Ncm104 11th CD III

jcmendiola_Achievers2013
Care of Clients with Problems In Inflammatory

& Immunologic Response, Perception & Coordination
(NCM104)
Patients With Communicable Diseases III
GIT Infectious Diseases
Cholera (El Tor)
(Asiatic Cholera / Epidemic Cholera)

Definition:
o Acute bacterial enteric
disease of the GIT
characterized by
diarrhea, vomiting,
massive loss
of fluid and electrolytes,
which can
lead to hypovolemic
shock,
acidosis
and death
o Acute bacterial enterotoxin (Responsible for secretion of electrolytes from the cell
out into the intestinal lumen)
Host: Children, squatters, crowded,
uneducated, poor economic level
Reservoir: Contaminated water BOIL!
Portal of Entry: GIT
Portal of Exit: GIT (Feces)
Etiologic Agent: Vibrio cholerae /
Vibrio coma
o Curved (Comma-shaped)
o Gram-negative
o Motile with polar flagellum
Pathognomonic Sign: Rice-water Stool = Odorless, colorless appearance of stools with
mucoid appearance like slime
Incubation Period:
o Ranges from A FEW HOURS to FIVE DAYS
o Usually ONE to THREE DAYS

PERIOD of Communicability
During the stool-positive stage and usually a few days after recovery
Note: Occasionally, carrier may have the organism for several months

MODE of TRANSMISSION (Water-borne Transmission)
1. Fecal transmission (Water, milk, food)
2. 5 Fs (Fomites, Finger, Food, Flies, Feces)
3. Flies, soiled hands, utensils also serve to transmit the infection

*** Life THREATENING!
- 24 48 Hours may kill client
Topics Discussed Here Are:
1. GIT Infectious Diseases
a. Cholera (El Tor) / Asiatic Cholera, Epidemic Cholera
b. Typhoid Fever
c. Amoebiasis (Amoebic Dysentery)
d. Botulism
e. Red Tide
f. Schistosomiasis (Bilharziasis / Snail Fever)
g. Bacillary Dysentery (Shigellosis / Bloody Flux)
2. Skin Diseases
a. Leprosy (Hansens Disease / Hansenosis)
b. Scabies
c. Pediculosis (Phthiriasis)
3. Respiratory Infective Diseases
a. Pulmonary Tuberculosis (PTB)
b. Severe Acute Respiratory Syndrome (SARS)
c. Pneumonia
d. Anthrax
e. Influenza (La Grippe)
f. Influenza A (H1N1) Virus
g. Pertussis (Whooping Cough)
h. Paragonimiasis (Lung Fluke)
LOOKY
HERE

PATHOGENESIS

CLINICAL MANIFESTATIONS
1. Acute, profuse, watery diarrhea
2. Initially, stool is brown; Later, becomes pale gray and rice water-like in appearance with
an inoffensive slightly fishy odor
3. Vomiting occurs after diarrhea
4. Complication: Dehydration = 1 30 Liters/day of fluid from diarrhea
5. Poor skin turgor, sunken eyes into orbits
6. Cold skin, wrinkled fingers and toes washerwomans hand
7. Imperceptible radial pulses and unobtainable blood pressure
8. Cyanosis
9. Hoarse voice, then is lost, patient speaks in whispers (Aphonia)
10. Rapid and deep breathing
11. Diminished peripheral circulation
12. Oliguria and even Anuria
13. Temperature could be normal at the onset, subnormal in later stages
14. DEEP SHOCK = Diarrhea STOPS!
15. Death may come four hours after onset, usually on the first or the second day

PRINCIPAL Deficits
1. Extracellular Volume = Loss of intestinal fluid due to enterotoxin adenylate cyclase, cAMP
2. Metabolic Acidosis = Due to loss of a large volume of HCO
3

3. Hypokalemia = Due to massive loss of potassium
4. Renal Failure = Decreased urine output
5. Convulsions and Tetany = Due to loss of magnesium
6. Hypoglycemia = Due to rapid loss of sugar
7. Corneal Scarring = Lost the wink reflex
8. Acute pulmonary Edema = Due to rapid infusion of IV

Diagnostic EXAMS
1. Rectal Swab
2. Darkfield / Phase Microscopy
3. Stool Exam

MODALITIES OF TREATMENT
Treatment Aims To: Correcting the basic abnormality without delay
1. IV Treatment
2. Oral Therapy (ORESOL, HYDRITES) Unless contraindicated

3. Maintenance of fluid and electrolyte volume
4. Antibiotics
o Tetracycline
500 mg q6 hours (Adults)
125 mg/kg body weight q6 hours for 72 hours (Children)
o Furazolidone
100 mg (Adults)
125 mg/kg q6 hours for 72 hours (Children)
o Chloramphenicol
500 mg (Adults)
18 mg/kg q6 hours for 72 hours (Children)
o Cotrimoxazole 8 mg/kg for 72 hours

NURSING MANAGEMENT
1. Medical Aseptic Protective Care (Handwashing!)
2. Enteric isolation
3. VS recorded accurately
4. I&O accurately measured
5. Careful personal hygiene
6. Proper disposal of excreta
7. Concurrent disinfection
8. Food must be properly prepared
9. Environmental sanitation
10. Weighing the client
11. Appropriate diet is given according to stage of recovery

PREVENTION
1. Food and water supply must be protected from fecal contamination by boiling at least 20
minutes
2. Water should be boiled or chlorinated
3. Milk should be pasteurized
4. Sanitary disposal of human excreta
5. Sanitary supervision is important

COMMON NURSING DIAGNOSES
High risk for fluid volume deficit
Impaired skin integrity
Altered nutrition: Less than body requirements
Altered tissue perfusion
Knowledge deficit
Diarrhea

Typhoid Fever
Bacterial infection transmitted by contaminated water, milk, shellfish and other foods affecting the
lymphoid tissues of the small intestines called Peyers Patches
Pathognomonic Sign: Rose spots appear on the abdominal wall (7
th
9
th
Day)

ETIOLOGIC AGENT: Salmonella typhosa / Salmonella typhi
- Gram-negative, motile and non-spore forming

INCUBATION PERIOD: 5 40 Days (With a mean of 10 20 Days)

