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Physiology Unit 6 > Adrenal Gland > Flashcards

Adrenal Gland Flashcards

1
Q

cortex

A
  • derived from mesoderm
  • secretes glucocorticoids, mineralcorticoids, androgens
  • essential for life- fatal in 4-14 days if lost
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2
Q

medulla

A
  • derived from NCC
  • epi, norepi. dopa, dopamine
  • modified post ganglionic SNS cells
  • total loss is not life threatening
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3
Q

steroid hormone synthesis in adrenal cortex

A
  • starts at cholesterol
  • to pregnenolone via 20,22 desmolase (P450 side chain cleavage enzyme)
  • rate limiting step
  • all enzymes are cyt P450 family except for cytosolic 3-b-hydroxysteroid dehydrogenase
  • then a bunch of other enzymes take it to final products
  • can get to cortisol in two pathways- through corticosterone (3b, 21a, 11b) and then 17a or use 17-a-hydroxylase first and then go through 3-b-hydroxysteroid DH, 21a and 11 b to cortisol
  • see picture please
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4
Q

aldosterone synthesis in zona glomerulosa

A
  • layer lacks 17-a-hydroxylase, but has aldosterone synthase
  • goes from pregnenolone to progesterone with 3-beta- hydroxysteroid DH
  • then to 11 deoxycorticosterone via 21a
  • then to corticosterone via 11b
  • then finally to aldosterone with aldosterone synthase
  • only this layer has that enzyme
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5
Q

aldosterone

A
  • no storage pool of pre-synthesized aldosterone
  • once secreted, 37% remains free in the plasma, rest weakly binds to CBG and albumin
  • stimulates kidney to reabsorb water and socium and enhance potassium secretion
  • increases transcription of Na/K pump and expression of apical sodium channels
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6
Q

synthesis of cortisol and androgens in zona fasciculata and reticularis

A
  • androgens down from pregnenolone or progesterone (3bDH), then down through 17a, 17,20 desmolase
  • cortisol as talked about above (17 first or last, then 3 bDH, 21a, 11b)
  • these layers don’t have aldosterone synthase but have 17a
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7
Q

DHEA

A
  • dehydroepiandroesterone and androstenedione are two adrenal androgens
  • far less potent than testosterone or dihydrotestosterone
  • andro can be converted to testosterone in peripheral tissues
  • DHEA peak production in the 20s, maintains sex drive in females after menopause
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8
Q

cortisol transport in plasma

A
  • 90% bound to cortisol binding protein
  • 7% bound to albumin
  • 3% circulates free
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9
Q

cortisol mechanism of action

A
  • free cortisol enters cell by diffusion
  • binds to cytoplasmic receptor
  • migrates to the nucleus
  • modulates gene transcription
  • cortisol inhibits expression of CRH and ACTH in the corticotrophs of ant pit
  • inhibits transcription of POMC gene
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10
Q

cortisol action

A
  • in muscle increases protein degradation and lipolysis
  • FA used for work, aa used for proteins elsewhere
  • in liver causes increased gluconeogenesis
  • blocks glucose uptake except in the brain
  • anti-IF and suppresses immune system
  • inhibits phospholipase A2, Cox1 and 2, also IL2 and its receptor
  • promotes fat deposition in face and trunk
  • decreases osteoblastic activity in bone and interferes with calcium absorption in gut
  • can cause emotional instability (receptors expressed in the brain)
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11
Q

Anti IF action of cortisol

A
  • inhibits production of cytokines
  • inhibits production of chemo-attractants
  • stabilizes lysosomal enzymes
  • contributes to vasoconstriction and decreased cap perm
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12
Q

immunosuppressive effects of cortisol

A
  • decreases lymphocyte proliferation
  • inhibits hypersensitivity reactions (histamine release from mast cells)
  • inhibits Fc receptor on macrophages
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13
Q

analogs

A
  • if cortisol potency for glucocorticoid and mineralcorticoid taken as 1 (g and m)
  • predisone increases G 3.5-5 and m 0.8
  • prednisolone g4, m 0.8
  • dexamethasone g 25-80, m 0
  • fludrocortisone acetate g 15, m 200
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14
Q

cellular action of CRH

A
  • exhibits effect on corticotroph
  • CRH binds to receptor
  • activates Gs, increases cAMP, activates PKA
  • PKA P a calcium channel, influx causes release of ACTH
  • also causes synthesis of new ACTH
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15
Q

cellular action of ACTH

A
  • ACTH binds to receptor
  • Gs activated, inc cAMP, increase PKA
  • PKA increases synthesis of enzymes and activity of P450SCC- the first enzyme in the cholesterol to hormone synthesis pathway
  • receptor called melanocortin 2
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16
Q

control of cortisol secretion

A
  • long feedback-cortisol from adrenal gland inhibits corticotrophs in ant pit (ACTH) and hypothal (CRH)
  • short feedback ACTH from ant pit inhibits hypothal
  • inhibits POMC gene in ant pit and exocytosis of ACTH
17
Q

