus, cold virus, Persistent extrainguinal areas for
influenza) generalized more than 3 mos.
lymphadenopathy
2. Cell-mediated Immune System (T cell) Stage IV
 Chronic bacterial infection (syphilis, Subgroup A Constitutional symptoms
TB) Subgroup B Neurologic disease
 Fungal infection Subgroup C Opportunistic infections
 Transplanted/transformed cells (PCP pneumonia,
(cancer) histoplasmosis,
cryptococcosis, PTB, herpes
II. Manifestations of Inflammation simplex)
A. Local Manifestations Subgroup D Secondary cancer (Kaposi’s
1. redness (rubor) – d/t hyperemia sarcoma, cervical Ca, NHL)
2. swelling (tumor) – caused by the fluid
exudates Laboratory Diagnostics
3. pain (dolor) – caused by pressure of 1. Enzyme-linked immunoabsorbent assay (ELISA)
fluid exudates and chemical irritation 2. Western blot assay
of nerve endings 3. CD4 count
4. loss of function (function laesa) – d/t 4. CD4/CD8 ratio
swelling and pain 5. CBC
6. Chest x-ray
B. Systemic Manifestations 7. Sputum culture
1. fever
- d/t endogenous pyrogens Medical Management
- part of defense mechanism; helps 1. Protease inhibitors
increase production of interferon 2. Nucleoside reverse transcriptase inhibitors
2. increased WBC 3. Non-nucleoside reverse transcriptase inhibitors
3. increased erythrocyte sedimentation 4. Antineoplastics
rate (ESR) – d/t increase in fibrogen 5. Antibiotics
6. Antifungals
7. Antidiarrheals
8. Antidepressants
HIV INFECTION AND AIDS 9. Appetite stimulants

1
Clinical Manifestations
Complications Blood disorders (anemia, leukemia, lymphopenia,
1. Cancer (Kaposi’s sarcoma, cervical Ca, NHL) thrombocytopenia)
2. PCP pneumonia Renal disorders
3. TB (M. avium, M. tuberculosis) Arthritis
4. Fungal infection (candidiasis, histoplasmosis, Immunologic disorder (anti-DNA antibody, (+) LE)
crytococcosis) Neurologic disorders
5. Protozoal infection (Toxoplasmosis) Serositis (pleuritis, pericarditis)
6. CMV (blindness) Oral ulcers
Antinuclear antibody
Nursing Process Photosensitivity
Malar rash
Diagnosis Discoid rash
1. High risk for infection related to decreased
immune response Diagnostics
2. Altered nutrition: less than body requirements 1. Antinuclear antibody (ANA) test
r/t chewing/swallowing difficulties 2. ESR
3. Coping, family: compromised r/t temporary 3. Serum complement
family disorganization and role changes 4. CBC
4. Social isolation r/t inadequate personal 5. Urinalysis
resources 6. LE prep
5. Fear r/t uncertainty of illness 7. 12 lead ECG
8. Chest x-ray
Nursing Interventions
1. Educate the client regarding the need for Medical Management
repeat testing at 3, 6 and 12 mos. if risk factors 1. Anti-inflammatory drugs (NSAIDs, salicylates)
are present even if the first diagnostic test is 2. Antimalarial drugs
negative. 3. Corticosteroids
2. Use universal precautions when there is 4. Cytotoxic drugs
potential for contact with blood and body fluids 5. Creams/emollients
known to transmit HIV.
3. Teach client regarding transmission of HIV and Nursing Process
methods for safer sex with uninfected partners.
4. Identify factors that may interfere with Nursing Diagnosis
nutrition (anorexia, nausea, vomiting, oral 1. Fluid volume excess r/t compromised
lesions, dysphagia). regulatory mechanism
5. Teach regarding self-administration of 2. High risk for infection r/t decreased immune
prescribed drugs, its side effects and response
compliance with drug therapy. 3. Knowledge deficit r/t lack of exposure to
6. Encourage activity and rest periods. information
7. Administer supplemental oxygen as needed. 4. Self-esteem disturbance r/t change in body
8. Teach client to report signs of infection appearance
immediately.
9. Encourage use of constructive coping Nursing Interventions
mechanisms. 1. Facilitating learning by educating client on:
10. Assist client with identification of support  Nature, course and treatment of disease
systems.  Appropriate balance of rest and activity
 Avoidance of sun exposure (use of
SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) sunscreen, sunglasses, wearing long-
 Autoimmune disease with no known cure or sleeved blouse, broad-brimmed hats)
cause  Application of cosmetics and wigs
 Characterized by periods of remissions and 2. Administer medications as prescribed.
exacerbations 3. Assist patient to gradually resume
 F>M independence in ADL.
4. Monitor signs and symptoms of complications.
Pathogenesis 5. Keep skin lesions clean and dry.
 Increase in autoantibody production as a result 6. Encourage close follow-up care.
of a decreased or abnormal T suppressor cell
function

