stomach and small intestine pathology

Question 1

1. Describe the differences between infantile and adult pyloric stenosis.

Answer 1

Infantile: Hyperplasia of pyloric muscularis propria obstructs gastric outflow. Presents in 2-3 week with regurg, projectile nonbilious vomiting, and abd mass. Adult: caused by antral gastritis or peptic ulcers close to pylorus.

Question 2

2. Describe the gastric “mucosal barrier.”

Answer 2

surface mucus, bicarb in mucus, mucosal blood flow, epithelial barrier, epithelial regenerative capacity, prostaglandins

Question 3

3. Define acute gastritis and describe its microscopic appearance and etiology.

Answer 3

mucosal inflammatory process with ulcers and erosions on endoscopy and neutrophils, erosions and ulcers on histology. Caused by NSAIDS, H pylori, stress related, chemicals

Question 4

4. Define chronic gastritis and describe its microscopic appearance and etiologies

Answer 4

Caused by H pylori in antrum or autoimmune gastritis. Lymphocytes and plasma cells in lamina propria, lymphoid aggregate with germinal center

Question 5

Pathogenesis of autoimmune chronic gastritis

Answer 5

Autoantibodies against parietal cells and intrinsic factor results in decreased acid and pernicious anemia (megaloblastic anemia due to B12 deficiency).

Question 6

H pylori pathogenesis

Answer 6

Ingested H.pylori reach gastric lumen → penetrate mucus layer overlying epithelium → attach to surface epithelium and penetrate intercellular spaces → organisms produce toxins, urease which causes alkalinization of local environment → presence of bacteria elicits infiltration by neutrophils and mononuclear cells → gastric mucosal damage and leakage of acid and pepsin into underlying lamina propria → peptic ulcer

Question 7

H pylori virulence factors

Answer 7

Flagella – allows motility in viscous mucin. Urease – generates ammonia from urea → elevates local gastric pH. Adhesins – enhance bacterial adherence to surface epithelium. Toxins – cytotoxin-associated gene A (CagA) involved in ulceration

Question 8

5. Define Peptic Ulcer Disease and list the factors that predispose to ulcer formation.

Answer 8

H pylori compromises mucosal defense and NSAIDs cause chemical irritation and suppression of prostaglandin. Cigarettes impair mucosal blood flow and healing

Question 9

H pylori associated diseases

Answer 9

1.) Acute and chronic gastritis. 2.) Gastric and duodenal ulcers (peptic ulcer disease) 3.) Gastric adenocarcinoma. 4.) MALT Lymphoma (mucosa associated lymphoid tissue)

Question 10

6. Describe the two most common types of polyps in the stomach.

Answer 10

Hyperplastic polyp: most common, located in antrum, H pylori associated. Polypoid gastritis: second most common, located in antrum, H pylori associated.

Question 11

Hyperplastic polyp

Answer 11

Inflammatory polyp associated with chronic gastritis. Exaggerated mucosal response to injury and inflammation. Caused by proliferation of Foveolar epithelium and lamina propria

Question 12

7. two main types of gastric carcinoma.

Answer 12

Adenocarcinoma: intestinal type forms masses and diffuse type is diffusely infiltrative. GIST: Stromal tumor derived from the Interstitial Cells of Cajal, located in the muscularis propria and serve as pacemaker cells for gut peristalsis

Question 13

adenocarcinoma epidemiology

Answer 13

intestinal type: M>F 2:1. predominates in Japan, s america and eastern europe. Precursor lesion present (adenoma). Diffuse type: M=F, younger people. No precursor lesion

Question 14

Adenocarcinoma risk factors

Answer 14

Chronic gastritis. Intestinal type: tobaco, diet, inherited cancer syndromes like FAP, HNPCC, Li Fraumeni. Diffuse: mutations in CDH1 (hereditary diffuse gastric cancer.

Question 15

Adenocarcinoma gross findings

Answer 15

Intestinal type: Ulcer with heaped-up borders. Diffuse type: “Linitis plastica” thickened wall with loss of rugal folds, leather bottle, signet ring cells

Question 16

GIST epidemiology

Answer 16

M=F, mean age 60

Question 17

Carneys triad

Answer 17

GIST, paraganglioma, pulmonary chondroma

Question 18

GIST symptoms

Answer 18

weight loss, anemia, dyspepsia

Question 19

Causes of GIST

Answer 19

80% are due to an activating mutation in the gene encoding the tyrosine kinase CKIT. KIT negative GIST: Majority are gastric/extraintestinal: PDGFRA mutated

Question 20

GIST gross findings

Answer 20

Arise from within the gastric wall (muscularis propria), and sometimes ulcerate the mucosa

Question 21

GIST treatment

Answer 21

resection and/or imatinib (tyrosine kinase inhibitor)

Question 22

GIST diagnosis

Answer 22

CKIT staining on histo

Question 23

pathogenesis of neuroendocrine tumor

Answer 23

Tumor derived from malignant proliferation of cells from the GI neuroendocrine system (enterochromaffin cells (“ECCs”)

Question 24

neuroendocrine tumor prognosis

Answer 24

Foregut (esophagus, stomach, duodenum): cured by resection, rarely metastasize. Midgut (jejunum, ileum): multiple, larger, more invasive. Hindgut (appendix, colorectum): proximal colon has worse prognosis

Question 25

MALT lymphoma predisposing factors

Answer 25

H Pylori gastritis, celiac dz, IBD, immunodeficiency

Question 26

MALT pathogenesis

Answer 26

Derived from malignant proliferation of B cells in the gastric lamina propria