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45 Cards in this Set
- Front
- Back
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Superficial erosion, Minimal inflammation
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acute Peptic Ulcer Disease
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Muscular wall erosion with formation of fibrous tissue
Present continuously for many months or intermittently |
gastric peptic ulcer disease
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Develop only in presence of acid environment
Excess of gastric acid not necessary for ulcer development Pepsinogen is activated to pepsin in presence of HCl and a pH of 2 to 3 Secretion of HCl by parietal cells has a pH of 0.8 pH reaches 2 to 3 after mixing with stomach contents At pH level 3.5 or more, stomach acid is neutralized Pepsin has little or no proteolytic activity Surface mucosa of stomach is renewed about every 3 days Mucosa can continually repair itself except in extreme instances Mucosal barrier prevents back diffusion of acid from gastric lumen through mucosal layers to underlying tissue |
etiology and pathophysiology of PUD
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Mucosal barrier can be impaired and back diffusion can occur
HCl freely enters mucosa when barrier is broken Injury to tissue occurs Result: cellular destruction and inflammation Histamine is released Vasodilation, ↑ capillary permeability Further secretion of acid and pepsin Ulcerogenic drugs inhibit synthesis of prostaglandins and cause abnormal permeability Corticosteroids ↓ rate of mucosal cell renewal thereby ↓ protective effects |
etiology and pathophysiology of PUD
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When mucosal barrier is disrupted, there is a compensatory ↑ in blood flow
Prostaglandin-like substances, histamines act as vasodilators Hydrogen ions are rapidly removed Buffers are delivered Nutrients arrive ↑ Mucosal cell replication When blood flow is not sufficient, tissue injury results |
etiology and pathophysiology of PUD
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Two mechanisms that protect
Mucus forms a layer that entraps or slows diffusion of hydrogen ions across mucosal barrier Bicarbonate is secreted Neutralizes HCl acid in lumen of GI tract |
etiology and pathophysiology of PUD
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↑ Vagal nerve stimulation results in hypersecretion of HCl acid
↑ HCl acid can alter mucosal barrier Duodenal ulcers are associated with ↑ acid |
etiology and pathophysiology of PUD
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Commonly found on lesser curvature in close proximity to antral junction
Less common than duodenal ulcers Prevalent in women, older adults, persons from lower socioeconomic class Characterized by A normal to low secretion of gastric acid Back diffusion of acid is greater (chronic) Critical pathologic process is amount of acid able to penetrate mucosal barrier |
Gastric Ulcer
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H. pylori is present in 50% to 70%
H. pylori is thought to be more destructive when noxious agents are used, or patient smokes Drugs can cause acute gastric ulcers Aspirin, corticosteroids, NSAIDs, reserpine Or known causative factors Chronic alcohol abuse, chronic gastritis |
Gastric Ulcer
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Occur at any age and in anyone
↑ Between ages of 35 to 45 years Account for ~80% of all peptic ulcers Associated with ↑ HCl acid secretion H. pylori is found in 90-95% of patients Direct relationship has not been found Diseases with ↑ risk of duodenal ulcers COPD, cirrhosis of liver, chronic pancreatitis, hyperparathyroidism, chronic renal failure Treatments used for these conditions may promote ulcer development account for 80% of all peptic ulcers |
Duodenal Ulcers
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Acute ulcers that develop following a major physiologic insult such as trauma or surgery
A form of erosive gastritis Gastric mucosa of body of stomach undergoes a period of transient ischemia in association with : Hypotension, Severe injury, Extensive burns, Complicated surgery Ischemia due to ↓ capillary blood flow or shunting of blood away from GI tract so that blood flow bypasses gastric mucosa Imbalance between destructive properties of HCl acid and pepsin, and protective factors of stomach’s mucosal barrier everyone in ICU should be on H2 blockers. At risk d/t decreased bloodflow to gut b/c blood goes to brain, heart and lungs |
Psychological Stress Ulcers
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Common to have no pain or other symptoms
Gastric and duodenal mucosa not rich in sensory pain fibers Duodenal ulcer pain Burning, cramplike Gastric ulcer pain Burning, gaseous |
Peptic Ulcer Disease: Clinical Manifestations
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3 major complications
Hemorrhage Perforation Gastric outlet obstruction Initially treated conservatively May require surgery at any time during course of therapy |
Peptic Ulcer Disease complications
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Most common complication of peptic ulcer disease
Develops from erosion of Granulation tissue found at base of ulcer during healing Ulcer through a major blood vessel |
Hemmorrhage
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Most lethal complication of peptic ulcer
Commonly seen in large penetrating duodenal ulcers that have not healed and are located on posterior mucosal wall Perforated gastric ulcers often located on lesser curvature of stomach Occurs when ulcer penetrates serosal surface Spillage of gastric or duodenal contents into peritoneal cavity Size of perforation directly proportional to length of time patient has had ulcer Sudden, dramatic onset |
Perforation
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Ulcers located in antrum and prepyloric and pyloric areas of stomach
Duodenum can predispose to gastric outlet obstruction ↑ contractile force needed to empty stomach results in hypertrophy of stomach wall Obstruction is not totally due to fibrous scar tissue Active ulcer formation is associated with edema, inflammation, pylorospasm All contribute to narrowing of pylorus Usually has a history of ulcer pain Short duration or absence of pain indicative of a malignant obstruction Vomiting is common and constipation May show swelling in upper abdomen |
Gastric Outlet Obstuction
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Endoscopy procedure most often used-tells size, location, if healing, if H. pylori present.