RHEUMATOID ARTHRITIS  Chronic systemic, inflammatory disorder that


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

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 Characterized by remissions and exacerbations Clinical Manifestations
 Etiologic Factors: Immune factors, genetic and 1. Non-specific symptoms (fever, weight loss,
metabolic factors, infection fatigue)
2. Bilateral and symmetrical swelling of joints
Pathogenesis 3. Morning stiffness
 Altered immune complexes that deposit in 4. Subcutaneous nodules
synovial fluid causing inflammation and tissue 5. Limitation of movement of affected joint
injury and subsequent joint destruction 6. Systemic manifestations (glaucoma,
splenomegaly, aortic valve disease, etc.)

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
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

Antigen-antibody response: production of normal immunoglobulins against the

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 Increased blood flow and
Degradation of joint tissues migration of capillary permeability

Attraction of more phagocytes


to ingest products of degradation

Chronic inflammatory joint


disease

Medical Management
1. Anti-inflammatory agents Nursing Process
2. Corticosteroids
3. Disease Modifying Anti-rheumatic drugs Diagnosis
(methotrexate, anti-malarials, sulfasalazine, 1. Knowledge deficit (r/t arthritis) d/t lack of
gold) exposure of information

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2. Self-care deficit r/t pain and musculoskeletal 2. Administer medications as prescribed.
impairments 3. Encourage frequent rest periods.
3. Fatigue r/t chronic systemic disease 4. Splint acutely inflammed joints.
4. Self-esteem disturbance d/t change in body 5. Encourage compliance with prescribed exercise
appearance program.
6. Encourage active ROM exercise.
7. Encourage use of cane, crutches or other
Nursing Interventions assistive devices.
1. 8. Apply
cold

Assess/monitor for: compress to acutely inflammed joints.


 Joints for pain, mobility, deformities and 9. Apply heat via shower, bath or moist warm
contractures packs as prescribed.
 VS 10. Provide emotional support and encouragement.
 Weight

