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GACTROINTESTINAL DISORDERS

Gastrointestinal system

Vibrio cholerae, 1. Gram negative, motile, curved rod. 2. Survive well in an ordinary temperature 2240 degrees 3. Survive longer in refrigerated foods 4. An enterotoxin, choleragen grow in the intestinal tract

Cholera

Transmitted by contaminated water/food 10000 organisms are sufficient to cause disease, depends on stomach pH. Profuse diarrhea and vomiting 35-60 hours after infection Rapid dehydration, electrolyte imbalance and acidosis. Treatment by oral rehydration therapy

Cholera
Transmission: Fecal - oral route
Bacterium transmitted via contaminated water, food Carriers: houseflies and other insects Person to person transmission
Period of communicability During stool positive stage few days after delivery

Incubation period: 1 3 days

Pathogenesis:
V. Eltor
Enterotoxin Stimulates adenylate cyclase Conversion of ATP (adenosine triphosphate adesine monophosphate (CAMP) Stimulate mucosal cell increase secretion of chloride (Water and bicarbonate loss) Toxin acts upon intact epithelium on vasculature of stomach Outpouring of intestinal fluid (5-10 % of body wt) Dehydration and metabolic acidosis Acute renal failure hypokalemia

Cholera
Symptoms: pathognomonic sign is RICE WATERY Stool Acute , profuse diarrhea diarrhea Sudden severe diarrhea Mucus and intestinal tissue visible in feces Muscle cramps Vomiting Loss of skin turgor Weak pulse skin is fold, fingers and toes are wrinkled assuming washer womans hand.

Cholera
Treatment: Chemotherapeutic Antibiotics (tetracycline) Immunological Local mucosal immune response to V. cholerae Serological antivibrio antibodies Antitoxin antibodies To Ease Symptoms Oral Rehydration Intraveneous Rehydration

Immunization Active Immunity induced by:attenuated V. cholerae Toxoid (not good antigen) Preventing contamination of food and water e.g. boiling water, covering food Education Personal and domestic hygiene Prevention of contamination of water supplies Improvement of sewage systems

Typhoid fever
A systemic infection characterized by continued fever, malaria, anorexia, slow pulse,diarrhea. A usual fatality of 10% is reduced to 2 or 3 % b antibiotic therapy. Infection agent: Salmonella typosa,typhoid bacillus
gram-negative enteric bacillus belongs to the family Enterobacteriaceae. It is a motile, facultative anaerobe that is susceptible to various antibiotics

Typhoid fever
Transmission: direct or indirect contact with patient or carrier. Vehicle: food and water Vector: flies Incubation period: average 2wks.

Pathogenesis:
V. Eltor
Enterotoxin Stimulates adenylate cyclase Conversion of ATP (adenosine triphosphate adesine monophosphate (CAMP) Stimulate mucosal cell increase secretion of chloride (Water and bicarbonate loss) Toxin acts upon intact epithelium on vasculature of stomach Outpouring of intestinal fluid (5-10 % of body wt) Dehydration and metabolic acidosis Acute renal failure hypokalemia

S/s Headache, chilly sensation, aching all over the body. Diarrhea 4th & 5th day High fever in the morning and afternoon

Typhoid fever
Communicability:
As long as typhoid bacilli appear in excreta.

Prevention and control:


Same w/ cholera

Typhoid fever
Nsg. Intervention:
Demonstrate to the family how to give bedside care. Any bleeding, abdominal pain, restlessness,hypothermia should be reported. Take TPR & teach family member to take record.

Hepatitis
Widespread inflammation of the liver tissue caused by viruses, bacterial infection or continuous exposure to alcohol, drugs.

Types of Hepa
Type A
Oral-anal sex Contaminated food Fecal-oral route 2 to 6wks. Household contact Sexual contact

Type B
skin or mucus membrane break Sexual contact 6 wks. To 6months Sexual contact Medical personnel Multiple blood transfusion recipients Bld & body fluid precaution

Type C
Blood products Sexual contact

2 wks to 6 months Same as Hepa B

Enteric precaution

Bld & body fluid precaution

Assessment
Hepatitis B Hepatitis A Young children & young Contact with serum adult. Blood transfusion Crowded living Saliva & semen Food handlers All ages Contaminated water Primary route: Fecal - oral

Clinical Manifestation(phases)
Preicteric
Anorexia nausea RUQ discomfort Malaise Headache Low grade fever
hepatomegaly

Icteric
Dark urine Pruritus Liver remains enlarged Stool will be light or clay colored

Postcteric

Anicteric

Malaise Frequently Easily fatigued occurs in children hepatomegaly Unexplained fever GI disturbance Anorexia malaise

Diagnosis: ATP Normal or protein Prolonged PT Presence of HBsAg in serum of hepa B client Treatment: No specific meds Diet modification: calories, CHON, CHO as tolerated, fat activity

Nsg. Intervention
Hepa A Hygiene Health education Identification of infected indvl. Administer IgG w/ in 2 wks of exposure. Enteric precaution Abstinence when affected Hepa B Identification of infected indvl. Abstinence when affected Administration of hepa B vaccineat high risk Administration oh HBIG to pt. w/ one time exposure. Enteric precaution & needle precaution.