PERIOD OF COMMUNICABILITY: Variable, as long as the patient is excreting the
microorganism, he is capable of infecting others

SOURCES OF INFECTION:
1. Person who just recovered from the disease or has recently taken care of a diseased patient
with typhoid
2. Ingestion of shellfish (oysters) from contaminated waters
3. Stool / Vomitus (Reptile feces)

MODE OF TRANSMISSION
1. Fecal-oral Transmission
2. Through the 5 Fs
3. Contaminated food, water and milk

PATHOGENESIS

1. Onset
a. Headache, chilly sensation and aching all over the body Body reacting
b. N/V, diarrhea
c. All symptoms are WORST 4
th
and 5
th
Day
d. Fever is higher in the morning than in the afternoon
e. Breathing is accelerated, furred tongue, hot and dry skin, distended and tender
abdomen
f. 7
th
9
th
Day Rose spots appear on the abdominal wall
g. 2
nd
Week: Symptoms become more aggravated. Temperature becomes stable, rose
spots are more prominent due to massive hemorrhage / apposes
DENGUE IS DIFFERENT
2. Typhoid State
a. Decline of symptoms
b. Tongue protrudes, dry and brown Dehydration and wrinkles
c. Teeth and lips are dirty-brown, collection of dried mucus (Sordes)
d. Staring blankly (Coma vigil)
e. Twitching of tendons, especially those of the wrist (Subsultus tendinum)
f. Mutters deliriously (Carphologia)
g. Tendency to slip down to the foot part of the bed
h. Severe Cases: Rambling delirium ending in DEATH

COMPLICATIONS
1. Hemorrhage or Perforation [Secretin III Secretion] = Most dreaded complications
2. Peritonitis
3. Bronchitis and Pneumonia
4. Meteorism or Excessive distention of the bowels (tympanites)
5. Thrombosis and embolism
6. Early heart failure
7. Typhoid Spine or neuritis
8. Septicemia
9. Reiters Syndrome Joint pain, eye irritation, painful urination can lead to chronic arthritis

DIAGNOSTIC PROCEDURE
1. Typhidot Confirmatory (Injection of antigen of typhoid
2. ELISA
3. Widal Test
4. Rectal Swab
5. Mouse Bioassay

1. Chloramphenicol (DRUG OF CHOICE!)
2. Ampicillin
3. Co-trimoxazole
4. Ciprofloxacin or Ciftriaxone
5. Does not respond to Chloramphenicol, 3
rd
and 4
th
Generation Drugs are used

NURSING MANAGEMENT
1. Medical aseptic technique
2. Restore F&E by small quantities at frequent intervals
3. Monitor VS
4. Prevent further injury (If with typhoid psychosis)
5. Personal hygiene and mouth care
6. Cooling measures
7. WOF: Intestinal bleeding
8. Terminal and concurrent disinfection

PREVENTION and CONTROL
1. Boil water up to 40C , COOK it, PEEL it/Forget it
2. Supervision of food handlers
3. Enteric isolation
4. Adequate amounts of safe drinking water
5. Reporting of cases
6. Detection and monitoring
7. Education on the mode of transmission

Fluid volume (Diarrhea)
Hyperthermia
Self-care deficit
Constipation
Anxiety
Knowledge deficit
High risk for injury (Typhoid psychosis)

Amoebiasis (Amoebic Dysentery)
- Protozoal infection of human beings which involves the colon, spreading to the soft tissues
commonly to the liver and lungs by contiguity or hematogenous / lymphatic dissemination
- Host: People who commonly eat STREET FOODS

ETIOLOGIC AGENT
Entamoeba histolytica
o Has two Developmental Stages
1) Trophozoites / Vegetative Form Cant survive in tropical environment
2) Cyst Infective stage of E. histolytica
INCUBATION PERIOD
Severe infection: 3 Days
Sub-acute and Chronic Form: Several Months
Average Cases: Varies from 3 4 Weeks (For life Amoebiasis)

PERIOD OF COMMUNICABILITY: Entire Duration of the ILLNESS

1. Fecal-oral Transmission
2. Direct contact: Sexual contact by orogenital, oroanal and proctogenital sexual activity
3. Indirect Contact: Uncooked leafy vegetables, foods contaminated with fecal material

PATHOPHYSIOLOGY

1. Acute Amoebic Dysentery
a. Slight attack of diarrhea, period of constipation accompanied by Tenesmus
Abnormal contraction of anal sphincter
b. Diarrhea, watery and foul-smelling stools often containing blood-streaked mucus
c. Colic and gaseous distention of lower abdomen Bloated / Inflamed
d. Nausea, flatulence, abdominal distension and tenderness in the right iliac region over
the colon
2. Chronic Amoebic Dysentery
a. Several days, usually succeeded by constipation
b. Tenesmus

c. Anorexia, weight loss, and weakness
d. Liver may be enlarged If protozoa
e. First are semifluid, but soon become water, bloody and mucoid
f. Vague abdominal distress, flatulence, constipation or irregularity of bowel
movement
g. Mild toxemia, constant fatigue and lassitude Feeling of exhaustion
h. Abdomen loses its elasticity when picked up between the fingers
i. Scattered ulceration with whitish/yellowish and erythematous borders
j. Gangrenous Type (Fatal), large sloughs of intestinal tissues in the stools,
accompanied by hemorrhage
3. Extraintestinal Forms
HEPATIC
a. Pain in upper right quadrant with tenderness of the liver
b. Jaundice
c. Intermittent fever
d. Loss of weight or anorexia
e. Abscess through the lungs; patient coughs anchovy-sauce sputum

DIAGNOSTIC EXAM
1. Stool exam
2. Blood exam
3. Proctoscopy / Sigmoidoscopy

TREATMENT MODALITIES
1. Metronidazole (Flagyl) 800 mg TID x 5 days
2. Tetracycline 250 mg q6 hours
3. Ampicillin, Quinolone, Sulfadiazine
4. Streptomycin SO
4
, Chloramphenicol
5. F&E replaced

NURSING MANAGEMENT
1. Isolation and enteric precaution
2. Health education: Food and water management
3. Proper collection of stool specimen As long as client has diarrhea, NO TO ANTI-
DIARRHEAL DRUGS and NO TO DAIRY PRODUCTS
4. Skin Care
5. Mouth Care
6. Provide optimum comfort
7. Diet Forced fluids

