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
transports cholesterol into mitochondria
StAR
26
how does desmolase modify cholesterol in rate limiting step
shortens hydrocarbon chain and hydroxylates steroid nucleus.
27
what does the rate limiting step of steroid synthesis require
NADPH and O2
28
hormone secreted from zona glomerulosa
aldosterone
29
hormone secreted from zona fasiculata
cortisol
30
hormones secreted from zona reticularis
dihydrotestosterone, estradiol
31
peptide that signals cortisol release
ACTH
32
peptide that signals aldosterone release
Ang II or Ang III
33
peptide that signals estradiol release
FSH
34
peptide that signals progesterone and testosterone release
LH
35
how is cortisol transported in the blood
bound to transcortin and albumin
36
raises bp & fluid volume. increases Na+ reabsorption
aldosterone
37
precursor to testosterone and estradiol
DHEA, and androstenedione
38
patient has buffalo hump, hyperglycemia, abnormal hair growth
cushings (too much cortisol)
39
disorder that is the opposite of cushings
addisons.
40
CAH that presents with patient unable to make glucocorticoids, mineralocorticoids, and androgens
3-beta-hydroxysteroid dehydrogenase deficiency. (Unable to take pregnenolone to progesterone)
41
CAH that presents with patient unable to make glucocorticoids and androgens. patient has normal aldosterone
17-alpha-hydroxylase deficiency. (unable to take progesterone to 17-a-hydroxyprogesterone)
42
CAH that presents with patient unable to make glucocorticoids and mineralocorticoids. patient overproduces androgens
21-alpha-hydroxylase deficiency (unable to take progesterone to 11-deoxycortiocosterone) (unable to take 17-alpha-hydroxyprosterterone to 11-deoxycortisol)
43
CAH that presents with patient unable to make glucocorticoids and mineralocorticoids. patient overproduces androgens. also have increased deoxycorticosterone
11-beta1- hydroxylase deficiency (unable to take 11-deoxycortisol to cortisol) (unable to take 11-deoxycortiocosterone to corticosterone)