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NURSINGMANAGEMENT

OFGIT

PROBLEMS

GASTRIC ANDDUODENALDISORDERS

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GASTRITIS

Inflammation of the gastric mucosa. Often caused by dietary indiscretion or misuse

of

gastric irritating medications (aspirin, NSAIDs),

excessive alcohol intake, bile reflux and radiation

therapy.

Chronic gastritis and prolonged inflammation of

the stomach may be caused by either benign or

malignant ulcers of the stomach, or by the

bacteria Helicobacter pylori.

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GASTRITIS

The gastric mucous membrane becomes edematous and hyperemic and undergoes

superficial erosion.

Gastric mucosa secretes a scanty amount of

gastric juice, containing normal amount of

acid,

but very little mucus, and superficial erosions

may occur and can lead to hemorrhage.

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GASTRITIS

Clinical Manifestations: Abdominal discomfort

Headache, lassitude

Nausea, anorexia Vomiting

Singultus

Pyrosis

Belching

Sour taste in the mouth

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GASTRITIS

Diagnosis can be obtained by endoscopy,upper

GI radiographic studies, and histologic

examination of a tissue specimen obtained by

biopsy.

In addition to biopsy, other diagnosticmeasures

for detecting H. pylori include serologic testing

for antibodies against H. pylori antigen.

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GASTRITIS

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GASTRITIS

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GASTRITIS

Medical Management:Refrain from alcohol and food untilsymptoms subsideNon-irritating dietFluids may need to be administeredparenterallyCommon antacids to neutralize acidsEmetics and lavage are avoided because ofthe danger of perforation and damage to theesophagus.

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GASTRITIS

Medical Management:

Nasogastric intubation

Analgesic agents and sedatives

Fiberoptic endoscopy may be necessary

Emergency surgery to remove gangrenous or

perforated tissue

Diet modification

H. pylori may be treated with antibiotics and a

proton-pump inhibitor and possibly bismuth salts

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GASTRITIS

Nursing Management:

Assessment

Nursing Diagnoses

Planning and Goals

Nursing Interventions:

1. Reducing anxiety

2. Promoting optimal nutrition

3. Promoting fluid balance

4. Relieving pain

Promoting home and community-based care

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GASTRIC AND DUODENAL ULCERS

A peptic ulcer is an excavation that forms in the

mucosal wall of the stomach, in the pylorus, in

the duodenum, or in the esophagus.

Peptic ulcers are more likely to be in the

duodenum than in the stomach.

As a result, gastric ulcers tend to occur alone, but

they may occur in multiples.

Chronic gastric ulcers tend to occur in the lesser

curvature of the stomach, near the pylorus.

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GASTRIC AND DUODENAL ULCERS

Peptic ulcer disease occurs with the greatest

frequency in people between the ages of 40 and

60 years.

In the past, stress and anxiety were thought to be

causes of ulcers.

Familial tendency may be a significant

predisposing factor.

People with blood type O are more susceptible to

peptic ulcers than are those with blood type A, B,

or AB.

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GASTRIC AND DUODENAL ULCERS

Microbiologic etiology: Helicobacter pylori

Other predisposing factors: chronic NSAID

intake, alcohol ingestion, and excessive smoking.

Rarely ulcers are caused by excessive amounts of

the hormone gastrin, produced by tumors

(Zollinger-Ellison syndrome): severe peptic

ulcers, extreme gastric hyperacidity, and gastrinsecreting

benign or malignant tumors of the

pancreas.

