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PEPTIC ULCER disease (PUD) Pathophysiology

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PEPTIC ULCER disease (PUD) Pathophysiology By ... Increased gastric acid secretion. Drugs: NSAI, Aspirin, cortisone and cytotoxic drugs.. Cigarette smoking. – PowerPoint PPT presentation

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Title: PEPTIC ULCER disease (PUD) Pathophysiology


1
PEPTIC ULCER disease (PUD) Pathophysiology
  • By
  • Dr. Abdelaty Shawky
  • Assistant professor of pathology

2
  • Anatomy of the stomach
  • The stomach is located in the upper part of the
    abdomen just beneath the diaphragm .
  • The stomach is distensible and on a free
    mesentery, therefore, the size, shape, and
    position may vary with posture and content.

3
  • An empty stomach is roughly the size of an open
    hand and when distended with food, can fill much
    of the upper abdomen and may descend into the
    lower abdomen on standing.

4
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5
  • The stomach may be divided into seven major
    sections. The cardia is a 12 cm segment distal
    to the esophagogastric junction.
  • The fundus refers to the superior portion of the
    stomach that lies above an imaginary horizontal
    plane that passes through the esophagogastric
    junction.

6
  • The antrum is the smaller distal one-fourth to
    one-third of the stomach. The narrow 12 cm
    channel that connects the stomach and duodenum is
    the pylorus.
  • The lesser curve refers to the medial shorter
    border of the stomach, whereas the opposite
    surface is the greater curve.

7
Histology of stomach
  1. Mucosa.
  2. Submucosa (with Meissner plexus).
  3. Muscularis propria (outer longitudinal layer,
    Auerbach/myenteric plexus, inner circular layer,
    innermost oblique layer).
  4. Serosa.

8
  • Gastric mucosa has two compartments 1.
    Superficial foveolar compartment, relatively
    uniform throughout, consists of surface
    epithelial / foveolar cells lining the entire
    mucosal surface and pits 2. Deep glandular
    compartment, varying composition and thickness in
    different regions containing gastric glands

9
  • The gastric mucosa is very metabolically active
  • The entire mucosa is replaced every 2 to 8 days.
  • Mucous neck cells at the base of foveola are
    progenitors of surface epithelium and gastric
    glands, mitotically active, site of gastric
    carcinogenesis.
  • Ratio of foveola to gland volume differs by
    region cardia/antrum 50/50 fundus 25/75

10
Cardia
  • Branching mucous glands without parietal cells.

11
Antrum
  • Branching mucus glands, cytoplasm may be bubbly,
    vacuolated, granular or glassy

12
Fundus
  • Straight glands composed of tightly packed chief
    cells, parietal cells, endocrine cells, mucus
    cells
  • Higher ratio of glands to foveola than antrum

13
Parietal cells
  • Primarily in fundus/body.
  • Have eosinophilic cytoplasm.
  • Produce acid via H/K ATPase pump.
  • Also secrete intrinsic factor which binds luminal
    Vitamin B12.
  • Stimulated by vagus nerve, binding of gastrin
    receptor by gastrin from antral cells, binding of
    H2 receptor by histamine from enterochromaffin-lik
    e cells.

14
Mucous cells
  • Produce neutral mucin.
  • Lightly eosinophilic or clear cytoplasm and
    bubbly

15
Chief cells
  • Scattered in fundus/body.
  • Have basophilic cytoplasm.
  • Release pepsinogen I and II, which are activated
    by low luminal pH to pepsin

16
Endocrine cells
  • Scattered in fundus/body.
  • Have clear cytoplasm.
  • Produce
  • Histamine (enterochromaffin-like).
  • Gastrin (G cells).
  • Serotonin (enterochromaffin cells).
  • Somatostatin (D cells).

