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ER Week 2 > Adrenal Physiology > Flashcards

Adrenal Physiology Flashcards

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1
Q

What hormone is released by the hypothalamus to activate the adrenal axis?

A

corticotropin releasing hormone (CRH)

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2
Q

Where are the cells have have the receptor for CRH (CRHR1)?

A

anterior pituitary corticotrophs

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3
Q

What kind of receptor of the CRFR1?

A

a Gs GPCR with adenylate cyclase activity

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4
Q

What types of mediators will promote release of CRH?

A

proinflammatory cytokines and chronic stress

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5
Q

What is the preprohormone that is synthesized to make ACTH?

A

pro-opiomelanocortin (POMC)

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6
Q

What are the two other products of POMC?

A

melanostimulating hormone and lipotropin

note that other tissues can further break down ACTH and lipotropin into other types of MSH and some other things

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7
Q

What cells synthesize POMC?

A

the anterior pituitary corticotrophs

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8
Q

What receptor does ACTH prefer to bind to? Where?

A

the melanocortin-2 receptor in adrenal cortical cells

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9
Q

What type of receptor is the melanocortin 2 receptor?

A

Gs-alpha protein, which elevates cAMP to initiate a signal transduction cascade

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10
Q

What does ACTH binding to MC2 receptor do?

A

it rapidly promotes side-chain cleavage enzyme synthesis in the adrenal cortex

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11
Q

Why is this side-chain cleavage enzyme so important?

A

It converts cholesterol to pregnenolone, which is the first and rate-limiting step in all adrenal steroid synthesis

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12
Q

What receptor is the primary melanocortin receptor in the skin? What does it regulate?

A

MC1 receptor

it regulates pigmentation

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13
Q

What does MC1-R prefer to bind - ACTH or MSH?

A

It prefers most MSH isoforms, but ACTH at high levels can also bind to it

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14
Q

So what are the two ways that excessive POMC levels can stimulate hyperpigmentaiton?

A
  1. excess POMC will make excess MSH

2. the excess PMC will make ACTH, which can also activate MC1 at high concentrations

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15
Q

Where is MC3-R expressed?

A

the brain

regulates food intake and energy homeostasis

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16
Q

Where is MC4-R expressed?

A

central nervous system (mainly hypothalamus)
GI tract (it’s the primary melanocortin receptor for regulating food intake)
Placenta

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17
Q

Where is MC5-R expressed?

A

adrenals, skin, stomach, lung and spleen

involved in sebum preduction

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18
Q

What is the primary active glucocorticoid?

A

cortisol

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19
Q

What do the glucocrticoids do in terms of glucose?

A
  1. mobilizes amino acids from protein for the liver to use i gluconeogenesis
  2. so raises blood glucose
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20
Q

What receptor does cortisol prefer to bind to?

A

the glucocorticoid receptor

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21
Q

What is the primary mineralocorticoid?

A

aldosterone

22
Q

What are the three main sex steroids produced in the adrenals?

A

dehydroepiandrosterone (DHEA)
androstenedione
testosterone

only a very minor site for estrogen synthesis

23
Q

What percentage of cortisol is free in the blood? What binds the bound stuff?

A

10% circulates free

of the 90% that’s bound, 60% is bound to corticotropin binding globulin (transcortin), and 30% is bound to albumin

24
Q

What is the half life for the glucocorticoids like cortisol?

A

70-90 minutes (longer than the peptide hormones)

25
Q

What are two situtations where the total cortisol hormone level is varied by the amount of transcorting that’s produced?

A

Transcortin is decreased in liver cirrhosis or elevated cortisol

Transcortin is increased in pregnancy and other times of high estrogen

26
Q

The glucocorticoid receptors belong to what receptor family?

A

the nuclear receptor superfamily

27
Q

What hormone has the highest affinity and potency for the glucocorticoid receptors?

A

cortisol

other glucocorticoids will bind but have less affinity and potency

28
Q

What tissues are the mineralocorticoid receptor located?

