Thug’s

PEPTIC ULCER DISEASE

OBJECTIVES

Acute gastritis (def- causes)

Chronic gastritis (causes-types)

Helicobacter pylori associated disorders

Chronic peptic ulcer (pathogenesis- morphology- complications)

NORMAL STOMACH 1) Cardia : mucus cells only

2) Body : Parietal (HCL+ intrinsic factor) and Chief cells (pepsin)

3) Antrum : Mucin secretion and G-cells that secrete gastrin

Thug’s

ACUTE GASTRITIS

- Transient mucosal inflammatory process that

may be asymptomatic

- cause variable degrees of epigastric pain,

nausea, and vomiting.

- In more severe cases there may be

mucosal erosion

ulceration

hemorrhage

hematemesis, melena

(rare)massive blood loss.

- Acute gastritis is a major cause for

hematemesis especially in alcoholics

- Erosions affect the superficial mucosa and

can heal rapidly as opposed to ulceration.

CAUSES INCLUDE:

Heavy use of Non-steroidal anti-inflammatory

drugs particularly aspirin

Excessive Alcohol

Heavy smoking

ttt with Cancer chemotherapy

Hypovolemia

Ischemia and Shock

Severe Stress (burns, surgery, strokes, post

infarction)

Uremia

Enterogastric reflux

Corrosives (may cause perforation)

Mechanical trauma

ACUTE ERROSIVE GASTRITIS

The superficial part is affected.

Thug’s

CHRONIC GASTRITIS

DEFINITION - Chronic gastritis is defined histologically as an

increase in the number of lymphocytes and

plasma cells in the gastric mucosa.

- In contrast to acute gastritis, the symptoms

associated with chronic gastritis are typically

less severe but more persistent.

- Nausea and upper abdominal discomfort may

occur, sometimes with vomiting, but

hematemesis is uncommon

- The mildest degree of chronic gastritis is chronic

superficial gastritis, which involves the

subepithelial region around the gastric pits.

- More severe cases involve the glands in the

deeper mucosa; this is commonly associated

with gland atrophy (chronic atrophic gastritis)

and intestinal metaplasia.

CAUSES:

1- Helicobacter pylori: G-ve bacilli; Noble prize in

Medicine 2005, for Barry Marshal & Robin Warren…

Type B chronic gastritis

Helicobacter pylori is present in 70-90% of patients

with gastric and duodenal ulcers, respectively

2- Autoimmune: auto-antibodies to parietal cells

(decreased acid and intrinsic factor)…Type A chronic

gastritis

3- psychologic stress, caffeine, alcohol, and tobacco

use were considered the primary causes of gastritis

TYPES OF CHRONIC GASTRITIS

TYPE A TYPE B

autoimmune gastritis that primarily involves the body

primarily involves the antrum

associated with pernicious anemia

associated with Helicobacter pylori infection.

CHRONIC SUPERFICIAL

GASTRITIS

CHRONIC ATROPHIC

GASTRITIS

HELICOBACTER PYLORI

MECHANISMS OF H. PYLORI-INDUCED

PATHOLOGY - Although the organism is not invasive, it induces

intense inflammatory and immune response:

cytokines and B-cell activation.

- Enhances gastric acid secretion

- Bacterial products such as urease, lipases and

proteases induce epithelial injury

HELICOBACTER PYLORI ASSOCIATED DISORDERS

1. Chronic gastritis 2. Peptic (gastric

and duodenal) ulcers

3. Gastric adenocarcinoma, intestinal type

4. Gastric lymphoma

Thug’s

PEPTIC ULCER

Thug’s

CHRONIC PEPTIC ULCER

- Peptic ulcers are ulcers occurring in any part of the

gastrointestinal tract exposed to the action of acidic

gastric juice.

SITES

1- First part of duodenum

2- Stomach

3- Lower esophagus

4- Meckel's diverticulum

5- Stomal (marginal) ulcer

(gastro-jujenostomy)

PATHOGENESIS -The gastric mucosa is protected by a variety of

mechanisms from the erosive effect of gastric acid,

these include

1. The anatomic integrity of the mucosa:

- The mucosal cells have a specialized apical

surface membrane that resists the diffusion of

acid into the cell.

2. Gastric mucus:

- Mucin and HCO3 secreted by surface epithelial

cells create a mucous layer that has a pH

gradient which is very acid in the lumen to

nearly neutral near the cell surface.

3. Prostaglandins (E series)

- synthesized and secreted by gastric mucosal

cells.

- Have a cytoprotective effect on the

gastroduodenal mucosa.

- Act to increase bicarbonate secretion, gastric

mucus production, mucosal blood flow, and the

rate of mucosal cell regeneration.

4. Mucosal blood flow:

- Ischemia of the mucosa decreases mucosal

resistance.

MORPHOLOGY 1. Usually solitary, round-to-oval in shape

2. Often large (larger than 1 cm, rarely larger than

5 cm) and usually found on the lesser curvature

or pyloric antrum

3. Margins are either flush with the mucosal

surface or slightly raised because of edema. The

edge is punched out, the floor of the ulcer is

smooth, and its base is thick and firm because

of fibrosis.

4. The mucosa around the ulcer is either normal

or—in the stomach—shows changes of chronic

gastritis.

5. The mucosal folds around the ulcer appear to

radiate outward from it, which is an effect of

fibrous contraction of the base of the ulcer

Thug’s

MORPHOLOGY MICROSCOPICALLY the base of a chronic peptic ulcer is composed of :-

1. A surface of necrotic layer

2. Acutely inflamed layer

3. A zone of granulation tissue.

4. Extensive fibrosis of the base, with extension of

fibrosis into the muscle wall.

5. The epithelium at the edge of the ulcer shows

regenerative hyperplasia, which frequently

demonstrates marked cytologic atypia,

mimicking neoplastic change.

GASTRIC ULCER DUODENAL ULCER Occur in stomach Occur in duodenum

Epigastric pain 1-2 hrs after eating

2-5 hrs after eating

Can cause hematemesis & melena

Can cause melena & hematochezia

Heartburn, Chest disfomfort & early satiety commonly seen

Heartburn, Chest disfomfort & early satiety less common but may be seen

Can cause gastric carcinoma (mostly in elderly)

Pain may awaken patient at night

CLINICAL FEATURES:

Epigastric pain (worse at night and relieved by

food)

Bleeding (30%)

Perforation (5%; accounts for 2/3 of deaths).

COMPLICATIONS: 1- Hemorrhage

2- Perforation, penetration.

3- Fibrosis: stenosis, hour-glass stomach

4- Duodenal diverticulum

5- Malignancy, rare, gastric not deudenal