gastritis and peptic ulcer 30 5-2016
TRANSCRIPT
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GASTRITIS AND PEPTIC ULCER
Dept of path ology, C
HR
I.
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STOMACH - ANATOMY
Types of glands Cardiac glands – mucus secreting
cellsGastric or Oxyntic or Fundic glands –
found in fundus and body contain parietal cells, chief cells & a few endocrine cells
Antral/pyloric glands – contain mucus secreting & endocrine cells
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MUCOSAL PROTECTION
Mucus secretion – secretion of mucus with a low diffusion coefficient for H+
Bicarbonate secretion – secreted by surface epithelial cells
Epithelial barrier – intercellular tight junctions Rich mucosal blood flow Prostaglandin synthesis – PG inhibits acid secretion,
promotes bicarbonate and mucin secretion and improves blood supply
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ACUTE GASTRITIS
Definition: acute mucosal inflammatory process, usually transient & self-limited
NEUTROPILS PRESENT
↑sed acid secretion ↓sed HCO3 ( H.PYLORI, UREMIA) DECREASED PROSTAGLANDINS reduced blood flow (ELDERLY)
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Dept of path ology, C
HR
I.
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ACUTE GASTRITIS
Asymptomatic epigastric pain nausea & vomiting painless bleeding
Gross diffusely hyperemic mucosa superficial, circular, small erosions
(<1 cm); dark brown due to acid digestion of extravasated blood
Erosion denotes loss of epithelium
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ACUTE GASTRIC ULCER STRESS ULCER
CURLING’S ULCER
CUSHING’S ULCER
Reduced splanchnic blood flow in ischemic / shock
Less than 1cm, sharply defined normal rugal folds , resolves completely
No scarring 10
Dept of path ology, C
HR
I.
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Dept of path ology, C
HR
I.
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CHRONIC (NON-EROSIVE) GASTRITIS
Definition: chronic inflammatory infiltration of gastric mucosa, often accompanied by mucosal gland atrophy and INTESTINAL metaplasia
Types of Chronic Gastritis• Autoimmune Gastritis (type A or Fundic)• Type B gastritis (H. Pylori and other causes)
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AUTOIMMUNE (TYPE A OR FUNDIC TYPE)
Involves body & fundus (~10% chronic gastritis)
Auto-antibodies to parietal cells, H+,K+-ATPase, gastrin receptor & intrinsic factor lead to loss of parietal cells, acid secretion, mucosal atrophy
Hyperplasia of the G cells with hypergastrinemia.
↑sed risk for gastric carcinoma & carcinoids
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TYPE B CHRONIC GASTRITIS
Predominantly Antral type with high acid secretion and increased risk of PEPTIC ulcer
Pan-gastritis with multifocal gastric atrophy, low acid secretion and increased risk for adenocarcinoma
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CHRONIC H.PYLORI GASTRITIS
Helicobacter pylori Spiral shaped curved organisms Colonise the mucus layer(don’t invade) Chronic than acute Flagella, urease, cytotoxins Symptoms: abdominal pain Complication: peptic ulcer INCREASED RISK OF ADENOCA
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CHRONIC (NON-EROSIVE) GASTRITISActive Inflammation(LYMPHOID AGGREGATES IN
LAMINA PROPRIA)
INTRAEPITHELIAL NEUTROPHILS
PIT ABCESS
Intestinal metaplasia
H.PYLORI IN LUMEN
Atrophic gastritis
Normal
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PEPTIC ULCER
Includes duodenal and gastric ulcerCHRONIC M:F = 3:1 for DU & 1.5-2:1 for GUThey are remitting, relapsing lesions
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PEPTIC ULCER
The imbalances of mucosal defenses and damaging forces that cause chronic gastritis are also responsible for PUD
NSAID H.pylori Zollinger ellison syndrome
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HELICOBACTER PYLORI
Infection is present in 90% of patients with chronic gastritis in all duodenal ulcer patients & 70% of gastric ulcer patients; but is
limited to stomachOnly 10-20% of infected develop peptic ulcer
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Stomach – usually antrum- LESSER CURVATURE (II most common)Duodenum – first portion (most common site)Multiple in patients with Zolinger-Elison syndrome
SITES OF PEPTIC ULCER
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DUODENAL ULCER
4 times more common than gastric ulcers
Peak incidence is in 40's
Most duodenal ulcers occur within a few centimetres from pyloric ring
Anterior wall is affected more often than posterior wall
Irregular dietary habits
Pain releived with food intake
Weight gain
Contrasts wit gastric ulcer- increased risk of ca
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PEPTIC ULCER - GROSS Over 50% of ulcers are <2cm
• Round to oval• Punched-out area with clean
base• Margins are usually level with
surrounding mucosa or slightly elevated due to edema
• no heaping up of margins
• Gastric rughae converge upto the margin of ulcer( spoke wheel /cartt wheel appearance)
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DIFFEREWNCE BETWEEN PEPTIC AND MALIGNANT GASTRIC ULCER
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ULCER – MICROSCOPIC FEATURES
Four zones:1. Superficial necrotic debris2. Zone of non-specific
inflammation with neutrophils predominating
3. Active granulation tissue with mononuclear infiltration
4. Zone of fibrosis
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HELICOBACTER PYLORI- DIAGNOSIS
Diagnostic tests: 1. serologic test for Ab 2. faecal bacterial detection 3.urea breath test 4. finding organisms or its DNA in tissues/culture
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COMPLICATIONS OF PEPTIC ULCER DISEASE
Bleeding – most frequent complication; occurs in 15 – 20% of patients; accounts for 25% of ulcer deaths; may be the first manifestation
Perforation, penetration & peritonitis; Obstruction Intractable pain
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Thank you!
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