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ENRE > Steroid Biosynthesis > Flashcards

Steroid Biosynthesis Flashcards

1
Q

How do you make steroid hormones from cholesterol?

A

cholesterol – desmolase –> pregnenolone –> progesterone

then either corticosteroids = aldosterone and cortisol

or sex hormones = testosterone and estradiol

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2
Q

How is progesterone related to pregnancy?

A

regulates voltage-gated Ca channels on spermatozoa

prepares uterus for implantation

causes smooth muscle relaxation

decreases maternal immune response

decrease in progesterone precedes menstruation, labor, and lactation

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3
Q

How are glucocorticoids linked to infant respiratory distress syndrome?

A

in normal-term babies: burst of glucocorticoids during delivery –> surfactant, normal lung expansion

in preterm babies, this is lost –> give mothers glucocorticoids to prevent

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4
Q

What is the significance of cortisone?

A

target tissues of mineralcorticoids have receptors w/ affinity for both gluco and mineralcorticoids

avoid excessive Na and H2O retention from cortisol by metabolizing cortisol – 11Beta-hydroxysteroid dehydrogenase –> cortisone = lower affinity

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5
Q

Why can licorice cause hypertension?

A

natural licorice has isoflavones = inhibitors of 11beta-dehydrogenase

cant convert cortisol to cortisone –> excess Na and H2O retention –> HTN

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6
Q

How is testosterone metabolized for signalling?

A

Testosterone – 5alpha-reductase –> DHT = higher affinity for T receptor, potentiates T effects

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7
Q

What does finasteride do?

A

inhibits 5alpha-reductase that converts T to DHT

used to treat male pattern baldness and benign prostate hyperplasia

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8
Q

What is CBG?

A

human corticosteroid-binding globulin

involved in the transport and release of the majority of plasma glucocorticoid hormones and also progesterone

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9
Q

What is SHBG?

A

sex hormone binding globuline

transports sex steroids (T, DHT, and estradiol)

only partially saturated in women

binding sites are mostly occupied by testosterone in men

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10
Q

How do glucocorticoids suppress the immune system?

A

induce i-KBA inhibitory protein –> sequestors NF-KB (needed for cytokines)

also promotes T cell apoptosis

decreased IL-2 and receptor –> inhibition of clonal expansion of B cells

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11
Q

What is significant about the CYP3A4 enzyme?

A

nearly 60% of all drugs are metabolized by it in the liver

have to consider interactions w/ this enzyme and how it might affect other drugs a pt is taking

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12
Q

What is significant about desmolase (cyp11A1)?

A

catalyzes cholesterol –> pregnenolone = 1st and rate limiting step of steroid synthesis

Positively regulated by ACTH

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13
Q

How does cortisol affect ACTH release?

A

negative feedback to hypothalamus and Ant pit = inhibits release

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14
Q

What are the short-term actions of ACTH?

A

stimulates lipoprotein uptake into cortical cells

increases bioavailability of cholesterol in adrenal cortex

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15
Q

What are the long-term actions of ACTH (hours)?

A

stimulation of transcription of the genes coding for steroidogenic enzymes

P450scc

11Beta-hydroxylase

associated e- transfer proteins

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16
Q

What type of receptor does ACTH bind?

A

Gs

17
Q

What can occur in a tumor that secretes cortisol?

A

PKA that is normally signaled by ACTH binding Gs is always active –> get too much cortisol and cell proliferation

18
Q

What in general, does cortisol do?

A

Binds and activates glucocorticoid receptor (GR)

increases gluconeogenesis and BP

anti-inflammatory

19
Q

What, in general, does aldosterone do?

A

binds and activates mineralcorticoid receptor (MR)

increases Na and H2O retention

raises BP

20
Q

What receptor does testosterone bind?

A

androgen receptor (AR)

21
Q

What do women with congenital adrenal hyperplasia present with?

A

hirsuitism

general oligomenorrhea = infrequent or very light menstruation

infertility

22
Q

What are the 3 main enzyme deficiencies that can lead to congenital adrenal hyperplasia?

A

21alpha-hydroxylase = 95%

11beta hydroxylase = 5%

17alpha-hydroxylase = unknown %

23
Q

What occurs biochemically in CAH due to mutant 11-beta-hydroxylase?

A

cant do 11-deoxycorticosterone –> corticosterone (don’t make aldosterone)

can’t do 11-deoxycortisol –> cortisol

get buildup of precursors –> excess androgen production

increased DOC –> has mineralcorticoid activity –> high BP

low K+ (bc of water retention)

24
Q

What occurs to cause hypertension in CAH w/ mutant 11-beta-hydroxylase?

A

get buildup of 11-deoxycortisol –> can bind to MR w/ high affinity –> HTN

25
Q

What do you see clinically in CAH due to mutant 11-beta-hydroxylase?

A

masculinization

virilization

high BP

low potassium

26
Q

What occurs biochemically in CAH due to mutant 21-alpha-hydroxylase?

A

can’t do progesterone –> 11-DOC (can’t make aldosterone)

can’t do 17-alpha-hydroxyprogesterone –> 11-DOC (can’t make cortisol)

get buildup of precursors –> shunted to androgen production

27
Q

What do you see clinically in CAH due to mutant 21-alpha-hydroxylase?

A

low aldosterone and cortisol

increased androgens –> masculinization

low BP

high K

28
Q

What occurs in CAH due to mutant 17-alpha-hydroxylase?

A

can’t do progesterone –> 17-alpha-hydroxyprogesterone –> can’t make cortisol

buildup of progesterone –> shifted to aldosterone synthesis

29
Q

What do you see clinically in CAH due to mutant 17-alpha-hydroxylase?

A

high aldosterone

low cortisol

decreased androgens –> lack of secondary sex characteristics

high BP

low serum K

30
Q

where are CBG and SHBG made?

A

in the liver

31
Q

What do FSH and LH do in females?

A

promote production of estradiola and progesterone

32
Q

What do FSH and LH do in men?

A

FSH –> stimulates inhibin production

LG –> stimulates testosterone production

33
Q

What enzyme catalyzes Vit D3 –> 25 OH Vit D?

Where does this occur?

A

25-hydroxylase

in the liver

34
Q

What enzyme catalyzes 25-OH Vit D –> 1,25 Vit D (calcitriol)?

Where does this occur?

A

1-alpha hydroxylase

in the kidneys

35
Q

What occurs with an excess of vitamin D?

A

elevated blood and urine Ca

dazed, loss of apepetite

ENRE (21 decks)

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