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 Acquired Acquired Pneumonia
Pneumonia Pneumonia
Preventing Infection in the Community Occur either Also called Refers to
1. Sanitation techniques Charac- in the nosocomial pulmonary
2. Regulated health practices teristics community or infection consequences
3. Vaccination programs 48 hours Onset of resulting from
before symptoms the entry of
a. Passive immunization – temporary
hospitalizatio more than 48 endogenous or
protection afforded by the acquisition of n hours after exogenous
preformed antibodies hospitalizatio substances
2 types: n into the lower
a.1. Natural passive immunization airway
a.2. Artificial passive immunization Streptococcu P.aeruginosa, Streptococcus
Etiologic s Staphylo- pneumoniae,
b. Active immunization – provides long term Factors pneumoniae, coccus H.influenza,
H.influenza, pneumoniae, Staphylo-
immunity by giving either a killed or a live
Mycoplasma Klebsiella coccus
attenuated vaccine, thus stimulating either pneumoniae pneumoniae, pneumoniae,
the humoral or cell mediated immunity E.coli gastric
Ex: killed vaccine – DPT contents
live attenuated vaccine – MMR
Risk Factors
1. Conditions that produce mucus or bronchial
Contraindications obstruction
1. previous anaphylaxis or anaphylactic-like - smoking
reaction 7 days after DPT vaccination - cancer, COPD
2. encephalopathy 2. Immunosuppressed patients
3. fever ≥ 40oC within 48 hours of vaccination 3. Prolonged immobility
4. seizure of shock-like manifestations 3 days 4. Depressed cough reflex (medication,
after immunization debilitated state, weak respiratory muscles,
5. live attenuated vaccines should not be decreased LOC)
given to immunosuppressed patients 5. Alcohol intoxication
6. MMR contraindicated for pregnant women 6. Respiratory therapy with improperly cleaned
instruments
Preventing Infection in the Hospital Setting 7. Aging – may either be a primary problem or as
1. Handwashing before and after each patient a complication of a chronic disease
contact - clinical manifestations are usually atypical
2. Use sterile gloves when handling contaminated
body fluids and secretions Pathophysiology
3. Use aseptic technique when cleaning wounds Normal Patho- Clinical Manifestation
4. Changing of infusion sets, catheters and Function physiology
solutions regularly Mucociliary Hypertrophy Increased sputum
5. Handle all sharps and needles with care system of mucous production and cough
6. Use of masks when taking care of patients with membrane  anaerobic –
infections transmitted via airborne or droplet lining of the foul smelling
lungs specimen
RESPIRATORY INFECTIONS resulting in  Klebsiella –
hypersec- currant jelly color
I. Pneumonia: acute inflammation of lung retion  Staphylococcu
tissue s – creamy yellow
 Pseudomonas
Classification of Pneumonia – green
Community Hospital Aspiration  Viral – muco-

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purulent  Offer small, frequent feedings with diet high in
Broncho- carbohydrates and protein
spasm from  Localized or  Monitor for signs and symptoms of
increased diffuse wheezing; complications (hypotensive shock, atelactasis,
secretions dyspnea pleural effusion)
Alveolo- Decreased  chest X-ray
capillary surface area films: consolidated II. Pulmonary Tuberculosis
membrane for gas or diffused/patchy  Caused by Mycobacterium tuberculosis
exchange appearance  Spreads via airborne transmission (generally
 Hypoxemia particles 1 to 5 micrometers in diameter)
Pleura Inflamma-  chest pain
tion of the  pleural Risk Factors
pleura effusion 1. Close contact with someone who has active TB
 dullness on 2. Immunocompromised status
percussion 3. Substance abuse
 decreased 4. Any person without adequate health care
breath sounds 5. Pre-existing medical conditions
6. Living in overcrowded, substandard housing
 decreased
7. Health care providers
vocal fremitus
Respiratory Hypoventi-  decreased
muscles lation chest expansion
 respiratory
acidosis
Lung Bacteremia  Elevated WBC
Defense  tachypnea,
System fever Pathophysiology

Laboratory and Diagnostics Inhalation of mycobacterium


1. Complete Blood Count (CBC) ↓
2. Chest X-ray Multiplication of bacteria in lower airways
3. Blood culture ↓
4. Sputum Examination Transmission of bacteria to other parts
5. Arterial Blood Gas (ABG) (lymph nodes, kidneys, brain)

Nursing Process Immune system activated

Nursing Diagnosis Formation of primary tubercle
1. Ineffective airway clearance r/t copious ↓
tracheobronchial secretions Caseation necrosis
2. Impaired gas exchange r/t alvelocapillary ↓
membrane changes Cavitation
3. Risk for fluid volume deficit r/t fever and
dyspnea Classification of PTB
4. Altered nutrition: less than body requirements Class Description Medical Therapy
r/t increased metabolic needs 0 No TB exposure, None
not infected
Nursing Interventions 1 (+) TB exposure Preventive
 Monitor for increased respiratory distress (-) infection chemotherapy
 Administer oxygen therapy via nasal cannula 2 (+) TB exposure, INH for 1 year
 Assist patient to cough effectively (+)infection, (<35 years old)
 Suction airway using sterile technique (-)disease
 Assist with nebulizer therapy 3 Active disease Anti-Koch’s
 Do chest physiotherapy medications for 6
 Administer antibiotics and bronchodilators as months
ordered 4 TB not clinically None
 Ensure adequate fluid intake active
 Assist with ADL, pacing activities to prevent 5 TB suspect Preventive
fatigue and respiratory distress chemotherapy with
 If comatose, reposition patient q 2 h and do INH may be
passive ROM q 4 h instituted
 Encourage deep breathing exercises q 2 h
Nursing Process

