Lect 19 - Steroid Hormone Metabolism Flashcards

Jan 28, 2019 (32 cards)

1
Q

How many carbons do gluco- and mineralo-corticoids have?

A

21 carbons

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2
Q

How many carbons do estrogens have?

A

18 carbons

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3
Q

How many carbons do progestins have?

A

21 carbons

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4
Q

How many carbons do androgens have?

A

19 carbons

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5
Q

How many carbons are in cholesterol?

A

27 carbons

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6
Q

Where are steroid hormones NOT produced ever?

A

the liver!

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7
Q

The first reaction that converts cholesterol to pregnenolone is catalyzed by which enzyme? What are the three names of this enzyme?

A

1) desmolase
2) cholesterol side-chain cleavage enzyme (CYP450scc)
3) CYP11A

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8
Q

How does the body regulate levels of free steroid hormone?

A

Through binding to binding proteins in the blood

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9
Q

Does free steroid hormone or hormone bound to binding protein enter the cell?

A

free steroid hormone

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10
Q

Steroid hormones are degraded where? Excreted where?

A

Degraded in liver. Excreted in urine.

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11
Q

What are the organs where there is de novo synthesis of steroid hormones?

A

1) testes/ovaries
2) adrenal cortex
3) corpus luteum

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12
Q

What hormone is the main glucocorticoid?

A

cortisol

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13
Q

What hormone is the main mineralocorticoid?

A

aldosterone

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14
Q

Cholesterol is turned into pregnenolone by which enzyme?

A

CYP11A

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15
Q

What is another name for CYP11A?

A

Desmolase or side-chain cleavage enzyme

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16
Q

What enzyme turns angiotensin I into angiotensin II?

17
Q

What enzyme turns angiotensinogen into angiotensin I?

18
Q

What is the rate-limiting enzyme in steroid hormone synthesis? What is the regulated enzyme?

A

Regulated: StAR

Rate-limited: CYP11A

19
Q

At what point in the day is cortisol synthesis/release the highest?

A

In the AM right before waking up

20
Q

What are the four major targets of cortisol?

A

1) liver
2) fat
3) muscle
4) inflammatory response

21
Q

Cortisol affects the liver by stimulating what?

A

long term gluconeogenesis

22
Q

What activated StAR?

23
Q

3-beta hydroxysteroid DHG deficiency:

  • — DHEA
  • — androstenedione
  • — aldosterone
  • — cortisol
A

↑ DHEA
↓ androstenedione
↓ aldosterone
↓ cortisol

24
Q

CYP17 deficiency:

  • — DHEA
  • — androstenedione
  • — aldosterone
  • — cortisol
  • — 11-deoxycorticosterone
  • — 11-deoxycortisol
A
↓ DHEA
↓ androstenedione
↑ aldosterone
↓ cortisol
↑ 11-deoxycorticosterone
↑ 11-deoxycortisol
25
CYP 21 deficiency: - --- DHEA - --- androstenedione - --- aldosterone - --- cortisol
↑ DHEA ↑ androstenedione ↓ aldosterone ↓ cortisol
26
Which is the most common cause of congenital adrenal hyperplasia? What percentage of cases?
CYP21 deficiency, 90-95% of cases
27
What are the symptoms of 3 beta-hydroxysteroid DHG deficiency?
1) low fasting blood glucose 2) natriuresis 3) deficiencies of glucocorticoids and mineralocorticoids 4) ambiguous genitalia may be possible 5) hypotension
28
What are the symptoms of CYP17 defiency?
1) no cortisol or weak androgens 2) hypertension (due to build up of the mineralocorticoid 11-deoxycorticosterone) 3) low fasting blood glucose 4) female-like genitalia
29
What are the symptoms of CYP21 deficiency?
1) hypotension 2) "salt crisis" 3) low fasting blood glucose 4) ambiguous male-like genitalia in females
30
What are the symptoms of CYP11B defiency?
1) mild hypertension 2) low fasting blood glucose 3) male-like genitalia
31
Where does the conversion of tesosterone to DHT take place? Which hormone catalyzes this reaction? What is another name for this hormone?
1) Sertoli cells 2) 5-alpha reductase 3) aromatase
32
Follicular granulosa cells produce _______ by catalysis with ________ under stimulation of _______ receptors.
1) estrogens 2) 5-alpha reductase 3) FSH