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Pharmacology 200 > 3 - adrenocorticosteroids > Flashcards

3 - adrenocorticosteroids Flashcards

1
Q

where is adrenaline released? (cortex or medulla)

A

medulla

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2
Q

where are steroid hormones released? (cortex or medulla)

A

cortex

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3
Q

what are the three layers for the adrenal cortex

A

zone glomerulosa, fasciculata, reticularis

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4
Q

where is catecholamine/aa hormone released? (cortex or medulla)

A

medulla

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5
Q

where are mineralocorticoids released

A

zone glomerulosa

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6
Q

where are glucocorticoids released

A

zone fasciculata

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7
Q

where are andogens released

A

zone reticularis

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8
Q

name an example of a mineralocorticoid

A

aldosterone

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9
Q

name an example of a glucocorticoid

A

cortisol

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10
Q

name an example of an androgen

A

DHEA

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11
Q

what is DHEA

A

precursor for strong androgens (testosterone) and estrogens

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12
Q

what is the order going inwards of the 4 layers of the adrenal gland

A

zone glomerulosa, fasciculata, reticularis, adrenal medulla

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13
Q

what is the role of mineralocorticoids

A

salt balance

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14
Q

what is the role of glucocorticoids

A

metabolic and immune effects

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15
Q

what is the common precursor for all adrenal steroids

A

cholesterol

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16
Q

what is the HPA axis

A

hypothalamus, anterior pituitary, adrenal cortex

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17
Q

what does the HPA axis control

A

cortisol release from the zona fasciculata

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18
Q

where is ACTH released from

A

the anterior pituitary

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19
Q

what does ACTH stimulate

A

steroid production

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20
Q

when is ACTH stimulated

A

after meals, just before waking (circadian rhythm)

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21
Q

where is CRH released from

A

hypothalamus

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22
Q

what is ACTH released controlled by

A

CRH from the hypothalamus

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23
Q

what kind of hormone is cortisol

A

steroid

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24
Q

how are steroid hormones stores

A

cant be stored in vesicles, regulated at point of synthesis

lipophilic

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25
Q

what stimulates cortisol synthesis

A

ACTH

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26
Q

where does cortisol give negative feedback to and what does it cause
(where and what is less released)

A

onto the hypothalamus and anterior pituitary to reduce the release of CRH and ACTH

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27
Q

what does ACE do

A

converts AT1 to AT2

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28
Q

what does AT2 trigger

A

aldosterone release

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29
Q

what is the role of aldosteron

A

promotes sodium and water reabsorption in the kidneys

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30
Q

what is the mineralocorticoid response

A

water and sodium reabsorption

31
Q

what is the primary role of the RAAS

A

control of blood pressure and volume

32
Q

what is GRE and what does it do

A

glucocorticoid receptor/response element

33
Q

what happens once a steroid hormone binds to its receptor

A

the receptor dissociates from Hsp90 complex, transport to nucleus, change gene transcription

34
Q

what is the spectrum of receptors for corticosteroids

A

some have more affinities for glucocorticoids while others have affinities for mineralocorticoids

35
Q

what does 11beta-hydroxysteroid dehydrogenase type 1 do?

A

it activates cortisol

turns it from a ketone to an alcohol

36
Q

what does corticosteroid specificity arise from? (2 things)

A

affinity to receptor and metabolism in target tissues (11beta-hydroxysteroid dehydrogenase)

37
Q

where is there a lot of 11beta-hydroxysteroid dehydrogenase type 1

A

in glucocorticoid target tissues (adipose, muscle, liver)

38
Q

is prednisone or prednisolone better to take topically and why

A

prednisolone because it is the active form (has an OH group)

39
Q

can prednisone work orally

A

yes, it is metabolized to prednisolone in the liver and in glucocorticoid receptor tissues

40
Q

which receptors does cortisol have affinity for

A

same affinity for glucocorticoid and mineralocorticoid receptors

41
Q

why does cortisol have weak mineralocorticoid effects

A

kidney cells (mineral.. targets) have [11beta-hydroxysteroid dehydrogenase type 2] which inactivates cortisol

