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GI Final Exam > Biochemistry > Flashcards

Biochemistry Flashcards

1
Q

What is well developed in hepatocytes?

A

ER system; smooth for lipids and rough for proteins

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2
Q

Give a brief description of each of the following cells types: hepatocytes, endothelial cells, kupffer cells

A
  • hepatocytes: carry out most metabolic functions of liver
  • endothelial cells: allow exchange of materials between hepatocytes and blood
  • kupffer cells: macrophages that line sinusoids and protect the liver from gut derived microbes
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3
Q

Give a brief description of each of the following cell types: hepatic stellate cells, pit cells, cholangiocytes

A
  • hepatic stellate cells: storage site for vitamin A and other lipids
  • pit cells: NK cells that protect against viruses and tumors
  • cholangiocytes: line bile ducts, control bile flow rate and bile pH
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4
Q

Why does the liver have low portal blood pressure?

A

maximizes access of blood to hepatocytes - more time to take up nutrients

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5
Q

What is used to make a 5C isopentenyl pyrophosphate (IPP)?

A

3 acetyl CoA (2C compound)

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6
Q

What does IPP serve as the building block of?

A

isoprenoids

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7
Q

What are 3 examples of isoprenoids?

A
  • steroids (cholesterol, bile acids, hormones)
  • lipid soluble vitamins (ADEK)
  • ubiquinone
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8
Q

What do 6 IPP molecules form?

A

tetracyclic (4 ring) sterane ring -> backbone of most steroids

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9
Q

Which carbon of a cholesterol compound has a hydroxyl group (OH)?

A

C3

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10
Q

What is cholesterol a precursor for (3)?

A
  • bile salts and acids
  • vitamin D
  • steroid hormones
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11
Q

How are cholesterol biosynthesis and dietary intake related?

A

inversely proportional; if you ingest less cholesterol, your body makes more

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12
Q

What is the main purpose of the 2 phases of cholesterol synthesis?

A

phase 1: acetyl CoA -> IPP

phase 2: IPP -> cholesterol

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13
Q

What are the 5 intermediates of phase 1 of cholesterol synthesis?

A

acetyl CoA -> acetoacetyl CoA -> HMG CoA -> mevalonate -> IPP

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14
Q

What is the rate limiting step of cholesterol synthesis? What targets this step?

A
  • HMG CoA reductase: HMG CoA -> Mevalonate

- targeted by statins

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15
Q

What are the 4 intermediates of phase 2 of cholesterol synthesis?

A

IPP -> squalene -> lanosterol -> cholesterol

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16
Q

What do azoles (antimycotics) inhibit?

A

inhibit fungal formation of cholesterol; can inhibit mammalian production at high doses and long term use (blocks lanosterol -> cholesterol)

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17
Q

How do statins work?

A

competitive inhibitors of HMG CoA reductase (rate limiting step) and lead to maturation of SREBP that transcribe LDL receptor that internalize cholesterol from plasma

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18
Q

What effect do statins have on ubiquinone (CoQ 10)

A

ubiquinone has a role in ETC in mitochondria -> long term statin use causes depletion of muscle levels of ubiquinone (fatigue)

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19
Q

What is the fate of cholesterol in the GI tract?

A

used to synthesize bile acids

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20
Q

What activates HMG CoA reductase?

A

insulin

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21
Q

What inhibits HMG CoA reductase?

A

thyroxine, glucagon, sterols, high AMP, vitamin E, statins, phosphorylation

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22
Q

What are SRE, SREBP, and SCAP?

A
  • SRE - promotor of HMG CoA reductase
  • SREBP - transcription factor
  • SCAP - SREBP activating protein
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23
Q

Explain transcriptional control of HMG CoA reductase

A
  • in cholesterol present, SREBP-SCAP bind to INSIG in ER
  • when cholesterol absent, SREBP-SCAP released form ER -> cleaved to mature SREBP -> binds to SRE to promote cholesterol synthesis
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24
Q

What does ketoconazole do?

A

inhibits 7-a hydroxylase which is the RLS of the pathway that converts cholesterol to bile acids

25
Q

What do epileptogenic drugs do?

A

inhibit conversion of squalene to lanosterol and impairs cholesterol trafficking

26
Q

What is used to form bile acids and bile salts? Where are they synthesized?

A

hepatic cholesterol is used; made in hepatocytes

27
Q

What is the rate limiting step in the synthesis of bile acids?

A

7a-hydroxylase: adds a 2nd -OH group to cholesterol

28
Q

What are the 2 primary bile acids produced by hepatocytes?

A

cholic acid (3 OHs); chenodeoxycholic acid (2 OHs)

29
Q

What 2 amino acids conjugate w/ bile acids?

A

Taurine and Glycine

30
Q

What does it mean when a bile acid has a lower pKa?

A

lower pKa makes them more ionized and better at emulsifying fats in the small intestine (lower pH than small intestine)

31
Q

What are the primary conjugated bile acids made from cholic acid?

A

glycocholic acid; taurocholic acid

32
Q

What are the primary conjugated bile acids made from chenodeoxycholic acid?

