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MOD 1 Quiz 1 > Physiology: Adrenal Glands > Flashcards

Physiology: Adrenal Glands Flashcards

1
Q

Primarily steroids in circulation are bound to what protein?

A

Corticosteroid-binding protein (CBP)

And/or other plasma proteins (albumin)

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2
Q

3 cellular layers of the adrenal cortex?

A

glomerulosa
fasiculata
reticularis

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3
Q

glomerulosa creates what steroids? what do they do?

A

mineralcorticoids (aldosterone)

promotes salt and water retention by the kidney

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4
Q

fasiculata makes what steroids? what do they do?

A

glucocorticoids (cortisol)

increase plasma glucose levels

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5
Q

reticularis makes what steroids?

A

androgens/ sex steroids

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6
Q

The adrenal medulla makes what steroids?

A

catecholamines (Epinephrine, Norepinephrine)

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7
Q

chromaffin cells?

A

produce epinephrine or adrenaline (catecholamine)

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8
Q

Amino acid needed to synthesize epinephrine?

A

tyrosine

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9
Q

definiceny in cortisol can lead to?

A

hypoglycemia

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10
Q

3 major classes of steroid hormones?

A

glucocorticoids
mineralcorticoids
sex steroids

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11
Q

how does cortisol increase plasma glucose?

A

enhances mobilization of amino acids from proteins in many tissues and to enhance the ability of the liver to convert these amino acids into glucose and glycogen by activating gluconeogenesis

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12
Q

Other actions of glucocorticoids

A

potent immunosupressive and anti-inflammatory activity, effects on protein and fat metabolism, behavioral effects on the CNS, and important effects on calcium and bone metabolism

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13
Q

Excess glucocorticoid secretion

A

Cushing syndrome

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14
Q

glucocorticoid deficiency

A

Addison disease

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15
Q

glucocorticoid excess is commonly seen because of?

A

individuals receiving treatment for a chronic inflammatory or neoplastic disorder

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16
Q

less common glucocorticoid excess?

A

cortisol producing adrenal tumor, secondary to a pituitary tumor

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17
Q

Symptoms of overproduction of glucocorticoid? aka?

A

truncal adiposity, hypertenstion, loss of subcutaneous adipose and CT in the extremities associated easy brusing, loss of bone mineral, muscle weakness and wasting and hyperglycemia

Cushing Syndrome

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18
Q

If pituitary gland is responsible for cushing syndrome it’s called?

A

Cushing disease

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19
Q

Common cause of glucocorticoid deficiency?

A

autoimmune adrenal disease

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20
Q

Etiology of glucocorticoid deficiency?

A

increase ACTH and other products of POMC

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21
Q

Cause hyperpigmentation of skin?

A

alpha MSH and gama MSH

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22
Q

lack of glucocorticoid predisposes patient to?

A

hypoglycemia

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23
Q

combined glucocorticoid and mineralcorticoid leads to?

A

hypotension

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24
Q

Aldosterone deficiency leads to?

A

hyperkalemia

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25
Q

2 sources of cholesterol for steroid hormone synthesis?

A
  1. LDL receptor-mediated endocytosis

2. synthesize cholesterol de novo from acetate

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26
Q

Which pathway for cholesterol to synthesize hormone is more important?

A

LDL cholesterol circulating

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27
Q

Except for 3B-HSD all enzymes are found where for steroid synthesis?

A

mitochondria or smooth endoplasmic reticulum

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28
Q

Adrenal adnrogens?

A

dehyroepiandrosterone and androstenedione

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29
Q

21alpha Hydroxylase deficiency?

A

inadequate production of glucocorticoid and mineralcorticoid

hypotension, dehydration, hypoglycemia

excess ACTH

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30
Q

Excess ACTH will cause? (21alpha Hydroxylase deficiency?)

A

enhanced growth of adrenal gland
excessive production of androgens

females- ambiguous genitalia at birth

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31
Q

effect of glucocorticoid use on the body?

A

Moon facies- increase in supraclvaicular and dorsal interscapular fat, rounding of the face
wasting of fat in extremities produces thining of skin and fragility of cutaneous blood vessels
osteopenia, osteoporosis
glucose intolerant

32
Q

CRH?

A

corticotropin-releasing hormone

travels via hypophyseal portal venous plexus to the anterior pituitary

33
Q

CRH receptor

A

G protein coupled receprot on corticotroph cells

Galphas- adenylyl cyclase,cAMP, protein kinase A, increase Ca2+

34
Q

arginine vasopressin

A

role in cortisol production under stress

35
Q

ACTH

A

secreted by corticotroph cells of the anterior pituitary

melanocortin (as well as a, b, gamma MSH)

36
Q

ACTH receptor

A

ACTH binds to MC2R in the fasculata cells of the adrenal cortex

37
Q

Only source of CYP11b2

A

glomerulosa layer of cortex

38
Q

Neg feedback for ACTH?

A

glucocorticoids neg regulate corticotrophs (release ACTH) and hypothalamus (release CRH)

39
Q

stAR?

A

steroidogenic acute regulatory protein

mediates the transfer of cholesterol into the mitochondria for steroidogenesis

40
Q

cortisol at the pituitary?

