Small group question Flashcards
what is the release of pepsinogen promoted by?
HCl, Ach, gastrin, secretin, CCK
what are some abnormalities that raise gastrin levels?
- hyposecretion of gastric acid destroys negative feedback (pH of stomach is too high)
- hyperplasia (abnormal amounts) of g cells in antrum
what is a likely cause of steatorrhea in a patient with high gastrin secretion?
inactivation of lipase at acidic pH
what causes a patient’s diarrhea with a gastrinoma?
1) osmotically active fats
2) fatty acids hydoxylated by intestinal bacteria which induce fluid/electrolyte secretion
3) gastrin induces secretion and inhibits absorption
T/F You would expect gastrin to increase in a patient with a gastrinoma following a test meal if the gastrinoma is due to hyperplasia of g cells in the antrum
TRUE
what is the effect of secretin on HCl secretion?
strongly supresses gastric HCl secretion by inhibiting parietal cells & inhibiting gastrin release
main way gastrin effects HCl secretion?
causes the release of histamine from the ECL cells to act on H2 receptors
what does omeprazole do?
forms a covalent bond with the H/K ATPase and inhibits it irreversibly
what is the likely cause of steatorrhea in a patient with pancreatitis? creatorrhea? hypoalbunemia?
lack of lipases of pancreatic origin; lack of proteases; no digestion of proteins used to make albumin (protein indigestion)
explain the secretin test
assesses the ability of the exocrine pancreas to release a high volume (2mL/kg/hr), HCO3 rich (>90meq/L) pancreatic secretion
where is the main site of carbohydrate (lactose) absorption?
distal duodenum & proximal jejenum
what are the primary sources of carbs in the diet?
starches, lactose, sucrose
where are oligosaccharidases found?
brush border of intestinal mucosal clels
how are glucose and galactose transported from lumen to blood?
- SGLT1 (against gradient)
- GLUT2 (leave cell)
what is the osmolarity of chyme entering the duodenum? what is it in the ileum?
- can be hyper/iso/hypoosmotic
- is iso-osmotic by mid-jejenum
is there cross-talk between the duodenum and the stomach regarding osmolarity?
- osmoreceptors in duodenum activate hormonal and neuronal signaling pathways in response to hyper-osmotic chyme (CCK1, vagus)
changes that occur when there is hyperosmotic chyme
- less gastric motility
- less gastric emptying
- increases duodenal motility
role of ileum in bile acid physiology?
ASBT- symporter that absorbs 90% of bile acids (conjugated) in terminal ileum
how much bile salts are lots in stool?
200-400mg
what does cholestyramine do?
- binds to and sequesters bile acids
- makes them osmotically inactive
- blocks bile-acid mediated fat absorption
what is jaundice caused by?
bilirubin elevated above 2 mg/100 mL
what is pruitus caused by?
cholesterol bile salts build up and deposit in the skin
what do increased levels of AST/ALT represent? alkaline phosphatase?
AST/ALT- enzymes normally in hepatocytes, liver damage
alkaline phosphatase- enzyme in biliary epithelium, stasis in bile duct
how can liver disease cause encephalopathy?
failure to detoxify ammonia in urea cycle
major constituents of bile
bile acids- 65% phospholipids- 20% proteins- 5% electrolytes- 3-6% cholesterol-4% bilirubin- 0.3%
what are bile salts?
conjugates of bile acids with taurine or glycine
2 functions of bile
1) emulsify lipids
2) excrete cholesterol
major component of most gallstones
cholesterol - water insoluble
major site of ammonia production
- large intestine & terminal ileum by bacterial urease
- amino acid release (kidney, liver, muscle, stomach, small intestine)
what does neomycin do?
kills intestinal bacteria & reduces NH3 production as a result of bacterial urease
what 2 pathways does glucose 6 phosphate dehydrogenase deficiency disrupt?
pentose phosphate pathway + reduction of glutathione using NADPH
Hyperlipidemia IIa results from
defective LDL receptors or mutation in the ligand-binding region of Apo-b-100
the mechanism of action of Lovastatin
- is a statin
- inhibits HmG-CoA reductase, the rate limiting enzyme; leads to increased synthesis of LDL receptors
the GSD where glycogen content increases and the structure has short outer branches, occurs in liver and muscle
GSD-3; Cori
How would you be able to tell if glycogen enzyme deficiency were present in the liver?
- check fasting glucose levels
reaction where you exchange an NH2 for a double bond O
transamination
what is the guthrie inhibition assay test used for?
test for PKU- high levels of phenylalanine= high levels of bacterial growth
what can excess phenylalanine be transaminated to?
phenylpyruvic acid
what is diet soda bad for people with PKU?
aspartame degraded in SI into phenylalanine
what does the drug carbaglu do?
takes the place of n-acetylglutamate and activates carbamoyl phosphate synthase I in the urea cycle
what is the enzyme deficiency if you can’t degrade hypoxanthine to IMP?
HGPRT-ase
how do sulfa drugs work?
inhibit synthesis of folic acid, which is required for purine + dTTP; inhibit bacterial cell growth
how does lesch-nyhan lead to gout?
deficient in HGPRTase, don’t salvage purines, instead make uric acid
how does leukemia lead to gout?
have accelerated production & destruction of leucocytes, increased DNA synthesis & degradation; increased purine degredation
how does von girke’s lead to gout?
deficiency in g6phosphatase; increases ribose-5-phosphate, increases purines, increases uric acid
if you have elevated purine nucleosides, what enzyme would you be deficient in?
purine nucleoside phosphorylase
what converted ribose to deoxyribose? how would inhibiting this enzyme slow tumor growth?
ribonucleotide reductase; doxyriboses are needed for DNA synthesis