A

kidney, colon, sweat glands, heart, hippocampus, brown adipose

29
Q

The mineralocorticoid receptor has about equal affinity for what two hormones?

A

aldosterone and cortisol

30
Q

So if it has equal affinity for both, how do tissues make sure to only respond to the aldosterone - like the kidney?

A

The kidney will have enzymes that inactivate the cortisol (convert to cortisone) such that the aldosterone can act on the MC receptor

31
Q

What enzyme will do intracellular conversion of active glucocorticoid ot inactive steroid?

A

11 beta hydroxylase type 2

32
Q

WHat enzymes will do intracellular conversion of inactive steroids to active steroids?

A

11 beta hydroxylase type 1

33
Q

How is it determined whether steroid hormone will be enzymatically activated or inactivated?

A

the tissue location of 11 beta hydroxylase type 1 and type 2 will define the net result in that particular tissue

34
Q

True or false: most synthetic glucocorticoids are already in the active form and thus do not require any of the hydoxylase activity.

A

false - many needs to be reduced to their 11beta hydroxy derivatives to attain biological activity

35
Q

Most metabolism of glucocorticoids occurs in what organ?

A

the liver - will be conjugated to form tetrahydrocortisone and tetrahydrocortisol glucuronid eof sulfate

these are then excreted by the kidneys (what we measure in 24 h urine collections)

36
Q

What will happen to urinary nitrogen excretion if glucocorticoids are on board?

A

increase - because they promote proteolysis to free up AA for gluconeogenesis in the liver

so you get muscular atrophy

37
Q

Again, what is the first and rate limiting step in adrenal hormone synthesis?

A

side chain cleavage hormone converts cholesterol to pregnenolone

38
Q

What is the hydroxylase that promtoes conversion of pregnenolone to the sex hormones?

So where in the cortex will this enzyme have the highest activity?

A

17alpha hydroxylase (or CYP17)

highest in the zona reticularis (the inner layer), while the zona glomerulosa (outer layer) has none

39
Q

What is the most common adrenal enzyme deficiency? second most common?

A

21alpha hydroxylase is the most common

11beta hydoxylase is the second most comon

40
Q

What syndromes do 21 hydroxylase deficiency and 11beta hydrosylase deficiency cause?

A

congenital adrenal hyperplasia

41
Q

So we use pregnenolong to make progesteron derivatives which are then used to make both cortisol and aldosterone. Which works in thei pathway first - 21 or 11 hydroxylase?

A

21 works first

42
Q

What does 21 turn the progesterone into?

A

11-deoxycortisol

43
Q

True or false: 11-deoxycortisol is inactive.

A

false

it does have some mineralocorticoid effects

44
Q

What does the 11 hydroxylase do to the 11 deoxycortisol?

A

converts it to cortisol

45
Q

So if you have a 21 hydroxylase deficiency, what will the level of cortisol be? aldosterone? sex hormones?

A

decreased cortisol and decreased aldosterone (can’t even get to the 11-deosycortisol)

you have an increase in ACTH, enzymes, precurors, and androgen synthesis

46
Q

So what are the symptoms of a 21 hydroxylase deficiency?

A

virilization and hypotension

47
Q

How about if you have an 11 hydroxylase deiciency - what will the hormone levels be like?

A

decreased cortisol, corticosteron and aldosteron

however, you get increased deoxycorticosteroid and 11 deoxycortisol, which have mineralocorticoid activity!!!

increased ACTH and sex hormones as well

48
Q

So what are the symptoms of an 11 hydroxylase defiiency?

A

virilization and HYPERTENSION (because of the excess mineralocorticoid activity of deoxycorticosterone and 11 doexycortisol

49
Q

True or false: aldosterone feeds back to inhibit the axis like cortisol does?

A

false

50
Q

Normal ACTH is tonic to aldosterone production, but at high levels it is stimulatory. What else is stimulatory for aldosterone production?

A

angiotensin II

ER Week 2 (10 decks)

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