A

decrease synthesis of CRH receptor

decrease synthesis of ACTH

41
Q

cortisol at the hypothalamus?

A

decrease synthesis and release of CRH

42
Q

Glucorticoid receptors?

A

intracellular, nuclear receptors

heat shock proteins, influence gene transcription

43
Q

Inhibited by ANP?

A

stAR

stop cholesterol from making steroids

44
Q

Congential adrenal hyperplasia

A

hyposecretion of glucocorticoids
defect/ deletion in genes encoding stAR or steroidogenic enzymes
defects include
CYP21A1, CYP11B1, CYP17, stAR

45
Q

Overall effect of glucocorticoids?

A 
increase appetite
increase fetal maturation through synthesis of surfactant in the lung
omental adipose exrpession of GR
decrease osteoblast function
increase renal Ca expression
decrease intestinal Ca uptake 
decrease Ca absorption
increase secretion into aqueous humor
decrease GnRH release
decrease TSH, deiodinase conversion of T4 to T3
46
Q

Most common defect with congenital adrenal hyperplasia?

A

CYP21A2

47
Q

defect of CYP21A2 causes?

A

build up of precursors and a shunting to make androgens

48
Q

Defect of CYP11B1?

A

not as common, reduce final conversions

again shunt to androgens

49
Q

defect of CYP17?

A

very rare, no glucocorticoids and androgens

still make mineralcorticoids

50
Q

defect of stAR?

A

no steroids made

51
Q

Primary cause of hyposecretion of glucocorticoids?

A

adrenal disease, addison’s disease

52
Q

Addison’s disease?

A

autoimmune
infectious (TB)
congenital adrenal hyperplasia

53
Q

Can adrenal disease also affect mineralcorticoids and androgen production?

A

yes (congential adrenal hyperplasia for ex)

54
Q

hirsuitism?

A

abnormal hair growth in women

55
Q

Simulate mineralcorticoid release?

A

Angiotensin II
extracellular K
ACTH

56
Q

angiotensin II?

A

AT1 receptor, Gq, activation of calmodulin kinases, increase of CYP11B2

57
Q

extracellular k?

A

depolarize plasma membrane, open Ca channels, activate calmodulin kinases, increase CYP11B2

58
Q

renin-angiotensin-aldosteone and potassium-aldosterone negative feedback loops?

A

Decreased Na activates the acis, angiotensin II promotes renal retention of Na

decrease renal perfusion, aldosterone increases the expression of Na channel in apical membrane of cells in the the distal tubule of the kidneyand also a NA/K ATPase in the BM (promote Na reabsorption)

Aldosterone increases membrane permeabilty to K in the kidney tubule, facilitating the secretion of K into the tubule lumen

59
Q

Aldosterone elicits effects via

A 
mineralcorticoid receptor (type 1 GR)
conservation of sodium, secretion of potassium, increased water retention, and increased blood pressure.
60
Q

11bHSD on mineralcorticoids?

A

limits cortisol in kidney thereby reserving activation of type 1 GR for mineralcorticoids aka aldosterone

why aldosterone works in kidney vs cortisol

61
Q

Role of mineralcorticoids?

A 
salt and water retention
maintain K
blood pressure
elicit effects via mineralcorticoids receptor (type 1 GR)
excess aldosterone leads to hypertension
62
Q

Adrenal Androgens?

A

stimulated by ACTH
important contributor of circulating androgens in women, not in men (testes)
reticularis layer

63
Q

Catecholamines?

A

chromaffin cells in the adrenal medulla
Epi primary product, NE secondary
stored bound to granular proteins, chromogranins

64
Q

rate limit step in catecholamine production?

A

tyrosine hydroxylase

65
Q

catecholamines?

A

epi, ne, dopamine, L-DOPA

66
Q

Stim release of Epi?

A

preganglionic sympathetic axons terminate on chromaffin cells

67
Q

Catecholamine regulation: ACTH?

A

increase tyrosine hydroxylase, N-methyltransferase

68
Q

Catecholamine regulation: Cortisol?

A

increase N-methyltransferase

69
Q

Catecholamine regulation: Sympathetic stimulation?

A

increase tyrosine hydroxylase

chronic: increase N-methyltransferase

70
Q

Catecholamine regulation: Chromogranins?

A

vasostatin- vasoinhibitory effects on bv
catestatin- inhibit nicotinic actylcholine receptor, limit catecholamine secretion, suppressive on cardiomyocytes

used to eval tumors, hypertension, organ failure

71
Q

receptors for catecholamines: alpha 1?

A

Gq

vasconstriction, gluconeogenesis, glycogenolysis

72
Q

receptors for catecholamines: alpha 2?

A

Gi

vasoconstriction, decrease sympathetic outflow, simulate vagal outflow, decrease insulin secreation

73
Q

receptors for catecholamines: beta 1?

A

Gs

increase hear rate, myocardial contractilility, lipolysis, increase renin secretion

74
Q

receptors for catecholamines: beta 2?

A

Gs

vasodilate, bronchial relax, GI relax, stim renin secretion, gluyconenolysis, gluconeogeneis

75
Q

receptors for catecholamines: beta 3?

A

Gs

lipolysis

MOD 1 Quiz 1 (15 decks)

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