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GASTRIC AND DUODENAL ULCERSDUODENAL ULCER GASTRIC ULCER

AGE 30 60 years Usually 50 and over

MALE:FEMALE RATIO 2-3:1 1:1

INCIDENCE 80% of peptic ulcers 15% of peptic ulcers

STOMACH ACID Hypersecretion Normal or hyposecretion

BODY WEIGHT Normal or weight gain Weight loss

EPIGASTRIC PAIN 2-3 hrs post-meal, early

morning awakenings,

relieved by food intake

- 1 hr post-meal, rarely

occurs at night; food intake

aggravates pain

VOMITING Uncommon Common (relieves pain)

HEMORRHAGE Less common, melena More common,hematemesis

PERFORATION More common Less common

MALIGNANCY Rare Occasionally

RISK FACTORS H. Pylori, alcohol,

smoking, cirrhosis, stress

H. pylori, gastritis, alcohol,

smoking, NSAIDs, stress

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GASTRIC AND DUODENAL ULCERS:

Pathophysiology

Peptic ulcers occur mainly in the gastroduodenal

mucosa because this tissue cannot withstand the

digestive action of gastric acid and pepsin.

Erosion is caused by increased concentration or

activity of acid pepsin, or by decreased resistance

of the mucosa.

The use of NSAIDs inhibits the secretion of

mucus that protects the mucosa.

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GASTRIC AND DUODENAL ULCERS:

Pathophysiology

Stress ulcer is the term given to the acute

mucosal ulceration of the duodenal or gastric area

that occurs after physiologically stressful events,

such as burns, shock, severe sepsis and multiple

organ traumas.

As the stressful condition continues, the ulcers

spread. When the patient recovers, the lesions

are reversed.

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GASTRIC AND DUODENAL ULCERS:

Pathophysiology

Cushings ulcers are common in patients with

trauma to the brain. They may occur in the

esophagus, stomach or duodenum and are usually

deeper and more penetrating than stress ulcers.

Curlings ulcers are frequently observed about 72

hours after extensive burns and involves the

antrum of the stomach or the duodenum.

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GASTRIC AND DUODENAL ULCERS:

Assessment

Endoscopy is the preferred diagnostic procedure

because it allows direct visualization of

inflammatory changes, ulcers and lesions.

Stools may be tested periodically until they are

negative for occult blood.

H. pylori infection may be determined by biopsy

and histology with culture, as well as a breath test

and serologic test for H. pylori antibodies.

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GASTRIC AND DUODENAL ULCERS:

Assessment

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GASTRIC AND DUODENAL ULCERS:

Assessment

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Medical Management:

Once the diagnosis is established, the patient is

informed that the problem can be controlled.

Recurrence may develop; however, peptic ulcers

treated with antibiotics to eradicate H. pylori

have a lower recurrence rate than those not

treated with antibiotics.

Methods include medications, lifestyle

modification, and surgical intervention.

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Medical Management: Pharmacologic

Therapy

Most commonly used therapy is a combination of

antibiotics, proton pump inhibitors, and bismuth

salts that suppresses or eradicates H. pylori.

Histamine-2 (H2) receptor antagonists and proton

pump inhibitors are used to treat NSAID-induced

and other ulcers not associated with H. pylori

ulcers.

Patient is advised to adhere to the medication

regimen to ensure complete healing of the ulcer.

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Medical Management: Stress

Reduction and Test

Reducing environmental stress requires physical

and psychological modifications on the patients

part as well as the aid and cooperation of family

members and significant others.

Identify situations that are stressful and

exhausting.

Biofeedback, hypnosis (?), or behavior

modification may be helpful.

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Medical Management:

Smoking Cessation

Studies have shown that smoking decreases the

secretion of bicarbonate from the pancreas into

the duodenum, resulting in increased acidity of

the duodenum.

Patient is strongly encouraged to stop smoking.

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Medical Management:

Dietary Modification

The intent is to avoid oversecretion of acid and

hypermotility of the GI tract.

Avoiding extremes of temperature and

overstimulation from consumption of meat

extracts, alcohol, coffee (including decaffeinated

coffee) and other caffeinated beverages, and diets

rich in milk and cream.

Neutralize acid by eating three regular meals a

day.

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Surgical Management

Surgery is usually recommended for patients with

intractable ulcers (those that fail to heal after 12

to 16 weeks of medical treatment), lifethreatening

hemorrhage, perforation, or

obstruction, and for those with ZES that do not

respond to medications.

