Small group question

Question 1

what is the release of pepsinogen promoted by?

Answer 1

HCl, Ach, gastrin, secretin, CCK

Question 2

what are some abnormalities that raise gastrin levels?

Answer 2

• hyposecretion of gastric acid destroys negative feedback (pH of stomach is too high)
• hyperplasia (abnormal amounts) of g cells in antrum

Question 3

what is a likely cause of steatorrhea in a patient with high gastrin secretion?

Answer 3

inactivation of lipase at acidic pH

Question 4

what causes a patient’s diarrhea with a gastrinoma?

Answer 4

1) osmotically active fats
2) fatty acids hydoxylated by intestinal bacteria which induce fluid/electrolyte secretion
3) gastrin induces secretion and inhibits absorption

Question 5

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

Answer 5

TRUE

Question 6

what is the effect of secretin on HCl secretion?

Answer 6

strongly supresses gastric HCl secretion by inhibiting parietal cells & inhibiting gastrin release

Question 7

main way gastrin effects HCl secretion?

Answer 7

causes the release of histamine from the ECL cells to act on H2 receptors

Question 8

what does omeprazole do?

Answer 8

forms a covalent bond with the H/K ATPase and inhibits it irreversibly

Question 9

what is the likely cause of steatorrhea in a patient with pancreatitis? creatorrhea? hypoalbunemia?

Answer 9

lack of lipases of pancreatic origin; lack of proteases; no digestion of proteins used to make albumin (protein indigestion)

Question 10

explain the secretin test

Answer 10

assesses the ability of the exocrine pancreas to release a high volume (2mL/kg/hr), HCO3 rich (>90meq/L) pancreatic secretion

Question 11

where is the main site of carbohydrate (lactose) absorption?

Answer 11

distal duodenum & proximal jejenum

Question 12

what are the primary sources of carbs in the diet?

Answer 12

starches, lactose, sucrose

Question 13

where are oligosaccharidases found?

Answer 13

brush border of intestinal mucosal clels

Question 14

how are glucose and galactose transported from lumen to blood?

Answer 14

• SGLT1 (against gradient)

- GLUT2 (leave cell)

Question 15

what is the osmolarity of chyme entering the duodenum? what is it in the ileum?

Answer 15

• can be hyper/iso/hypoosmotic

- is iso-osmotic by mid-jejenum

Question 16

is there cross-talk between the duodenum and the stomach regarding osmolarity?

Answer 16

• osmoreceptors in duodenum activate hormonal and neuronal signaling pathways in response to hyper-osmotic chyme (CCK1, vagus)

Question 17

changes that occur when there is hyperosmotic chyme

Answer 17

• less gastric motility
• less gastric emptying
• increases duodenal motility

Question 18

role of ileum in bile acid physiology?

Answer 18

ASBT- symporter that absorbs 90% of bile acids (conjugated) in terminal ileum

Question 19

how much bile salts are lots in stool?

Answer 19

200-400mg

Question 20

what does cholestyramine do?

Answer 20

• binds to and sequesters bile acids
• makes them osmotically inactive
• blocks bile-acid mediated fat absorption

Question 21

what is jaundice caused by?

Answer 21

bilirubin elevated above 2 mg/100 mL

Question 22

what is pruitus caused by?

Answer 22

cholesterol bile salts build up and deposit in the skin

Question 23

what do increased levels of AST/ALT represent? alkaline phosphatase?

Answer 23

AST/ALT- enzymes normally in hepatocytes, liver damage

alkaline phosphatase- enzyme in biliary epithelium, stasis in bile duct

Question 24

how can liver disease cause encephalopathy?

Answer 24

failure to detoxify ammonia in urea cycle

Question 25

major constituents of bile

Answer 25

``` bile acids- 65% phospholipids- 20% proteins- 5% electrolytes- 3-6% cholesterol-4% bilirubin- 0.3% ```

Question 26

what are bile salts?

Answer 26

conjugates of bile acids with taurine or glycine

Question 27

2 functions of bile

Answer 27

1) emulsify lipids | 2) excrete cholesterol

Question 28

major component of most gallstones

Answer 28

cholesterol - water insoluble

Question 29

major site of ammonia production

Answer 29

- large intestine & terminal ileum by bacterial urease | - amino acid release (kidney, liver, muscle, stomach, small intestine)

Question 30

what does neomycin do?

Answer 30

kills intestinal bacteria & reduces NH3 production as a result of bacterial urease

Question 31

what 2 pathways does glucose 6 phosphate dehydrogenase deficiency disrupt?

Answer 31

pentose phosphate pathway + reduction of glutathione using NADPH

Question 32

Hyperlipidemia IIa results from

Answer 32

defective LDL receptors or mutation in the ligand-binding region of Apo-b-100

Question 33

the mechanism of action of Lovastatin

Answer 33

- is a statin | - inhibits HmG-CoA reductase, the rate limiting enzyme; leads to increased synthesis of LDL receptors

Question 34

the GSD where glycogen content increases and the structure has short outer branches, occurs in liver and muscle

Answer 34

GSD-3; Cori

Question 35

How would you be able to tell if glycogen enzyme deficiency were present in the liver?

Answer 35

- check fasting glucose levels

Question 36

reaction where you exchange an NH2 for a double bond O

Answer 36

transamination

Question 37

what is the guthrie inhibition assay test used for?

Answer 37

test for PKU- high levels of phenylalanine= high levels of bacterial growth

Question 38

what can excess phenylalanine be transaminated to?

Answer 38

phenylpyruvic acid

Question 39

what is diet soda bad for people with PKU?

Answer 39

aspartame degraded in SI into phenylalanine

Question 40

what does the drug carbaglu do?

Answer 40

takes the place of n-acetylglutamate and activates carbamoyl phosphate synthase I in the urea cycle

Question 41

what is the enzyme deficiency if you can't degrade hypoxanthine to IMP?

Answer 41

HGPRT-ase

Question 42

how do sulfa drugs work?

Answer 42

inhibit synthesis of folic acid, which is required for purine + dTTP; inhibit bacterial cell growth

Question 43

how does lesch-nyhan lead to gout?

Answer 43

deficient in HGPRTase, don't salvage purines, instead make uric acid

Question 44

how does leukemia lead to gout?

Answer 44

have accelerated production & destruction of leucocytes, increased DNA synthesis & degradation; increased purine degredation

Question 45

how does von girke's lead to gout?

Answer 45

deficiency in g6phosphatase; increases ribose-5-phosphate, increases purines, increases uric acid

Question 46

if you have elevated purine nucleosides, what enzyme would you be deficient in?

Answer 46

purine nucleoside phosphorylase

Question 47

what converted ribose to deoxyribose? how would inhibiting this enzyme slow tumor growth?

Answer 47

ribonucleotide reductase; doxyriboses are needed for DNA synthesis