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01b: Steroid Hormone Synthesis Flashcards

1
Q

List the five classes of steroid hormones.

A
  1. Glucocorticoids
  2. Mineralocorticoids
  3. Androgens
  4. Estrogens
  5. Progesterone
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2
Q

There are (X) classes of steroid hormones, which can be categorized/grouped into either (Y) or (Z).

A 
X = 5
Y = corticosteroids
Z = sex steroids
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3
Q

Sex steroid hormones are made from (X) and corticosteroids are made from (Y).

A

X = Y = cholesterol (all steroid hormones are)

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4
Q

Which symptom on a skin exam would be significant clue of a steroid hormone problem?

A

Hyperpigmentation

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5
Q

You suspect presence of steroid hormone problem in your patient. What would you do next? Be specific.

A

Order tests to examine levels of different steroid hormones and their precursors

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6
Q

The first step in steroid hormone synthesis is universally (X) conversion to (Y) via (Z) enzyme.

A 
X = cholesterol
Y = pregnenolone
Z = desmolase
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7
Q

Steroid hormone synthesis begins in (cytoplasm/ER/mito), specifically in (X).

A

Mitochondria;

X = IMM

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8
Q

StAR is crucial for:

A

Cholesterol entry into mitochondria

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9
Q

T/F: A mutation that makes StAR completely dysfunctional is one that’s incompatible with life.

A

True

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10
Q

What’s the rate-limiting step in cortisol biosynthesis?

A

Cholesterol transport into mito by StAR (rate-limiting for synthesis of ALL steroid hormones)

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11
Q

Cortisol synthesis: Prognenolone is converted into (X) via (Y) enzyme. Where does this occur?

A 
X = progesterone
Y = 3-beta-hydroxy steroid DH

Cytoplasm

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12
Q

T/F: Once progesterone is formed in cortisol biosynthesis, it moves out from mito into cytoplasm.

A

False - it’s formed in cytoplasm (pregnenolone moves out prior to progesterone formation)

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13
Q

Cortisol synthesis: Progesterone is converted into (X) via (Y) enzyme. Where does this occur?

A 
X = 17-alpha-hydroxyprogesterone
Y = 17-alpha-hydroxylase

ER

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14
Q

Cortisol synthesis: there are two paths that can be taken to arrive at (X) intermediate from (Y).

A 
X = 17-alpha-hydroxyprogesterone
Y = pregnenolone
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15
Q

Pregnenolone can be acted on by which two enzymes in steroid hormone biosynthesis? List the respective product of each.

A
  1. 3-beta-hydroxy steroid DH (progesterone)

2. 17-alpha-hydroxylase (17-alpha-hydroxypregnenolone)

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16
Q

Cortisol synthesis: 17-alpha-hydroxyprogesterone is converted into (X) via (Y) enzyme.

A 
X = 11-deoxycortisol
Y = 21-alpha-hydroxylase
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17
Q

The final (1/2/3) step(s) of cortisol biosynthesis occur in mitochondria. Which intermediate makes the trip back there?

A

1;

11-deoxycortisol

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18
Q

Cortisol synthesis: 11-deoxycortisol is converted into (X) via (Y) enzyme.

A 
X = Cortisol
Y = 11-beta-hydroxylase
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19
Q

In (X) steroid synthesis pathway, 17-alpha-hydroxylase acts twice. If its first reactant is pregnenolone, which two products are formed?

A

X = androgen

  1. 17-alpha-hydroxypregnenolone
  2. DHEA
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20
Q

DHEA is an important intermediate in (X) steroid biosynthesis. (Y) enzyme acts on it to produce (Z) product.

A 
X = androgen
Y = 3-beta-hydroxy steroid DH
Z = Androstenedione
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21
Q

Testosterone is formed directly from (X) via (Y) enzyme.

A 
X = Androstenedione
Y = 17-beta-hydroxy steroid DH
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22
Q

(X) intermediate can be acted in by either (Y) enzyme to form testosterone or (Z) enzyme to form:

A 
X = androstenedione
Y = testosterone
Z = aromatase

Estrone

23
Q

Testosterone, if acted on by (X) enzyme, will form (Y).

A 
X = aromatase
Y = estradiol
24
Q

(X) intermediate in androgen synthesis can be formed from either (Y) intermediate or from the cortisol synthesis intermediate, (Z). Which enzymes involved in each path?

A 
X = androstenedione
Y = DHEA (3-beta-hydroxy steroid DH)
Z = 17-alpha-hydroxyprogesterone (17-alpha-hydroxylase)
25
Q

T/F: Aldosterone can be an intermediate in one pathway for testosterone biosynthesis.

26
Q

T/F: Path for Aldosterone biosynthesis, like that for androgen synthesis, branches off at the pregnenolone step.

A

False - at progesterone step

27
Q

Aldosterone synthesis: Progesterone becomes (X) when acted on by (Y) enzyme.

A 
X = 11-deoxycorticosterone
Y = 21-alpha-hydroxylase
28
Q

Aldosterone synthesis: 11-deoxycorticosterone becomes (X) when acted on by (Y) enzyme.