Vagotomy, with or without pyloroplasty.

Billroth I (gastroduodenostomy) and Billroth II

(gastrojejunostomy) procedures.

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Follow-Up Care

Recurrence within a year may be prevented with

the prophylactic use of H2-receptor antagonists

given at a reduced dose. Not all patients require

maintenance therapy.

Likelihood of recurrence is reduced if th4e

patient avoids smoking, coffee and other

caffeinated beverages, alcohol, and ulcerogenic

medications.

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Follow-Up Care

Recurrence within a year may be prevented with

the prophylactic use of H2-receptor antagonists

given at a reduced dose. Not all patients require

maintenance therapy.

Likelihood of recurrence is reduced if th4e

patient avoids smoking, coffee and other

caffeinated beverages, alcohol, and ulcerogenic

medications.

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NURSINGMANAGEMENT

OFGIT

PROBLEMS

INTESTINALAND RECTALDISORDERS

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CONSTIPATION

Abnormal infrequency or irregularity of

defecation, abnormal hardening of the stools that

makes their passage difficult and sometimes

painful, a decrease in stool volume, or retention

of stool in the rectum for a prolonged period.

May be caused by certain medications, rectal or

anal disorders, obstruction, metabolic, neurologic

and neuromuscular conditions, endocrine

disorders, lead poisoning and connective tissue

disorders.

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CONSTIPATION: Pathophysiology

Poorly understood.

Interference with mucosal transport, myoelectric

activity, or processes of defecation.

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CONSTIPATION: Clinical Manifestations

Abdominal distention

Borborygmus

Pain and pressure

Decreased appetite

Headache, fatigue

Indigestion

Sensation of incomplete emptying

Passage of scybala

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CONSTIPATION: Assessment and

Diagnosis

Chronic constipation is usually considered

idiopathic, but secondary causes should be

eliminated.

Diagnosis is based on results of the patients

history, physical examination, possibly a barium

enema or sigmoidoscopy, and stool testing for

occult blood.

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CONSTIPATION: Assessment and

Diagnosis

Chronic constipation is usually considered

idiopathic, but secondary causes should be

eliminated.

Diagnosis is based on results of the patients

history, physical examination, possibly a barium

enema or sigmoidoscopy, and stool testing for

occult blood.

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CONSTIPATION: Complications

Hypertension

Fecal impaction

Hemorrhoids and fissures

Megacolon

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CONSTIPATION: Medical Management

Treatment is aimed at the underlying cause of

constipation and includes education, bowel habit

training, increased fiber and fluid intake, and

judicious use of laxatives.

Enemas and rectal suppositories are generally not

recommended for constipation and should be

reserved for the treatment of impaction or for

preparing the bowel for surgery or diagnostic

procedures.

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CONSTIPATION: Medical Management

Further studies are being carried out on

cholinergic agents (e.g., bethanechol),

cholinesterase inhibitors (e.g., neostigmine), and

prokinetic agents (e.g., metoclopramide) to

determine the role of these agents in treating

constipation.

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CONSTIPATION: Nursing Management

Elicit information about the onset and duration of

constipation, past and present elimination

patterns, the patients expectation of normal

bowel elimination, and lifestyle information

during health history review.

Past medical and surgical history, current

medications, and laxative and enema use are

important, as is information about the sensation

of rectal fullness or pressure, abdominal pain,

excessive straining at defecation and flatulence.

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CONSTIPATION: Nursing Management

Patient education and health promotion

Restoring and maintaining a regular pattern of

elimination

Ensuring adequate intake of fluids and high-fiber

foods

Teach methods to avoid constipation

Relieve anxiety about bowel elimination patterns

Avoid complications

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DIARRHEA

Increased frequency of bowel movements (more

than three per day), increased amount of stool

volume (more than 200 g per day), and altered

consistency (i.e., looseness) of stool.

Associated with urgency, perianal discomfort,

incontinence, or a combination of these factors.

