2 Flashcards
Acute Gastritis
Definition, Etiology
Definition: - Acute gastritis is an acute inflammation of gastric mucosa which may be associated with hemorrhage or erosion in severe cases.
Etiology: Acute gastritis is frequently associated with: 1- Drugs:
as heavy use of aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs)
& cancer chemotherapy
2- Excessive alcohol consumption
3- Excessive cigarette smoking
4- Systemic bacterial infection: as salmonellosis
5- Uremia
6- Severe stress :e.g. postsurgery, burns (Curling ulcer)
7- Irritant or spicy food.
8- Mechanical trauma as during endoscopic examination
Pathogenesis of Acute Gastritis
is poorly understood, one or more of the following may operate:
1- disruption of the adherent mucous layer,
2- stimulation of acid secretion with hydrogen ion back-diffusion into the
superficial epithelium,
3- decreased production of bicarbonate buffer by superficial epithelial cells,
4- reduced mucosal blood flow, and
5- direct damage to the epithelium.
Acute Gastritis
Microscopic, Clinical Features:
Microscopic: - mucosal edema and an inflammatory infiltrate of neutrophils and possibly by chronic inflammatory cells. - Regenerative replication of epithelial cells in the gastric pits is usually seen
Clinical Features:
- may be asymptomatic,
- may cause epigastric pain with nausea & vomiting, or
- may present with gastric hemorrhage as hematemesis and melena.
Chronic Gastritis
Definition, Etiology and Pathogenesis (1)
Definition:
chronic inflammation of the gastric mucosa which may finally lead to mucosal atrophy and epithelial metaplasia.
Etiology and Pathogenesis:
1- Autoimmune gastritis (Type A gastritis):
- represents less than 10% of cases of chronic gastritis, - affects the body and the fundus
- It is due to autoantibodies to parietal cells → gland destruction & mucosal atrophy leading to:
1- ↓ acid secretion (hypochlorhydria or achlorhydria). ↑ serum gastrin (hypergastrinemia) (loss of negative feedback)
2- ↓ intrinsic factor: → B12 malabsorption → pernicious anemia (megaloblastic anemia)
1- Autoimmune gastritis (Type A gastritis):
Gross, Micro ,Complication
Gross: loss of rugal folds in the body and fundus
Micro:
- Atrophy of gastric mucosa with loss of parietal cells - Chronic inflammatory cells (lymphocytes and plasma cells) - Intestinal metaplasia
Is the replacement of gastric epithelium with columnar & goblet cells of intestinal type.
Complication:
- Increased risk of gastric adenocarcinoma (2% - 4% of patients)
Second cause of Chronic Gastritis
Helicobacter pylori associated gastritis (Type B gastritis)
(Nonimmune gastritis):
The (mechanisms )by which H. pylori causes gastritis are, Complications
The mechanisms by which H. pylori causes gastritis are:
a- bacterial enzymes and toxins and
b- release of harmful chemical mediators by the attracted neutrophils.
Complications: peptic ulcer - Increased risk of gastric carcinoma - Increased risk of gastric lymphoma
Helicobacter pylori associated gastritis (Type B gastritis)
(Nonimmune gastritis):
Two patterns, Micro
1) Antral-type with high acid production & higher risk for peptic ulcer disease of the duodenum or stomach;
Over time, chronic antral H. pylori gastritis may progress to
2) Pangastritis (involving the body of stomach) with multifocal mucosal atrophy,
low acid secretion, intestinal metaplasia, & ↑ed risk for adenocarcinoma.
Micro: - H. pylori organisms are found within the mucus layer on top of surface
mucosal epithelium
- Chronic inflammation with Foci of acute inflammation
- may be variable gland loss and mucosal atrophy. - Intestinal metaplasia
Chronic Peptic Ulcers Peptic ulcer disease (PUD)
Definition, Sites
Definition: Peptic ulcer is a defect (break) in the mucosa extending into the submucosa or deeper that occur in any portion of the gastrointestinal tract exposed to the action of acid-pepsin secretion.
Sites: - At least 98%
- in the first )))jportion of the duodenum (80%)
- or in the stomach (18%),
- Less than 2% occur in:
1- Within a Barrett’s esophagus.
