gastritis (metab)

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GASTRITIS GERARD GABRIEL PASION-REOTUTAR, RM, MAN

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Page 1: Gastritis (metab)

GASTRITIS

GERARD GABRIEL PASION-REOTUTAR, RM, MAN

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Gastritis

The inflammation of the gastric or stomach mucosa

Gastritis may be acute, lastingseveral hours to a few days, or chronic, resulting from repeated exposure to irritating agents or recurring episodes ofacute gastritis.

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eating food that is irritating, too highly seasoned, orcontaminated with disease-causing microorganisms. overuse of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), excessive alcohol intake, bile reflux, and radiation therapy. ingestion of strong acid or alkali, which may cause the mucosa to become gangrenous or to perforate. may develop in acute illnesses, especially when the patient has had major traumatic injuries; burns; severe infection;hepatic, renal, or respiratory failure; or major surgery.

Acute gastritis

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benign or malignant ulcers of the stomach or by the bacteria Helicobacter pylori.associated with autoimmune diseases such as pernicious anemia; dietary factors such as caffeine; the use of medications such as NSAIDs or

bisphosphonates (eg, alendronate [Fosamax], risedronate [Actonel], ibandronate [Boniva]); alcohol and smoking; chronic reflux of pancreatic secretions and bile into the stomach.

Chronic gastritis

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Clinical Manifestations

abdominal discomfort, headache, lassitude,nausea, vomitinganorexia,hiccupping,

Acute gastritis

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Clinical Manifestations

anorexia, heartburn after eating, belching,a sour taste in the mouth, nausea and vomiting. intolerance to spicy or fatty foods

Chronic gastritis

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Assessment and Diagnostic Findings

Gastritis is sometimes associated with achlorhydria orhypochlorhydria (absence or low levels of hydrochloric acid [HCl]) or with hyperchlorhydria (high levels of HCl).

Diagnosis can be determined by:

upper GI x-ray seriesendoscopyhistologic examination of a tissue specimen obtained by biopsy.laboratory studies for detecting H. pylori infection

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The gastric mucosa is capable of repairing itself after anepisode of gastritis. As a rule, the patient recovers in about1 day, although the appetite may be diminished for an additional 2 or 3 days.

instruct the patient to refrain from alcohol and food until symptoms subsideif the symptoms persist, intravenous (IV) fluids may need to be administeredanalgesic agents and sedativesnasogastric (NG) intubation

Medical Management

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If gastritis is caused by ingestion of strong acids or alkalis, emergency treatment consists of diluting and neutralizing the offending agent.

To neutralize acids, common antacids (eg, aluminum hydroxide) are used;

To neutralize an alkali, diluted lemon juice or diluted vinegar is used;

If corrosion is extensive or severe, emetics and lavage are avoided because of the danger of perforation and damage to the esophagus.

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Emergency surgery may be required to remove gangrenous or perforated tissue.

A gastric resection or a gastrojejunostomy

(anastomosis of jejunum to stomach to detour

around the pylorus) may be necessary to treat pyloric obstruction, a narrowing of the pyloric orifice, which cannot be relieved by medical management.

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PUD

GERARD GABRIEL PASION-REOTUTAR, RM, MAN

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Peptic Ulcer Disease

an excavation (hollowed-out area) that forms in the mucosal wall of the stomach, in the pylorus (the opening between the stomach and duodenum), in the duodenum (the first part of the small intestine), or in the esophagus.

A peptic ulcer may be referred to as a gastric, duodenal, or esophageal ulcer, depending on its location.

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Erosion of a circumscribed area of mucous membrane is the cause. This erosion may extend as deeply as the muscle layers or through the muscle to the peritoneum.

Peptic ulcers are more likely to occur in the duodenum than in the stomach.

As a rule they 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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Risk Factorspeople between 40 and 60 years of age.

familial tendency also 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.

excessive secretion of HCl in the stomach may contribute to the formation of peptic ulcers. The ingestion of milk and caffeinated beverages, smoking, and alcohol also may increase HCl secretion.

chronic use of NSAIDs

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In the past, stress and anxiety were thought to be causes of ulcers, but research has documented that peptic ulcers result from infection with the gram-negative bacteria H. pylori, which may be acquired through ingestion of food and water.

Person-to-person transmission of the bacteria also occurs through close contact and exposure to emesis.

