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23 Cards in this Set

  • Front
  • Back
4 main cell types of intestine
Absorptive, Goblet, Endocrine, Paneth
intestinal Intra-epithelial lymphocytes:
CD8+ T cells
intestinal Lamina propria lymphocytes
CD4+ T cells, Educated B cells
Malabsorption: Most Common Causes in the USA
Celiac sprue,• Pancreatic insufficiency (Chronic pancreatitis Cystic Fibrosis); Crohn’s Disease
Celiac Sprue: Definition•
Relatively rare chronic mucosal lesion of small intestine  impaired nutrient absorption. Improves with withdrawal of wheat gliadins from diet. A disease of Caucasians
Celiac Sprue: Pathogenesis
CD4+ gliadin-sensitized cells• Exposure  intra-epithelial accumulation  enterocyte injury• Increased mitotic rate• Loss of villi
Dysentery: Commonest offenders:
Rotavirus; Norwalk Virus; Enterotoxigenic E. coli; Viral agents: WATERY diarrhea
Bacterial Enterocolitis: Three Pathogenetic Mechanisms
Ingestion of pre-formed toxin: s. aureus, vibrios, c. perfringens; Ingestion of toxigenic agents: E. coli, Campylobacter; Ingestion of entero-invasive organisms: Salmonella, Shigella, Campylobacter, Yersinia
Protozoan;• Fecally contaminated water; Attaches to enterocyte surface Does NOT invade Malabsorptive diarrhea; Blockade; Enterocyte injury;•Blunting of villi +increased lymphocytes
Small Intestine: Adenocarcinoma. Location, morphology, presentation•
Duodenum: Ampulla of Vater• “Napkin-ring” or polypoid• Presentation:– Obstruction– Fatigue from blood loss– Jaundice• Regional nodal and liver metastases
Small Intestine: Carcinoid Tumors. Age, location, cells of origin
Median age 60 yrs• Appendix, ileum; Arise from enterochromaffin cells• Tryptophan metabolites and neuropeptide production:– Serotonin, bradykinin, histamine, prostaglandins– Urinary 5-HIAA
Acute Pancreatitis•
Sudden enzymatic necrosis of pancreas;• 80% due to two causes:– Biliary disease (15%)• 35-60% have gallstones• 5% of those with gallstones get it • F:M 3:1– Alcoholism (65%)• M:F 6:1
Acute Pancreatitis: Histomorphology•
Edema• Fat necrosis– Fatty acids + Ca+2 =precipitation of salts;• Acute inflammation; Liquefactive necrosis;• Hemorrhage
Acute Pancreatitis: clinical features
Clinical Features• A disease of mid-life; Abdominal pain, shock, anemia• Elevated serum amylase and lipase• Acute abdomen; medical emergency• 10% have glycosuria• Some have hypocalcemia• Rx: Support vital functions and “rest” the pancreas
Chronic Pancreatitis: Causes (?)
Alcohol looms much larger than does biliary disease;• Hypercalcemia and hyperlipoproteinemia;• Cystic fibrosis;• 12%: pancreas divisum;• Familial disease• ;40%: IDIOPATHIC
Chronic Pancreatitis: Mechanisms (?)•
Hypertonic secretions  precipitation plugging• Loss of endogenous lithosuppressant proteins• Oxidative stress• Fibrotic alteration of secretory flow perpetuation theory)• Hereditary form:– Point mutation in trypsinogen  Loss of cleavage site in the activated enzyme  Inability to inactivate the enzyme
Chronic Pancreatitis:
Clinical Features• Repeated episodic moderate or mild abdominal and/or back pain OR• Continuous pain OR• NO symptoms until exocrine or endocrine insufficiency– Malnutrition– Diabetes mellitus• Calcification of pancreas by U/S or CT• Disabling; not life threatening
morphology of chronic pancreatitis
2 kinds: 1 chronic calcifying pancreatitis most common, seen in alcoholics. atrophy and fibrosis, and calcification. chronic inflammation, hard w/ palpable calcifications; can often be seen on x ray. 2 chronic obstructive pancreatitis, less common and results from stenosis of sphincter of oddi. fibrosis, inflammation, occur predominately in head of pancreas. more difficult diagnosis
complications of chronic pancreatitis
1 diabetes mellitus; 2 pancreatic insufficiency; pseudocyst; pancreatic carcinoma
Adenocarcinoma of the Pancreas: Clinical Features•
Weight loss, anorexia, malaise• Depression may be a prodrome• Pain results from abdominal wall and nerve infiltration• 10%: migratory thrombophlebitis: “Trousseau’s Sign”• Usually silent until impingement• Serum CA 19-9 elevated• Obstructive jaundice may be lifesaving but:– Only 15% are resectable at diagnosis– Surgery is the only potentially curative therapy• Endoscopic FNA has greatly aided diagnosis
Insulinoma: A Classic (Whipple’s) Triad of Clinical Features•
Hypoglycemic episodes, glucose < 50 mg/dL• CNS manifestations:– Confusion, stupor, syncope• Triggered by fasting or exercise; relieved by eating or IV glucose
Gastrinoma: “Zollinger-Ellison Syndrome”•
Gastrinoma may arise in:– Pancreas– Duodenum– Peripancreatic soft tissue• Gastrin is “ectopic” in terms of the pancreas• The sndrome = pancreatic islet cell tumors +gastric acid hypersecretion + severe peptic ulceration• 90-95% have ulcers; duodenal:gastric = 6:1
Islet Cell Tumors: Other hormones•