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Physiology > Unit 6 - Adrenal and Supradrenal gland > Flashcards

Unit 6 - Adrenal and Supradrenal gland Flashcards

1
Q

what is the adrenal cortex derived from? what does it secrete? what does it mean by “essential”?

A
  • derived from mesoderm
  • secretes glucocorticoids/androgens from zona fasciculata and reticularis, and mineralccorticoids from zona glomerulosa
  • essential b/c total loss of funcction is fatal in 4-14 days
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2
Q

what is adrenal medulla derived from? what does it secrete? is it essential for life?

A
  • derived from neural crest
  • secretes E, NE, dopa, dopamine
  • modified post-ganglionic sympathetic nerve cells
  • total loss is not life-threatening
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3
Q

what is the rate-limiting reaction in steroid hormone synthesis?

A

cholesterol to pregnenolone via 20,22 desmolase (AKA P450 side-chain cleavage enzyme)

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4
Q

how many enzymes in the “steroid hormone forming” pathway are of the P450 family?

A

all of them except cytosolic 3-beta hydroxysteroid dehydrogenase

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5
Q

is there a storage pool of aldosterone? what happens once it’s secreted?

A

no, since it’s a steroid hormone

  • secretion is limited by the rate at which glomerulosa can synthesize the hormone
  • once secreted, 37% are free in the plasma, and the rest weakly binds to CBG and albumin
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6
Q

what is the major action of aldosterone?

A
  • stimulate kidney (distal nephron segments) to reabsorb sodium and water, and enhance potassium secretion
  • -similar actions in colon, salivary glands, and sweat glands
  • increases activity of Na/K pump and expression of apical Na channels
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7
Q

what enzyme does the glomerulosa layer lack that the fasciculata and reticularis have?

A

it doesn’t have 17-alpha-hydroxylase, which is found in the SER of all other adrenal cortex layers
-so once it’s made in the other 2 layers, corticosterone can be moved to mitochondria of glomerulosa to be converted to aldosterone via aldosterone synthase

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8
Q

what enzyme does the fasciculata and reticularis lack that the glomerulosa has?

A

they don’t have aldosterone synthase, but they have 17-alpha-hydroxylase
-they also don’t have 17-keto-dehydrogenase, so androstenedione must be moved to testes to be converted to testosterone

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9
Q

cortisol transport in plasma

A

90% bound to cortisol binding PRO (CBP or transcortin)
7% to albumin
3% is “free”

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10
Q

androgen synthesis in adrenal gland

  • how strong are they?
  • when do they peak?
A

DHEA (dehydroepiandrosterone) and androstenedione are major adrenal androgens

  • less potent than testosterone or dihydrotestosterone, but androstenedione can be converted to testosterone in peripheral tissue
  • peak in 20’s, decline in early 30’s (75 yo has 20% of a 25 yo)
  • -important for maintaining sex drive in females after menopause
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11
Q

how does cortisol work once inside the cell?

A
  1. ‘free” cortisol enters target cell by diffusion
  2. binds to cytoplasmic receptor associated with heat shock proteins
    - cytoplasmic activation creates active GR monomer, which then dimerizes
  3. migrates to nucleus and enters as dimer
  4. modulates gene transcription via GRE
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12
Q

what does cortisol inhibit via feedback inhibition loop?

A

inhibits:

  • anterior pituitary: POMC expression, release of premade ACTH, expression of CRH receptor
  • hypothalamus: decreases mRNA and peptide levels of CRH, and release of premade CRH
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13
Q

what are metabolic effects of cortisol action?

A
  • stimulate gluconeogenesis in liver
  • enhance PRO breakdown in muscle to provide AA substrate for gluconeogenesis
  • stimulate lipolysis in adipose in periphery as alternative to glucose
  • -for some reason, fat is deposited centrally and on face
  • decreases osteoplastic activity in trabecular bone, and interferes with Ca++ absorption in gut
  • decrease GLUT in most tissues except brain to block glucose uptake
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14
Q

what are anti-inflammatory effects of cortisol action?

A
  • inhibits cytokine production
  • inhibits chemo-attractant molecule production
  • stabilizes lysosomal enzymes
  • contributes to vasoconstriction and decreased capillary permeability
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15
Q

what are immunosuppressive and neural effects of cortisol action?

A
  • decreases lymphocyte proliferation
  • inhibits hypersensitivity reactions (especially cell-mediated)
  • -inhibits IL (especially IL-2) and receptor expression
  • emotional instability (receptors are in brain)

immunosuppressive effects usually at high doses

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16
Q

how do glucocorticoid VS mineralocorticoid potency differ?

A

if something has good glucocorticoid potency, it generally has weaker mineralocorticoid potency, and vice versa

17
Q

what is the most important regulator of cortisol?

A

ACTH

18
Q

what does prolonged PKA expression in adrenal cortex cells do?

A

has ACTH-like effects

19
Q

how does CRH bind to receptor?

  • what happens if it binds
  • what happens if it is prolonged/
A

CRH is 41-AA neuropeptide made in paraventricular nucleus of hypothalamus

  • CRHR are GPCR on cell membrane of corticotrophs
  • hormone binding activates signaling thru second messengers for increased [Ca++] and exocytosis of preformed ACTH
  • prolonged CRH receptor activation leads to increased gene transcription and synthesis of ACTH precursor
20
Q

how does ACTH bind to receptor?

-what happens when it binds, and if prolonged?