Determines degree of ulcer healing after treatment Tissue specimens can be obtained to identify H. pylori and to rule out gastric cancer Tests for H. pylori Noninvasive tests Serum or whole blood antibody tests: Immunoglobin G (IgG) Urea breath test Invasive tests Biopsy of stomach Rapid urease test Barium contrast studies X-ray studies Ineffective in differentiating a peptic ulcer from a malignant tumor Laboratory analysis CBC Liver enzyme studies Serum amylase determination Stool examination |
peptic ulcer disease diagnostic studies
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Laboratory analysis
CBC-see if anemic Liver enzyme studies-see if increased risk of ulcers Serum amylase determination Stool examination |
Lab analysis of peptic ulcer disease
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Medical regimen consists of
Adequate rest Dietary modification Drug therapy Elimination of smoking Long-term follow-up care |
collaborative care PUD
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Aim of treatment program
↓ degree of gastric acidity Enhance mucosal defense mechanisms Minimize harmful effects on mucosa Moderation in daily activity is essential NSAIDs that are COX-2 inhibitors are used |
collaborative care PUD
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Includes use of
Antacids H2R blockers PPIs Antibiotics Anticholinergics Cytoproctective therapy Recurrence of peptic ulcer is frequent No drugs, unless prescribed by health care provider, should be taken Ulcerogenic effect |
Drug therapy for PUD
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Used to manage peptic ulcer disease
Block action of histamine ↓ HCl acid secretion ↓ conversion of pepsinogen to pepsin ↑ ulcer healing |
Histamine-2 receptor blocks (H2R blockers)
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Block ATPase enzyme that is important for secretion of HCl acid
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PPIs-proton pump inhibitors
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Eradicate H. pylori infection
No single agents have been effective in eliminating H. pylori |
antibiotic therapy
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Used as adjunct therapy for peptic ulcer disease
↑ gastric pH by neutralizing acid |
antacids
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Occasionally ordered for treatment
↓ cholinergic stimulation of HCl acid |
anticholinergic drugs
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used for short term treatments of ulcers
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cytoprotective drug therapy
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Dietary modifications may be necessary so that foods and beverages irritating to patient can be avoided or eliminated
Nonirritating or bland diet consisting of 6 small meals a day during symptomatic phase Include a sample diet with a list of foods that usually cause distress Hot, spicy foods and pepper, alcohol, carbonated beverages, tea, coffee, broth Foods high in roughage may irritate an inflamed mucosa Protein considered best neutralizing food Stimulates gastric secretions Carbohydrates and fats are least stimulating to HCl acid secretion Do not neutralize well Milk can neutralize gastric acidity and contains prostaglandins and growth factors Protects GI mucosa from injury |
nutritional therapy
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Treated with same regimen used for conservative therapy
Situation is more serious because of possible complications of perforation, hemorrhage, gastric outlet obstruction Accompanied by bleeding, ↑ pain and discomfort, nausea, vomiting Recurrent vomiting, gastric outlet obstruction NG tube placed in stomach with intermittent suction for about 24 to 48 hours Fluids and electrolytes are replaced by IV infusion until patient is able to tolerate oral feedings without distress Management is similar to that for upper GI bleeding Blood or blood products may be administered Careful monitoring of vital signs, intake and output, laboratory studies, signs of impending shock Endoscopic evaluation reveals degree of inflammation or bleeding and ulcer location 5-year follow-up program is recommended |
acute exacerbation-therapy related to complications of PUD
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Immediate focus to stop spillage of gastric or duodenal contents into peritoneal cavity and restore blood volume
NG tube is placed into stomach Placement of tube as near to perforation site as possible facilitates decompression Circulating blood volume must be replaced with lactated Ringer’s and albumin solutions Blood replacement in form of packed RBCs may be necessary Central venous pressure line, indwelling urinary catheter should be inserted and monitored hourly |
