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U6 Physiology > Adrenal Gland - RM > Flashcards

Adrenal Gland - RM Flashcards

1
Q

What is adrenal cortex derived from?

A

mesoderm

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2
Q

What are the three layers of adrenal cortex and what do they secrete?

A

zona glomerulosa-mineralocorticoids
zona fasiculata- glucocorticoids, some androgens
zona reticularis- androgens, some glucocorticoids

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3
Q

What is the adrenal medulla derived from?

A

neural crest

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4
Q

What does adrenal medulla secrete?

A

norepinephrine, epinephrine, DOPA, dopamine

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5
Q

Is the adrenal cortex or adrenal medulla essential for life?

A

adrenal cortex

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6
Q

What is the common precursor of all adrenal cortical hormones? Where does it come from?

A

cholesterol, from LDL in blood or de novo synthesis

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7
Q

What is the rate limiting step in cortical hormone synthesis? What enzyme catalyzes it?

A

conversion of cholesterol to pregnenolone by P450 side chain cleavage enzyme/20,22-desmolase (same enzyme, different names)

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8
Q

What enzyme is not part of the cyt.P450 oxidase complex?

A

3 beta hydroxysteroid dehydrogenase

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9
Q

What does 3beta hydroxysteroid dehydrogenase catalyze?

A

conversion of prenenolone to progesterone

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10
Q

What does 21 alpha hydroxylase catalyze? Where does this occur?

A

conversion of progesterone to 11-deoxycorticosterone

-in SER

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11
Q

What does 11 beta hydroxylase catalyze? Where does this occur?

A

conversion of 11-deoxycorticosterone to corticosterone

-in mitochondria

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12
Q

What oxidizes corticosterone to aldosterone?

A

aldosterone synthase

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13
Q

What synthesizes cortisol?

A

17 alpha hydroxylase

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14
Q

Because of its lack of substrate specificity, what does 17 alpha hydroxylase act on?

A

-acts on corticosterone, pregnenolone, and progesterone

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15
Q

What does 17,20-desmolase do?

A

generates DHEA and androstenedione (androgens)

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16
Q

How are 17 alpha hydroxylase and 17,20 desmolase related?

A

same enzyme but two different catalytic sites

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17
Q

Why can’t adrenal cortex make testosterone?

A

there is no 17 ketyl reductase to convert androstendione to testosterone

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18
Q

How is testosterone produced outside of the testes?

A

peripheral tissue has small amounts of 17 ketyl reductase in adipose tissue that can act on androstendione

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19
Q

Why is aldosterone the only thing produced in zona glomerulosa?

A
  • no 17 alpha hydroxylase expression so can’t produce cortisol or androgens
  • has aldosterone synthase
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20
Q

What does aldosterone do?

A

increases transcription of Na/K pump and expression of apical Na channels to increase Na reabsorption and K secretion to reabsorb water

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21
Q

Why isn’t aldosterone produced in zona fasiculata or reticularis?

A

no aldosterone synthase

22
Q

How is cortisol transported in plasma?

A

90% bound to cortisol binding protein (CBP/transcortin)
7% bound to albumin
3% free

23
Q

What is DHEA associated with?

A

aging, highest in 20s and declines after

24
Q

How does cortisol effect its changes?

A

free cortisol enters target cell by diffusion, binds cytosolic receptor, causes it to dissociate from heat shock proteins, transports to the nucleus, binds hormone response, modulates transcription

25
Q

Are steroid hormones stored?

A

No, once synthesized, they are secreted into blood

26
Q

How is cortisol release regulated?

A

feedback inhibition by cortisol on CRH and ACTH

  • CRH release inhibited, decreased CRH mRNA and peptide levels
  • ACTH release inhibited and transcription of POMC gene inhibited (from which ACTh is formed)
27
Q

What are the metabolic effects of cortisol?

A
  • stimulates gluconeogenesis in liver
  • enhances protein breakdown in muscle to provide amino acids for gluconeogenesis
  • stimulates lipolysis as alternate fuel for glucose
  • decreases osteoblastic activity and interferes with Ca absorption from gut
  • inhibits glucose transporters to block glucose uptake (except in brain)
28
Q

Why doesn’t cortisol inhibit glucose uptake in brain?

A

glut3 receptor doesnt respond to cortisol

29
Q

What are the antiinflammatory effects of cortisol?

A
  • inhibits production of cytokines and chemoattractant molecules
  • stabilize lysosomal enzymes
  • contributes to vasoconstriction and decreased capillary permeability
30
Q

What are the immunosuppressive effects of cortisol?

