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PHYSIO II > adrenal > Flashcards

adrenal Flashcards

1
Q

what type of neurons innervate the adrenal glands?

A

sympathetic postganglionic neurons

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2
Q

will the adrenal medulla regenerate?

A

no

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3
Q

will the adrenal cortex regenerate?

A

yes

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4
Q

where is the zona arcuata (aka glomerulosa) located?

A

superficial adrenal cortex

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5
Q

where is the zona fasciculata + reticularis located?

A

deep in the adrenal cortex

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6
Q

where is the site of mineralocorticoid synthesis?

A

zona arcuata

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7
Q

where is the site of glucocorticoid and sex hormone synthesis?

A

zona fasciculata + reticularis

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8
Q

is the zona arcuata responsive to ACTH?

A

no

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9
Q

is the zona fasciculata + reticularis responsive to ACTH?

A

yes

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10
Q

loss of ACTH does what to the adrenal cortex?

A

produces a thin adrenal cortex

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11
Q

T/F: the thickness of the zona glomerulosa is affected by loss of ACTH.

A

false

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12
Q

what is the non-specific response to injury or stress by the adrenal glad?

A

general adaption syndrome

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13
Q

adrenocortical hormones are derivatives of what?

A

cholesterol

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14
Q

what are the two sources of cholesterol?

A
  • synthesis in the adrenal cortex
  • plasma LDL cholesterol
  • (liver)
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15
Q

in the steroid nucleus of adrenocortical hormones, how many carbons are there?

A

C-21s

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16
Q

what enzyme does trilostane block?

A

3,b-dehydrogenase

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17
Q

the synthetic pathway of adrenocortical hormone involves what 2 organelles?

A
  • smooth endoplasmic reticulum

- mitochondria

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18
Q

do mineralocorticoids have a C17 hydroxyl group?

A

no

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19
Q

do glucocorticoids have a C17 hydroxyl group?

A

yes

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20
Q

where are binding proteins synthesized

A

the liver

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21
Q

what does total glucocorticoid in blood depend on?

A
  • secretion rate
  • metabolism
  • amount of carrier protein
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22
Q

how do steroid travel in aqueous solution (blood)?

A

binding protein carry the steroid

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23
Q

what are steroid binding proteins?

A
  • transcortin for cortisol
  • albumin
  • free hormone (no protein)
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24
Q

what is the reltaionshipt of [cortisol] to [aldosterone]?

A

[cortisol] is more than 10 fold higher than [adosterone]

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25
Q

what is the clearance of cortisol?

A

60 min half life

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26
Q

what is the clearance of aldosterone

A

20 min half life

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27
Q

what causes the differences in the half lives of cortisol and aldosterone?

A

the carrier protein

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28
Q

how/where are steroid hormones metabolized?

A
  • reduction in the liver
  • hormones rendered water soluble
  • excreted in urine
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29
Q

what is the importance of mineralcorticoids?

A

they are acutely critical for maintaining life

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30
Q

what is the most important mineralcorticoid?

A

aldosterone

31
Q

what does aldosterone protect against?

A
  • hypotension
  • hyopnatremia
  • potassium intoxication
32
Q

to prevent overstimulation of aldosterone receptor by cortisol, ______ converts ______ to inactive _____.

A
  • 11-b hydroxysteroid dehydrogenase
  • cortisol
  • cortisone
33
Q

can cortisone bind to the mineralcorticoid receptor?

A

no

34
Q

licorice can inhibit what?

leading to what?

A
  • 11-b hydroxysteroid dehydrogenase

- mineralcorticoid excess syndrome

35
Q

what are the physiological actions of aldosterone?

A
  • increases na+ reabsorption from urine, saliva and gastric juices
  • increases angiontensin II production
  • decreases K+ by increasing renal excretion
  • conservation of water follows the conservation of na+
36
Q

what behavior does aldosterone cause together with angiontensin II?

A

drives salt seeking behavior

37
Q

what regulates aldosterone?

A

-plasma K+ will stimulate aldosterone by a DIRECT EFFECT ON adrenal zona glomerulosa
-angiotensin II
-poorly regulated ACTH
suppressed by atrial natriuretic factor
-high plasma Na+ and K+ deficiency decrease aldosterone secretion

38
Q

aldosterone and angiotensin II act upon what?