Caused by increased intestinal secretions,

decreased mucosal absorption, or altered motility.

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DIARRHEA

Acute diarrhea is most often associated with

infection, and is usually self-limiting.

Chronic diarrhea persists for a longer period

(three weeks), and may return sporadically.

Diarrhea can be caused by certain medications,

tube feeding formulas, metabolic and endocrinedisorders, viral or bacterial infectious processes,

nutritional and malabsorptive disorders and anal

sphincter defects.

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DIARRHEA: Pathophysiology

Types of diarrhea: secretory, osmotic and mixed

diarrhea.

Secretory diarrhea is usually high-volume

diarrhea caused by increased production and

secretion of water and electrolytes by the

intestinal mucosa into the intestinal lumen. Osmotic diarrhea occurs when water is pulled

into the intestines by the osmotic pressure of

unabsorbed particles, slowing the reabsorption of

water.

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DIARRHEA: Pathophysiology

Mixed diarrhea is caused by increased peristalsis

(usually from IBD) and a combination of

increased secretion and decreased absorption in

the bowel.

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DIARRHEA: Clinical Manifestations

Increased frequency and fluid content of stools

Abdominal cramps and distention

Intestinal rumbling

Anorexia and thirst

Painful spasmodic contractions of the anus and

ineffectual straining (tenesmus) Watery stools are characteristic of small bowel

disease.

Loose, semisolid stools are associated more often

with disorders of the colon.

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DIARRHEA: Clinical Manifestations

Voluminous, greasy stools suggest intestinal

malabsorption.

Presence of mucus and pus suggests

inflammatory enteritis or colitis.

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DIARRHEA: Assessment and Diagnostic

Findings

Complete blood count

Chemical profile

Urinalysis

Routine stool examination

Stool examinations for parasitic or infectious

organisms, bacterial toxins, blood, fat andelectrolytes.

Barium enema may assist in identifying the

cause.

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DIARRHEA: Complications

Fluid and electrolyte imbalance (cardiac

dysrhythmias)

Renal failure

Multiorgan failure and death

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DIARRHEA: Medical Management

Primary management is directed at controlling

symptoms, preventing complications, and

eliminating or treating the underlying disease.

Certain medications may reduce the severity of

the diarrhea and treat the underlying disease.

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DIARRHEA: Nursing Management

Assess and monitor the characteristics and

pattern of diarrhea.

Encourage bed rest and intake of fluids and food

low in bulk until the acute attack subsides.

When food intake is tolerated, recommend a

bland diet of semisolid and solid food. Avoid caffeine, carbonated beverages and very

hot and very cold food.

Restrict milk products, fat, whole-grain products,

fresh fruits and vegetables for several days.

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DIARRHEA: Nursing Management

Administer antidiarrheal medications such as

diphenoxylate (Lomotil) and loperamide

(Imodium) as prescribed.

IV therapy for rapid rehydration especially for

the elderly and those with preexisting GI

conditions. Monitor serum electrolyte levels

Report immediately clinical evidence of

dysrhythmias or a change in the level of

consciousness.

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DIARRHEA: Nursing Management

The perianal area may be excoriated because

diarrheal stool contains digestive enzymes that

can irritate the skin. The patient should follow a

perianal skin care routine to decrease irritation

and excoriation.

Use skin sealants and moisture barriers asneeded.

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APPENDICITIS

The most common cause of acute abdomen in the

United States.

Males > females

Adolescents > adults

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APPENDICITIS: Assessment and

Diagnostic Findings

Diagnosis is based on results of a complete

physical examination and on laboratory and x-ray

findings.

Leukocytosis

Localized distention of the bowel or RLQ density

on abdominal x-ray films, sonographic ortomographic studies.

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APPENDICITIS: Complications

Perforation of the appendix

Peritonitis

Abscess

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APPENDICITIS: Medical Management

Surgery is indicated upon diagnosis.