A

glycochenodeoxycholic acid; taurochenocdeoxycholic acid

33
Q

How are secondary bile acids made? What are the 2 secondary bile acids and what do they derive from?

A
  • produced when bacteria in the gut deconjugate primary bile salts into secondary bile acids
  • deoxycholic acid (from cholic acid)
  • lithocholic acid (from chenodeoxycholic acid)
34
Q

What do resins such as cholestryamine do?

A

bind to bile acids and make them non-absorbable -> cause large increase in excretion of bile acids in feces

35
Q

How do resins result in lower plasma cholesterol levels?

A

more bile acids excreted -> rate of bile synthesis increases -> deplete liver cholesterol pool -> increase in hepatic uptake of LDL -> lower plasma cholesterol levels

36
Q

What causes cholelithiasis?

A

insufficient secretion of bile salts or phospholipids into gallbladder or excess cholesterol secretion into bile

37
Q

Metabolites vs Xenobiotics

A
  • metabolites: compounds made in the body (intermediates or end products of metabolism)
  • xenobiotics: compounds ingested from outside (pharmacologic agents, recreational drugs, food additives)
38
Q

Explain the detoxification process of xenobiotics

A
  • phase 1 reactions create a primary metabolite (more polar) using cytochrome P450 enzymes
  • phase 2 reactions add a functional group to metabolite and conjugate it for safe excretion
39
Q

What catalyzes the detoxification process for xenobiotics?

A

cytochrome P450 (CYP) enzymes -> helps make drugs more polar

40
Q

What will be the effect of agents that inhibit and stimulate CYP?

A
  • agents that inhibit CYP will increase drug levels

- agents that stimulate CYP will decrease drug levels

41
Q

Heredity of Crigler Najjar syndrome? What enzyme is affected in this disease and type of bilirubin that builds up`?

A

AR; UGT1A1; uncojugated

42
Q

What is the function of UGT1A1?

A

adds a sugar to bilirubin to conjugate it (makes it more polar and easily excreted)

43
Q

Crigler Najjar Type I vs Type II

A

Type I: UGT1A1 completely absent - sx at birth - lethal

Type II: some UGT1A1 activity - survive to adulthood

44
Q

What is kernicterus?

A

when uncojugated bilirubin builds up in brain; poor development/mental function; seen in crigler najjar type I

45
Q

What is the tx for Crigler Najjar Type I and II?

A

Type I: plasmapheresis; liver transplant

Type II: phenobarbital (UGT1A1 inducer)

46
Q

What is the cause of Gilbert’s syndrome? Type of bilirubin that builds up?

A

defect in gene promotor for UGT1A1; unconjugated

47
Q

What generally causes flair ups of Gilbert’s syndrome?

A

fasting, stress, EtOH intake

48
Q

What is the treatment for Gilbert’s syndrome?

A

no treatment needed; avoid irinotecan (anti-cancer drug detoxed by UGT1A1)

49
Q

What is mutated in Dubin-Johnson syndrome and what is its funciton? What is the hallmark of Dubin-Johnson syndrome?

A

MRP2 -> moves conjugated bilirubin from hepatocytes to bile; hallmark = black liver

50
Q

What is mutated in Rotor’s syndrome and what is its function? What sx is seen in Rotor’s syndrome and why?

A

Mutations in both OATP1B1 and OATP1B3 -> move bilirubin from blood into hepatocytes; bilirubinuria seen -> bilirubin backs up in blood and is excreted in urine

51
Q

Urine coproporphyrin levels in Rotor’s and DJS?

A
  • elevated in Rotor’s

- normal in DJS

52
Q

What is mutated in Wilson’s disease and what is it’s function?

A

ATP7B -> transports copper from liver to bile -> accumulates in liver if not working

53
Q

What is the function of ceruloplasmin?

A

transport protein for copper in blood -> free copper is toxic (similar to Fe)

54
Q

What type of sxs are hallmark in Wilson’s disease?

A

CNS sxs: parkinson like sxs, hemiballismus (flailing of limbs), dementia
Kayser-Fleischer rings (multicolored concentric rings around irises)

55
Q

What causes galactosemia? When in life is it seen?

A

deficiency in enzymes that transform galactose -> G6P (galactose builds up in blood) -> mainly GALT enzyme
- seen in newborns

56
Q

What does fructokinase deficiency cause?

A

disruption of fructose metabolism -> fructosuria (fructose in urine)

57
Q

What does aldolase B deficiency cause? How do pt’s present?

A
  • causes build up of fructose and fructose 1-phosphate (damages liver and kidneys)
  • pt’s have low serum levels of phosphorus and glucose
58
Q

Von Gierke’s disease vs glycogen storage disease 1B?

A
  • Von Gierke’s disease: deficiency of glucose 6 phosphatase (needed for release of glucose from liver)
  • Glycogen storage disease 1B: deficiency is in transport protein that moves G6P to ER lumen where glucose 6 phosphatase is
59
Q

What does PEPCK deficiency cause?

A

cannot catalyze conversion of OAA to PEP in carbohydrate metabolism -> academia (high acid levels in blood)

GI Final Exam (6 decks)

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