01b: Steroid Hormone Synthesis Flashcards by Nuna H

List the five classes of steroid hormones.

Glucocorticoids
Mineralocorticoids
Androgens
Estrogens
Progesterone

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

X = 5
Y = corticosteroids
Z = sex steroids

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

X = Y = cholesterol (all steroid hormones are)

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

Hyperpigmentation

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

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

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

X = cholesterol
Y = pregnenolone
Z = desmolase

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

Mitochondria;

X = IMM

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StAR is crucial for:

Cholesterol entry into mitochondria

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

True

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

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

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

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

Cytoplasm

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

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

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

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

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

X = 17-alpha-hydroxyprogesterone
Y = pregnenolone

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

3-beta-hydroxy steroid DH (progesterone)

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

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

X = 11-deoxycortisol
Y = 21-alpha-hydroxylase

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

11-deoxycortisol

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

X = Cortisol
Y = 11-beta-hydroxylase

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

X = androgen

17-alpha-hydroxypregnenolone
DHEA

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

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

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

X = Androstenedione
Y = 17-beta-hydroxy steroid DH

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

X = androstenedione
Y = testosterone
Z = aromatase

Estrone

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

X = aromatase
Y = estradiol

(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?

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

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

False

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

False - at progesterone step

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

``` X = 11-deoxycorticosterone Y = 21-alpha-hydroxylase ```

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

``` X = corticosterone Y = 11-beta-hydroxylase ```

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

``` X = Y = aldosterone Z = aldosterone synthase ```

Synthesis of aldosterone occurs in which gland?

Zona glomerulosa of adrenal cortex

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

X = testes Zona reticularis of adrenal cortex

Cortisol synthesis occurs in which gland?

Zona fasciculata of adrenal cortex

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

``` X = cortisol Y = Adrenocorticotropic hormone Z = anterior pituitary gland ```

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?

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

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).

``` Delta-5; Hydroxylation; X = pregnenolone Lyase; Y = 17-alpha-hydroxypregnenolone ```

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

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

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

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

T/F: Estrogens are made from androgens.

True

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

``` X = cytoplasm Y = HSP90 ```

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

``` X = estradiol Y = HSP90 Z = nucleus ``` Monomer (dimerizes inside nucleus)

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

X = ERE (esterogen response element) No

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

Antagonist; | X = Androgen

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

Antagonist; | X = Progesterone

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

1. Edema 2. Hypokalemia 3. CHF, HT

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

X = 3-beta-hydroxy steroid DH | Female

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?

X = 17-alpha-hydroxylase Female; Over-production; Na/fluid retention and HT

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

X = 21-alpha-hydroxylase | Masculinization of external F genitalia and early virilization in M

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?

X = 11-beta-hydroxylase; Masculinization of external F genitalia and early virilization in M; Deoxycorticosterone (fluid retention)

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

1. 17-alpha-hydroxylase | 2. 11-beta-hydroxylase

Deficiency in which steroid hormone synthesis enzymes is most common?

21-alpha-hydroxylase (over 90%)

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

X = some types of breast cancer Binds estrogen receptor (prevents estrogen from binding and inducing conformational change); prevents its association with co-activators

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

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

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

Inhibiting aromatase (preventing estrogen production in first place)