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Diagnosis
1. Ineffective airway clearance r/t increased and
tenacious sputum
2. Knowledge deficit about treatment regimen
and preventive health measures
3. Activity intolerance r/t fatigue and altered
nutritional status

Nursing Interventions
1. Increase fluid intake
2. Do chest physiotherapy
3. 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

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Clinical manifestations 4. High risk for injury due to altered clotting
1. Anorexia prothrombin time
2. Weight loss
3. Fatigue
4. Cough
5. Low-grade fever
6. Night sweats

Diagnostics
1. History and PE
2. Chest X-ray
3. Sputum smear and culture
4. Gastric aspirate
5. Tuberculin skin test

Medical Management
A. First line drugs
 INH and rifampicin for 6 months
 PZA, ethambutol/streptomycin for 2
months
B. Second line drugs

GASTROINTESTINAL INFECTIONS

I. Viral Hepatitis

Pathophysiology and Clinical Manifestations


Pathophysiology Clinical Manifestations
Necrosis and - Fever
inflammation of - Chills
hepatocytes - Nausea and vomiting
- Anorexia
- RUQ pain
- Murphy’s sign
- Hepatomegaly
- Elevated liver function
test
Circulating immune - Arthralgia
complexes and - Headache
complement system
activation
Impaired bilirubin - Jaundice
metabolism - Dark-colored urine
- Clay-colored stools
- Pruritus
- Bleeding tendencies
- Increased total,
conjugated and
unconjugated bilirubin

Diagnostics
1. History and PE
2. Liver function test
3. Serologic exam

Nursing Process

Nursing Diagnosis
1. Activity intolerance r/t fatigue
2. Knowledge deficit: diagnostic test,
manifestations, prophylaxis, treatment and
prevention
3. Altered nutrition: less than body requirements
r/t increased metabolic needs and anorexia

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Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E
Age group Older children Young adults All age groups Young adults All age groups
and young
adults
Transmission Fecal-oral Percutaneous Parenteral Same as Hepa B Fecal-oral
and permucosal
routes
Secretions that Stools: 2 weeks Blood, semen, Blood Blood Feces
have been found before jaundice saliva,
to contain nasopharyngeal
infective agent washings
Clinical onset abrupt insidious Insidious insidious Same as Hepa A
Diagnostic IgM anti- HAV HbsAg, HbeAg, Anti-HCV Anti-HDV Anti-HVE
serologic 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 Absent 10% 20-70% Frequent Unknown
chronic diseases
High-risk groups Staff and Drug addicts, Persons Same as for HBV Immigrants/trav
children at day- fetus of women receiving elers from HEV
care centers and with infected frequent blood epidemic areas
institutions mothers, transfusions
sexually active
people, health
care workers
Nursing Interventions • Common organisms: E. coli, Salmonella
1. Primary Prevention typhi, Shigella species, Campylobacter,
 immunization to high-risk individuals Giardia lamblia, Vibrio cholera
 administering immune globulins to those
exposed to Hepa A and B Clinical Manifestations
 Thorough blood screening 1. diarrhea
 Use of condoms during sexual activity 2. fever
2. Secondary Prevention 3. abdominal pain
 proper handwashing by patient and staff 4. nausea and vomiting
 contaminated needles and equipment 5. tachycardia
should be handled with great care 6. shock
 wearing of gloves when disposing infected
stool and blood Nursing Process
 proper cleansing, bagging and labeling of
Diagnosis
contaminated items such as bed linens and
1. Fluid volume deficit related to fluid lost through
bedpans
diarrhea
3. Intersperse rest periods in between activity to
2. Knowledge deficit about the infection and the
promote rest
risk of transmission to others
4. Encourage adequate fluid intake and promote
a well-balanced diet
Nursing Interventions
5. Assess for signs of progressive disease and
1. Assess degree of dehydration
report immediately to physician
2. Encourage patient to continue oral rehydration
6. Apply emollients and creams to reduce pruritus
therapy
7. Avoid activities that promote sweating and
3. Encourage mother to continue breastfeeding of
increased body temperature
infants
8. Administer antihistamines as ordered
4. Provide low residue, high calorie, high protein
9. Advise patient not to scratch skin or if not
diet
tolerated, use a soft cloth to rub skin
5. Educate patient on:
10. Monitor for signs of bleeding
11. Use of soft toothbrushes or swabs to avoid  Proper food handling and cooking
injury to gums and resultant bleeding  Importance of handwashing
12. Collect blood samples at one time to prevent  Importance of proper garbage and sewage
bleeding disposal
6. Monitor for signs and symptoms of
II. Infectious Diarrhea complications (bacteremia, shock)
• Transmitted through oral ingestion
LEPTOSPIROSIS

