Dept. of Surgery
Introduction
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Erosion of GI mucosa resulting from digestive
action of HCl and pepsin
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Site? Lower esophagus
? Stomach
? Duodenum
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? 10% of men, 4% of womenTypes
Acute
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? Superficial erosion? Minimal erosion
Chronic
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? Muscular wall erosion with formation of fibrous tissue? Present continuously for many months or intermittently
Etiology and Pathophysiology
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? Develop only in presence of acid environment? Excess of gastric acid not necessary for ulcer development
? Person with a gastric ulcer has normal to less than normal gastric acidity
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compared with person with a duodenal ulcer
? Some intraluminal acid does seem to be essential for a gastric ulcer to
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occur? Pepsinogen is activated to pepsin in presence of HCl
? Secretion of HCl by parietal cells has a pH of 0.8
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? pH reaches 2 to 3 after mixing with stomach contents
? At pH level 3. 5 or more, stomach acid is neutralized
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? Surface mucosa of stomach is renewed about every 3 days
? Mucosa can continually repair itself except in extreme
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instances? Mucosal barrier prevents back diffusion of acid from gastric
lumen through mucosal layers to underlying tissue
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? Mucosal barrier can be impaired and back diffusion can occurDiffusion of Acid
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Disruption of Gastric Mucosal Barrier
Protective Mechanism
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? Mucus forms a layer that entraps or slowsdiffusion of hydrogen ions across mucosal barrier
? Bicarbonate secreted Neutralizes HCl acid in
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lumen of GI tract
Gastric Ulcers
Characterized by
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? A normal to low secretion of gastric acid
? Back diffusion of acid is greater (chronic )
? Critical pathologic process is amount of acid able to
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penetrate mucosal barrier? H pylori is present in 50% to 70%
? Drugs --- Aspirin, corticosteroids, N SAIDs, reserpine,
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Chronic alcohol abuse, chronic gastritisDuodenal Ulcers
? Between ages of 35 to 45 years
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? Account for 8 0% of all peptic ulcers? Associated with HCl acid secretion
? H.pylori associated in 9 0- 9 5 % of cases
? Diseases with risk of duodenal ulcers
COPD, cirrhosis of liver, chronic pancreatitis,
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hyperparathyroidism, chronic renal failure
Clinical Features
? Common to have no pain or other symptoms
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? Gastric and duodenal mucosa not rich in sensory pain
fibers
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? Duodenal ulcer pain? Burning, cramplike
? Gastric ulcer pain
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? Burning, gaseous
Complications
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? 3 major complicationsvHemorrhage
vPerforation
vGastric outlet obstruction
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? Initially treated conservatively
? May require surgery at any time during course of
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therapyDiagnostic Studies
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? Endoscopy procedure? Determines degree of ulcer healing after treatment
? Tissue specimens can be obtained to identify H. pylori and to rule out
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gastric cancer
? Tests for H.pylori
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? Noninvasive tests? Serum or whole blood antibody tests
? Immunoglobin G (I g G)
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? Urea breath test
? C 14 breath test
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? Invasive tests? Biopsy of stomach
? Rapid urease test
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? Barium contrast studies? Widely used
? X- ray studies
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? Ineffective in differentiating a peptic ulcer from a
malignant tumor
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? Gastric analysis? Lab analysis
Treatment
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Medical regimen consists of? Adequate rest
? Dietary modification
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? Drug therapy
? Elimination of smoking
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? Long-term follow-up careAim of treatment pro g ram
? degree of gastric acidity
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? Enhance mucosal defense mechanisms
? Minimize harmful effects on mucosa
Drug Therapy
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? Antacids
? H2 receptor blockers
? PPIs
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? Antibiotics? Anticholinergics
? Cytoproctective therapy
Histamine receptor blocks (H2 R blockers)
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?Used to manage peptic ulcer disease
?Block action of histamine on H2 receptors
HCl acid secretion
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conversion of pepsinogen to pepsinulcer healing
Proton pump inhibitors
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? Block ATPase en zyme that is important for secretion of HCl acidAntibiotic therapy
? Eradicate H. pylori infection
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? No single agents have been effective in eliminating H. pylori? Antacids
? Used as adjunct therapy for peptic ulcer disease
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? gastric pH by neutralizing acid? Anticholinergic drugs
? Occasional y ordered for treatment
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? cholinergic stimulation of HCl acid
? Cytoprotective drug therapy
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? Serotonin reuptake inhibitorsNutritional therapy
? Dietary modifications may be necessary so that foods and
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beverages irritating to patient can be avoided or eliminated
? Nonirritating or bland diet consisting of 6 small meals a day
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during symptomatic phase? Protein considered best neutralizing food
? Stimulates gastric secretions
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? Carbohydrates and fats are least stimulating to HCl acid
secretion
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? Do not neutralize wellSurgical Treatment
? < 20% of patients with ulcers need surgical
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intervention? Indications for surgical interventions
vIntractability
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vHistory of hemorrhage, risk of bleedingvPrepyloric or pyloric ulcers
vMultiple ulcer sites
vDrug-induced ulcers
vPossible existence of a malignant ulcer
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vObstructionSurgical procedures
v Gastroduodenostomy
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v Gastrojejunostomy
v Vagotomy
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v PyloroplastyA. Billroth I Procedure
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B. Billroth II ProcedureGoals
vComply with prescribed therapeutic regimen
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vExperience a reduction or absence of discomfort related to
peptic ulcer disease
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vExhibits no signs of GI complicationsvHave complete healing
vLifestyle changes to prevent recurrence
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