Antibiotics and intravenous fluids are

administered until surgery is performed.

Analgesics may be administered in some patients

after the diagnosis is made.

Appendectomy is performed as soon as possibleto decrease the risk of perforation.

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APPENDICITIS: Nursing Management

Palliative Preoperative Care

Place patient in a comfortable position to relieve

abdominal pain and tension usually Fowlers

position.

See that the patient takes nothing by mouth to

decrease peristalsis and to allow stomach to emptypreparatory to surgery. Note time and nature of last

meal.

Place ice bag to right lower quadrant.

Do not administer cathartics.

Frequently evaluate vital signs.

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APPENDICITIS: Nursing Management

Operative

If diagnosis is established, a simple appendectomy is

performed.

Because relief is almost assured, patient usually

accepts surgery very willingly, which afford a smooth

recovery. Anesthetic may be general or spinal.

Incision may be McBurney, muscle splitting or gridiron,

or right rectus.

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APPENDICITIS: Nursing Management

Postoperative Care

Following recovery from anesthetic, Fowlers position

is maintained, analgesic is given every 3 or 4 hours as

needed, and fluids and food are given as tolerated.

Stitches are removed between 5th and 7th day (usually

in the physicians office).

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APPENDICITIS: Nursing Management

Goals: relieve pain, prevent fluid volume deficit,

reduce anxiety, eliminate infection, maintain skin

integrity, and attain optimal nutrition

Prepare patient for surgery

NGT insertion

Avoid enema Post-operative care

Instruction for wound care prior to discharge

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APPENDICITIS: Nursing Management

Goals: relieve pain, prevent fluid volume deficit,

reduce anxiety, eliminate infection, maintain skin

integrity, and attain optimal nutrition

Prepare patient for surgery

NGT insertion

Avoid enema Post-operative care

Instruction for wound care prior to discharge

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INFLAMMATORY BOWEL DISEASE

Refers to two chronic inflammatory GI disorders:

regional enteritis (i.e., Crohns disease or

granulomatous colitis) and ulcerative colitis.

The cause is still unknown.

Researchers think it is triggered by

environmental agents such as pesticides, foodadditives, tobacco, and radiation.

NSAIDs have been found to exacerbate IBD.

Allergies and immune disorders have also been

suggested as causes.

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INFLAMMATORY BOWEL DISEASE

CROHNS DISEASE ULCERATIVE COLITIS

COURSE Prolonged, variable Exacerbations, remissions

EARLY PATHOLOGY Transmural thickening Mucosal ulceration

LATE PATHOLOGY Deep, penetrating

granulomas

Mucosal minute ulcerations

LOCATION Ileum, right colon (usually) Rectum, left colon

BLEEDING Usually not, but may occur Common severe

PERIANAL

INVOLVEMENT

Common Rare mild

FISTULAS Common RareRECTAL

INVOLVEMENT

About 20% Almost 100%

DIARRHEA Less severe Severe

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INFLAMMATORY BOWEL DISEASE

CROHNS DISEASE ULCERATIVE COLITIS

RADIOGRAPHY Regional, discontinuous

lesions

Narrowing of colon

Thickening of bowel wall

Mucosal edemaStenosis, fistulas

Diffuse involvement

No narrowing of colon

No mucosal edema

Stenosis rare

Shortening of colonAbnormal inflamed mucosa

SIGMOIDOSCOPY May be unremarkable

unless accompanied by

perianal fistulas

Abnormal inflammed

mucosa

COLONOSCOPY Distinct ulcerations

separated by relatively

normal mucosa in the

right colon

Friable mucosa with

pseudopolypsor ulcers in

the left colon

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INFLAMMATORY BOWEL DISEASE

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COLORECTAL CANCER

The colorectal area is the third most common site

of new cancer cases and deaths.

Incidence increases with age and is higher for

people with a family history of colon cancer and

those with IBD or polyps.

