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45 Cards in this Set

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  • Back
Superficial erosion, Minimal inflammation
acute Peptic Ulcer Disease
Muscular wall erosion with formation of fibrous tissue
Present continuously for many months or intermittently
gastric peptic ulcer disease
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
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
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
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
↑ 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
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
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
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
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
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
3 major complications
Gastric outlet obstruction
Initially treated conservatively
May require surgery at any time during course of therapy
Peptic Ulcer Disease complications
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
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
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
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
Liver enzyme studies
Serum amylase determination
Stool examination
peptic ulcer disease diagnostic studies
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
Medical regimen consists of
Adequate rest
Dietary modification
Drug therapy
Elimination of smoking
Long-term follow-up care
collaborative care PUD
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
Includes use of
H2R blockers
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
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)
Block ATPase enzyme that is important for secretion of HCl acid
PPIs-proton pump inhibitors
Eradicate H. pylori infection
No single agents have been effective in eliminating H. pylori
antibiotic therapy
Used as adjunct therapy for peptic ulcer disease
↑ gastric pH by neutralizing acid
Occasionally ordered for treatment
↓ cholinergic stimulation of HCl acid
anticholinergic drugs
used for short term treatments of ulcers
cytoprotective drug therapy
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
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
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
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
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
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
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
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
Gradual onset
Constant NG aspiration of stomach contents may relieve symptoms
Regular irrigation of NG tube
gastic outlet obstruction
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
< 20% of patients with ulcers need surgical intervention
Indications for surgical interventions
History of hemorrhage, ↑ risk of bleeding
Prepyloric or pyloric ulcers
Multiple ulcer sites
Drug-induced ulcers
Possible existence of a malignant ulcer
surgical therapy
surgial therapy for PUD
Dumping syndrome
Postprandial hypoglycemia
Bile reflux gastritis
postoperative complications of PUD
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
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
Prolonged contact of bile causes damage to gastric mucosa
Administration of cholestyramine relieves irritation
Also, aluminum hydroxide antacids
bile reflux gastritis
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
↑ 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