METHODS OF PREVENTION
1. Health education
2. Sanitary disposal of feces
3. Protect, chlorinate, and purify drinking water
4. Observe scrupulous cleanliness in food preparation and food handling
5. Detection and treatment of carriers
6. Fly control (Can serve as vectors)

Botulism
A rare but serious paralytic illness caused by a potent neurotoxin

ETIOLOGIC AGENT:
Clostridium botulinum
o Gram-positive, spore-forming, anaerobic organism

Three Human Forms of Botulism
1) Foodborne Ingestion of inadequately cooked contaminated food, low acid content
2) Wound Botulism (Cutaneous Botulism) Ulcers with sharply demarcated edges
3) Infant Botulism Aged 3 20 weeks. Hypotonic (floppy) infant syndrome

PATHOPHYSIOLOGY

CLINICAL CHARACTERISTICS
1. Flaccid paralysis and descends via the bulbar musculature
2. Somatic musculature is the next part which will result in generalized weakness
3. Neurological Symptoms:
a. Diplopia and blurred vision
b. Ptosis, dry mouth, dysphagia and Dysarthria
4. Classic Symptoms:
a. Double vision, blurred vision, drooping eyelids
b. Slurred speech, difficulty swallowing and dry mouth
c. Muscle weakness
d. Infants:
i. Lethargic appearance, feed poorly, usually constipated due to peristalsis
of smooth muscles
ii. Weak cry and poor muscle tone
e. If untreated, can cause paralysis of arms, legs, trunk and respiratory muscles
f. Foodborne Botulism:
i. Symptoms usually begin 18 36 hours after eating contaminated food
ii. Symptoms continue to cause paralytic ileus with severe constipation and to
body paralysis
iii. Respiratory muscles are affected, DEATH (Respiratory failure)

COMPLICATIONS
1. Pneumonia
2. UTI
3. Pulmonary Embolism
4. Decubitus ulcer
5. Flexion contractures

TREATMENT / MANAGEMENT
1. Supportive care especially to respiratory and nutritional needs
Clostridium botilinum enters
the body through the wound
Wound Botulism
Produces toxins in traumatized
and necrotic tissue
Formation of ulcers with sharply demarcated edges
and a membranous base from the deposition of toxin
Ingestion of C. Botulinum
(Improper processed canned foods,
inadequate cooked contaminated foods)
Food Borne
Produces toxins to
the bowel lumen
Hematogenously disseminated to
peripheral cholinergic synapses
(Irreversible bond)
Blocks acetylcholine ACh
Produces impaired autonomic and voluntary
neuromuscular transmission and muscular paralysis

2. Food Borne Botulism: Emetics and gastric lavage is recommended
3. Wound Botulism: Exploration and debridement

1. Health education on proper preparation of food, especially on home canning
2. Infant Botulism can be prevented by NOT giving infants HONEY
3. Promptly report Foodborne botulism outbreak

Impaired physical mobility
Potential impairment of skin integrity
Alteration in bowel elimination
Pain and discomfort
Altered Nutrition: Less than body requirements
Anxiety

Red Tide
Caused by a population explosion of toxic, naturally occurring microscopic phytoplanktons
(toxin), specifically a subgroup known as Dinoflagellates

ETIOLOGIC AGENT
Gonyaulax, Protogonyaulax, and Gessnerium. Presently, known by the accepted name
Alexandrium sp.
1. Alexandrium tamarense = Atlantic Coast
2. Alexandrium catanella = Pacific West Coast
3. Ptychodiscus brevis = Gulf of Mexico, West Florida Coast

TYPES OF SHELLFISH THAT ARE PRONE FOR TOXIC ACCUMULATION
1. Quahogs
2. Soft Shell Clamps
3. Oysters
4. Mussels
5. Scallops
6. Moon Snails

FOUR SYNDROMES OF SHELLFISH POISONING
1. Paralytic shellfish poisoning
2. Diarrheal shellfish poisoning
3. Amnestic shellfish poisoning
4. Neurologic shellfish poisoning FIRST TARGET

PATHOPHYSIOLOGY

REMEMBER:
Toxic shell fish taste and
appear no different from non-
toxic shellfish!!
Cooking DOES NOT destroy
the organism

CLINICAL MANIDESTATIONS
1. Initial Sign: Tingling of the lips and tongue which spreads to the face, neck and fingertips and
toes
2. HA, dizziness and nausea follow (May be mistaken as being a drunken condition)
3. Symptoms are aggravated by alcohol consumption
4. In severe cases, muscular paralysis and difficulty of breathing in 5 12 hours due to paralysis
of the diaphragm, can only survive with the aid of a respirator
5. Fatalities have been reported due to respiratory arrest

1. Induced to vomit
2. Charcoal hemoperfusion
3. Alkaline fluids (Na HCO
3
)
4. Artificial respiration

1. Monitoring program for all shellfish-producing areas
2. Year-round testing of shellfish and shellfish-growing areas
3. Seek medical attention if accidental ingestion of toxic shellfish is suspected
4. Pay close attention if hot season, look for posted warnings about red tide

Schistosomiasis (Bilharziasis / Snail Fever)
Slowly, progressive disease caused by blood flukes of class Trematoda
A chronic wasting disease common among farmers and their families in certain parts of the
Philippines

ETIOLOGIC AGENT
Schistosoma japonicum
o Three Major Types
1) Schistosoma japonicum
Infects the intestinal tract (Katayama disease)
Also known as oriental schistosomiasis
2) Schistosoma mansoni
Also affects the intestinal tract
3) Schistosoma haematobium
Affects the urinary tract

INCUBATION PERIOD: At least two months

SOURCES OF INFECTION
1. Feces of infected persons
2. Dogs, pigs, carabaos, cows, monkeys and wild rats serve as hosts

1. Ingestion of contaminated water
2. Skin pores
3. Through an intermediary host, a tiny snail called Oncomelania quadrasi

