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Drew 921 > 5_Adrenal > Flashcards

5_Adrenal Flashcards

1
Q

What are the effects of epinephrine?

A

primarily fight-or-flight

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2
Q

What are the effects of norepinephrine

A

strong vasoconstrictor to increase BP

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3
Q

What is the outermost layer and thinnest of the adrenal cortex?

A

zona glomerulosa

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4
Q

What is the middle and thickest layer of the adrenal cortex?

A

zona fasciculate

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5
Q

What is the innermost layer of the adrenal cortex?

A

zona reticularis

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6
Q

What hormones does the zona fasciculate release?

A

glucocorticoids

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7
Q

What hormones does the zona reticularis secrete?

A

adrenal androgens (DHEA and androstenedione)

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8
Q

What hormones does the zona glomerulosa release?

A

aldosterone

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9
Q

How is the zona glomerulosa regulated?

A

by AngII and K+

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10
Q

How is the zona fasciculate regulated?

A

ACTH

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11
Q

How is the zona reticularis regulated?

A

ACTH

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12
Q

What is a pheochromocytoma?

A

a medullary tumor that causes a sporadic secretion in response to palpation or anesthetics

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13
Q

What are the clincal consequences of a pheochromocytoma?

A

postural hypotension: prolonged increase in catecholamines downregulates GPCRs to cause a reduction in sympathetic tone

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14
Q

Describe the cellular make-up of the adrenal medulla.

A

post-ganglionic neurons (“chromaffin cells”) that secrete the catecholamines epinephrine and norepinephrine

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15
Q

Where are the chromaffin cells derived?

A

they are sympathoadrenal & derived from the neural crest

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16
Q

How are norepi and epi synthesized?

A

from tyrosine - l-dopa - dopamine - norepi - epi

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17
Q

Where is norepi primarily converted to epi?

A

in the adrenal gland

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18
Q

What is the reaction catalyzed by cholesterol desmolase?

A

cholesterol P450 side-chain-cleavage to yield pregnenolone

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19
Q

What is the RLS in steroidogenesis?

A

cholesterol desmolase P450 scc

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20
Q

What is required for CD450scc activation?

A

ACTH

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21
Q

How does ACTH activate CD450scc?

A

activates G-alpha-S pathway

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22
Q

What factors increase aldosterone synthesis?

A

AngII and K+

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23
Q

What factors decrease aldosterone synthesis?

A

increased Na (mild decrease in synthesis)

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24
Q

Where is renin secreted?

A

JG cells

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25
Q

Upon response to what factors is renin secreted?

A

decreased pressure, beta-1 stimulation, decreased NaCl

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26
Q

What are the effects of AngII?

A

1) thirst, 2) vasoconstriction, 3) aldosterone

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27
Q

What are the major & minor mineralocorticoids?

A

major: aldosterone; minor: deoxycorticosterone, cortisone

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28
Q

What are the synthetic mineralocorticoids?

A

agonist: 9-alpha-fludrocortisone; antagonist: spironolactone

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29
Q

For what diseases is 9-alpha-fludrocortisone used?

A

addisons

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30
Q

For what disease is spironolactone used?

A

CHF

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31
Q

How does spironolactone work?

A

prevents aldosterone-MR binding

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32
Q

How does amiloride work?

A

prevents formation of new Na channels

33
Q

Where do the mineralocorticoids act (cell types)?

A

principle cells of CT, also DT and CD

34
Q

What are the effects of the mineralocorticoids?

A

Na/H2O reabsorption and K secretion

35
Q

What are the symptoms of hypokalemia?

A

muscle weakness and paralysis

36
Q

What are the symptoms of hyperkalemia?

A

cardiac toxicity

37
Q

What are the axes of the RFC?

A

sodium intake (x normal) vs. BP

38
Q

What is aldosterone effect?

A

short-term aldosterone effects due to pressure di-/natriuresis after 24-48h

39
Q

Where does aldosterone bind its receptor?

A

binds MR in cytoplasm

40
Q

What is aldosterone’s receptor?

A

the mineralocorticoid receptor (a nuclear receptor)

41
Q

How does the aldosterone-MR complex initiate cell changes?

A

1) MR-Ald releases HSP, 2) MR-Ald translocates to nucleus, 3) MR-Ald is phosphorylated, 4) MR-Ald forms a homodimer, 5) 2 MR-Ald binds to GRE in promoter regions

42
Q

What are aldosterone’s effects on its target cells?

A

1) increases Na/K ATPase, 2) increases Enac (epithelial sodium channel), 3) increases mitochondria

43
Q

What are the major/minor glucocorticoids?