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 caused by spirochetes; clinical manifestations Nursing Interventions
may range from asymptomatic to fulminant 1. Monitor for hemorrhagic manifestations;
 mode of transmission: direct contact with monitor PT and PTT
infected urine, blood or tissue 2. Assess level of consciousness and cognitive
level
Pathogenesis 3. Provide safe environment (pad side rails,
 Leptospires enter the skin through abrasions or remove obstacles in rooms, prevent falls)
via mucous membranes 4. Observe each stool for color, consistency, and
 Leptospiremia develops amount
5. Observe during blood transfusions
 Vasculitis develops causing:
6. Administer Vit K as indicated
- Renal – interstitial nephritis and tubular
7. Encourage gentle blowing of nose
necrosis (oliguria, proteinuria, hematuria,
8. Use small gauge needles for protection
uremia)
9. Encourage oral fluid intake
- Liver – centrilobular necrosis (jaundice,
10. Monitor IV fluids, central venous lines or
increased liver function tests, dark-colored
arterial monitoring lines
urine, clay colored stool, hepatomegaly)
11. Assess for signs of dehydration
- Lungs – pulmonary hemorrhage
12. Monitor intake and output
(hemoptysis, chest pain, cough)
13. Administer antibiotics as prescribed
- Skeletal muscles – swelling and focal
14. Apply cool sponges or icebag for elevated
necrosis (calf pain, rashes)
temperature
Clinical Manifestations
DENGUE HEMORRHAGIC FEVER
1. Influenza-like symptoms
 caused by a Flaviviridae virus; transmitted by
 fever
Aedes aegypti mosquito
 retroorbital pain
 contains 4 subtypes
 photophobia
 calf pain Clinical Manifestations
 conjunctival suffusion 1. fever
 lymphadenopathy 2. myalgia
 mild jaundice 3. retroorbital pain
 hepatomegaly/ splenomegaly 4. back pain
 mental confusion 5. lymphadenopathy
 maculopapular rashes 6. petecchiae
2. Weil’s syndrome 7. bleeding diathesis
 jaundice 8. renal failure
 renal dysfunction 9. maculopapular rash
 hemorrhagic diathesis
Diagnostics
Laboratory Diagnostics 1. IgM ELISA
1. isolation of leptospires 2. Tourniquet test
2. microscopic agglutination test (MAT) 3. Serial CBC
3. urinalysis
4. BUN, creatinine, electrolytes Nursing Process
5. AST, ALT, bilirubin, alkaline phosphatase
6. CBC Nursing Diagnosis
7. Chest X-ray 1. Altered tissue perfusion r/t bleeding
8. PT, PTT tendencies
2. Knowledge deficit about the disease and
Medical Management risk for spread of infection or re-infection
1. Antibiotics 3. Potential for fluid volume deficit r/t
2. Supportive treatment (dialysis, endotracheal bleeding
intubation, blood transfusion)
Nursing Interventions
Nursing Process 1. Monitor VS regularly
2. Handle patient gently so as to prevent
Diagnosis injury
1. High risk for injury r/t altered clotting 3. Use soft-bristled toothbrush to prevent
mechanisms and mental confusion gum bleeding
2. Altered body temperature: hyperthermia r/t 4. Encourage patient to increase fluid intake
inflammatory processes of leptospirosis 5. Avoid intramuscular injections as much as
3. Fluid volume deficit r/t compromised regulatory possible
mechanisms 6. Advise patient to avoid using NSAIDs or
aspirin to prevent GI bleeding