PATHOPHYSIOLOGY

CLNICAL MANIFESTATIONS
Signs and Symptoms depend on the site of infection, but these are common
1. Pruritic rash, swimmers itch At the site of penetration
2. Low-grade fever, myalgia and cough
3. Abdominal discomfort due to Hepatomegaly, Splenomegaly and Lymphadenopathy
4. Bloody-mucoid stools
5. Icteric and jaundice (Obstructive jaundice)
6. Later, belly becomes big because of an inflamed liver, from the accumulation of eggs in
the organ
7. Chronic disease: Weak and pale and marked muscle wasting
8. When parasites reach the brain, victim experiences severe HA, dizziness, and convulsions

COMPLICATIONS
1. Liver cirrhosis and portal hypertension
2. Cor pulmonale and pulmonary hypertension

3. Heart failure
4. Ascites
5. Hematemesis as a result from rupture of esophageal varices
6. Renal failure
7. Cerebral schistosomiasis Crossed the Blood Brain Barrier

DIAGNOSTIC PROCEDURES
1. Fecalysis or direct stool exam
2. Kato-Katz Technique
3. Liver and rectal biopsy
4. Enzyme-linked Immunosorbent Assay (ELISA)
5. Circumoval precipitin test (COPT) Confirmatory diagnostic test

Treatment is effective when given EARLY in the course of the disease
1. Praziquantel tablet for 6 months
o 1 tab BID for 3 months, then
o 1 tab a day for another 3 months
2. Fuadin injection given either IM or IV, should consume 360 mg for entire treatment

To prevent Schistosomiasis , one must know:
- How the disease spreads
- How to interrupt the life cycle of the worm
- How to protect people from infection
1. Stool examination
2. Reduce snail density
3. Diminish infection rate
4. Health education on the disease process, mode of transmission and prevention

Body image disturbance
Altered role function
Altered urinary elimination (S. hematobium)
Social isolation
Self-esteem disturbance
Knowledge deficit
Risk for infection

Bacillary Dysentery (Shigellosis / Bloody Flux)
- Acute bacterial infection of the intestines characterized by diarrhea, fever and associated with
passing out of bloody-mucoid stools accompanied by tenesmus

ETIOLOGIC AGENT
E Shigella group
- Short, non-motile, gram-negative organism
- Four Serologic Groups:
1. Shigella flexneri (Group B)
2. Shigella boydii
3. Shigella connei
4. Shigella dysenteriae

INCUBATION PERIOD: 7 HOURS to 7 DAYS (With an average of 3 5 DAYS)

PERIOD OF COMMUNICABILITY: During the acute infection until negative feces

1. Ingestion of contaminated food or water or milk
2. Flies or through other objects contaminated by the feces
3. Fecal-oral

PATHOPHYSIOLOGY

1. Fever, specially in children
2. Tenesmus, nausea, vomiting and headache
3. Colicky or cramping abdominal pain with anorexia and body weakness
4. Diarrhea with blood-mucoid stools that are watery at first
5. Rapid dehydration

COMPLICATIONS
1. Rectal prolapse (Particularly in undernourished children)
2. Respiratory Complications (Cough and pneumonia)
3. Non-suppurative arthritis and peripheral neuropathy

1. Fecalysis or microscopic examination of stools
2. Isolation of the causative organism from rectal swab or culture
3. Peripheral blood examination
4. Blood culture
5. Sheets of polymorphonuclear leukocytes seen in staining with methylene blue

MODALITIES of TREATMENT
1. Ampicillin, tetracycline and Cotrimoxazole may be useful in severe cases
2. F&E Management (Prevent dehydration with NSS)
3. Low-residue diet is recommended
4. Anti-diarrheal drugs are CONTRAINDICATED = They delay fecal excretion can lead to
prolonged fever (Also dairy products are contraindicated)

NURSING MANAGEMENT
1. Maintain F&E balance
2. Keep client warm and comfortable
3. Restrict food until N/V subsides
4. Isolation
5. Personal hygiene maintained
6. Proper disposal of excreta
7. Concurrent and terminal disinfection should be employed

8. Return to normal activities must be gradual, relapse may occur

METHODS of PREVENTION and CONTROL
1. Sanitary disposal of human feces
2. Sanitary supervision of processing, preparation and serving of food particularly those eaten
raw
3. Adequate provision of safe washing facilities
4. Fly control and protection
5. Isolation of client during acute stage
6. Protection and purification of public water supply
7. Persons known to be infected should be excluded from handling food for public consumption

Skin Diseases
Leprosy (Hansens disease / Hansenosis)
1. Chronic disease that mainly affects the skin, peripheral nerves, eyes, and mucosa of the upper
respiratory tract and eventually producing deformities
- Host - Immune response, crowded places, related to tuberculosis, poverty, malnutrition
- Agent: Mycobacterium leprae
- Reservoir Nasal secretions of infected persons
- Portal of Entry Respiratory / skin
- Portal of Exit Respiratory / skin
- Mode of Transmission Droplet / direct contact
2. Pathognomonic Sign: Weakness

1. Droplets
2. Inoculation through skin breaks and mucous membranes

THREE DISTINCT FORMS
1. Lepromatous Leprosy (Multibacillary)
a. Most serious type, most infectious
b. Damage to the respiratory tract, eyes and testes as well as the nerves and the skin
c. Lepromin test is negative but the skin lesion contains large amounts of Hansens
bacillus
d. Gradual thickening of the skin with development of a granulomatous condition
e. Lesions appear as macules and become nodular (Leproma)
f. Slow involvement of the peripheral nerves, with some degree of anesthesia, loss of
sensation and gradual destruction of the nerves
g. Atrophy of the skin and muscles, melting or absorption of small bones, primarily
hands and feet
h. Ulceration of the mucous membrane of the nose
i. Due to melting or absorption of small bones and ulceration, natural amputation may
occur
2. Tuberculoid Leprosy
a. Affects the peripheral nerves and sometimes surrounding skin (face, eyes, and
testes), nerves, skin
b. Lepromin test is positive but the organism is rarely isolated from the lesions
The concentration is in the blood! NOT in the tissues
c. Elevated macules, with clearing at the center, more clearly defined than in the
lepromatous form
d. Anesthesia is present, involvement of the peripheral nerves occurs more rapidly than
in the lepromatous form
3. Borderline (Dimorphous) Leprosy
a. Has characteristics of both Lepromatous and Tuberculoid leprosy
b. Diffused and poorly defined