17
Peptic Ulcer Disease
18
  • Definition
  • Ulceration of any part of the G.I.T exposed to
    the gastric juice.

19
  • Acute peptic ulcers
  • (stress ulcers)

20
  • Etiology
  • I. Infective Salmonellosis staph. Food
    poisoning.
  • II. Non infective
  • Drugs NSAI, cytotoxic drugs and cortisone.
  • Alcoholism.
  • Cigarette smoking.
  • Uremia.
  • Severe stress.
  • Chemical irritation by strong alkalis, acids.
  • Mechanical trauma during endoscopic examination.

21
  • Sites stomach 1st part of duodenum.
  • Pathology hemorrhagic inflammation and
    superficial ulceration.
  • Fate usually heal by regeneration.

22
Acute gastritis
23
Chronic peptic ulcer disease
24
Sites of peptic ulcer
  • Duodenum First portion usually toward the
    anterior wall is more often affected.
  • Stomach Usually antrum toward the Lesser
    curvature.
  • At the margins of a gastroenterostomy (stomal
    ulcer)
  • In the duodenum, stomach or jejunum of patients
    with Zollinger-Ellison syndrome.
  • Within Meckels diverticulum that contains
    ectopic gastric mucosa.

25
  • Etiology
  • Genetic factors Genetic factors play a role in
    the pathogenesis of ulcer disease. The lifetime
    prevalence of developing ulcer disease in
    first-degree relatives of ulcer patients is about
    three times greater than the general population.
    Approximately 2050 of duodenal ulcer patients
    report a positive family history.  

26
  • 2. Hormonal factors evident in in cases of
    Zollinger Ellison syndrome.
  • 3. Environmental factors cigarette smoking,
    coffee and alcoholism.
  • 4. Emotional stress evident with duodenal ulcer.
  • 5. Associated diseases Chronic bronchitis,
    emphysema, liver cirrhosis, renal failure.

27
  • Pathogenesis
  • 1. Duodenal ulcer
  • Due to increased gastric juice secretion Rapid
    emptying of stomach into duodenum
  • Causes
  • Increased vagus nerve stimulation.
  • Increased number of parietal cell (as in tall
    thin patient).
  • Increase hormonal stimulation (Z.E syndrome)
    Gastrinoma ? Gastrin.
  • Increase the responsiveness of parietal cells to
    secretory stimuli.
  • ? psychosomatic stimuli.

28
  • 2. Gastric ulcer.
  • Due to decreased mucosal defense mechanisms or
    increasing damaging forces

29
Mucosal defense mechanisms
  • Bicarbonate secretion
  • Mucous secretion
  • Tight adherence between epithelial cells to
    prevent any acid leakage to the inside.
  • Good blood supply to the mucosa
  • Renewal of damaged epithelial cells.

30
Damaging agents
  • H. pylori infection.
  • Increased gastric acid secretion.
  • Drugs NSAI, Aspirin, cortisone and cytotoxic
    drugs..
  • Cigarette smoking.
  • Chronic alcoholism.

31
Break for 10 minutes
32
H. Pylori infection
  • H. pylori is the etiologic factor in most
    patients with peptic ulcer disease and may
    predispose individuals to the development of
    gastric carcinoma. H. pylori colonizes in the
    human stomach.

33
  • The method of H. pylori transmission is unclear,
    but seems to be person-to-person spread via a
    fecal-oral route. The prevalence of H. pylori in
    adults appears to be inversely related to the
    socioeconomic status. It is also thought that
    water is a reservoir for transmission of H.
    pylori.

34
  • H. pylori infection is present in almost all
    patients with duodenal ulcers and 70 of cases
    with gastric ulcers.
  • Mechanism
  • 1. H. pylori secretes urease (generates ammonia),
    protease (breaks down glycoprotein in the gastric
    mucus) and phospholipases.

35
  • 2. Bacterial lipopolysaccharide attracts
    inflammatory cells to the mucosa. Chronically
    inflamed mucosa are susceptible to injury.
  • 3. A bacterial platelet-activating factor
    promotes thrombotic occlusion of surface
    capillaries.