Risk factors:

Increasing age

Past and family history of colon cancer, polyps, IBD

High-fat, high-protein, low-fiber diet

Genital or breast cancer (in women)

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COLORECTAL CANCER:

Pathophysiology

Predominantly (95%) adenocarcinoma.

Usually starts as a benign polyp but may become

malignant, invade and destroy normal tissues,

and extend into surrounding structures.

Cancer cells may break away from the primary

tumor and spread to other parts of the body (most

often the liver).

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COLORECTAL CANCER:

Clinical Manifestations

Determined by the location of the cancer, the

stage of the disease, and the function of the

intestinal segment in which it is located.

Change in bowel habits

Passage of blood in the stools

Unexplained anemia, anorexia, weight loss and

fatigue

Dull abdominal pain and melena (right colon)

Abdominal pain, cramping, narrowing stools,

constipation and distention (left colon)

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COLORECTAL CANCER:

Clinical Manifestations

Tenesmus, rectal pain, feeling of incomplete

evacuation after a bowel movement, alternating

diarrhea and constipation and bloody stool (rectal

lesions)

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COLORECTAL CANCER:

Assessment and Diagnosis

Abdominal and rectal examination

Fecal occult blood testing

Barium enema

Proctosigmoidoscopy and colonoscopy with

biopsy or cytology smears

CEA studies for prognostication

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COLORECTAL CANCER:

Assessment and Diagnosis

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COLORECTAL CANCER:

Assessment and Diagnosis

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COLORECTAL CANCER:

Medical Management

Depends on the stage of the disease

Surgery to remove the tumor

Supportive therapy

Adjuvant therapy

Chemotherapy

Radiation therapy

Immunotherapy

Multimodality therapy

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ANORECTAL DISEASES:

Hemorrhoids

Dilated portions of veins in the anal canal

Internal hemorrhoids vs external hemorrhoids

Cause itching and pain and the most common

cause of bright red bleeding with defecation

Symptoms and discomfort can be relieved by

good personal hygiene and by avoiding excessive

straining during defecation.

High residue diet that contains fruit and bran

along with an increased fluid intake may be all

the treatment that is necessary.

A O C AL IS AS S

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ANORECTAL DISEASES:

Hemorrhoids

Warm compresses, sitz baths, analgesic

ointments and suppositories, astringents, and bed

rest allow the engorgement to subside.

Nonsurgical treatments: infrared

photocoagulation, bipolar diathermy and laser

therapy, sclerosing solutions

Surgical treatment: rubber band ligation,

cryosurgery, hemorrhoidectomy

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NURSINGMANAGEMENT

OFGIT

PROBLEMS

HEPATIC,BILLIARY

SYSTEM ANDPANCREAS

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HEPATITIS

Hepatitis is an inflammation of the liver caused

by a variety of factors; most infectious etiologies

are viral in nature.

Significance:

From a community health perspective, one is

concerned with ease of disease transmission and

morbidity.

From a socioeconomic viewpoint, one is concerned

with prolonged loss of time from school and

employment.

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HEPATITIS

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HEPATITISHAV HBV HCV HDV HEV

Incubation(days) 15-45,mean 30 30-180, mean60-90 15-160,mean 50 30-180,mean 60-90 14-60,mean 40

Onset Acute Insidious or

acute

Insidious Insidious or

acute

Acute

Age

preference

Children,

young

adults

Young

adults,

babies,toddlers

Any age,

but more

commonin adults

Any age

(similar to

HBV)

Young

adults

(20-40years)

Transmission Fecal-

oral

Percutaneous

Perinatal

Sexual

Similar to

HBV

Similar to

HBV

Fecal-oral

Severity Mild Occasionallysevere Moderate Occasionallysevere Mild

Fulminant 0.1% 0.1-1% 0.1% 5-20% 1-2%

Progression to

chronicity

None Occasional (1-

10%, 90%

of neonates)

Common Common None

HEPATITIS

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HEPATITIS

HAV HBV HCV HDV HEV

Carrier None 0.1-30% 0.5-1% Variable None

Cancer None + (neonatal

infection)