PATHOPHYSIOLOGY

1. Neural Involvement
The earliest manifestations (Nerve Damage)
a. Atrophy of muscles of the hands which extends to the thenar, hypothenar and
forearm muscles, resulting in clawhand
b. Nerves involved are: Ulnar, median, radial, lateral popliteal and facial
c. Paralysis and peripheral anesthesia
d. Secondary consequences of nerve involvement include: Malperforant, clawhand,
ocular complications incident (corneal insensitivity or paralysis of the eyelids)
2. Skin
Lepromatous and Tuberculoid leprosy differ greatly in their Cutaneous manifestations:
a. Lepromatous Leprosy:
o Multiple early lesions, symmetrical, and erythematous, macules or
papules with smooth surfaces
o Later, enlarged lesions and forms plaques or nodules on the earlobes,
nose, eyebrows and forehead (Leonine appearance)
o Loss of eyebrows and eyelashes
o Loss of function of sweat and sebaceous glands makes skin dry and
hairless
b. Tuberculoid Leprosy
o Purely neural or may simultaneously affect the skin
o Raised, large erythematous plaques appear on the skin
3. Eye
a. Ocular manifestations Found only in LEPROMATOUS and BORDERLINE
Leprosy
b. Conjunctiva, sclera, cornea and iris are affected, sparing the retina and optic nerve
c. Photophobia, conjunctivitis and iridocyclitis frequently occurs, opacity of the cornea,
insensitivity and ulceration can lead to blindness
4. Upper Respiratory Tract
a. Nose, mouth, pharynx, larynx, trachea, and esophagus involved in LEPROMATOUS
LEPROSY
b. Epistaxis, ulceration of the uvula and tonsils, septal formation and nasal collapse
5. Visceral Leprosy
a. Heaviest concentration of lesions in the organs representing the reticuloendothelial
system, the lymph system and liver
M. leprae attacks
peripheral nerves
Nerves of Ulnar, radial, posterior
popliteal, anterior-tibial and facial nerves
When bacilli damage the skins fine nerves, they
cause anesthesia, anhydrosis and dryness
If they attack a
large nerve trunk,
Motor nerve damage,
weakness and pain occur,
Followed by peripheral anesthesia, muscle
paralysis and atrophy

b. Testicular damage occurs in almost all moderately advanced cases of Lepromatous
Leprosy

1. Identification of the Signs and symptoms
2. Tissue biopsy Confirmatory
3. Tissue smear Confirmatory (+) M. leprae
4. Blood tests (Increased RBC and ESR, Decreased Serum Ca, Albumin and Cholesterol levels)

1. Sulfone Therapy
2. Rehabilitation, recreational and occupational therapy
3. Multiple Drug Therapy (MDT)
a. Combinations of:
i. Rifampicin (600 mg once a month)
ii. Clofazimine (50 mg daily)
iii. Dapsone (100 mg daily) For Multibacillary Leprosy
iv. And Rifampicin and Dapsone Pausibacillary Type
b. Among these, Rifampicin is the most important ant-leprosy drug and is therefore
included in the treatment of both types of leprosy
c. Treatment of leprosy with only one anti-leprosy drug will always result in the
development of DRUG RESISTANCE
d. Treatment of leprosy with Dapsone or any anti-leprosy drug used as monotherapy
should be considered as an UNETHICAL PRACTICE
e. For Multibacillary Leprosy:
i. Rifampicin 600 mg is given once a month
ii. Dapsone 100 mg is given daily
iii. Clofazimine 50 mg daily for 12 months
f. For Paucibacillary Leprosy:
i. Give Rifampicin 600 mg once a month
ii. Dapsone once daily
iii. Duration of treatment is 6 months
g. Clofazimine causes black discoloration and dryness of skin (Disappears within a few
months after treatment)
h. MB and PB patients should have fixed-duration treatment, which means:
i. MB Px: After 12 monthly doses of MDT (Cured and removed from
register)
ii. PB Px: After 6 monthly doses of MDT (Cured and discharged)

NURSING MANAGEMENT
1. Respiratory isolation and medical asepsis
2. Moral support and encouragement
3. Diet full! WHOLESOME and NUTRITIOUS!
4. Terminal disinfection

PREVENTION
1. Report suspects of leprosy
2. Newborn infants should be separated from leprous mothers
3. BCG protective if given during 1
st
6 months of life
4. Health education on mode of transmission

Social isolation
Ineffective coping

Knowledge deficit
Anxiety
Impaired body image

Scabies
An age-old skin infection caused by a female itch mite, which penetrates the skin, forming
burrows

ETIOLOGIC AGENT
Sarcoptes scabiei

INCUBATION PERIOD: Itch mite may burrow under the skin and lay ova within 24 hours of the
original contact

PERIOD OF COMMUNICABILITY: Entire period that the host is infected

MODE of TRANSMISSION
1. Direct Through infected individual
2. Sleeping on an infested bed or wearing infested clothing
3. Anyone can become infected or re-infected
4. Contact with dogs, cats, and other small animals
5. Scabies on dogs is called mange
6. But human scabies gets worse and worse if untreated

PATHOPHYSIOLOGY

SIGNS and SYMPTOMS
1. Itching, more pronounced at night when
the client has retired (Since the increased
warmth of the skin has a stimulating
effect on the parasite)
2. The itch is subtle for the first week,
gradually becomes more intense after a
month or two (Sleep becomes almost
IMPOSSIBLE)
3. Secondary lesions like vesicles, papules,
pustules, excoriations and crusts may be
found on the affected site
4. Bacterial superinfection results from
constant excoriation

A drop of mineral oil placed over the
burrow, followed by superficial scraping
and examination of expressed material
under a low-power microscope

1. Application of pediculicide, such as permethrin cream or lindane lotion left on for 10 12
hours [Miticide Drugs]
2. Crotamiton Cream for 5 consecutive nights
3. Neosporin ointment (Rubbed onto the affected skin 4 5 times a day)
4. Eurax and Kwell lotion (Prove effective in some patients)
5. Antihistamines like diphenhydramine (Benadryl) Relief from the itch
6. All clothes used before and during the treatment period should be disinfected (Dry cleaning or
boiling)

