62: Adrenal Agents Flashcards

(34 cards)

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
MOA mifepristone
high dose - glucocorticoid receptor antagonist used to treat pt. with ectopic ACTH or adrenal carcinoma
26
mechanisms of anti-inflammatory effects of corticosteroids (6)
- 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
first line tx with patients with persistent asthma
inhaled corticosteroids
28
MOA fluticasone in asthma
- reduces leaky vascual endothelial cells - decreases adhesion molecules in airway - increases epithelial integrity - decreases growth of airway smooth muscle cells
29
reciprocal interactions b/w inhaled corticosteroids and B2 receptor agonists
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
individuals with liver disease or chronic inflammatory disease can decrease serum prtns, therefore...
decrease the dosage of glucocorticoids because without binding to prtns, more will be free and active
31
doses less than ___-- have not been associated with impaired growth
400 ug/d
32
concurrent use of glucorticoid and cyclosporin?
increase levels of each other by inhibiting metabolism
33
why is it necessary to taper a pt off long term glucocorticoid therapy slowly?
to reduce HPA axis suppression and allow body to make its own cortisol to respond to stress
34
what is the mechanism by which high doses cortisol can lead to HTN or hypokalemia? would this same mechanism be observed with dexamthasone?
Mineralocorticoid receptor effects no- it doesn't hit those receptors