A

ACTH is 39-AA peptide hormone made by corticotrophs of anterior pituitary

  • made by post-translational processing of preprohormone (POMC)
  • ACTHR is GPCR called melanocortin-2 receptor
  • increased cAMP activates PKA, which phosphorylates many PRO
  • rapid effect is to stimulate rate-limiting step in cortisol formation (20,22 desmolase for cholesterol –> pregnenolone)
  • prolonged increases synthesis of PRO involved in cortisol synthesis
21
Q

how is ACTH processed? in anterior pituitary VS intermediate pituitary?

A

post-translational processing of POMC

  • AP: makes ACTH and beta-LPH (lipotropin)
  • IP: makes alpha-MSH (anoxygenic hormone) and beta-endorphin (among other things; usually done in fetal life and pregnancy)
22
Q

how is cortrisol secretion related to the circadian rhythm?

A

diurnal variation with highest levels in early morning, and lower levels in evening

  • info about light/dark cycle is transmitted from retina to suprachiasmatic nucleus of hypothalamus that controls circadian rhythms of body
  • CRH release is in pulses, causing ACTH in pulses
  • thus, rhythmic ACTH directly controls diurnal variation of cortisol production
23
Q

how is cortisol secretion and stress related?

A

physical, psychological, and biochemical stress enhance CRH secretion, thus enhanced ACTH secretion, thus more cortisol
-this happens in hypoglycemia, which then raises blood glucose levels

24
Q

21-alpha-hydroxylase deficiency symptoms

A

most common form of congenital adrenal hyperplasia (1:7000)

  • decreased aldosterone synthesis
  • -loss of salt, hypotension, dehydration
  • decreased cortisol synthesis
  • -hypoglycemia, adrenal hyperplasia (since increased ACTH due to no negative feedback from cortisol)
  • increased androgen production
  • -ambiguous genitalia in females, virilizing effect in males
25
Q

21-alpha-hydroxylase deficiency diagnosis and treatment

A
  • have elevated 17-hydroxyprogesterone before and after ACTH stimulation test
  • -diagnosis should be confirmed by molecular genetic analysis of CYP21 gene
  • provide glucocorticoids (prednisolone, dexamethasone) to replace cortisol and reduce ACTH (which also reduces hyperplasia and androgen overproduction) and mineralcorticoids (fludrocortisone) to prevent salt-wasting or increased renin
26
Q

17-alpha-hydroxylase deficiency symptoms

A

increased aldosterone synthesis
-HTN, hypokalemia
decreased cortisol synthesis
-hyperplasia of adrenal gland (but no hypoglycemia, because increased corticosterone can provide enough)
decreased androgen synthesis
-sexual infantilism in both, pseudohermaphroditism in males
-deccreased estrogen synthesis in ovary

27
Q

17-alpha-hydroxylase deficiency treatment

A
  • HTN and mineralocorticoid excess treated with glucocorticoid replacement
  • genetic females given estrogen
  • genetic males given surgery or testosterone treatment
28
Q

Cushing syndrome VS disease

A

syndrome: excess cortisol of any etiology
- hypercortisolism or hyperadrenocorticism
disease: only hypercortisolism secondary to excess production of ACTH from pituitary gland adenoma

29
Q

what are some causes of Cushing’s syndrome?

A
  • prolonged use of immunosuppression drugs (prednisone)
  • adrenal tumors
  • things that increase ACTH like pituitary adenomas (Cushing’s disease) or ectopic ACTH syndromes
30
Q

what are symptoms of Cushing’s sydrome?

A
  • change in fat distribution
  • -moon face (b/c cortisol increases fat on face)
  • -upper body obesity
  • -increased fat on neck
  • -skin thinning and fragility
  • florid complexion (red face)
  • thinning of arms and legs (muscle wasting/weakness b/c cortisol increases PRO breakdown)
  • osteopenia (b/c cortisol decreases Ca++ absorption and collagen I)
  • increased frequency and severity of infections (b/c high cortisol has immunosuppressing effects)
  • glucose intolerance
  • hypokalemia and HTN (from high aldosterone)
  • increased facial hair in women (b/c more androgens)
31
Q

how is Cushing’s disease diagnosed? what do the results mean?

A
  • 24 hour urinary or salivary cortisol measurement
  • Dexamethasone (potent synthetic glucocorticoid) suppression test
  • -will act as cortisol and provide negative feedback to pituitary to suppress ACTH action
  • -if high cortisol and low ACTH, is adrenal tumor
  • -if high cortisol and ACTH, is ACTH-producing tumor
  • -if low cortisol and ACTH, is normal
32
Q

how is Cushing’s disease treated?

A
  • surgery to remove adrenal adenoma or ACTH-producing adenoma
  • -if both removed, need hydrocortisone or prednisolone
  • inhibit cortisol synthesis with asketoconazole and metyrapone (limited efficacy)
33
Q

what are symptoms of Addison’s disease?

A

hypoadrenal function (from autoimmune, TB, or infection; usually autoAbs VS 21-hydroxylase)

  • lack of aldosterone causes hypotension, hyperkalemia
  • lack of cortisol causes hypoglycemia, weakness, weight loss, poor tolerance to stress
  • if primary adrenal disease, has increasd ACTH that cause hyperpigmentation of the skin and mucous membranes
34
Q

diagnosis of Addison’s disease

A
  1. determine whether cortisol levels are insufficient (can use dexamethasone test)
  2. ACTH stimulation test: blood and/or urine cortisol are measured before and after synthetic ACTH is given via injection
    - normal response is rise in blood and urine cortisol levels
    - adrenal insufficiency causes poor response or none at all
  3. CRH stimulation test: synthetic CRH is injected intravenously
    - cortisol and ACTH are measured before and after injection
    - if primary adrenal insufficiency, have high ACTH but no cortisol
    - if secondary adrenal insufficiency, have deficient responses of both cortisol and ACTH

Physiology (60 decks)

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