perforation
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Decompress stomach
Correct any existing fluid and electrolyte imbalances Improve patient’s general state of health NG tube inserted in stomach, attached to continuous suction to remove excess fluids and undigested food particles Continuous decompression allows Stomach to regain its normal muscle tone Ulcer can begin to heal Inflammation and edema subside When aspirate falls below 200 ml, within normal range, oral intake of clear liquids can begin Watch patient carefully for signs of distress or vomiting IV fluids and electrolytes are administered according to degree of dehydration, vomiting, electrolyte imbalance |
gastric outlet obstruction
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Identify patients at risk
Early detection and ↓ morbidity Encourage patients to take ulcerogenic drugs with food or milk Teach patients to report symptoms related to gastric irritation to health care provider |
health promotion
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Identify patients at risk
Early detection and ↓ morbidity Encourage patients to take ulcerogenic drugs with food or milk Teach patients to report symptoms related to gastric irritation to health care provider |
acute intervention
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Changes in vital signs, ↑ in amount and redness of aspirate signal massive upper GI bleeding
↑ amount of blood in gastric contents ↓ pain because blood helps neutralize acidic gastric contents Keep blood clots from obstructing NG tube |
hemorrhage
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Sudden, severe abdominal pain unrelated in intensity and location to pain that brought patient to hospital
Indicated by a rigid, boardlike abdomen Severe generalized abdominal and shoulder pain Shallow, grunting respirations Ensure any known allergies are reported on chart Antibiotic therapy is usually started Surgical closure may be necessary if perforation does not heal spontaneously |
perforation
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Gradual onset
Constant NG aspiration of stomach contents may relieve symptoms Regular irrigation of NG tube |
gastic outlet obstruction
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General instructions should cover aspects of disease, drugs, possible lifestyle changes, regular follow-up care
Patient motivation ↑ when they understand why they should comply with therapy and follow-up care |
ambulatory home care
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< 20% of patients with ulcers need surgical intervention
Indications for surgical interventions Intractability History of hemorrhage, ↑ risk of bleeding Prepyloric or pyloric ulcers Multiple ulcer sites Drug-induced ulcers Possible existence of a malignant ulcer Obstruction |
surgical therapy
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Gastroduodenostomy
Gastrojejunostomy Vagotomy Pyloroplasty |
surgial therapy for PUD
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Dumping syndrome
Postprandial hypoglycemia Bile reflux gastritis |
postoperative complications of PUD
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Direct result of surgical removal of a large portion of stomach and pyloric sphincter
↓ reservoir capacity of stomach Associated with meals having a hyperosmolar composition Experienced by one-third to one-half of patients after peptic ulcer surgery |
Dumping syndrome
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Considered a variant of dumping syndrome
Result of uncontrolled gastric emptying of a bolus of fluid high in carbohydrate into small intestine Release of excessive amounts of insulin into circulation same symptoms as dumping syndrome |
postprandial hypoglycemia
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Prolonged contact of bile causes damage to gastric mucosa
Administration of cholestyramine relieves irritation Also, aluminum hydroxide antacids |
bile reflux gastritis
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Start as soon as immediate postoperative period is successfully passed
Patient should be advised to eliminate drinking fluid with meals Diet should consist of Small, dry feedings daily Low in carbohydrates Restricted in sugars Moderate amounts of protein and fat 30 minutes of rest after each meal Interventions are diet instruction, rest, and reassurance |
nutritional therapy
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↑ patients > 60 years of age
↑ use of NSAIDs First manifestation may be frank gastric bleeding or ↓ hematocrit Treatment similar to younger adults Emphasis placed on prevention of both gastritis and peptic ulcers |
gerontological considerations
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