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 increased
Tuberculoi Borderline Lepromatous
lacrimation
d
 fever
Number of Single Several Many
 postural
skin lesions
hypotension
Hair
growth on Absent Slightly Not affected
skin lesions decreased
Sensation Glove and Brainstem  diplopia
in lesions Completely Moderately stocking dysfunction  facial palsies
of the lost lost peripheral  difficulty with
extremities neuropathy deglutition
Acid fast  hydrophobia
bacilli in None Several Innumerable  coma
skin  apnea
scrapings Death  Death
Lepromin Strongly No reaction No reaction
skin test positive Diagnostics
7. Monitor for signs of complications (IC 1. History and PE
bleeding, viremia) 2. Viral culture
8. Provide high residue, high carbohydrate 3. Histologic and microscopic examination of
and high protein diet Negri bodies in postmortem brain
9. Advise patient to avoid Valsalva maneuver
10. Advise patient on preventive measures Medical Management
 constantly remove waters in jars, vases 1. Post-exposure prophylaxis
and discarded containers a. Local wound therapy – mechanical and
 apply anti-repellant on skin especially chemical cleansing of infected site
during the day time b. Passive immunization – Human rabies
immune globulin (HRIG)
RABIES 2. Active immunization – give 5 doses of
 acute viral illness of the CNS antirabies vaccine within 28 days
 transmitted via infected secretions, usually
saliva or through transplantation of infected Nursing Process
tissues
 caused by the rabies virus Diagnosis
 mortality is almost 100% 1. Potential for injury related to seizures
2. Ineffective breathing pattern related to
Pathogenesis neuromuscular impairment
3. Impaired swallowing related to neuromuscular
Inoculation of virus in the epidermis onto mucous impairment
membrane
↓ Nursing Interventions
replication in striated muscle 1. Monitor VS regularly
↓ 2. Assess for signs of respiratory distress. Closely
ascends to the CNS monitor for breath sounds, rate and character
↓ of respiration.
dissemination to autonomic nerves 3. Have a plastic airway readily available on
bedside.
Stages and Clinical Manifestations 4. Have suction and oxygen available at bedside
Stages Clinical Manifestations 5. Note any changes in behavior
6. Provide a quiet environment
Prodromal  fever
7. Provide long side rails and pad the rails
period  headache 8. If comatose, monitor for signs and symptoms
 malaise of complications
 anorexia 9. If with fever, administer acetaminophen as
 nausea and prescribed
vomiting 10. Keep skin clean and dry. Make sure that linens
Encephallic  confusion are not crumpled.
phase  hallucinations
 combativeness LEPROSY
 muscle spasm  Chronic granulomatous infection that affects
 meningismus superficial tissues
 seizures  Involve cooler areas of the body (face, eyes,
peripheral nerves, testes)
 opisthotonus

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 Caused by Mycobacterium leprae; grows slowly
 Mode of transmission: direct human to human
contact

Types of Leprosy
1. enlarged peripheral nerves
2. leonine facies
3. thinning of lateral eyebrows
4. saddlenose deformity
5. hypesthesia followed by anesthesia
6. (-) sweating on site of lesion
7. infertility
8. keratitis, blindness
9. muscle atrophy

