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Medical Physiology > Adrenal Cortex: Mineralocorticoids > Flashcards

Adrenal Cortex: Mineralocorticoids Flashcards

1
Q

what releases CRH

A

paraventricular nuclei

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2
Q

what innervation does the adrenal gland have

A

only sympathetic innervation

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3
Q

what products are made from POMC

A

ACTH, gamma lipotropin, beta endorphin, MSH

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4
Q

what stimulates ACTH

A
  1. decreased blood cortisol
  2. sleep-wake transition
  3. stress, hypoglycemia, surgery, trauma)
  4. psychiatric disorders
  5. ADH (aldosterone)
  6. alpha adrenergic agonists
  7. beta adrenergic antagonists
  8. serotonin
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5
Q

what inhibits ACTH

A
  1. increased blood cortisol levels
  2. opioids
  3. somatostatin
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6
Q

what occurs once ACTH binds to receptor

A

cAMP increases

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7
Q

what causes the immediate response to ACTH

A

steroidogensis activator peptide

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8
Q

what is the immediate response to ACTH

A
  1. increased cholesterol esterase
  2. decreased cholesterol ester synthase
  3. increased cholesterol transport into mitochondria
  4. increased cholesterol binding to P450
  5. increased pregnenolone production
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9
Q

what causes the subsequent response to ACTH

A

steroid hormone inducing protein

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10
Q

what is the subsequent response to ACTH

A

increased gene transcription of P450scc, c17, c11 and LCL receptor (cholesterol capturing to transport into cells)

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11
Q

what causes the long term response to ACTH

A

IGF-2

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12
Q

what is the long term response to ACTH

A
  1. increased size and functional complexity of organelles and increased size and number of cells
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13
Q

what turns cholesterol into pregnenolone

A

P450scc

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14
Q

what turns pregnenolone into progesterone

A

3-beta-hydroxysteroid dehydrogenase

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15
Q

what turns pregnenolone and into 17a hydroxypregnenolone

A

17alpha hydroxylase

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16
Q

what turns progesterone into deoxycorticosterone?

A

21-hydroxylase

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17
Q

what turns progesterone into 17a hydroxy progesterone?

A

17a-hydroxylase

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18
Q

what turns 17a hydroxy progesterone into 11-deoxycortisol

A

21 hydroxylase

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19
Q

what turns 17ahydroxypregnenolone into DHEA

A

17.20 lyase

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20
Q

what turns 17a hydroxyprogesterone into androstendione

A

17.20 lyase

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21
Q

what turns deoxycorticosterone into corticosterone

A

11beta hydroxylase

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22
Q

what turns 11 deoxycortisol into cortisol

A

11beta hydroxylase

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23
Q

what turns corticosterone into aldosterone

A

aldosterone synthase

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24
Q

what turns androstenedione into estrone

A

aromatase

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25
Q

what turns androstenedione into testosterone

A

17beta HSD

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26
Q

what turne DHEA into androstenediol

A

17beta HSD

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27
Q

what turns DHEA into androstenedione

A

3beta hydroxysteroid dehydrogenase

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28
Q

what turns testosterone into dihydrotestosterone

A

5a reductase

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29
Q

what turns testosterone into estradiol

30
Q

what is total cholesterol for low heart disease risk

A

less than 200

31
Q

LDL for low heart disease risk

A

less than 130

32
Q

HDL for low heart disease risk

A

more than 60

33
Q

TG for low heart disease risk

A

less than 150

34
Q

what makes glucocorticoids

A

zona fasiculata

35
Q

what makes mineralocorticoids

A

zona glomerulosa

36
Q

what makes the androgens

A

zona reticularis

37
Q

how do LDL particles get into the cell

A

absorbed into the cytoplasm via receptor mediated endocytosis

38
Q

how many carbons on estrogens

39
Q

how many carbons testosterone/androgens

40
Q

what are the 21 carbon steroids

A

progesterone, aldosterone, cortisone

41
Q

where is the OH group on glucocorticoids

42
Q

what if there is an OH group at carbon 17?

A

steroid will be involved in electrolyte activity

43
Q

what if there is an aldehyde (CHO) at carbon 18?

A

steroid is a potent mineralcorticoid

44
Q

what is the most potent naturally occuring mineralcorticoid in humans

A

aldosterone

45
Q

where is aldosterone metabolized

46
Q

what is transcortin?

