Cholesterol & Steroids Flashcards

1
Q

cholesterol synthesis requires

A

acetyl CoA, NADPH, & ATP

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2
Q

rate limiting enzyme for cholesterol synthesis

A

HMG CoA reductase

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3
Q

where does cholesterol synthesis occur

A

cytoplasm

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4
Q

steps of acetyl coA to HMG coA

A

2 acetyl CoA to acetylacyl CoA via thiolase. acetylacyl CoA to HMG CoA via HMG CoA synthase

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5
Q

function of HMG CoA reductase

A

takes HMG CoA to mevalonate. uses 2 NADPH. irreversible step because it releases CoA

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6
Q

inhibitors of HMG CoA reductase

A

cholesterol, statins, glucagon.

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7
Q

activator of HMG CoA reductase

A

insulin

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8
Q

explain sterol independent inactivation of HMG CoA reductase

A

high levels of AMP activate AMPkinase to phosphorylate HMG CoA reductase and render it inactive.

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9
Q

statins are what kind of inhibitors of HMG CoA reductase

A

competitive

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10
Q

low cholesterol promotes the release of which stimulatory protein

A

SREBP (causes the liver to produce more HMG CoA reductase)

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11
Q

degradation of HMG CoAR due to high levels of cholesterol or Mevalonate, is done by

A

proteosomes tagging with ubiquitin

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12
Q

lipoprotein with highest amount of cholesterol

A

LDL

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13
Q

increases the amount of LDL receptors on the cell surface to lower serum LDL

A

statins

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14
Q

converts cholesterol to cholesterol ester for storage

A

ACAT

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15
Q

enzyme needed for double bond formation in the b ring of cholesterol

A

7-dehydrocholesterol reductase

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16
Q

disorder associated with absent 7-dehydrocholesterol reductase

A

SLOS- causes severe mental retardation

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17
Q

some cholesterol is modified by bacteria to form

A

cholestanol & coprostanol

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18
Q

most abundant organic components of bile

A

PC and bile salts

19
Q

primary bile acids

A

cholic acid & chenodeoxycholic acid

20
Q

rate limiting enzyme for synthesis of bile acids

A

7-alpha-hydroxlase (puts OH on carbon 7)

21
Q

7-alpha-hydroxlase is inhibited by

A

cholic acid

22
Q

amino acids involved in bile salt formation

A

taurine and glycine

23
Q

four functions of bile

A

eliminates excess cholesterol in feces, prevents gallstone formation, help with digestion of TAGs and help absorb vitamins

24
Q

rate limiting step for steroid synthesis

A

conversion of cholesterol to pregnenolone via desmolase (cyp11a, p450)

25
Q

transports cholesterol into mitochondria

A

StAR

26
Q

how does desmolase modify cholesterol in rate limiting step

A

shortens hydrocarbon chain and hydroxylates steroid nucleus.

27
Q

what does the rate limiting step of steroid synthesis require

A

NADPH and O2

28
Q

hormone secreted from zona glomerulosa

A

aldosterone

29
Q

hormone secreted from zona fasiculata

A

cortisol

30
Q

hormones secreted from zona reticularis

A

dihydrotestosterone, estradiol

31
Q

peptide that signals cortisol release

A

ACTH

32
Q

peptide that signals aldosterone release

A

Ang II or Ang III

33
Q

peptide that signals estradiol release

A

FSH

34
Q

peptide that signals progesterone and testosterone release

A

LH

35
Q

how is cortisol transported in the blood

A

bound to transcortin and albumin

36
Q

raises bp & fluid volume. increases Na+ reabsorption

A

aldosterone

37
Q

precursor to testosterone and estradiol

A

DHEA, and androstenedione

38
Q

patient has buffalo hump, hyperglycemia, abnormal hair growth

A

cushings (too much cortisol)

39
Q

disorder that is the opposite of cushings

A

addisons.

40
Q

CAH that presents with patient unable to make glucocorticoids, mineralocorticoids, and androgens

A

3-beta-hydroxysteroid dehydrogenase deficiency. (Unable to take pregnenolone to progesterone)

41
Q

CAH that presents with patient unable to make glucocorticoids and androgens. patient has normal aldosterone

A

17-alpha-hydroxylase deficiency. (unable to take progesterone to 17-a-hydroxyprogesterone)

42
Q

CAH that presents with patient unable to make glucocorticoids and mineralocorticoids. patient overproduces androgens

A

21-alpha-hydroxylase deficiency (unable to take progesterone to 11-deoxycortiocosterone) (unable to take 17-alpha-hydroxyprosterterone to 11-deoxycortisol)

43
Q

CAH that presents with patient unable to make glucocorticoids and mineralocorticoids. patient overproduces androgens. also have increased deoxycorticosterone

A

11-beta1- hydroxylase deficiency (unable to take 11-deoxycortisol to cortisol) (unable to take 11-deoxycortiocosterone to corticosterone)