CRH and CRH receptor

A
  • CRH from paraventricular nucleus

- receptors are G coupled receptors

18
Q

ACTH

A
  • comes from POMC gene in corticotroph

- trophic for cortex cells

19
Q

POMC

A
  • precursor protein called pro-opiomelanocortin
  • ACTH and alphaMSH come from here
  • beta lipotropin
  • MSH and beta endorphin during pregnancy
20
Q

MSH

A
  • melanin stimulating hormone

- anorexogenic

21
Q

diurnal variation in ACTH

A
  • highest levels in early morning and lower levels in the evening
  • information about light/dark transmitted from retina to suprachiasmatic nucleus of hypothal which controls circadian rhythms of body
  • CRH release from hypothal is in pulses, results in pulsatile secretion of ACTH
22
Q

stress and cortisol secretion

A
  • physical, psychosocial and biochemical stress enhances CRH secretion and enhanced ACTH secretion which result in increased secretion of cortisol
  • hypoglycemia stimulates both, cortisol raises blood glucose levels
23
Q

21-a-hydroxylase deficiency

A
  • can’t get to corticosterone or cortisol
  • salt losing hypotension/dehydration/ hyperkalemia
  • common for genetic disease
  • decreased cortisol and aldosterone, increased ACTH, adrenal hyperplasia, increased androgen production, ambiguous genitalia in females
  • diagnosis by elevation of 17-hydroxyprogesterone before and after ACTH stimulation test
  • molecular analysis of CYP21 gene
24
Q

hormone replacement therapy for 21

A
  • glucocorticoids like prenisolone and dexamethason provied reliable sub
  • reduces ACTH levels
  • reducing ACTH reduces stimulus for hyperplasia
  • mineralcorticoids are replaced in all infants with salt wasting and in most patients with elevated renin levels
  • fludrocortisone only one available
25
Q

consequences of 21a deficiency

A
  • decreased aldosterone- loss of salt, hypotension, dehydration
  • decreased cortisol synthesis-hypoglycemia, increased size of adrenal gland
  • increased androgen synthesis-virilizing effect in males, ambiguous genitalia in females
26
Q

17 a dehydroxylase deficiency

A
  • reduced cortisol and androgens
  • increased corticosterone (weak glucocorticoid, mitigates adrenal insufficiency)
  • increased aldosterone, hypertension and hyperkalemia
  • reduced estrogen synthesis in ovary

-hormone replacement-hypertension and mineralcorticoid excess treated with glucocorticoid replacement, genetic females need estrogen, genetic males need testosterone or surgery

27
Q

clinical features of 17 a deficiency

A
  • hypertension
  • hyperkalemia
  • sexual infantilism in genetic females
  • pseudohermaphroditism and sexual infantilism in genetic males
  • increased size of adrenal gland due to increased corticosterone
28
Q

cushing’s syndrome

A
  • exposed to too much cortisol for long periods of time
  • prolonged use of immunosuppressive drugs (prednisone), adrenal tumors, tumors that increase ACTH (pit), ectopic ACTH syndromes
  • disease is pit tumor that increases ACTH
  • syndrome is excess cortisol of any etiology
29
Q

symptoms of cushings syndrome

A
  • moon face, florid complexion, upper body obesity, rounded face, increased fat around the neck, thinning arms and legs
  • change in body fat distribution
  • skin thinning and fragility
  • osteopenia
  • increased freq and severity of infections
  • muscle wasting and weakness
  • glucose intolerance
  • hypokalemia and hypertension
  • females can grow hair on their face
30
Q

diagnosis of cushing’s

A
  • urinary or salivary cortisol measurement
  • dexamethason suppression test
  • if adrenal tumor, cortisol high and ACTH low
  • if ACTH producing tumor, both will remain high
  • dexa provides negative feedback- should stop ACTH (if pit tumor secreting, it won’t, if adrenal tumor, it will, but cortisol will stay high because adrenal gland messed up)
  • treated with surgery to remove adrenal adenoma or ATCH producing adenoma
  • if both adrenals removed need to replace with hydrocortisone
  • alternatively can inhibit cortisol synthesis, limited efficacy
31
Q

addison’s disease

A
  • hypoadrenal function
  • AI, TB, infection
  • lack of aldosterone results in hypotension, hyperkalemia
  • lack of cortisol results in hypoglycemia, weakness, weight loss and in general a poor tolerance to stress
  • primary adrenal disease and increased ACTH causes hyperpigmentation of skin and mucous membranes
32
Q

diagnosis of addisons

A
  1. determine if levels of cortisol are sufficient
  2. ACTH stim test- blood cortisol, urine cortisol, or both measured before and after a synthetic form of ACTH given by ijection
  3. CRH stimulation test- inject CRH, measure cortisol and ACTH before and after
    - primary adrenal problem have high ACTH but not cortisol, secondary problem have no ACTH or cortisol
    - treat by replacing cortisol and fludrocortisone if necessary for aldosterone

Physiology Unit 6 (12 decks)

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