A 
X = corticosterone
Y = 11-beta-hydroxylase
29
Q

Corticosterone is an intermediate in (X) steroid hormone biosynthesis. It becomes (Y) when acted on by (Z) hormone.

A 
X = Y = aldosterone
Z = aldosterone synthase
30
Q

Synthesis of aldosterone occurs in which gland?

A

Zona glomerulosa of adrenal cortex

31
Q

Testosterone primarily produced in (X), but its synthesis also occurs in which gland?

A

X = testes

Zona reticularis of adrenal cortex

32
Q

Cortisol synthesis occurs in which gland?

A

Zona fasciculata of adrenal cortex

33
Q

Synthesis of (X) occurs in response to ACTH, aka (Y), release from (Z).

A 
X = cortisol
Y = Adrenocorticotropic hormone
Z = anterior pituitary gland
34
Q

The two key steps that make up the delta-4 and delta-5 pathways of (X) synthesis are essentially carrying out which functions? What’s the difference between the pathways?

A

X = androgen
Hydroxylation, then lyase activity (BOTH via 17-alpha-hydroxylase);
Starting at different intermediates (either pregnenolone or progesterone)

35
Q

Delta-(4/5) pathway tends to dominate. In the two key steps of this pathway, (hydroxylation/lyase) of (X) is followed by (hydroxylation/lyase) of (Y).

A 
Delta-5;
Hydroxylation;
X = pregnenolone
Lyase;
Y = 17-alpha-hydroxypregnenolone
36
Q

Metabolism of testosterone: in (X) tissue/organ, testosterone is metabolized to (Y) by (Z) enzyme.

A 
X = any of its target
Y = DHT (dihydrotestosterone)
Z = 5-alpha-reductase
37
Q

One treatment for BPH (benign prostatic hyperplasia) is (X), which will (stimulate/inhibit) metabolism of (Y).

A

X = 5-alpha-reductase inhibitors;
Inhibit;
Y = testosterone

38
Q

T/F: Estrogens are made from androgens.

39
Q

Esterogen receptor is located in (X) compartment of cell and associated with (Y) protein when inactivated.

A 
X = cytoplasm
Y = HSP90
40
Q

Estrogen Receptor: When (X) enters cell, it displaces (Y) and binds estrogen receptor. The complex moves to (Z) compartment as (monomer/dimer/trimer/other).

A 
X = estradiol
Y = HSP90
Z = nucleus

Monomer (dimerizes inside nucleus)

41
Q

Estrogen receptor: the H-R complex binds to (X) of DNA. In absence of ligand, can estrogen receptor bind DNA?

A

X = ERE (esterogen response element)

No

42
Q

Prostate cancer can be treated by (agonist/antagonist) to (X) receptor.

A

Antagonist;

X = Androgen

43
Q

One method of contraception is an (agonist/antagonist) to (X) receptor.

A

Antagonist;

X = Progesterone

44
Q

You’d expect an aldosterone receptor antagonist to be treatment for which array of symptoms/diseases?

A
  1. Edema
  2. Hypokalemia
  3. CHF, HT
45
Q

A deficiency in (X) enzyme of steroid hormone biosynthesis would cause patient to have virtually no steroid hormones and (male/female)-like genitalia.

A

X = 3-beta-hydroxy steroid DH

Female

46
Q

A deficiency in (X) enzyme of steroid hormone biosynthesis would cause patient to have virtually no sex hormones or cortisol and (male/female)-like genitalia. You’d expect (over/under)-production of mineralocorticoids and which symptoms?

A

X = 17-alpha-hydroxylase
Female;
Over-production;

Na/fluid retention and HT

47
Q

A deficiency in (X) enzyme of steroid hormone biosynthesis would cause patient to have virtually no mineralocorticosteroids and glucocorticoids and (male/female)-like genitalia.

A

X = 21-alpha-hydroxylase

Masculinization of external F genitalia and early virilization in M

48
Q

A deficiency in (X) enzyme of steroid hormone biosynthesis would cause patient to have decreased serum cortisol, aldosterone, and corticosterone and (male/female)-like genitalia. There’s be an increased production of which specific intermediate?

A

X = 11-beta-hydroxylase;
Masculinization of external F genitalia and early virilization in M;

Deoxycorticosterone (fluid retention)

49
Q

Deficiency in which steroid hormone synthesis enzymes would cause fluid retention/edema?

A
  1. 17-alpha-hydroxylase

2. 11-beta-hydroxylase

50
Q

Deficiency in which steroid hormone synthesis enzymes is most common?

A

21-alpha-hydroxylase (over 90%)

51
Q

Tamoxifen is a drug used to treat (X). What’s its general mechanism of action?

A

X = some types of breast cancer

Binds estrogen receptor (prevents estrogen from binding and inducing conformational change); prevents its association with co-activators

52
Q

Tamoxifen, though a drug that blocks (X) in breast cell, may be a cause for (Y) because it (activates/inhibits) (Z).

A

X = estrogen receptor
Y = uterine cancer;
Activates
Z = estrogen receptor in uterus (endometrial proliferation)

53
Q

Instead of blocking the estrogen receptor, some FDA drugs decrease effect of estrogens via:

A

Inhibiting aromatase (preventing estrogen production in first place)

Endo/Repro (15 decks)

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