+ + or - None

Prognosis Excellent Worse with

age, debility

Moderate Acute, Good

Chronic,

poor

Good

Prophylaxis IG

vaccine

HBIG

Recombinant

vaccine

None HBV vaccine

(none for

HBV

carriers)

Unknown

Therapy None Interferon

40% effective

Interferon

50%

response;

sustained

response

< 15%

Unknown None

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HEPATITIS A

Epidemiology

RNA virus of the enterovirus family

Mode of transmission:

Feca-oral route; respiratory route possible

Poor sanitation; person-to-person (epidemic type)

Contaminated food, milk, polluted water, or shell fish

Blood transfusion rarely

Incubation: 3 to 7 weeks; average 4 weeks

Occurrence:

Worldwide

Usually children and young adults

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HEPATITIS B

Epidemiology

Double-shelled virus containing DNA

Causative agent is composed of:

Antigenic material in an outer coat hepatitis B surface

antigen (HBsAg)

Antigenic material in an inner coat hepatitis B core antigen

(HBcAg)

An independent protein circulating in the blood (HBeAg)

Antibody:

Anti-HBs produced early after infection

Anti-HBc noted later in convalescence

Anti-Hbe noted later in convalescence

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HEPATITIS B

Epidemiology

Double-shelled virus containing DNA

Causative agent is composed of:

Antigenic material in an outer coat hepatitis B surface

antigen (HBsAg)

Antigenic material in an inner coat hepatitis B core antigen

(HBcAg)

An independent protein circulating in the blood (HBeAg)

Antibody:

Anti-HBs produced early after infection

Anti-HBc noted later in convalescence

Anti-Hbe noted later in convalescence

HEPATITIS B

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HEPATITIS BCOMMONLY ENCOUNTERED SEROLOGIC PATTERNS OF HEPATITIS B INFECTION

HBsAg Anti-HBs Anti-HBc HB-eAG Anti-HBe Interpretation

+ - IgM + - Acute HBV infection, high

infectivity

+ - IgG + - Chronic HBV infection, high

infectivity

+ - IgG - + Late-acute or chronic HBVinfection, low infectivity

+ + + + or - + or - 1. HBsAg of one

subtype and

heterotypic anti-

HBs (common)

2. Process ofseroconversion

- - IgM + or - + or - 1. Acute HBV

infection

2. Anti-HBc window

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HEPATITIS B

Epidemiology

Mode of transmission:

Oral-oral via saliva

Parenterally or via intimate contact with carriers

Male homosexuals

Blood, saliva, semen, vaginal secretions

Incubation: 2 to 5 months

Occurrence: affects all ages but mostly young adults

worldwide

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HEPATITIS B

Assessment

Resembles Hepatitis A clinically.

Symptoms insidious and variable.

Arthralgias and rashes may be observed; fever and

respiratory symptoms are rare.

Jaundice may or may not be present.

Anorexia, abdominal pain, generalized ailing, malaise

may be noted.

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HEPATITIS B

Nursing Management

Provide adequate fluids, nutrition and bed rest.

Administer alkalis, belladonna and antiemetics if

these agents are required to control dyspepsia and

malaise.

A newly available gamma globulin with a high titer of

anti HBs seems to reduce severity of hepatitis

following needle-stick exposure or contact.

Recognize that recovery and convalescence are slow

and prolonged, sometimes taking 3 to 4 months;

provide psychosocial stimulation.

Hepatitis vaccination

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HEPATITIS CIRRHOSIS

Cirrhosis of the liver is a chronic disease in

which there has been diffuse destruction of

parenchymal cells followed by degeneration and

increase in connective tissue.

Classification:

Laennecs cirrhosis alcoholic

Postnecrotic

Biliary

Posthepatitic

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HEPATITIS CIRRHOSIS

Nursing Management

Instruct and prepare patient for the very many

laboratory studies.

Evaluate nutritional status and needs.

