gastritis and peptic ulcer 30 5-2016

GASTRITIS AND PEPTIC ULCER

Dept of path ology, C

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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

© 2008 Chettinad Hospital & Research Institute

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


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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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


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


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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)


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


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


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

CHRONIC (NON-EROSIVE) GASTRITISActive Inflammation(LYMPHOID AGGREGATES IN

LAMINA PROPRIA)

INTRAEPITHELIAL NEUTROPHILS

PIT ABCESS

Intestinal metaplasia

H.PYLORI IN LUMEN

Atrophic gastritis

Normal


PEPTIC ULCER

Includes duodenal and gastric ulcerCHRONIC M:F = 3:1 for DU & 1.5-2:1 for GUThey are remitting, relapsing lesions


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

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


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

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


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)


DIFFEREWNCE BETWEEN PEPTIC AND MALIGNANT GASTRIC ULCER

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


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


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


Thank you!


gastritis and peptic ulcer 30 5-2016

Health & Medicine