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(OMS1) GIGU Exam > Lecture 29: Steroid Biosynthesis > Flashcards

Lecture 29: Steroid Biosynthesis Flashcards

1
Q

Why is progesterone important in pregnancy?

A

It regulates voltage Ca2+ channels on spermatozoa, prepares uterus for implantation, causes SM relaxation and decreases maternal immune response

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2
Q

What role do glucocorticoids play on infant respiration?

A

Glucocorticoid surge during delivery to enhance surfactant production

impaired process in premies leading infant respiratory distress syndrome

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3
Q

How do tissues limit Na/H2O retention?

Why does licorice stimulate Na/H2O retention?

A
  • Since glucocorticoids induce Na/H2O retention, the tissues metabolize them to cortisone to block the glucocorticoid receptor and block retention
  • Licorice has isoflavones that inhibit 11B dehydrogenase which turns cortisol to cortisone
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4
Q

What major pathways depend on cholesterol?

A
  1. Vitamin D3 (from 7 dehydrocholesterol)
  2. Steroid hormone synthesis
  3. Steroid degradation
  4. Bile acid biosynthesis
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5
Q

Draw the pathway of steroid hormone biosynthesis in the adrenal cortex

A

Ok

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6
Q

What hormone induces steroid biosynthesis?

A

ACTH (induces conversion of cholesterol to pregnenolone)

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7
Q

What is the rate limiting enzyme of steroid biosynthesis and what is the major mechanism?

A

desmolase (removes 6 carbons from cholesterol and replaces with carbonyl group)

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8
Q

What steroid hormones can be synthesized from pregnenolone?

A

Progesterone, Aldosterone, Cortisol, Testosterone, Estradiol

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9
Q

What proteins transport steroid hormones in the blood and what do they specifically transport?

A

CBG - most glucocorticoids + progesterone

SHBG and albumin - sex hormones (Testosterone, DHT, Estradiol)

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10
Q

Review: Be able to draw the RAAS pathway and the effects of ACE inhibitors and vasopressin

A

Ok

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11
Q

What is the main defect in Adrenal Hyperplasia?

What is the main treatment?

A
  • deficiency in 21 hydroxylase or 11B hydroxylase leading to accumulation of hormone precursors in affected pathway
  • hormone replacement therapy
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12
Q

How do adrenal hyperplasia patients present?

A

hirsutism, general oligomenorrhea (infrequent/light menses), infertility

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13
Q

How would you test a fetus for risk in developing congenital adrenal hyperplasia?

A
  1. Human leukocyte antigen (HLA) haplotype test

2. Presence of excess cortisol precursors in the amniotic fluid

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14
Q

AH due to 21- hydroxylase (Cyp21A2) deficiency

AH due to 11-B hydroxylase (Cyp11B1) deficiency

A
  • leads to accumulation of progesterone and 17-hydroxyprogesterone
  • accumulation of 11 deoxycorticosterone and 11-deoxycortisol (also a mechanism of hyperaldosteronism)
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15
Q

What receptor is important for aldosterone to mediate its effects on target cells in the adrenal gland?

A

Mineralocorticoid receptor (MR) - part of a receptor superfamily that binds steroid hormones in the nucleus

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16
Q

What is Conn Syndrome?

A

excessive secretion of aldosterone > overstimulation of zona glomerulosa > too much Na and water retention = HTN

17
Q

What hormones can also activate MR and cause Na retention (thus high BP)?

A

11 deoxycorticosterone
testosterone
hydrocortisone (cortisol)
cortisone

18
Q

How does 11-B hydroxylase deficiency cause HTN?

A
  • accumulation of 11-deoxycorticosterone and 11-deoxycortisol > both bind the MR receptor like aldosterone > increase HTN
  • basically the products that accumulate have capabilities of mimicking aldosterone effects because they bind the same receptor
19
Q

How do glucocorticoids cause immunosuppression?

A

they induce i-kBa which makes NF-KB inactive

20
Q

Review: Be able to draw the HPA axis

A

Ok

21
Q

What is the mechanism of ACTH?

A

ACTH > binds to ACTH receptors on adrenal cortex cells > Gs > AC > cAMP > PKA > phosphorylation of CREB > cell proliferation and cortisol production in target cell

22
Q

What happens to ACTH signaling in tumor cells?

A

-stimulation of proliferation and cortisol production even without ACTH stimulation > process in constantly turned on

23
Q

What are the short term (within minutes) actions of ACTH?

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

A
  • cholesterol taken to MT where desmolase is

- gene transcription of enzymes needed for aldosterone and cortisol synthesis

24
Q

What is 17,20 lyase (CYP17A1) deficiency?

A

-associated with 17,20 lyase and 17a hydroxylase deficiency > testosterone synthesis pathway blocked > leading to pseudohemaphroditism and adrenal hyperplasia

25
Q

Review: Be able to draw the pathway of Vitamin D synthesis

A

Ok

(OMS1) GIGU Exam (40 decks)

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