Monitor intake and output accurately.

Adjust nutritional offerings if the patient has ascites

and edema.

Assist the patient in overcoming anorexia, weight loss

and fatigue.

Observe skin and control pruritus.

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HEPATITIS CIRRHOSIS

Nursing Management

Recognize the effect of esthetic factors.

Eliminate alcohol but encourage high caloric intake.

Give supplementary vitamins.

Be cognizant of signs of hematemesis and melena.

Anticipate manifestations of hemorrhage.

Recognize signs of increasing stupor.

Health education

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HEPATITIS ENCEPALOPATHY

Nursing Management

Recognize the effect of esthetic factors.

Eliminate alcohol but encourage high caloric intake.

Give supplementary vitamins.

Be cognizant of signs of hematemesis and melena.

Anticipate manifestations of hemorrhage.

Recognize signs of increasing stupor.

Health education

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HEPATITIS ENCEPALOPATHY

Precipitating Factors

Progressive hepatocellular disease

Increased sources of ammonia in the blood

Infections, paracentesis, acute alcoholism,

hypotension, shock, general anesthesia, minor

surgery, hypokalemia, alkalosis, administration of

sedatives or narcotics.

Portocaval shunts

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HEPATITIS ENCEPALOPATHY

Nursing Management

Evaluate the patients vital functions.

Arrest gastrointestinal bleeding and reduce

intraintestinal nitrogen.

Reduce and possibly eliminate all sedatives and

analgesics.Administer only those specifically

prescribed.

Prevent complications.

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GALLBLADDER DISEASE

Types

Cholecystitis (inflammation of the gall bladder)

Cholelithiasis (stones in the gall bladder)

Choledocholithiasis (stones in the common bile duct)

Assessment and Clinical Manifestations

History of episodic and usually colicky epigastric or

RUQ pain associated with nausea and vomiting.

Jaundice (?)

Murphys sign

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GALLBLADDER DISEASE

Treatment

Surgery is advised if gallstones are present.

In older patients, the risk of surgery must be evaluated

in relation to other disease conditions present.

Chenodeoxycholic acid can decrease the size of an

existing stone and prevent new stones from forming.

For acute cholecystitis, provide hospitalization, bed

rest, withholding of oral fluids, and insertion of

nasogastric tube with suction.

Administer IV fluids to correct electrolyte imbalances,

maintain adequate UO and provide nutritional needs.

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GALLBLADDER DISEASE

Treatment

Administer medication for pain and infection control.

Prepare for laboratory studies.

Record vital signs every 4 hours and prepare for

surgery.

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ACUTE PANCREATITIS

Acute pancreatitis is an inflammation of the

pancreas brought about by the digestion of this

organ by enzymes.

Etiology

Unknown

Associated with excessive intake of alcohol

Associated with blockage of the ampulla of Vater by

gallstones

Associated with spasm and edema of the ampulla of

Vater following duodenitis or after treatment with

opiates.

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ACUTE PANCREATITIS

Etiology

May occur as a complication of mumps or bacterial

disease.

Some congenital hyperlipidemias appear to be related

to acute pancreatitis.

Clinical Manifestations

Abdominal and back pain

Nausea, vomiting and fever

Tenderness across upper abdomen often minimal

Elevated lipase and amylase

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ACUTE PANCREATITIS

Nursing Management

Relieve discomfort and pain to control restlessness

Give meperidine (Demerol)

Encourage patient to assume position of comfort

Decrease pancreatic secretions by reducing

stimulation

NPO

Anticholinergic medications

NGT insertion

Maintain comfort of the intubated patient

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ACUTE PANCREATITIS

Nursing Management

Monitor patient for signs of respiratory failure.

Provide medications to correct deficiencies and

prevent complications

Parenteral fluids, electrolytes, blood and plasma; accurate I

and O.

Antimicrobials

Control of hyperglycemia

Support cardiopulmonary system

Surgical intervention (controversial)

Health education and discharge planning