Peptic ulcers are found in rare cases in patients withtumors that cause secretion of excessive amounts of thehormone gastrin. The Zollinger-Ellison syndrome (ZES)consists of severe peptic ulcers, extreme gastric hyperacidity, and gastrin-secreting benign or malignant tumors of the pancreas.

Risk Factors

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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.

Cushing’s ulcers are common in patients with head injury and brain trauma. They may occur in the esophagus, stomach, or duodenum and are usually deeper and more penetrating than stress ulcers.

Curling’s ulcer is frequently observed about 72 hours after extensive burns and involves the antrum of the stomach or the duodenum.

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Assessment and Diagnostic Findings

physical examination may reveal pain, epigastric tenderness, or abdominal distention. barium study of the upper GI tract may show an ulcer;

endoscopy is the preferred diagnostic procedure because it allows direct visualizationof inflammatory changes, ulcers, and lesions.

occult blood test.

gastric secretory studies are of value in diagnosing achlorhydria and ZES.

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Assessment and Diagnostic Findings

H. pylori infection may be determined by:

endoscopy and histologic examination of atissue specimen obtained by biopsy,

serologic testing for antibodies against the H. pylori antigen,

stool antigen test,

urea breath test

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Medical Management

Antibiotics to eradicate H. pylori

Bismuth salts

Histamine-2 (H2) receptor antagonists and proton pump inhibitors

Rest, sedatives, and tranquilizers may be added for the patient’s comfort and are prescribed as needed.

Research is being conducted to develop a vaccine against H. pylori

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For patients with ZES, hypersecretion of acid may be controlled with:

high doses of H2 receptor antagonistsoctreotide (Sandostatin), a medication that suppresses gastrin levels

Patients at risk for stress ulcers (eg, patients with head injury or extensive burns) may be treated

IV H2 receptor antagonists cytoprotective agents (eg, misoprostol, sucralfate) because of the risk of upper GI tract hemorrhage.

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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), life-threatening hemorrhage, perforation, or obstruction and for those with ZES that is unresponsive to medications.

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Surgical procedures include:

vagotomy, with or without pyloroplasty (transecting nerves that stimulate acid secretion and opening the pylorus)antrectomy, which is removal of the pyloric (antrum) portion of the stomach with anastomosis (surgical connection) to either the duodenum (gastroduodenostomy or Billroth I) or jejunum (gastrojejunostomy or Billroth II)

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Dumping Syndrome

an unpleasant set of vasomotor and GI symptoms that sometimes occur in patients who have had gastric surgery or a form of vagotomy causing too rapid passage of food from the stomach remnant into the jejunum

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Early symptoms include: sensation of fullness, weakness,faintness, dizziness, palpitations, diaphoresis, crampingpainsdiarrhea

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Later, there is a rapid elevation of blood glucose, followed by increased insulin secretion. This results in a reactive hypoglycemia. Vasomotor symptoms that occur 10 to 90 minutes after eating includes:

pallor, perspiration, palpitations,headache, and feelings of warmth, dizziness, and drowsiness. Anorexia because the person may be reluctant to eat.Steatorrhea is partially the result of rapid gastric emptying, which prevents adequate mixing with pancreatic and biliary secretions.

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Reducing the intake of fat and administering an antimotility medication (eg, loperamide [Imodium]) may control steatorrhea.

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a. Gastricenteromab. Gastro-intestinal polypsc. Gastroenteritisd. Gastremesis

1. Inflammation of the membrane lining the intestines and the stomach, caused by a viral infection and resulting in diarrhea and vomiting

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a. bacterial infectionb. viral infectionc. ingestion of toxic substancesd. allergic reactionse. severe diarrhea

2. The following are causes of gastroenteritis except

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a. chest discomfortsb. constipationc. increase appetited. nausea and vomiting

3. Symptoms of gastroenteritis includes

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a. guaiac examb. occult blood examc. fecalysisd. urinalysis

4. diagnostics for gastroenteritis is

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a. BROW dietb. CRAM diet- Cereal, Rice, Applesauce and Milk

c. BRAT dietd. DAT

5. diet of patient with gastroenteritis should include

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a. antiemeticsb. antibioticsc. antiviralsd. anti-inflammatorye. anticoagulants

6. Pharmacological management for gastroenteritis include the following but one