Complications
1. secondary infections
2. trauma
3. contractures

Laboratory Diagnostics
1. Skin scrapings
2. Skin biopsy
3. Lepromin test

Medical Management
1. Dapsone for 24 months
2. Rifampicin for 6 months
3. Clofazimine

Nursing Process

Diagnosis
1. Potential for injury related to decreased tactile
sensation
2. Fear related to stigmatization and to prognosis
and complications
3. Knowledge deficit about the infection and the
risk of transmission to others

Nursing Interventions
1. Advise patient to regularly inspect skin for
redness, abrasions or any signs of infection and
trauma
2. Always keep fingernails short and clean
3. Encourage both active and passive ROM

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

SEXUALLY TRANSMITTED DISEASES

Syphilis Gonorrhea Chlamydia Herpes Condyloma


trachomatis Simplex Type Acuminata
2
Signs and 1° syphilis – chancre • Increased • Dyspareuni • Vesicular • Wart-like
Symptoms 2° syphilis – vaginal a eruptions on cauliflower-
hematogenous secretions • Increased the penile like lesions
spread • Increased vaginal shaft, on the penis
• Rashes vaginal pruritus vagina, and vulva
• Condyloma lata pruritus • Increased vulva or
• Fever, malaise • Penile vaginal cervix
• Lymphadenopath discharge secretions
y • Dysuria • Infertility
• Weight loss • 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 Pharmacokinetics Adverse Effects Therapeutic Effects


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

BETA-LACTAMASE INHIBITORS

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

II. Carbapenems
• Imipenem Inhibits bacterial • IV or IM • Nausea & • Gram (-) & (+)
• Meropenem cell wall synthesis • Renal excretion vomiting • Anaerobes
• Allergy
• 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 • Oral or IV • Bone marrow • Bacterial
ribosomal sub-unit • Metabolized by depression meningitis in
and inhibits the liver • Gray baby infants
protein synthesis • Excreted via syndrome (cyanosis, • Ricketsial
kidney vomiting, green infection in
stools & vasomotor children &
collapse) pregnant women
Clindamycin Same • Oral or IV • Pseudomembranou • Anaerobes
• Excreted from s colitis (peritonitis, PID)
bile and urine • Gram (+)
organisms if
allergic to
penicillins and
cephalosporins
• Toxoplasma
gondii
Erythromycin Same • Oral or IV • Reversible • Chlamydia
• Concentrated cholestatic hepatitis trachomatis
in the liver • Epigastric distress • Bordatella
• Transient reversible pertussis
deafness with very • Mycoplasma
high doses pneumoniae
• Candida vaginits • Corynebacterium
diphtheriae
• Strep & Staph
infection for
allergic to
penicillin
Tetracycline Binds to 30S • Food and milk • GI irritation • Chlamydia
Doxycycline ribosomal sub-unit impairs oral • Renal and hepatic trachomatis
and inhibits absorption toxicity • Mycoplasma
protein synthesis Excretion • Fanconis syndrome pneumoniae
• Urine- • Teratogenic • Entamoeba
tetracycline histolytics
• Stool- • Treponema
doxycycline pallidum
Aminoglycosides Same as above • IV or IM • Nephrotoxic • Gram (-) enteric
• Diffuses • Ototoxic organisms
inflamed • Mycobacterium
meninges tuberculosis
• Synergistic
with 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 infections
Levofloxacin penetration cartilage • Chronic
Ofloxacin • Renal excretion • CNS symptoms infections
Sparfloxacin • Diarrhea caused
by enteric
organisms
Vancomycin Inhibits cell wall IV Red man syndrome • MRSA
synthesis if infused rapidly • Enterococcus
Trimethoprim/ Inhibits • GI upset • GUT infections
Sulfamethoxazole tetrahydrofolate Oral or IV • Skin rashes • Pneumocystis
synthesis • Bone marrow carinii
suppression
• Not used in 1st
trimester –
increased fetal
bilirubin
• Macrocytic
anemia