Steroids Flashcards

1
Q

What are the 5 classes of steroid hormones

A
  1. Progestagens (C21)
  2. Glucocorticoids (C21)
  3. Mineralocorticoids (C21)
  4. Androgens (C19)
  5. Estrogens (C18)
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2
Q

What is the effect of angiotensin II on the adrenal gland

A

Stimulates the adrenal gland zona glomulerosa to produce aldosterone

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3
Q

What is the effect of ACTH on the adrenal gland?

A

Stimulates the release of cortisol from the zona fasciulata and androgens from the zona reticularis

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4
Q

What kind of receptor does angiotensin II act on

A

G-protein coupled receptor that activates phospholipase C, which converts PIP2 to DAG And IP3. DAG stimulates PKC and IP3 increases Ca2+ release from the ER

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5
Q

What kind of receptor does ACTH/FSH/LH act on

A

G-protein coupled receptor that activates adenylyl cyclase (leading to eventual activation of PKA)

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6
Q

What does this mean to you: SALT, SUGAR, SEX

A

Divisions of the adrenal gland, from outside to inside: 1. SALT: Zona glomerulosa produces aldosterone, “salt steroid” that controls water and electrolyte balance

  1. SUGAR: Zona fasciculata produces cortisol – “sugar steroid” that affects fuel metabolism and immune response
  2. SEX: Zona reticularis produces androgens – “sex steroids” that control development of male sexual traits
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7
Q

What are 3 things that occur when you don’t have enough glucocorticoids?

A
  1. Hypoglycemia: because cortisol usually inhibits insulin and stimulates glucagon.
  2. Weakness/fatigue: due to #1 and lack of normal gluconeogenic pathway
  3. Infections: natural control of inflammation gone
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8
Q

How does aldosterone help you maintain BP? What stimulates its release?

A

It increases Na+ (and its buddy H2O) reuptake and excretion of K+ in the distal tubules of the kidney, increasing blood volume and cardiac output. Its release it stimulated by angiotensin II, which senses low blood Na+ and high blood K+

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9
Q

What is the main mineralocorticoid?

A

Aldosterone

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10
Q

What does testosterone do? I know, its a soft ball. You got it

A
  1. Anabolic effects: muslce mass and bone growth
  2. Androgenic effects: 2’ sexual characteristics in males during puberty
  3. Promotes spermatogonia differentiation
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11
Q

Where is progesterone made, what does it do and what stimulates its release?

A
  1. Made in corpus luteum and placenta
  2. Prepares uterine lining during ovulation, maintains pregnancy
  3. Stimulated by FSH
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12
Q

What are 3 types of estrogens and what is their significance? Rate their potencies

A
  1. Estrodiol (E2): #1 in ovaries
  2. Estriol (E3): made in placenta
  3. Estrone (E1): major source of estrogens in post-menopausla women. Made in adipose and ovary and can serve as reservoir for estradiol

Potency: Estradiol>Esterone>Estriol

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13
Q

What is the precursor for ALL steroid hormones

A

Cholesterol (C27)

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14
Q

Where does the cholesterol that fuels all steroid synthesis come from?

A
  1. De novo synthesis from acetyl-coA in cytoplasm and ER
  2. Cholesterol ester droplets
  3. LDL
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15
Q

What enzyme catalyzes the rate limiting step in steroid synthesis? What is the product of this reaction?

A

Rate limiting enzyme: 20,22 desmolase aka side-chain cleaving enzyme

Reaction: cholesterol–> pregnenolone

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16
Q

What is the precursor for mineralocorticoid/glucocorticoid synthesis? What about sex hormone synthesis?

A

Mineralocorticoid/glucocorticoid: progesterone

Sex hormone: androstenedione

17
Q

Describe testosterone synthesis. Ugh these questions are the worrrrst

A
  1. Cholesterol (C27) to pregnenolone (C21)
  2. Pregnenolone (C21) to DHEA (C19) by two different P450 enzyme reactions that replace the C17 aldehyde with a ketone, making it less active. Occurs in adrenals, ovaries, testes
  3. DHEA to androstenedione (C19). Ketone at C3
  4. Androstenedione to testosterone (alcohol at p17)
18
Q

How is testosterone converted to estradiol?

A
  1. The A ring is aromatized and demethylated
  2. The ketone on C3 is converted to an alcohol (estradiOL is an alcohOL)
19
Q

How is dihydrotestosterone (DHT) formed?

A

5a reductase can produce a more potent testosterone called dihydrotestosterone (DHT), which occurs in target tissues

20
Q

How is estrone formed?

A
  1. Cholesterol (C27) to pregnenolone (C21)
  2. Pregnenolone (C21) to DHEA (C19) by two different P450 enzyme reactions that replace the C17 aldehyde with a ketone, making it less active. Occurs in adrenals, ovaries, testes
  3. DHEA to androstenedione (C19). Ketone at C3
  4. The A ring is aromatized and demethylated, and the C3 ketone is converted to an alcohol (still have ketone at C17 so estrONE is still a ketONE)
21
Q

How is Aldosterone formed?

A
  1. Cholesterol (C27) to pregnenolone (C21)
  2. Pregnenolone to progesterone (C21)
  3. Progesterone to aldosterone through a series of P450 reactions that put an ALDehyde on C13
22
Q

How is cortisol formed?

A
  1. Cholesterol (C27) to pregnenolone (C21)
  2. Pregnenolone to progesterone (C21)
  3. Progesterone to cortisol through 2 P450 enzyme reactions that puts alcohols on C11 and C17.
23
Q

What is congenital adrenal hyperplasia and what is the most common form?

A

An autosomal recessive deficiency of steroid biosynthetic enzymes. Most common deficiency is CYP21.

24
Q

What changes in steroid hormone levels will you see in CYP21 deficiency

A
  1. Increased progesterone (can’t convert to aldosterone or cortisol)
  2. Decreased Aldosterone
  3. Decreased Cortisol
  4. Increased androgens (all the pregnenalone is converted to DHEA)
25
Q

What changes in steroid hormone levels will you see in CYP11β1 deficiency?

A
  1. Increased DOC (an intermediate in the aldosterone synthesis pathway).
  2. Over-activation of MC receptors by DOC causes hypertension (vasoconstriction)
  3. Decreased cortisol levels cause more ACTH release which increases DOC levels more
  4. Increase androgens
26
Q

What changes in steroid hormone levels will you see in CYP17 deficiency?

A
  1. Decreased cortisol
  2. Increase aldosterone (more progesterone converted to aldosterone)
  3. Increased DOC (same as #2) (hypertension)
  4. Increased ACTH
27
Q

What is a good way to suppress ACTH production and treat CAH?

A

Prednisone