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Pharm Exam 5 > 62: Adrenal Agents > Flashcards

62: Adrenal Agents Flashcards

1
Q

mineralocorticoid =

A

aldosterone

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2
Q

glucocorticoid =

A

hydrocortisone

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3
Q

medulla releases. ..

A

epi

NE

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4
Q

action of aldosterone/mineralcorticoid

A
  • increases sodium reabsorption at renal collecting tubule
  • increases excretion of K+
  • plays important role in regulating blood pressure
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5
Q

action of cortisol/glucocorticoid

A
  • restores homeostasis after exposure to stress
  • released in circadian rhythm and with stress
  • increases blood glucose
  • antiinflammatory
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6
Q

action of androgens (DHEA and androstenedione)

A
  • can be converted to testosterone

- major source of female adrogens

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7
Q

HPA axis starts in hypothalamus with CRH –>

A

ant. pit —> ACTH —> Adrenal cortex –> cortisol and adrenal androgens

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8
Q

aldosterone production is regulated by…

A

angiotensin II

blood K+

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9
Q

glucocorticoid and mineralocorticoid receptors are…

A

nuclear hormone receptors –> change gene expression

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10
Q

converts active cortisol into inactive cortisone

A

11B - HSD2

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11
Q

cortisone is converted into cortisol by..

A

11B-HSD1

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12
Q

hydroxylation of cortisone and prednisone by _____ in necessary to activate into active form

A

11B-HSD1

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13
Q

primary adrenal insufficiency =

A

addison’s disease

deficiency in cortisol, aldosterone, and androgens

observe elevated ACTH and CRH due to loss of negative feedback

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14
Q

treatment for addison’s disease

A

oral cortisol

fludrocortiosne

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15
Q

increase or decrease supplementary cortisol in times of stress?

A

increase - to prevent hypotension and shock

dosing regimen is usually 2/3 morning 1/3 afternoon

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16
Q

describe pituitary disease

A
  • decrease in ACTH causes increase in CRH

- decrease in cortisol

17
Q

describe hypothalamic disease

A
  • decrease in CRH causes decrease in ACTH

- decrease in cortisol

18
Q

treatment secondary adrenal insufficiency

A

just cortisol, no fludrocortisone

19
Q

chronic cortisol excess –>

A

cushing’s syndrome

20
Q

causes of elevated cortisol (4)

A
  • chronic glucocorticoid therapy
  • pit tumor that causes hypersecretion of ACTH
  • ectopic hypersecretion of ACTH by non-pit tumors
  • adrenal tumor that hypersecretes cortisol
21
Q

Increased Cortisol AND

– decreased CRH with increased ACTH

– decreased CRH and ACTH

A

– pituitary hypersecretion of ACTH or ectopic ACTH production

– adreanl adenoma

22
Q

dexamethasone suppression test – 50% reduction in cortisol

A

must be pit. hypersecretion of ACTH

adrenal adenoma and ectopic ACTH would show no reduction in cortisol

23
Q

MOA ketoconazole

A

inhibits 17alpha

used to treat cushings

can induce liver toxicity

24
Q

MOA metyrapone

A

inhibits 11B

diagnositc agen used to evaluate ACTH production

off-label cushings treatment

25
Q

MOA mifepristone

A

high dose - glucocorticoid receptor antagonist

used to treat pt. with ectopic ACTH or adrenal carcinoma

26
Q

mechanisms of anti-inflammatory effects of corticosteroids (6)

A
  • inhibition of phospholipase A2 activity
  • inhibition ofcyclooxygenase induction
  • inhibition of NO synthase induction
  • inhibition of cytokine production
  • inhibition of mast cell activity and reduction of mast cell number
  • vasoconstriction
27
Q

first line tx with patients with persistent asthma

A

inhaled corticosteroids

28
Q

MOA fluticasone in asthma

A
  • reduces leaky vascual endothelial cells
  • decreases adhesion molecules in airway
  • increases epithelial integrity
  • decreases growth of airway smooth muscle cells
29
Q

reciprocal interactions b/w inhaled corticosteroids and B2 receptor agonists

A

corticosteroids: - increase B2 receptor expression to prevent desensitization of B2 receptors

B2 agonists:
- increase nuclear translocation of GRs to increase binding of GR to GREs on genes

30
Q

individuals with liver disease or chronic inflammatory disease can decrease serum prtns, therefore…

A

decrease the dosage of glucocorticoids because without binding to prtns, more will be free and active

31
Q

doses less than ___– have not been associated with impaired growth

A

400 ug/d

32
Q

concurrent use of glucorticoid and cyclosporin?

A

increase levels of each other by inhibiting metabolism

33
Q

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

A

to reduce HPA axis suppression and allow body to make its own cortisol to respond to stress

34
Q

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

A

Mineralocorticoid receptor effects

no- it doesn’t hit those receptors

Pharm Exam 5 (11 decks)

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