42
Q

where is there 11beta-hydroxysteroid dehydrogenase type 2

A

in cells that dont want cortisol to work

43
Q

what is pseudohypoeraldosteronism

A

when cortisol affects the aldosterone target tissues (mineralocorticoid)

44
Q

how does pseudohypoeraldosteronism happen

A

11beta-hydroxysteroid dehydrogenase type 2 is inhibited by something like licorice

45
Q

what is apparent mineralocorticoid excess

A

mutations in 11beta-hydroxysteroid dehydrogenase type 2

46
Q

what does glucocorticoids do to carbohydrate metabolism and glucose

A

increases circulating glucose

47
Q

do glucocorticoids have an overall catabolic or anabolic effect

A

catabolic

48
Q

how does adipose tissue change with clucocorticoids

A

adipose redistributes from limbs to trunk

49
Q

how is fat affected directly and indirectly with glucocorticoids

A

fat metabolism so higher circulating fatty acids and glycerol, increased circulating insulin, promotes fat deposition

50
Q

what do glucocorticoids do to arachionic acid and how

A

they inhibit it because they inhibit phospholipase A2

51
Q

what are 3 main targets of glucocorticoid mediated inflammation

A

arachidonic acid
prostanoid
COX2 (not antagonist!)

52
Q

how do glucocorticoids affect prostanoid synthesis

A

inhibit it

because less arachidonic acid

53
Q

what is the role of COX2

A

early step of metabolism of arachidonic acid to various prostanoids

54
Q

how do glucocorticoids regulate COX2

A

suppress transcription of the COX2 gene
they DO NOT DIRECTLY ANTAGONIST OR INHIBIT COX2 ACTIVITY
it binds to a glucocorticoid receptor which causes a decrease in transcription

55
Q

what is annexin A-1

A

anti-inflammatory protein

56
Q

how does annexin A-1 do its thing (2 ways)

A

anti-inflammatory by
1-directly effects on leukocytes to inhibit inflammation
2-suppress phospholipase A2

57
Q

what are the annexin repeats proteins

A

lipocortins/annexins

58
Q

what macromolecule is lipocortin

A

protein

59
Q

how does lipocortin affect phospholipase A2?

A

inhibits

60
Q

how does glucocorticoids affect annexin A-1 pathway

A

glucocorticoids promotes annexin A-1 which inhibits PLA2

61
Q

what is addisons disease caused by

A

chronic adrenocortical insufficiency

low production of glucocorticoids and often mineralocorticoids too

62
Q

how can you treat addisons disease

A

with glucocorticoids/mineralocorticoids supplementation (hydrocortisone)

63
Q

what is cushings syndrome caused by

A

adrenal overactivity leading to excess cortisol

64
Q

what can cause cushings disease

A

tumors (adrenal, pit…)

65
Q

what are symptoms of cushings disease

A

round face, fat tummy

bone and muscle catabolism

66
Q

what kind of things can glucocorticoids be used for

A

anti-inflammatory, allergic, pain, asthma, GI, organ transplants (immunosuppression to avoid rejection)

67
Q

what causes addison-LIKE symptoms

A

administration of glucocorticoids creating negative of CRH and ACTH

68
Q

what are the side effects of addison-LIKE symptoms

A

hypoglycemia, hyponatremia (sodium), hyperkalemia(potassium), low bp

69
Q

why do you need to taper off glucocorticoids

A

addison-LIKE symptoms

70
Q

what happens if you use glucocorticoids for a long time

A

cushingOID

71
Q

what are the effects of cushingOID

A

hyperglycemia, high bp, low immune, muscle and bone wasting

72
Q

what are the two main receptors with different affinities for corticosteroids

A

glucocorticoid receptor and mineralocorticoid receptor

73
Q

what does 11beta-hydroxysteroid dehydrogenase type 2 do

A

inactivates cortisol (alcohol into ketone)

Pharmacology 200 (29 decks)

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