A
  • decrease lymphocyte proliferation
  • inhibits hypersensitivity reactions (esp. cell mediated)
  • inhibits expression of interleukins (esp IL-2) and IL receptors and Fc receptors on macrophages
31
Q

What cortisol analog has no mineralcorticoid activity? What is its glucocorticoid potency?

A

dexamethasone

25-80x glucocorticoid potency

32
Q

What is the intracellular signaling pathway of CRH? What does prolonged CRH exposure cause?

A
  • binds GPCR CRH receptor to increase adenylyl cyclase, cAMP, PKA, intracellular calcium, and exocytosis of ACTH in vesicles
  • prolonged exposure causes ACTH synthesis in corticotrophs
33
Q

What is the intracellular signaling pathway of ACTH?

A
  • binds melanocortin 2 receptor, increases adenylyl cyclase, cAMP, PKA, P450 side chain cleavage enzyme/20,22 desmolase
  • activates and increases synthesis of cortisol
34
Q

Why is ACTH the most important regulator of cortisol?

A

stimulates rate limiting step enzyme of cortisol synthesis

35
Q

What acts as a trophic factor for adrenal cortex?

A

ACTH

36
Q

What does the POMC gene code for in anterior pituitary?

A

ACTH, beta-lipotropin

37
Q

What does POMC gene code for in intermediate pituitary lobe in fetuses and pregnancy?

A

alpha-MSH, beta-endorphin

38
Q

Why does cortisol have diurnal (daily) variation?

A

info about light/dark cycle conveyed to hypothalamus which regulates pulsatile secretion of CRH and ACTH

39
Q

When are levels of cortisol highest? What do peaks follow pulses of?

A

cortisol highest in the early morning, rhythmic secretion of ACTH before each peak

40
Q

What is the most common form of congential adrenal hyperplasia?

A

21 alpha hydroxylase deficiency

41
Q

What does 21 alpha hydroxylase deficiency present with?

A

Decreased cortisol
-hypoglycemia, increase ACTh production–>adrenal hyperplasia (negative feed from cortisol is gone)
Decreased aldosterone
-loss of salt, hypotension, dehydration
Increased androgen secretion
-virilization in males, ambigious genitals in female

42
Q

How is 21 alpha hydroxylase deficiency diagnosed?

A

elevation of 17 hydroxyprogesterone before and after ACTH stimulation

43
Q

How is 21 alpha hydroxylase deficiency treated with hormone replacement therapy?

A

analogs of cortisol (prednisolone or dexamethasone) to reduce ACTH, adrenal hyperplasia and excess androgens
-mineralcorticoids replaced by fludrocortisone

44
Q

What does 17 alpha hydroxylase deficiency present with?

A
  • reduced cortisol and androgen synthesis
  • increased aldosterone–>causes hypertension and hypokalemia
  • reduced estrogen synthesis
  • increased corticosterone (weak glucocorticoid), which mitigates adrenal insufficiency so no hypoglycemia
45
Q

What is Cushing’s syndrome?

A

hyperadrenal function
-excessive levels of cortisol caused by prolonged immunosuppression drugs, adrenal tumors, ACTH secreting tumors, ectopic ACTH syndromes

46
Q

What is Cushing’s disease?

A

hypercortisolism secondary to ACTH excess from pituitary adenoma

47
Q

What are the symptoms of Cushing’s syndrome?

A

moon face, increased fat around neck, thinning of arms (change in body fat distribution), osteopenia, increased frequency and severity of infections, muscle wasting, hypokalemia, hypertension

48
Q

How do you diagnose Cushing’s disease?

A
  • dexamethasone suppression test
  • analog of cortisol so should lower ACTH by feedback inhibition
  • won’t see that in ACTH producing tumor though
49
Q

What is Addison’s disease?

A

hypoadrenal function

  • failure to produce enough cortisol–>hypoglycemia, weakness, weight loss, poor tolerance to stress
  • lack of aldosterone–>hypotension, hyperkalemia
50
Q

How do you diagnose Addison’s disease?

A
  1. test cortisol levels
  2. ACTH stimulation test–won’t show increased cortisol
  3. CRH stimulation–ACTh should increase but cortisol won’t
51
Q

How will primary and secondary adrenal insufficiency present differently in CRH stimulation test?

A

primary- high ACTH, low cortisol

secondary- low cortisol, but absent or delayed ACTH response

U6 Physiology (13 decks)

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