A

distal tubule and collecting duct

39
Q

what happens when aldosterone and angiotensin II are acting on the kidney?

A
  • resorption of renal sodium and water

- excretion of potassium

40
Q

where is renal renin released?

A

from the juxtaglomerular apparatus (JG)

41
Q

do aldosterone and angiotensin II synergize?

A

yes

42
Q

the JG complex acts as what?

A

a baroreceptor

43
Q

what is the most important glucocorticoid in most species?

A

cortisol

44
Q

what is the most important glucocorticoid in rabbits, mice and rats?

A

corticosterone

45
Q

what is the main physiological effect of cortisol?

A

to stimulate gluconeogenesis -> amino acids to glucose, glycogen to glucose

46
Q

cortisol acts on ____ to release ____.

A
  • liver

- gluconeogenic enzymes

47
Q

what are the 7 effects of cortisol?

A
  1. stimulate gluconeogenesis
  2. stimulate protein and fat catabolism
  3. redistribution of body fat
  4. water and electrolyte distribution
  5. trace mineral distribution
  6. blocks inflammatory responses
  7. suppresses immune system
48
Q

what is the most clinically important effect of cortisol?

A

that it blocks inflammatory responses

49
Q

how is cortisol regulated?

A

by negative feedback

50
Q

what is the most important hormone of the pars intermedia?

A

alpha-MSH

51
Q

what is the most potent glucocorticoid?

A

cortisol

52
Q

what are three ways you can test adrenocortical function?

A
  1. plasma [cortisol]
  2. ACTH response test
  3. dexamethasone suppression test
53
Q

what are 4 clinical uses of glucocorticoid?

A
  1. inhibition of inflammatory response
  2. immunosuppressant
  3. palliative therapy for arthritis, arthrosis
  4. replacement therapy for hypoadrenocorticism
54
Q

what animals are most prone to hypoadrenocorticism?

A

older, female, small breed dogs

55
Q

what is the common term for hyperadrenocorticism?

A

Cushing’s-like syndrome

56
Q

what causes cushing’s disease?

A

secondary to pituitary release of excess ACTH

-pituitary dependent

57
Q

what causes cushing’s syndrome?

A

primary hyperadrenocorticism due to adrenal tumor

-adrenal dependent

58
Q

what is cushings sydrome?

A
  • excessive glucocorticoid synthesis

- secondary to excessive ACTH

59
Q

what is the common name for hyperaldosteronism?

A

conn’s syndrome

60
Q

primary conn’s syndrome is caused by what?

A

adrenal tumor

adenoma

61
Q

secondary conn’s syndrome is caused by what?

A

renovascular disease leading to ang II increase

62
Q

what is PPID in horses?

A
  • equine cushing’s

- pituitary pars intermedia dysfunction

63
Q

what is a key sign of hypoadrenocorticism?

A
  • bradycardia/widened QRS complex
64
Q

what causes hypoadrenocorticism?

A

deficiency of mineralocorticoids (aldosterone)

65
Q

cells of the adrenal medulla are innervated by what type of nerve fibers?

A

pre-ganglionic sympathetic nerve fibers

66
Q

cells of the adrenal medulla are modified by what type of nerve fibers?

A

post-ganglionic nerve fibers

67
Q

what are the primary hormones synthesized by the adrenal medulla?

A

epinephrine and norepinephrine

68
Q

what is the key precursor for catecholamine synthesis?

A

tyrosine

69
Q

tyrosine is inhibited by what?

A

NE and EPI

70
Q

the actions of catecholamines are mediated by?

A

alpha- and beta-adrenergic receptors

71
Q

the actions of catecholamines by alpha-receptors are?

A
  • vasoconstriction by NE

- liver glycogenolysis

72
Q

the actions of catecholamines by beta-receptors are?

A
  • increased heart rate/contractility
  • bronchodilator
  • adipose tissue lipolysis
  • vasodilation by epinephrine
73
Q

sympathetic tone is regulated by what?

A

baroreceptors

74
Q

what is pheochromocytoma?

A
  • means dusky tumor
  • neoplasm (often adenoma) in adrenal medulla
  • can release catecholamines

PHYSIO II (33 decks)

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