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Endo Exam 1 > Adrenal Gland > Flashcards

Adrenal Gland Flashcards

1
Q

adrenal medulla

A

neuronal tissue

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2
Q

cortisol

A

suppresses neuron formation
promotes Epinephrine production

blood flow from cortex to medulla

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3
Q

action of cortisol on NE?

A

increases PNMT activity

NE > E

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4
Q

ACTH

A

stimulates production of DOPA

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5
Q

ACh

A

stimulates secretion of stored catecholamines

from preganglionic sympathetics

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6
Q

catecholamines

A

secreted into blood as hormones

80% E
20% NE

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7
Q

cathecholamine synthesis pathway

A

tyrosine > L-dopa > dopamine > E > NE

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8
Q

action of catecholamines

A

brief with fast degradation

GPCR - on adrenergic receptors

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9
Q

alpha 1 receptors

A

increase vascular smooth muscle contraction

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10
Q

alpha 2 receptors

A

inhibit NE and insulin release

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11
Q

beta 1 receptors

A

increase cardiac output

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12
Q

beta 2 receptors

A

increase hepatic glucose output, decrease contraction of vessels and uterus

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13
Q

beta 3 receptors

A

increase hepatic glucose output, increase lipolysis

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14
Q

degradation of catecholamines

A

COMT and MAO

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15
Q

to measure catecholamine production

A

catecholamine
metanephrine
vanillylmandelic acid (VMA)

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16
Q

mineralocorticoids

A

21 carbons

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17
Q

glucocorticoids

A

21 carbons

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18
Q

androgens

A

19 carbons

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19
Q

zona glomerulosa

A

lacks 17 alpha hydroxylase - only produces mineralocorticoids

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20
Q

action of aldosterone

A

increase Na reabsorption

increase K and H secretion

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21
Q

low aldosterone

A

hyperkalemia
hypotension
metabolic acidosis

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22
Q

high aldosterone

A

hypokalemia
HTN
metabolic alkalosis

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23
Q

kidneys and cortisol

A

convert it to cortisone - low affinity for aldosterone receptors

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24
Q

aldosterone regulation

A

major is RAAS

not under control of ACTH like cortisol

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25
Q

renin

A

released with low blood volume

stimulates angiotensinogen to ANG I

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26
Q

ACE

A

in lung

ANG I to ANG II

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27
Q

ANG II

A

increased Ca levels and triggers aldosterone synthesis

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28
Q

increased potassium

A

triggers aldosterone synthesis

influx of Ca bc of depolarized cells

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29
Q

ACTH

A

controls conversion of cholesterol to pregnenolone

induces secretion of cortisol, corticosterone, and DOC

  • mineralcorticoids
  • HTN with too high ACTH
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30
Q

cortisol

A

binds nuclear receptors - promotes gene transcription

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31
Q

actions of cortisol

A

increased gluconeogenesis, protein catabolism, lipolysis, decreased insulin sensitivity

