Pathology of GIT- Stomach

Pathology of GITStomach

Oct. 4. 2015 Prof. Dr. Faeza Aftan Col of Med. Aliraqia University

Normal Esophagus & Stomach

Stomach

Microscopic Anatomy of the Stomach

Microscopic Anatomy of the Stomach


CONGENITAL ABNORMALITIES Diaphragmatic Hernia, Omphalocele, and Gastroschisis Ectopia. (Gastric heterotopia, ectopic gastric mucosa in the small bowel or colon). Pyloric Stenosis

3-4 times more in males occurs 1/ 300 - 900 live births. genetic basis. presents in 2nd or 3rd week as regurgitation and projectile vomiting. O/E; hyperperistalsis and a firm, ovoid mass. Acquired pyloric stenosis Rx: myotomy
Congenital hypertrophic pyloric stenosis



ACID PROTECTION
MUCUS HCO3- EPITHELIAL BARRIERS BLOOD FLOW PROSTAGLANDIN E, I

ACUTE GASTRITIS NSAIDs Stress Others asymptomatic pain, N & V. ACUTE, HEMORRHAGIC mucosal erosion, ulcer, Hge, hematemesis, melena, blood loss

Acute Peptic Ulceration

NSAIDs. Stress less than 1 cm Multiple Superficial nausea, vomiting, coffee-ground hematemesis. Bleeding in 1% to 4% perforation,

ACUTE” ULCERS

NSAID cyclooxygenase inhibition prevents synthesis of PG. PG; HCO3- secretion, mucin synthesis, & vascular perfusion. HCL secretion. intracranial injury ___vagal nuclei, __increase HCL

Chronic Gastritis

H. Pylori; 90% of cases H. Pylori H. Pylori H. Pylori H. Pylori H. Pylori Autoimmune; 10%

Chronic Gastritis

Helicobacter pylori Antrum Chronic antral H. pylori gastritis increased acid secretion NO EROSIONS, NO HEMORRHAGE PU Gastric Ca Gastric Lymphoma.

Lymphocytes, +/- PMN lymphoid folliclesMETAPLASIA, intestinalATROPHY, mucosal “thinning”DYS-PLASIA Chronic Gastritis

Helicobacter pylori

Helicobacter pylori
H. pylori virulence: Flagella, Adhesins, Urease, Urea _Urease_ Amonia (Increase local pH) Toxins, encoded by cytotoxin-associated gene A (CagA), that may be involved in ulcer or cancer

Helicobacter pylori:

Gram negative, Spiral bacilli SpirochetesDo not invade cells – only mucousBreakdown urea - ammoniaBreak down mucosal defenseChronic Superficial inflammation

Helicobacter pylori

Causes chronic gastritis Causes 80 % of gastric peptic ulcers Causes 100% of duodenal peptic ulcers Causes gastric carcinomas Causes MALT lymphomas

H. pylori–Associated and Autoimmune Gastritis

H. pylori–Associated Autoimmune
Location
Antrum
Body
Acid production
Increased
Decreased
Gastrin
Normal to decreased
Increased
Serology
Abs to H. pylori
Abs to parietal cells (H+, K+-ATPase, intrinsic factor)
Sequelae
Peptic ulcer, adenocarcinoma
Atrophy, pernicious anemia, adenocarcinoma, carcinoid tumor
Associations
Low socioeconomic status, poverty, residence in rural areas
Autoimmune disease; thyroiditis, diabetes mellitus, Graves disease

PEPTIC ULCERS

PEPTIC ULCERS
PU are 4 times more in proximal duodenum than in stomach. Duodenal ulcers occur within a few cm of the pyloric valve & involve anterior duodenal wall. Gastric ulcers are located along lesser curvature near the interface of the body & antrum. PU are solitary in more than 80%. Classic PU is a round, sharply punched-out defect

H. pylori & NSAID., are the primary causes of PUD. Although more than 70% of individuals with PUD are infected by H. pylori, fewer than 10% of H. pylori–infected individuals develop PU.Clinical picture Young - middle-aged or older adultsepigastric pain (burning or aching, 1-3 hrs after meals & worse at night, is relieved by alkali or food). PEPTIC” ULCERS

PEPTIC ULCERS

The base of active ulcer; Thin layer of fibrinoid debris PMN infiltrate. Granulation tissue Fibrous scar forms the ulcer base. Vessel walls within the scarred area are thickened. Size and site do not differentiate benign and malignant ulcers. However, the gross appearance of chronic PU is virtually diagnostic

Chronic gastric ulcer Malignant gastric ulcer

chronic NSAID smoking, impairs mucosal bl flow & healing corticosteroids, suppress PG synthesis & healing. stress, increase gastric acid production. Ch Dis; alcoholic cirrhosis & ch. obstructive pulmonary dis. Ch. renal failure, and hyperparath, hypercalcemia, stimulates gastrin and increases acid secretion.
Cofactors in PUD

PEPTIC ULCERS

Complications. Bleeding Occurs in 15% to 20% of patients Accounts for 25% of ulcer deaths Perforation Occurs in about 5% of patients Accounts for two thirds of ulcer deaths Obstruction from edema or scarring Occurs in about 2% of patients Most often due to pyloric channel ulcers Fe. Def. Anemia Malignant transformation of peptic ulcers is very rare.


Acute gastric perforation in a patient presenting with free air under the diaphragm. A, Mucosal defect with clean edges. B, The necrotic ulcer base (arrow) is composed of granulation tissue

Zollinger-Ellison syndrome

Multiple peptic ulcerations in the stomach, duodenum, & even jejunum gastrin-secreting tumor of the pancreas (Gastrinoma), that stimulates acid-secreting cells of the stomach to maximal activity, with consequent GIT mucosal ulceration. ZES may occur sporadically or as part of an AD familial syndrome (MEN 1).


Rare, acquired, premalignant disease of the stomach Massive gastric folds, excessive mucous production protein loss, little or no acid production.
RUGAL PROMINENCE (cerebriform)
HYPERPLASIA of MUCOSA

BEZOARS

PHYTO-bezoar (plant material) TRICHO-bezoar (hairball) NON-food material in PSYCH patients pins nails razor blades coins Gloves A large obstructive bezoar usually takes on the shape and contour of the stomach