NURSING MANAGEMENT
1. Instruct the patient to apply the cream at bedtime, neck down to the toes (Covering the entire
body)
2. Dry cleaned or boil contaminated clothing or bedclothes
3. Report any skin irritation
4. Close contacts of the patient be checked for possible symptoms
5. Handwashing technique or use gloves while performing nursing procedures
6. Terminal disinfection

1. Good personal hygiene
2. Avoid contact with infected persons
3. Household members and close contacts should be treated
4. After treatment, beddings and clothing should be properly laundered

Alteration in comfort; itchiness / risk for infection
Altered role performance
Knowledge deficit
Social isolation

Pediculosis (Phthiriasis)
Infestation of the hairy parts of the body / clothing with eggs;
larvae / adult lice

Direct contact
Lice feed on the blood
Lice stay close to skin for
moisture, food, and warmth
Fertilized female louse lays about 10
eggs/day for upto a month until it dies
Eggs (nits) attached to the hair shafts are close to the skin
surface where the temperature is optimal for incubation
Eggs hatch after about
7 14 days of incubation

ETIOLOGIC AGENT
1. Pediculus humanos var. capitis Head lice
2. Pediculus humanos var. corporis Body lice
3. Phthirus pubis or pubic lice Crab lice
a. Feed on human blood and lay eggs in hairs
and clothing fibers
b. After hatching, lice must feed within 24
hours or else it will die
c. Mature in about 2 3 weeks
d. When a louse bites, it injects toxins into the
skin (Producing mild irritation and a purpuric
spot)
e. Repeated bites cause sensitization to the
toxin, leading to more serious inflammation

PATHOPHYSIOLOGY

1. The Head Louse
a. Common in females, more in children than adults
b. Itching is the predominant symptom
c. If neglected, irritation, excoriation and crusting ensue, foul-smelling mass (Matted
hairs, nits, ova, pus, crusts and pediculi) Plica polonica
2. Body Louse
a. Gray-white active insect 3 4 mm long
b. Mouth parts (adapted to sucking blood), Leg parts (Adapted to grasping hair)
c. Lifespan of females is about 1 month, she lays about 8 10 eggs per day
d. Eggs hatch in 8 days, releasing nymphs that will mature in 8 days
e. Initial lesions are minute red spots
f. Spot swells much like a mosquito bite
g. Head and body lice are closely related, interbreedable variants of the same species
3. Crab Lice
a. Rounder, stubbier insect, 2 3 mm long, difficult to see unless filled with blood
from a recent meal
b. 4 of its 6 legs terminate in its sturdy crab-like claws
c. Lifespan: 3 4 weeks, female lays a maximum of 3 eggs/day
d. Unusual, persistent itching in the pubic region and in the other affected areas is the
chief symptom
e. Presence is unsuspected, until nits become apparent on the hair, or until detached and
seen on fingers due to scratching
f. Grayish pigmented spots (Maculae caeruleae) found on the surface of inner thighs or
the abdomen

TREATMENT
1. Head Louse
a. Dusting the scalp with 1% malathion powder
b. Thoroughly massage gamma-benzene hexachloride shampoo in the scalp for 4
minutes then rinse
2. Body Louse
a. Launder (dry clean) or Boil the clothing and beddings
b. Good body hygiene
3. Crab Louse
a. Apply Kwell or Gamene (Lindane) cream or lotion
b. Rub crotamiton (Eurax, Geigy) onto affected area
c. Repeat after one week
d. Treat a person who has had sexual contact with the patient
e. Remove remaining nits mechanically
f. Infestations in the eyelids of children treated with yellow oxide of mercury, apply to
eyelids BID for a few days

COMPLICATIONS
Pigmentation and honey crusts of
secondary pyoderma
Vagabondia Combination of
extensive excoriation, hypo- and
hyper pigmentation with
lichenification
Enlargement of the Nuchal and
cervical nodes with febrile episodes
which can lead to micrococcal
infection
Blepharitis

PREVENTION
1. Good personal hygiene
2. Avoiding contact with persons
suffering from pediculosis

Alteration in comfort
Risk for infection
Sleep disturbance

Respiratory Infective Diseases
Refer to OLD NOTES on RESPI
Pulmonary Tuberculosis (PTB)
Severe Acute Respiratory Syndrome (SARS)
Pneumonia

Anthrax
1. An infection caused by Bacillus anthracis that occurs primarily in herbivores
2. Use in biological warfare or bioterrorism

ETIOLOGIC AGENT
Bacillus anthracis
o Large, aerobic, spore-forming, gram (+), rod-shaped microorganism that is
capsulated and non motile
o Can be destroyed by boiling in 10 minutes, but can survive for years in the dry soil

HUMAN CASES are CLASSIFIED AS:
1. Agricultural Cases
a. Contact with animals that are infected
b. Consumption of contaminated meat
2. Industrial Cases
a. Exposure to contaminated hides, goat hair, wool or bones

MODES of TRANSMISSION
1. Direct Contact with infected animals or contaminated animal products
2. Indirect Animal bites and ingestion of contaminated meat
3. Airborne Inhalation of contaminated or polluted air

TYPES
1. Cutaneous Anthrax
a. Incubation period is 9 hours 2 weeks (2 7 days)

Entrance of
Bacillus anthracis
2 3 Days
Pimple or Macule appears
Ring / Vesicle develops
around the papule
4
th
Day
Edema!!
Painful lymph adenitis may
occur in inguinal area
Papules ulcerate and
form Eschar
5
th
7
th
Day
Edema extends from lesion
SEVERE CASES
Face, neck or chest
High fever Toxemia
Regional painful
lymphadenopathy
Extensive
edema
Shock/death

2. Inhalation Anthrax (Woolsorters Disease)
a. Resembles those of severe viral respiratory diseases

3. Gastrointestinal Anthrax
a. Inadequately-cooked meat from animals with anthrax

COMPLICATIONS
1. Anthrax Meningitis Intense inflammation of the meninges of the brain and spinal cord
a. CSF Pressure with bloody CSF, with loss of consciousness
b. 100% Fatality rate
2. Anthrax Sepsis
a. Develops after lymphohematogenous spread of B. anthracis from primary lesion
b. Clinical features: High fever, toxemia and shock, with DEATH following in a short time