anti-inflammatory

immune suppression

vascular response to catecholamines

inhibit bone formation

increased GFR

decreased REM

32
Q

acute high cortisol

A

low I:G ratio

give body energy in times of stress

33
Q

chronic high cortisol

A

high I:G ratio

ex/ cushings

34
Q

cortisol release

A

diurnal
lowest before sleep
highest before awakening

35
Q

decreased ACTH

A

atrophy in zona fasciculata and reticularis

36
Q

excess ACTH

A

hyperpigmentation

-cross-reaction with MCR-1 on melanocytes with excess MSH

37
Q

androgens in male and female

A

female - majority from adrenal

male - majority from testes

38
Q

CRH

A

from paraventricular hypothalamus to anterior pituitary

increases ACTH secretion from corticotrophs

39
Q

cortisol feedback

A

negative feedback on CRH from hypothalamus

40
Q

cortisol deficiency

A

high ACTH

41
Q

cortisol excess

A

decreased ACTH

42
Q

dexamethasone suppression test

A

administer synthetic cortisol

-used to determine if hypercortisolism is from ACTH tumor or cortisol tumor

43
Q

ACTH tumor

A

DST - only high dose suppresses cortisol

44
Q

cortisol tumor

A

DST - neither low or high dose suppress cortisol

45
Q

11-beta hydroxysteroid DH

A

converts cortisol to cortisone

in kidney

46
Q

overproduction of adrenal androgens

A

increased urinary 17-ketosteroids

47
Q

excess cortisol

A

hyperglycemia

48
Q

excess aldosterone

A

hypokalemia

49
Q

hirsutism

A

masculinization in females

50
Q

addisons disease

A

adrenocortical insufficiency

  • autoimmune destructon all adrenal cortex
  • decreased cortisol, aldosterone, androgens

hypoglycemia, anorexia, weight loss, N/V, hypotension, hyperkalemia, hyperpigmentation**

51
Q

secondary adrenocortical insufficiency

A

low CRH or ACTH
-decreased cortisol

low ACTH levels, no hyperpigmentation, aldosterone normal

52
Q

cushings

A

excess cortisol

hyperglycemia, muscle wasting, central obesity, round face, osteoporosis

53
Q

cushings disease

A

hypersecretion ACTH (pituitary tumor)

54
Q

cushings syndrome

A

defect in adrenal cortex

-low ACTH

55
Q

conns syndrome

A

primary hyperaldosteronism
-aldosterone secreting tumor

HTN, hypokalemia, metabolic alkalosis

decreased renin levels

56
Q

21 hydroxylase deficiency

A

increased 17 ketosteroids in urine

high ACTH

57
Q

17 alpha hydroxylase deficiency

A

cannot produce cortisol or androgens
overproduction of mineralocorticoids

hypertension, hypokalemia, metabolic alkalosis

58
Q

pheochromocytoma

A

tumor of chromaffin tissue
-produce excess catcholamines

HA, sweating, palpitations** triad

HTN and orthostatic hypotension

59
Q

pounding heart

A

beta 1

60
Q

increased HR

A

beta 1

61
Q

increase BP

A

alpha 1

62
Q

cold hands and feet

A

alpha 1

63
Q

to control high BP

A

alpha 1 antagonist

64
Q

ACTH dependent

A

tumor ACTH

responds to DST

65
Q

ACTH independent

A

tumor cortisol

no response to DST

66
Q

factitious cushings

A

overreplacement of cortisol

67
Q

approach to cortisol diagnosis

A

exclude exogenous steroid use
DST test - synthetic cortisol
24 hour cortisol

68
Q

findings with cushings

A

central obesity, muscle wasting, striae in skin
decreased bone density
increased glucose - insulin resistance
increased BP - increased PNMT > increased E

69
Q

other cortisol effects

A

decreased LH, FSH = female menstrual abnormal
decreased TSH
decreased GH

70
Q

11beta hydroxysteroid DH

A

cortisol > cortisone

breaks cortisol down in kidney so it won’t act as a mineralocorticoid

this is why you get metabolic alkalosis with hypercortisolism

71
Q

addisons disease

A

primary adrenal insufficiency

-mainly autoimmune - 21 hydroxylase

72
Q

primary vs. secondary adrenal insufficiency

A

primary - problem adrenal gland
secondary - problem pituitary

primary has hyperpigmentation - high ACTH causes MSH rxn (MRC-1 in skin**)

secondary has no hyperpigmentation

73
Q

MCR2

A

adrenal glands

-bind ACTH

74
Q

primary hyperaldosteronism

A

HTN
hypokalemia
hypomagnesemia
metabolic alkalosis

75
Q

aldosterone:renin ratio

A

to determine aldosterone levels

76
Q

infusion of saline and aldosterone assay

A

to try to suppress it

77
Q

sodium escape

A

chronic aldosterone

  • sodium lost (mechanism not important)
  • not as elevated as you may think**

Endo Exam 1 (10 decks)

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