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Year 2 Pharmacology > Adrenal agents > Flashcards

Adrenal agents Flashcards

1
Q

what are the drug targets of corticosteroids?

A

17a-hydroxylase

11B-hydroxylase

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2
Q

17a-hydroxylase is responsible for catalyzing what reactions?

A

pregnenolone to 17-hydroxypregnenolone

progesterone to 17-hydroxyprogesterone

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3
Q

11B-hydroxylase is responsible for catalyzing what reaction?

A

deoxycortisone to cortisone

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4
Q

what enzyme is responsible for catalyzing the reactions

pregnenolone to 17-hydroxypregnenolone
progesterone to 17-hydroxyprogesterone?

A

17a-hydroxylase

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5
Q

what enzyme is responsible for catalyzing the reaction

deoxycortisone to cortisone?

A

11B-hydroxylase

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6
Q

what types of receptors are glucocorticoid and mineralocorticoid?

A

nuclear hormone receptors

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7
Q

cortisol binds to what receptors?

A

glucocorticoid

mineralocorticoid

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8
Q

does cortisone bind to mineralocorticoid receptors?

A

no

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9
Q

where is cortisone converted to cortisol? what is the enzyme?

A

liver

11B-HSD1

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10
Q

which enzyme is responsible for converting cortisol back to cortisone?

A

11B-HSD2

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11
Q

what type of drug is fludrocortisone? what effects does it have?

A

mineralocorticoid

heavy salt retaining
anti-inflammatory

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12
Q

what enzyme is important in converting prodrugs into their active forms?

A

11B-HSD1

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13
Q

what are the causes of primary adrenal insufficiency (addison’s disease)?

A

autoimmune

TB

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14
Q

what are the results of primary adrenal insufficiency (addison’s disease)?

A

deficiency in cortisol, aldosterone, androgens

hypotension from unresponsiveness of vascular smooth muscle to catecholamines

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15
Q

primary adrenal insufficiency (addison’s disease) is treated with what agents?

A

cortisol

fludrocortisone

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16
Q

secondary adrenal insufficiency are due to what causes?

A

pituitary - 1) decrease in ACTH causing increase in CRH, 2) decrease in cortisol

hypothalamic - 1) decrease in CRH causes increase in ACTH, 2) decrease in cortisol

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17
Q

secondary adrenal insufficiency (addison’s disease) is treated with what agent?

A

cortisol (fludrocortisone NOT needed)

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18
Q

chronic glucocorticoid (cortisol) excess leads to what condition?

A

Cushing’s syndrome

19
Q

Cushing’s syndrome is a result of elevation of what compound?

A

chronic glucocorticoid (corticoid) excess

20
Q

why does increased levels of cortisol cause HTN?

A

activation of mineralocorticoid receptors

21
Q

determination of the cause of cushing’s syndrome is made by what compound?

A

dexamethasone

22
Q

what will be the levels of CRH and ACTH in pituitary hypersecretion of ACTH? upon dexamethasone administration?

A

low CRH
high ACTH

usually 50% reduction in cortisol upon dexamethasone

23
Q

what will be the levels of CRH and ACTH in adrenal adenoma? upon dexamethasone administration?

A

low CRH
low ACTH

no reduction in cortisol upon dexamethasone (has nothing to do with cortisol)

24
Q

what will be the levels of CRH and ACTH in ectopic ACTH production? upon dexamethasone administration?

A

low CRH
high ACTH

no reduction in cortisol upon dexamethasone

25
Q

what class of drug is ketoconazole? what is the MOA? what is it used to treat?

A

antifungal

inhibits 17a-hydroxylase

cushing’s syndrome

26
Q

what is the adverse effect of ketoconazole?

A

significant liver toxicity

27
Q

what is the clinical application of metyrapone? for what condition is it used to treat?

A

diagnostic agent used to evaluate ACTH production

cushing’s syndrome

28
Q

what drugs are used to treat cushing’s syndrome?

A

ketoconazole

metyrapone

29
Q

what is the MOA of mifepristone? for what condition is it used to treat?

A

glucocorticoid receptor antagonist

inoperable patients with ectopic ACTH secretion or adrenal carcinoma

30
Q

what drug is used to treat inoperable patients with ectopic ACTH secretion or adrenal carcinoma?

A

mifepristone

31
Q

what are the effects of glucocorticoids on the immune cells?

A

macrophage - decrease activation
neutrophils - stabilize lysosomal membrane
mast cells - decrease release of histamine
eosinophils - decrease release of granules
T cells - decrease number and activation

32
Q

what are the anti-inflammatory mechanisms of corticosteroids?

A

inhibition of phospholipase A2

COX inhibition

33
Q

inhaled corticosteroids are the first line treatment for what condition? when should they be used?

A

asthma

patients who take inhaled B2 agonists more than twice a week

34
Q

what is the MOA of inhaled corticosteroids on asthma?

A

reduce vascular permeability
reduce growth of airway SMCs
reduce adhesion molecules in airway epithelial cells
increase epithelial integrity

35
Q

what is the importance of using inhaled glucocorticoids in conjuction with B2 agonists?

A

corticosteroids - 1) increase B2 receptor expression, 2) prevent desensitization of B2 receptors

B2 agonists - 1) increase nuclear translocation of GRs, 2) increase binding of GRs to GREs on genes

36
Q

what is the importance of dexamethasone administration for glucocorticoid effect?

A

dexamethasone has low affinity for blood proteins - higher free levels in serum

37
Q

what is the effect of glucocorticoids on stomach acid and pepsin production?

A

gastic acid - stimulation

pepsin - stimulation

38
Q

what is the adverse effect of glucocorticoids on the endocrine system?

A

HPA axis suppression

39
Q

what is the effect on estrogens and androgens on glucocorticoids?

A

increased effect

40
Q

why is it necessary to taper a patient off long term glucocorticoid therapy?

A

reduce HPA axis suppression

41
Q

what is the mechanism by which high doses of cortisol can lead to hypotension or hypokalemia? would this same mechanism be observed with dexamethasone?

A

aldosterone (mineralocorticoid) receptor effects

no - no mineralocorticoid receptor action

42
Q

what is the principle behind the high dose dexamethasone test?

A

pituitary tumor - dex has some effect of inhibiting ACTH

adrenal adenoma - dex isn’t regulated by ACTH at all

ectopic ACTH production - dex doesn’t inhibit ACTH production in lung (does not have the same responsive capabilities)

43
Q

what is the therapeutic use and MOA of ketoconazole?

A

inhibition of 17a-hydroxylase

Year 2 Pharmacology (70 decks)

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