TREATMENT
1. Parenteral Penicillin G
2 million units q6 hours until edema subsides
Subsequent administration of oral penicillin for 7 10 days
2. Patients who are sensitive to penicillin can be treated with erythromycin, tetracycline or
chloramphenicol

NURSING MANAGEMENT
1. History taking
2. Physical examination
3. Skin care, psychological and emotional support
4. Supportive measures and geared toward the type of anthrax exposure
5. Report to health authorities any type of anthrax

- Anxiety
- Altered nutrition
- Altered body temperature
- Impaired physical mobility
- Alteration in bowel elimination
- Altered nutrition: less than body requirements

Influenza (La Grippe)
1. Generalized, acute, febrile disease associated with upper and lower infection

ETIOLOGIC AGENT
RNA-containing myxoviruses, types A, A-prime, B and C

INCUBATION PERIOD: 24 48 Hours

PERIOD of COMMUNICABILITY: Until 5
th
Day of illness (Up to 7
th
day in children)
1. Airborne
2. Direct contact with infected droplet
3. Persists for hours in dried mucus

PATHOPHYSIOLOGY

1. Tissue culture
2. Blood examination
3. Swabs
4. Viral serology

1. Chilly sensation, hyperpyrexia, malaise, sore
throat, coryza, Rhinorrhea, myalgia and HA
2. Severe aches and pain, associated with severe
sweating
3. Sometimes GI symptoms and vomiting
4. Worst Symptoms: 3 5 days before the condition
improves
5. Most people recover

COMPLICATIONS
1. Directly related to primary viral infection
a. Hemorrhagic pneumonia
b. Encephalitis and other neurologic
syndromes
c. Reyes Syndrome
d. Myocarditis can lead to Cardiac failure
e. SIDS
f. Myoglobinuria
2. Superimposed bacterial infections due to
Streptococcus pneumoniae, Haemophilus
influenzae, Streptococcus pyogenes and
Staphylococcus aureus
a. Otitis media
b. Sinusitis
c. Pneumonia

a. Complement fixation test
b. Hemo-agglutination test
c. Neutralization test

MANAGEMENT
Advice the client to:
1. Stay home
2. Drink plenty of fluids
3. Medications to relieve fever and HA
a. Paracetamol
b. Aspirin (Unless contraindicated)
c. Ibuprophen or other anti-inflammatory drugs
4. Sponge down with tepid water
Also, make sure to:
1. Isolate
2. Limit strenuous activity
3. WOF Complications

PREVENTIVE MEASURES
1. Immunization
2. Avoidance of crowded places
3. Educate the public and health care personnel regarding personal hygiene
4. Vaccine annually:
a. Elderly
b. Poor immunity
c. People with diseases such as diabetes, and lung, kidney, heart or liver disease

Influenza A (H1N1) Virus
New virus
Almost all people are susceptible
More contagious than seasonal influenza
- 22 33% Attack rate vs. 5 15%
Mild illness in healthy people (Except in Mexico)
Younger age group are affected

WHAT IS the INFLUENZA AH1N1 VIRUS THAT HAS BEEN CAUSING RECENT
OUTBREAKS GLOBALLY?
` The specific type of H1N1 virus causing illness now is new/novel
` This virus is able to infect humans and be passed from person to person
` Caused by a novel virus that resulted from the triple reassortment of pigs, humans, and avian
influenza A strain
` Characteristics:
- RNA Virus
-

Two Surfaces Protein of the Virus
e Haemagglutinin (H)
o Glycoprotein enables virus to attach to host cell
o 15 exists in water
o H1H2 and H3 most commonly associated with human infection
e Neuraminidase (N)
o Glycoprotein enzyme essential for virus replication
o N1 and N2 most commonly associated with human infection

Fighting of bacteria:
Stimulates Sympathetic Nervous System
o Releases cortisol (Immunosuppressant)
o Stimulates Catechol

Antigenic Shift
+ Type A Infective virus undergo frequent change in their surface antigen / protein enabling the
virus to cause epidemics / pandemics

What Should I know About HIV?
L They spread through infected droplets from breathing passages
o Droplets are expelled by talking, spitting, coughing, sneezing
L Droplet spread about 1 meter (3 feet) from the infected person, either direct
L Virus can live for several hours in hard surfaces / on a cloth / paper
L If healthy people touch infected hands, doorknobs, keys, telephones etc.
L Virus can spread through the air
L An infected person is most likely to spread the virus when he/she has a cough and fever
L It is possible that a person can transmit during the incubation period

Individuals at HIGH RISK For Hospitalization / Death
Elderly greater than 65 years old
Children less than 2 years old
Certain chronic diseases
Pregnant women

PATHOPHYSIOLOGY
` Similar to influenza
System Signs and Symptoms
Respiratory System Cough / runny nose, sneezing
Respiratory failure
Circulatory System Fever / Extensive cold
GI System N/V
Musculoskeletal System Fatigue, sore joints
EENT Loss of smell
Nasal coughs
Sire throat
Reddened eyes
Skin, mouth, throat

Signs and Symptoms
Fever
Chills
Lethargy

INCUBATION PERIOD
: Although the precise incubation period has not been established for H1N1, Influenza A
infection is 1 week

Case Defense
A confirmed case of Influenza A Virus
An acutely febrile respiratory illness and lab confidence origin infection

1) Real Time Reverse Transcriptase Polymeric Chain Reaction (rRT PCR)
2) Viral Culture

A Probable Case of Influenza A (H1N1) Virus infection is defined as:
Acute febrile respiratory illness in a person who is positive for influenza A

INFECTIOUS PERIOD
Confirmed diagnosis

Close Contact
History with a convention with a person positive for A H1N1
Within 6 feet of an ill person
Acute Respiratory Illness
o Not confirmed but has symptoms

WHAT IS THE DIFFERENCE BETWEEN SEASONAL and PANDEMIC INFLUENZA ? LOL

MEDICAL MANAGEMENT
Supportive care
Strict isolation
Quarantine
Drugs of Choice
o Oseltamivir Pills
o Inhaled Zanamivir

NURSING DIAGNOSES
: Impaired gas exchange
: Risk for infection

NURSING INTERVENTIONS
W Nursing History
o Recent contact within 24 hours with someone known to have
W Onset of any cold / flu type symptom
W Physical Assessment
o Check VS
o Palpate: Cervical lymph nodes
o Percussion
o Auscultate: Presence of rales, crackles
W Improve Gas Exchange
W Monitor breath sounds, rate and dyspnea
W Manage rest and avoid exhaustion

