stomach and small intestine pathology Flashcards
- Describe the differences between infantile and adult pyloric stenosis.
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.
- Describe the gastric “mucosal barrier.”
surface mucus, bicarb in mucus, mucosal blood flow, epithelial barrier, epithelial regenerative capacity, prostaglandins
- Define acute gastritis and describe its microscopic appearance and etiology.
mucosal inflammatory process with ulcers and erosions on endoscopy and neutrophils, erosions and ulcers on histology. Caused by NSAIDS, H pylori, stress related, chemicals
- Define chronic gastritis and describe its microscopic appearance and etiologies
Caused by H pylori in antrum or autoimmune gastritis. Lymphocytes and plasma cells in lamina propria, lymphoid aggregate with germinal center
Pathogenesis of autoimmune chronic gastritis
Autoantibodies against parietal cells and intrinsic factor results in decreased acid and pernicious anemia (megaloblastic anemia due to B12 deficiency).
H pylori pathogenesis
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
H pylori virulence factors
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
- Define Peptic Ulcer Disease and list the factors that predispose to ulcer formation.
H pylori compromises mucosal defense and NSAIDs cause chemical irritation and suppression of prostaglandin. Cigarettes impair mucosal blood flow and healing
H pylori associated diseases
1.) Acute and chronic gastritis. 2.) Gastric and duodenal ulcers (peptic ulcer disease) 3.) Gastric adenocarcinoma. 4.) MALT Lymphoma (mucosa associated lymphoid tissue)
- Describe the two most common types of polyps in the stomach.
Hyperplastic polyp: most common, located in antrum, H pylori associated. Polypoid gastritis: second most common, located in antrum, H pylori associated.
Hyperplastic polyp
Inflammatory polyp associated with chronic gastritis. Exaggerated mucosal response to injury and inflammation. Caused by proliferation of Foveolar epithelium and lamina propria
- two main types of gastric carcinoma.
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
adenocarcinoma epidemiology
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
Adenocarcinoma risk factors
Chronic gastritis. Intestinal type: tobaco, diet, inherited cancer syndromes like FAP, HNPCC, Li Fraumeni. Diffuse: mutations in CDH1 (hereditary diffuse gastric cancer.
Adenocarcinoma gross findings
Intestinal type: Ulcer with heaped-up borders. Diffuse type: “Linitis plastica” thickened wall with loss of rugal folds, leather bottle, signet ring cells
GIST epidemiology
M=F, mean age 60
Carneys triad
GIST, paraganglioma, pulmonary chondroma
GIST symptoms
weight loss, anemia, dyspepsia
Causes of GIST
80% are due to an activating mutation in the gene encoding the tyrosine kinase CKIT. KIT negative GIST: Majority are gastric/extraintestinal: PDGFRA mutated
GIST gross findings
Arise from within the gastric wall (muscularis propria), and sometimes ulcerate the mucosa
GIST treatment
resection and/or imatinib (tyrosine kinase inhibitor)
GIST diagnosis
CKIT staining on histo
pathogenesis of neuroendocrine tumor
Tumor derived from malignant proliferation of cells from the GI neuroendocrine system (enterochromaffin cells (“ECCs”)
neuroendocrine tumor prognosis
Foregut (esophagus, stomach, duodenum): cured by resection, rarely metastasize. Midgut (jejunum, ileum): multiple, larger, more invasive. Hindgut (appendix, colorectum): proximal colon has worse prognosis
MALT lymphoma predisposing factors
H Pylori gastritis, celiac dz, IBD, immunodeficiency
MALT pathogenesis
Derived from malignant proliferation of B cells in the gastric lamina propria