36
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37
Non-steroidal Anti-Inflammatory Drugs (NSAIDS)
  • Risk factors for the development of
    NSAID-associated gastric and duodenal ulcers
    include advanced age, history of previous ulcer
    disease, higher doses of NSAIDs.
  • NSAIDs initiate mucosal injury topically by their
    acidic properties.

38
  • Systemic effects of NSAIDs appear to play a
    predominant role through the decreased synthesis
    of mucosal prostaglandins. The precursor of
    prostaglandins, arachidonic acid, is catalyzed by
    the two cyclo-oxygenase isoenzymes,
    cyclo-oxygenase-1 and cyclo-oxygenase-2.

39
  • Literature suggests that the anti-inflammatory
    properties of NSAIDs are mediated through
    inhibition of cyclo-oxgenase-2, and adverse
    effects, such as gastric and duodenal ulceration,
    occur as a result of effects on the
    constitutively expressed cyclo-oxygenase-1.

40
Zollinger-Ellison Syndrome
  • The classic triad of Zollinger-Ellison syndrome
    involves
  • Peptic ulcers in unusual locations (the jejunum)
    in addition to duodenal and gastric sites.
  • Massive gastric acid hypersecretion.
  • Gastrin-producing islet cell tumor of the
    pancreas (gastrinoma).

41
Gross features
  • Site Gastric ulcers are located at the antrum
    toward the lesser curvature. The duodenal ulcer
    is usually located at the 1st part anteriorly.
  • Shape Round, oval.
  • Size Usually less than 4 cm in diameter.

42
  • Depth of the ulcer
  • - Superficial ulcer penetrate the mucosa reaching
    up to the muscularis mucosa.
  • - Deeply excavated ulcers having their bases on
    the muscularis propria.

43
  • When the entire wall is penetrated, the base of
    the ulcer may be formed by adherent pancreas,
    omental fat, or liver. Free perforation into the
    peritoneal cavity may occur.

44
  • Edge
  • - Sharp edge.
  • Floor
  • Clean
  • Base of ulcer
  • - Firm (formed of bundles of muscles and fibrous
    tissue).
  • Margin (Surrounding gastric mucosa)
  • - Edematous and reddened due to gastritis.

45
GU
46
Gastric ulcer
47
Duodenal ulcer
48
Biopsy of peptic ulcer
  • Biopsy is necessary to distinguish between benign
    and malignant ulcers.
  • Biopsy should be taken from the ulcer edge, at
    least from each quadrant.
  • Up to 10-12 biopsies may be taken to exclude
    cancer.

49
Microscopic features
  • Active peptic ulcer shows
  • Superficial zone fibrinoid necrosis
    neutrophils.
  • Intermediate zone chronic inflammatory cells
    granulation tissue.
  • Deep zone fibrous tissue, muscle remnants.

50
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51
Microscopic picture of peptic ulcer
52
Superficial zone fibrinoid necrosis
neutrophils.
53
Intermediate zone chronic inflammatory cells
granulation tissue.
54
Deep zone fibrous tissue, muscle remnants.
55
  • Chronic gastritis is virtually universal among
    patients with peptic ulcer disease, occurring in
    85 to 100 of patients with duodenal ulcers and
    in 65 with gastric ulcers.
  • H. pylori infection is almost always demonstrable
    in patients with gastritis.

56
  • Gastritis remains after the ulcer has healed
    recurrence of the ulcer does not appear to be
    related to progression of the gastritis.
  • This feature is helpful in distinguishing peptic
    ulcers from acute erosive gastritis or stress
    ulcers, since the adjacent mucosa is generally
    normal in the latter two conditions.

57
Complications of PUD
  • 1. Hemorrhage hematemesis or melena.
  • 2. Perforation
  • 3. Healing by fibrosis causing gastric or
    duodenal obstruction.
  • 4. Malignant transformation rare (0.5 of
    gastric peptic ulcer).

58
References Robbins and Cotrans Pathologic
Basis of Disease. Seventh edition.
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