A

major: cortisol (hydrocortisone); minor: corticosterone

44
Q

What are the synthetic glucocorticoids?

A

1) cortisone, 2) prednisone, 3) dexamethasone

45
Q

What are the 5 stages of inflammation?

A

1) release of pro-inflammatory mediators, 2) erythema, 3) increased capillary permeability, clotting, and non-pitting edema/swelling, 4) leukocyte infiltration, 5) tissue remodeling and healing

46
Q

How do glucocorticoids oppose inflammation?

A

1) stabilizes lysosomal membranes, 2) decreases capillary permeability (by inhibiting COX2), 3) opposis leukocyte infiltration (chemotaxis via stopping leukotrienes), 4) suppresses T-lymphocytes, 5) decreases IL-1 (decreases fever)

47
Q

What are the immune effects of glucocorticoids?

A

1) decreased allergy inflammatory response, 2) decreased eosinophils & lymphocytes, 3) increased lymphoid atrophy, 4) increased RBCs

48
Q

What systems do the glucocorticoids affect?

A

muscle, liver, adipose, immune/inflammation

49
Q

What are the glucocorticoid effects on muscle?

A

muscle wasting & t2dm via inhibiting GLUT4 translocation

50
Q

What are the glucocorticoid effects on the liver?

A

increases glycogen, increases gluconeogenesis, increases insulin

51
Q

What are the effects of glucocorticoids in adipose?

A

lipolysis, but insulin overpowers to cause lipogenesis

52
Q

What enzyme converts cortisone to cortisol?

A

11-beta-HSD

53
Q

What is a Type 1 receptor?

A

the MR

54
Q

What is a type 2 receptor?

A

GR

55
Q

Where and when is CRF released?

A

by PVN of hypothalamus under stress

56
Q

What is the function of PC1?

A

splits POMC to ACTH and beta-lipotropin; in the anterior pituitary

57
Q

What is the function of PC2?

A

splits PC1 products to MSH and inactivated ACTH; in the hypothalamus

58
Q

What is MSH?

A

melanocyte stimulating hormone

59
Q

What are the effects of MSH?

A

1) melanin formation and dispersion, 2) decreased food intake/water consumption, 3) increased blood flow to brain, 4) increased tissue respiration

60
Q

From what pre-prohormone is ACTH derived?

A

POMC (proopiomelanocortin)

61
Q

What are the feedback loops in CRF/ACTH/cortisol?

A

cortisol inhibits CRF and ACTH (short and long loops)

62
Q

What percentage of the adrenal gland is the medulla?

A

10-20%

63
Q

Where is the type 1 (MR) receptor present?

A

in the kidney tubule

64
Q

What are the relative affinities of corticosterone and aldosterone for the type 1 (MR) receptor?

A

they are equal

65
Q

What are the relative affinities of corticosterone and aldosterone for the type 2 (GR) receptor?

A

corticosterone has greater affinity

66
Q

Why does cortisone have aldosterone effects at high concentrations?

A

if 11-beta-HSD is overwhelmed, cortisol is not converted to cortisone and cortisol can trigger aldosterone-like (HTN) effects

67
Q

What enzymes must be present to synthesize aldosterone?

A

aldosterone synthase

68
Q

What enzymes must be present to synthesize the glucocorticoids?

A

17-alpha, but NOT 17,20

69
Q

What enzymes must be present to synthesize the adrenal androgens?

A

17-alpha, AND 17,20

70
Q

What are the adrenal androgens and what role do they play?

A

weak androgens that play large role in fetal development

71
Q

What do adrenal androgens cause in males?

A

precocious puberty and stunted growth

72
Q

What do adrenal androgens cause in females?

A

masculinization

73
Q

What causes primary aldosteronism?

A

zona glomerulosa tumor

74
Q

What is the treatment for primary aldosteronism?

A

surgery then aldosterone replacement

75
Q

What is another term for addison’s disease?

A

hypoadrenalism

76
Q

What is another term for cushing’s disease?

A

hyperadrenalism

77
Q

What are the causes of Cushing’s?

A

1) too much CRF: dysfuntional HT; 2) too much ACTH: anterior pituitary adenoma; actopic ACTH tumor; 3) too much cortisol: cortical adenoma; glucocorticoid therapy

78
Q

What are the treatments for Cushings?

A

1) surgery, 2) block steroidogenesis with ketoconazole, 3) block ACTH secretion (serotonin antagonists and GABA-TA inhibitors)

79
Q

What are the symptoms of Cushings?

A

buffalo torso (upper body fat), moon face, acne, hirsuitism, hyperglycemia

Drew 921 (33 decks)

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