2- ln the margins of gastrojejunostomy.
3- Within a Meckel’s diverticulum containing ectopic gastric mucosa.
Chronic Peptic Ulcers Etiology,
Etiology: 1- H. pylori infection
2- NSAIDs
Other Causes:
a- Gastric hyperacidity: Zollinger-Ellison syndrome (= Pancreatic gastrin secreting tumor called gastrinoma → hyperacidity → multiple peptic ulcers)
caused by uncontrolled release of gastrin by a tumor and the resulting massive acid production.
b- Cigarette smoking. c- Alcohol directly
d- Corticosteroids. e- Personality & psychological
f- Genetic predisposition: Familial tendency, commonly in blood group O persons
The mechanisms of H. pylori infection in the development peptic ulcers of duodenum & stomach:
1- induces an intense inflammatory response → ↑ed cytokines by mucosal epithelial cells (IL-1, IL-6, TNF, IL-8) → attract and activates neutrophils.
2- Several bacterial toxic products → epithelial injury & inflammation.
3- secretes a urease → breaks down urea → toxic compounds as ammonium chloride → Toxic to mucosa
4- secretes phospholipases → damage surface epithelial cells.
5- secretes proteases → break down glycoprotein in the gastric mucus
6- Decreased production of bicarbonate buffer by superficial epithelial cells
7- H. pylori increases gastric acid secretion
Chronic Peptic Ulcers Clinical Features, Gross
-The most common symptom: eroding or burning epigastric pain which is typically relieved by antacids or food,
Duodenal ulcer pain often occurs hungry & classically pain tends to be worse at night and occurs usually 1 to 3 hours after meals during the day. Duodenal ulcer pain often awakens the patient at night.
- Gastric ulcer pain worsen with eating
- Other symptoms such as nausea, heartburn, flatulence, vomiting
- Symptoms of complications such as hemorrhage or perforation.
Gross: (gastric or duodenal ulcer) - Favored sites are: 1- duodenal ulcer: the anterior or posterior walls of the first part of the duodenum
2- gastric ulcer: the pyloric antrum at lesser curvature of the stomach.
- Most ulcers are round or oval in shape, - sharply demarcated “punched-out” ulcer, - 2 - 4 cm in diameter
- The surrounding mucosal folds are radiating
- The ulcer base is clean due to peptic digestion of the inflammatory exudate and necrotic tissue
Chronic Peptic Ulcers Microscopically, Complications
Four layers in sequence are noted in histologic sections of peptic ulcers:
1- a thin layer of necrotic debris
2- a zone of nonspecific inflammatory infiltration with neutrophils
3- granulation tissue, deep to which is 4- Fibrosis
Complications:
1- Bleeding is the main complication (40%), → hematemesis and melena.
2- Perforation (in about 5%) → localized or generalized peritonitis
3- Pyloric obstruction (rare) due to fibrosis.
4- Malignant transformation occurs in about 2% of gastric ulcers.
Duodenal ulcers are Not precancerous.
Diagnosis of Helicobacter pylori infection
Non-invasive methods
Serological tests detect IgG antibodies : diagnosis and in epidemiological studies. not useful for confirming eradication or the presence of a current infection.
13C Urea breath test: quick and easy way of detecting the presence, following treatment.
Stool Antigen test.
-diagnosis of H. pylori infection and
-for monitoring efficacy of eradication therapy.
- used as a screening test (cheaper than urea breath test).
Diagnosis of Helicobacter pylori infection
Invasive (endoscopy)
Rapid urease test: (Test to detect urease in a gastric biopsy) high Sensitivity and specificity
Histology: Giemsa) stained
Culture:
Tumors of The Stomach (Gastric Tumors)
A) Benign Tumors:
Gastric Polyps: Types:
1) Hyperplastic polyps (85%): hyperplastic mucosal epithelium & inflamed stroma
2) Fundic gland polyps (10%): collections of dilated glands
Incidence has increased markedly as a result of the use of proton pump inhibitors.
3) Adenomatous polyps (Adenoma) (5%):
- Microscopy: Proliferated mucosal glands showing dysplasia
- It is precancerous → adenocarcinoma, which increases with polyp size
