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Peptic Ulcer Disease.

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Presentation on theme: "Peptic Ulcer Disease."— Presentation transcript:

1 Peptic Ulcer Disease

2 Peptic Ulcer Disease Condition characterized by
Erosion of GI mucosa resulting from digestive action of HCl and pepsin

3 Peptic Ulcer Disease Ulcer development Lower esophagus Stomach
Duodenum 10% of men, 4% of women

4 Types Acute Superficial erosion Minimal erosion Chronic
Muscular wall erosion with formation of fibrous tissue Present continuously for many months or intermittently

5 Peptic Ulcer Disease Etiology and Pathophysiology
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 compared with person with a duodenal ulcer

6 Peptic Ulcer Disease Etiology and Pathophysiology
Some intraluminal acid does seem to be essential for a gastric ulcer to occur 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

7 Peptic Ulcer Disease Etiology and Pathophysiology
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

8 Peptic Ulcer Disease Etiology and Pathophysiology
Mucosal barrier prevents back diffusion of acid from gastric lumen through mucosal layers to underlying tissue Mucosal barrier can be impaired and back diffusion can occur

9 Back-Diffusion of Acids

10 Peptic Ulcer Disease Etiology and Pathophysiology
HCl freely enters mucosa when barrier is broken Injury to tissue occurs Result: cellular destruction and inflammation

11 Peptic Ulcer Disease Etiology and Pathophysiology
Histamine is released Vasodilation, ↑ capillary permeability Further secretion of acid and pepsin

12 Peptic Ulcer Disease Etiology and Pathophysiology
Ulcerogenic drugs inhibit synthesis of prostaglandins and cause abnormal permeability Corticosteroids ↓ rate of mucosal cell renewal thereby ↓ protective effects

13 Peptic Ulcer Disease Etiology and Pathophysiology
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

14 Disruption of Gastric Mucosal Barrier

15 Peptic Ulcer Disease Etiology and Pathophysiology
When blood flow is not sufficient, tissue injury results

16 Peptic Ulcer Disease Etiology and Pathophysiology
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

17 Peptic Ulcer Disease Etiology and Pathophysiology
↑ Vagal nerve stimulation results in hypersecretion of HCl acid ↑ HCl acid can alter mucosal barrier Duodenal ulcers are associated with ↑ acid

18 Gastric Ulcers 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

19 Gastric Ulcers Characterized by
A normal to low secretion of gastric acid Back diffusion of acid is greater (chronic)

20 Gastric Ulcers Critical pathologic process is amount of acid able to penetrate mucosal barrier H. pylori is present in 50% to 70%

21 Gastric Ulcers H. pylori is thought to be more destructive when noxious agents are used, or patient smokes

22 Gastric Ulcers Drugs can cause acute gastric ulcers
Aspirin, corticosteroids, NSAIDs, reserpine Or known causative factors Chronic alcohol abuse, chronic gastritis

23 Duodenal Ulcers Occur at any age and in anyone
↑ Between ages of 35 to 45 years Account for ~80% of all peptic ulcers

24 Duodenal Ulcers Associated with ↑ HCl acid secretion
H. pylori is found in 90-95% of patients Direct relationship has not been found

25 Duodenal Ulcers 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

26 Psychological Stress Ulcers
Acute ulcers that develop following a major physiologic insult such as trauma or surgery A form of erosive gastritis

27 Psychological Stress Ulcers
Gastric mucosa of body of stomach undergoes a period of transient ischemia in association with Hypotension Severe injury Extensive burns Complicated surgery

28 Psychological Stress Ulcers
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

29 Peptic Ulcer Disease Clinical Manifestations
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

30 Peptic Ulcer Disease Complications
3 major complications Hemorrhage Perforation Gastric outlet obstruction Initially treated conservatively May require surgery at any time during course of therapy

31 Peptic Ulcer Disease Hemorrhage
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

32 Peptic Ulcer Disease Perforation
Most lethal complication of peptic ulcer Commonly seen in large penetrating duodenal ulcers that have not healed and are located on posterior mucosal wall

33 Peptic Ulcer Disease Perforation
Perforated gastric ulcers often located on lesser curvature of stomach

34 Peptic Ulcer Disease Perforation

35 Peptic Ulcer Disease Perforation
Occurs when ulcer penetrates serosal surface Spillage of their gastric or duodenal contents into peritoneal cavity Size of perforation directly proportional to length of time patient has had ulcer Sudden, dramatic onset

36 Peptic Ulcer Disease Gastric Outlet Obstruction
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

37 Peptic Ulcer Disease Gastric Outlet Obstruction
After longstanding obstruction stomach enters decompensated phase Results in dilation and atony

38 Peptic Ulcer Disease Gastric Outlet Obstruction
Obstruction is not totally due to fibrous scar tissue Active ulcer formation is associated with edema, inflammation, pylorospasm All contribute to narrowing of pylorus

39 Peptic Ulcer Disease Gastric Outlet Obstruction
Usually has a history of ulcer pain Short duration or absence of pain indicative of a malignant obstruction

40 Peptic Ulcer Disease Gastric Outlet Obstruction
Vomiting is common Constipation is a common complaint Dehydration, lack of roughage in diet May show swelling in upper abdomen

41 Peptic Ulcer Disease Diagnostic Studies
Endoscopy procedure most often used Determines degree of ulcer healing after treatment Tissue specimens can be obtained to identify H. pylori and to rule out gastric cancer

42 Peptic Ulcer Disease Diagnostic Studies
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

43 Peptic Ulcer Disease Diagnostic Studies
Barium contrast studies Widely used X-ray studies Ineffective in differentiating a peptic ulcer from a malignant tumor

44 Peptic Ulcer Disease Diagnostic Studies
Gastric analysis Identifying a possible gastrinoma Determining degree of gastric hyperacidity Evaluating results of therapy

45 Peptic Ulcer Disease Diagnostic Studies
Laboratory analysis CBC Urinalysis Liver enzyme studies Serum amylase determination Stool examination

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