Nsg. Intervention
Bed rest w/ BRP Nutritional intake Avoid alcohol Regular check up Do not donate blood

Dysentery
An acute bacterial infection of the intestine characterized by diarrhea, fever, and in severe cases bloody and mucoid stools. Infection agent: Shigella(dysentery bacillus)

Dysentery
Transmission:
Eating contaminated food Drinking contaminated water Hand to mouth transfer. Flies; object soiled by feces of a carrier
Incubation period: 1 day, usually less than 4 days.

Dysentery
Communicability: During acute infection and until microorganism is absent from feces. A few individuals become carriers for a year or two and rarely longer. Susceptibility: Common and more severe in children.

Prevention & control


Sanitary disposal of feces Sanitary preparation of food. Adequate safe washing Fly control Control of infected individual contacts Reporting to local health officer Isolation of patient Rigid personal precaution by personnel

Dysentery
Nsg. Intervention: Hospitalization if facilities are available Health education Obtain stool specimen from any person found w/ undiagnosed diarrhea Diet: low fiber plenty of fluids, easy digestible food

Amoebiasis
Most infections are asymptomatic. Intestinal disease varies from acute dysentery with fever, chills and bloody diarrhea to mild abdominal discomfort with diarrhea containing blood or mucous alternating with periods of constipation or remission Infection agent:Entamoeba histolytica is a protozoan parasite

Amoebiasis
Transmission: fecal-oral Incubation: 2 4 weeks Communicability: The disease is communicable for as long as the infected person excretes E. histolytica cysts, which may continue for years.

Amoebiasis
Preventive Measures: Health Education To prevent future exposures, recommend that individuals: Always wash their hands thoroughly with soap and water before eating or preparing food, after using the toilet, and after changing diapers. After changing diapers, wash the childs hands as well as their own.

Amoebiasis
Dispose of feces in a sanitary manner. When caring for others with diarrhea, scrub hands with plenty of soap and water after helping the persons use the toilet, or changing diapers, soiled clothes or soiled sheets. especially before handling food, before eating and after toilet use. Avoid sexual practices that may permit fecal-oral transmission.

Amoebiasis

GI Poisoning
General principle(SIRES) Stabilize Initiate the ABCs of CPR Terminate exposure to the substance Identify Obtain accurate history and retrieve available substance. Notify local poison center

Reverse the substance effect


Shower or wash off substance Antidotes- drug overdose Ingested- emesis, adsorbents

Eliminate substance from the body


Induce emesis- administer syrup of ipecac Emesis is contraindicated if pt. Is comatose, severe shock, ingested strong corrosive substance

Support client physically & psychologically


If suicide attempt, refer for psychiatric evaluation If accidental poisoning w/ a child, parents often demonstrate guilt, and elf approach in regard to their parenting role

Salicylate poisoning
Toxic amounts affect the respiratory center with direct stimulation of the medulla resulting in hyperventilation, loss of carbon dioxide and precipitating respiratory alkalosis.

Salicylate poisoning
Clinical manifestation: Hyperventilation Nausea, vomiting temperature Tinnitus Excitability seizure Diagnostic: Serum salicylate level Electrolytes Signs of toxicity Ringing in the ear Dizziness Hearing & visual problem Delirium & sweating

Salicylate poisoning
Treatment: Induce vomiting w/ syrup of ipecac or gastric lavage ff. by activated charcoal. Vit. K to reduce bleeding tendencies IV fluids & NaHCO3 to treat acidosis and increase the excretion of hydrogen ion. Severe cases: peritonial or hemodialysis

Salicylate poisoning
Nsg. Intervention:
Focus on ABC Induce vomiting VS, LOC Health education

Acetaminophen poisoning
Primary toxic effect are on the liver No known antidote Assessment: Assymptomatic Anorexia Nausea & vomiting RUQ pain Jaundice

Acetaminophen poisoning
Treatment:
Emesis w/ ipecac

Nsg. Intervention: same w/ salicylate

Lead poisoning
An acquired condition in which blood levels of lead are above normal causing damage first in the hematologic system, renal system and the central nervous system.

Assessment
Etiology - ingestion of lead from chewing on wood w/ a lead base paint, glazed glassware, mexican pottery. Advance stage Encephalopathy Drowsiness Ataxia seizure Chronic stage Brain damage Poor school performance Delayed devt. Blue lead lines on gums

Lead poisoning
Treatment: Chelating agent to prevent absorption and aid in excretion of kidneys Nsg. Intervention: Assist in screening and diagnosis Administer chelating agent Health education Assist to identify measures to prevent occurrence .

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