A

transporter that 17% of aldosterone binds to, also corticosterone, progesterone and some testosterone and estradiol

47
Q

how does aldosterone circulate?

A

17% binds to transcortin

47% is bound to albumin

48
Q

half life of aldosterone

A

20min aka long

49
Q

what promotes aldosterone synthase activity

A

angiotensin II

50
Q

what is the transitional enzyme from mineralocorticoid to glucocorticoid

A

17alpha hydroxylase

51
Q

what is the transitional enzyme from glucocorticoid to androgen

A

17.20 lyase

52
Q

what is the transitional enzyme from androgen to estrogen?

53
Q

what is the transitional enzyme from androgen to DHT?

A

5a reductase

54
Q

describe the steps of aldosterone release

A

cholesterol comes into the plasma membrane via LDL receptor mediated endocytosis–>acetyl coa binds to cholesterol to make vacuole or go into mitochondria–>cholesterol made into 5 pregnenolone by mitochondrial P450 enzymes–>pregnenolone goes to ER to be make into progesterone by 3betahydroxysteroid dehydrogenase –>progesterone made into 11 deoxycorticosterone by 21 hydroxylase –>11 deoxycorticosterone goes back to mito to be made into corticosterone by 11beta hydroxylase and then aldosterone by aldosterone synthase–>freely passes out of the cell

55
Q

what stimulates aldosterone release

A
  1. ACTH
  2. increase K in blood
  3. RAAS
56
Q

what does aldosterone do on the late distal tubule and collecting ducts (principal cells)

A
  1. increases reabsorption of NaCl by increasing ENaC channels
  2. increase K secretion by increasing K channels
57
Q

what does aldosterone do on the late DCT and collecting ducts? (alpha intercalated cells)

A
  1. increase reabsorption of K by increasing H-K ATPase

2. increase secretion of H by increasing H ATPase

58
Q

what does aldosterone do in the kidneys?

A

increase K secretion, Na reabsorption, and H secretion

59
Q

what does binding of aldosterone stimulate

A
  1. production of ENac channels (Na)
  2. production of Na/K ATPase
  3. production of mitochondrial enzymes to man the Na/K ATPase
60
Q

where does aldosterone act

A

DCT and Collecting duct

61
Q

where are the ENaC channels

62
Q

where are the Na/K ATPase

A

basolateral

63
Q

net effect of aldosterone

A

increased urine K and decreased urine Na, decreased plasma K and increased plasma Na
leads to increased ECF and increased BP

64
Q

what is the effect of angiotensin II on adrenal glomerulosa cells

A

binds to Gq triggers PLC–>IP3 binds to SR–>releases Ca
DAG and Ca activate PKC–>P Proteins–>increase cholesterol into the mito–>pregnenolone–>smooth ER–>progesterone–>11deoxycorticosterone–>back to mito–>aldosterone then released

65
Q

what does hypoaldosteronism cause

A

hyperkalemia (little K excretion) — decreased Na and Cl resorption and increased water loss, decrease in ECF, CO and BP – hypovolemic shock. also decreased H and K excretion, acidosis. also causes partial depolarization

66
Q

what does hyperaldosteronism cause

A

hypokalemia (too much K excretion) – muscle weakness bc cell hyperpolarized, increased Na and Cl resorption causes increased plasma osmolarity, thrist, water resorption, intake and increased ECF – increased BP and alkalosis (increases H pumps out)

67
Q

EKG changes with hypokalemia

A
  1. slightly peaked P wave
  2. slightly prolonged PR interval
  3. ST depression
  4. shallow T wave
  5. prominent U wave
68
Q

what pattern occurs with hyperkalemia

A

sine wave pattern, decreased strength of myocardial AP cannot fully depolarize

69
Q

what occurs with acidosis

A

H+ in blood, go into cell, K out of cell–hypokalemia–hyperpolarized RMP, difficult to stimulate, CNS depression, confusion, disorientation, coma

70
Q

what occurs with alkalosis

A

decreased H in blood, H into blood K into cell–>hyperkalemia–>depolarized RMP, nerves overstimulated->spasms, tetany, convulsions, respiratory paralysis

Medical Physiology (21 decks)

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