GIT 2 Flashcards
Routes for pyogenic bacteria to reach liver and form hepatic abscess
> Biliary tract infection (ascending cholangitis)
Portal vein pyemia (bowel or peritoneal sources)
Hepatic artery (hematogenous seeding, direct route)
Direct invasion from adjacent source (peritonitis, cholecystitis)
Penetrating trauma/injury
Why is Rifamixin useful in patients w/ Hepatic encephalopathy?
Rifamixin is a nonabsorbable antibiotic that alters GI flora to decrease intestinal production of ammonia.
It’s sometimes given w/ Lactulose, w/c dec. colonic pH and inc. conversion of ammonia to nonabsorbable ammonium.
Where in the GIT would an biopsy specimen be taken to diagnose Hirschsprung disease?
Biopsy of the rectum (narrowed segment) should include the submucosa to show absence of ganglionic cells. The rectum is always involved in Hirschsprung dse.
What is the MOA of Ribavirin (tx for HepC, RSV)?
Ribavirin interferes w/ duplication of viral genetic material by several mechs:
>lethal hypermutation
>inhibits RNAp and IMP dehydrogenase (dec. GTP)
>defective 5’-cap on viral mRNA
>inc. Th1 cell-mediated immunity, dec. Th2 cytokine prodn.
If you have an elevated ALP of unclear etx, how do you differentiate b/w hepatic origin or boney origin?
Follow-up w/ gamma-glutamyl transpeptidase, which signifies hepatic origin.
What is toxic megacolon a common complication of?
Toxic megacolon can result from IBD (UC > CD). It’s due to colonic smooth muscle paralysis caused by a release of inflammatory mediators, bacterial products, and inc. NO. This leads to colonic distention and wall thinning, predisposing to perforation.
What is the preferred diagnostic for suspected toxic megacolon? What studies are contraindicated?
Plain abdominal xray to show colonic dilation w/ possible multiple air-fluid levels.
Contraindicated are barium contrast studies and colonoscopy – risk perforation.
How can gallbladder infection occur in patients w/ acute calculous cholecystitis?
Persistent outflow obstruction (gallstone) can promote mucosal destruction by lysolecithins – bile salt irritation of luminal epith. – PG release w/ transmural inflammation – hypomotility – inc. intraluminal pressure, ischemia – bacterial invasion.
Ethanol induces proteinaceous pancreatic secretions w/ low fluid content, forming plugs that can obstruct pancreatic ductules and cause pancreatitis. How do you differentiate alcohol-related pancreatitis from other causes?
Macrocytosis and AST:ALT > 2 are indirect indicators of chronic alcohol consumption. Otherwise, alcohol-related pancreatitis is indistinguishable from other causes.
How to porcelain gallbladder manifest from chronic cholecystitis?
There is dystrophic intramural deposition of Ca salts. Grossly, the thickened wall has a “crunchy” texture. Microscopically, there are calcified plaques in the muscularis, or spotty calcification in mucosa.
What is the most common GI manifestation of Cystic fibrosis?
Pancreatic insufficiency. Patients are unable to absorb fats and fat-soluble vitamins – steatorrhea, failure to thrive.
They would require pancreatic enzyme supplements.
What is a medication therapy for treating gallstone?
Since bile acids solubilize cholesterol, giving hydrophilic bile acids (Ursodeoxycholic acid) can reduce biliary cholesterol and inc. biliary bile acid secretion – gallstone dissolution.
*Cholecystectomy is preferred tx for symptomatic gallstone.
What part of the stomach does H.pylori most commonly colonize and how can this lead to duodenal ulceration?
H.pylori is often associated w/ antral gastritis and chronic inflammation, w/c can decrease the number of somatostatin-producing delta cells. As such, there is inc. gastrin and H+ secretion. Gastric fluid then becomes too acidic for duodenal and pancreatic HCO3 to neutralize.
Crohn disease often involves the terminal ileum, w/c is responsible for reabsorbing bile acids. What complications may manifest?
Bile acids help reabsorb fats and fat-soluble vitamins – steatorrhea, fat-soluble vitamin deficiencies.
>Vit K def: bruising, bleeding, hematoma after minor trauma.
>Vit A def: night blindness, hyperkeratosis (thick, dry skin).