PREVENT TRANSMISSION of INFECTION
1. Universal Precaution and droplet precaution
2. Basic Infection Control
a. Hand hygiene
b. Appropriate use of masks
c. Cough etiquette
d. General measures

Pertussis (Whooping Cough)
Infectious disease characterized by repeated attacks of spasmodic coughing which consists of a
series of explosive expirations
Ending in a long-drawn forced inspiration producing a crowing sound
Whoop and is usually followed by vomiting (Client coughs 5 10 times before inspiration)

ETIOLOGIC AGENT
Bordatella pertussis
o Non-motile, Gram-negative bacillus
o Easily destroyed by light, heat and drying

INCUBATION PERIOD: 7 14 Days

PERIOD of COMMUNICABILITY: 7 Days after exposure to 3 weeks after typical paroxysms

1. Direct Contact and Droplet
2. Indirectly soiled linens and other articles contaminated

SOURCES of INFECTION
Secretions from nose and throat of infected persons

INCIDENCE
Infants are highly susceptible
One attack produces lifetime immunity
Second attack may be due to other microorganisms causing whooping cough syndrome

PATHOPHYSIOLOGY

COMPLICATIONS
l Interstitial pneumonia Inflamed bronchioles
l Atelectasis Due to mucus plugs
l Convulsions Due to lack of O
2

l Umbilical hernia
l Otitis media
l Bronchopneumonia MOST DANGEROUS COMPLICATION
l Severe malnutrition and starvation Due to persistent vomiting

1. Catarrhal Stage
a. Non-specific symptomatology, there is mucoid
rhinorrhea, sneezing, Lacrimation and dry bronchial
cough
b. Cough is irritating, hacking, nocturnal and more
severe
c. Stage where disease is MOST COMMUNICABLE
d. Lasts about 1 2 Weeks
2. Paroxysmal Stage
a. Occurs on the 7
th
14
th
Day
b. Cough is spasmodic and recurrent with excessive
explosive outbursts in a rapid series
(5 10 rapid coughs in one expiration)
c. Ends in a loud, crowing Inspiratory whoop, and
choking on mucus that causes vomiting
d. Paroxysmal coughing induces nose bleeding, venous
pressure, periorbital edema, conjunctival hemorrhage
and hemorrhage of the anterior chamber of the eye
e. During a paroxysm, face becomes cyanotic, veins of
face and neck are distended, eyes bulge or pop out of
the eyeballs, tongue protrudes
f. Profuse sweating, involuntary urination, lethargy and
exhaustion
g. Cough provoked by crying, eating, drinking or
physical exertion
h. Convulsions occur due to intracranial hemorrhage
i. Between paroxysms, no physical signs and seems well
j. Stage lasts from 4 6 Weeks
3. Convalescent Stage (Recovery Stage)
a. Gradual decrease in the paroxysms of coughing,
vomiting ceases
b. Attack subsides after about 6 weeks from the onset

1. Nasopharyngeal swabs
2. Sputum culture
3. CBC (Leukocytosis)

1. Supportive therapy
a. F&E Replacement
b. Adequate nutrition
c. O
2
Therapy
2. Erythromycin and Ampicillin
3. Hyperimmune convalescent serum or gammaglobulin

NURSING MANAGEMENT
Major Objective: Prevent complications
Isolation and medical asepsis
During a paroxysm, patient should NOT be LEFT ALONE (Suctioning equipment should be
ready)
Sunshine and fresh air
Kept as still and quiet as possible
Warm baths and keep bed dry (Free from soiled linens)
I&O closely monitored

1. Report at once any case of pertussis
2. Immunize children
3. Isolated 4 6 weeks from onset of illness
4. Public education for active immunization and early diagnosis

Ineffective airway clearance
Altered nutrition: Less than body requirements
Risk for infection / complication
Sleep pattern disturbance
Alteration in comfort

Paragonimiasis
Lung Fluke
o Chronic parasitic infection contracted by the consumption of fresh water crabs or crayfish

CAUSATIVE AGENT
Paragonimus westermani
Subspecies (Philippineses)

INTERMEDIATE HOST in PHILIPPINES: Antemelenia asperata

INCUBATION PERIOD: 9 12 Weeks

PERIOD of COMMUNICABILITY: May persist for 20 years for humans

MODE OF TRANSMISSION:
Ingestion of raw or insufficiently cooked crabs
Contamination of foods / utensils with Metacercariae
Inadequately cooked meal of animal reservoir
Drinking of contaminated water with infected larvae (Metacercariae)

PATHOPHYSIOLOGY

General Intervention
> Treatment of infected persons
> Disinfection
> Sanitary disposal of excreta
> Anti-mollusk campaigns
> Health education on mode of transmission
> Avoid infected foods
> Avoid bathing in infected water

NURSING DIAGNOSES
~ Ineffective airway clearance
~ Alteration in comfort: Pain
~ Hyperthermia

Acute Phase
o Invasion and migration
o Diarrhea, abdominal pain, fever, cough,
urticaria, hepato-splenomegaly
Chronic Phase
o Pulmonary manifestations Cough,
expectoration of discolored sputum,
hemoptysis and chest radiography
abnormality

MEDICAL MANAGEMENT
1. Drugs
a. Praziquantel (Biltricide) DRUG of
CHOICE!
b. Bithionol (Bitin) Alternative
2. Surgical removal for heterotrophic cases
DIAGNOSTIC TESTS
` Sputum Examination
` Immunology
` Cerebral Paragonimiasis Fluke in CNS
` Effusion fluid test / Biopsy

Ncm104 11th CD III

Transféré par

Informations du document

Copyright

Formats disponibles

Partager ce document

Partager ou intégrer le document

Options de partage

Avez-vous trouvé ce document utile ?

Ce contenu est-il inapproprié ?

Droits d'auteur :

Formats disponibles

Ncm104 11th CD III

Transféré par

Droits d'auteur :

Formats disponibles

jcmendiola_Achievers2013

Care of Clients with Problems In Inflammatory

Vous aimerez peut-être aussi