Lect 19 - Steroid Hormone Metabolism Flashcards

Jan 28, 2019

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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?

A

ACE

17
Q

What enzyme turns angiotensinogen into angiotensin I?

A

renin

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?

A

PKA

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
Q

CYP 21 deficiency:

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

↑ DHEA
↑ androstenedione
↓ aldosterone
↓ cortisol

26
Q

Which is the most common cause of congenital adrenal hyperplasia? What percentage of cases?

A

CYP21 deficiency, 90-95% of cases

27
Q

What are the symptoms of 3 beta-hydroxysteroid DHG deficiency?

A

1) low fasting blood glucose
2) natriuresis
3) deficiencies of glucocorticoids and mineralocorticoids
4) ambiguous genitalia may be possible
5) hypotension

28
Q

What are the symptoms of CYP17 defiency?

A

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
Q

What are the symptoms of CYP21 deficiency?

A

1) hypotension
2) “salt crisis”
3) low fasting blood glucose
4) ambiguous male-like genitalia in females

30
Q

What are the symptoms of CYP11B defiency?

A

1) mild hypertension
2) low fasting blood glucose
3) male-like genitalia

31
Q

Where does the conversion of tesosterone to DHT take place? Which hormone catalyzes this reaction? What is another name for this hormone?

A

1) Sertoli cells
2) 5-alpha reductase
3) aromatase

32
Q

Follicular granulosa cells produce _______ by catalysis with ________ under stimulation of _______ receptors.

A

1) estrogens
2) 5-alpha reductase
3) FSH