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Physiology > Small group question > Flashcards

Small group question Flashcards

1
Q

what is the release of pepsinogen promoted by?

A

HCl, Ach, gastrin, secretin, CCK

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2
Q

what are some abnormalities that raise gastrin levels?

A
  • hyposecretion of gastric acid destroys negative feedback (pH of stomach is too high)
  • hyperplasia (abnormal amounts) of g cells in antrum
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3
Q

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

A

inactivation of lipase at acidic pH

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4
Q

what causes a patient’s diarrhea with a gastrinoma?

A

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

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5
Q

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

A

TRUE

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6
Q

what is the effect of secretin on HCl secretion?

A

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

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7
Q

main way gastrin effects HCl secretion?

A

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

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8
Q

what does omeprazole do?

A

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

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9
Q

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

A

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

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10
Q

explain the secretin test

A

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

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11
Q

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

A

distal duodenum & proximal jejenum

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12
Q

what are the primary sources of carbs in the diet?

A

starches, lactose, sucrose

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13
Q

where are oligosaccharidases found?

A

brush border of intestinal mucosal clels

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14
Q

how are glucose and galactose transported from lumen to blood?

A
  • SGLT1 (against gradient)

- GLUT2 (leave cell)

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15
Q

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

A
  • can be hyper/iso/hypoosmotic

- is iso-osmotic by mid-jejenum

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16
Q

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

A
  • osmoreceptors in duodenum activate hormonal and neuronal signaling pathways in response to hyper-osmotic chyme (CCK1, vagus)
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17
Q

changes that occur when there is hyperosmotic chyme

A
  • less gastric motility
  • less gastric emptying
  • increases duodenal motility
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18
Q

role of ileum in bile acid physiology?

A

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

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19
Q

how much bile salts are lots in stool?

A

200-400mg

20
Q

what does cholestyramine do?

A
  • binds to and sequesters bile acids
  • makes them osmotically inactive
  • blocks bile-acid mediated fat absorption
21
Q

what is jaundice caused by?

A

bilirubin elevated above 2 mg/100 mL

22
Q

what is pruitus caused by?

A

cholesterol bile salts build up and deposit in the skin

23
Q

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

A

AST/ALT- enzymes normally in hepatocytes, liver damage

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

24
Q

how can liver disease cause encephalopathy?

A

failure to detoxify ammonia in urea cycle

25
Q

major constituents of bile

A 
bile acids- 65%
phospholipids- 20%
proteins- 5%
electrolytes- 3-6%
cholesterol-4% 
bilirubin- 0.3%
26
Q

what are bile salts?

A

conjugates of bile acids with taurine or glycine

27
Q

2 functions of bile

A

1) emulsify lipids

2) excrete cholesterol

28
Q

major component of most gallstones

A

cholesterol - water insoluble

29
Q

major site of ammonia production

A
  • large intestine & terminal ileum by bacterial urease

- amino acid release (kidney, liver, muscle, stomach, small intestine)

30
Q

what does neomycin do?

A

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

31
Q

what 2 pathways does glucose 6 phosphate dehydrogenase deficiency disrupt?

A

pentose phosphate pathway + reduction of glutathione using NADPH

32
Q

Hyperlipidemia IIa results from

A

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

33
Q

the mechanism of action of Lovastatin

A
  • is a statin

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

34
Q

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

A

GSD-3; Cori

35
Q

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

A
  • check fasting glucose levels
36
Q

reaction where you exchange an NH2 for a double bond O

A

transamination

37
Q

what is the guthrie inhibition assay test used for?

A

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

38
Q

what can excess phenylalanine be transaminated to?

A

phenylpyruvic acid

39
Q

what is diet soda bad for people with PKU?

A

aspartame degraded in SI into phenylalanine

40
Q

what does the drug carbaglu do?

A

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

41
Q

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

A

HGPRT-ase

42
Q

how do sulfa drugs work?

A

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

43
Q

how does lesch-nyhan lead to gout?

A

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

44
Q

how does leukemia lead to gout?

A

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

45
Q

how does von girke’s lead to gout?

A

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

46
Q

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

A

purine nucleoside phosphorylase

47
Q

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

A

ribonucleotide reductase; doxyriboses are needed for DNA synthesis

Physiology (22 decks)

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