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Pharm Final > Endocrine > Flashcards

Endocrine Flashcards

1
Q

cushings disease =

A

hyperadrenocorticism

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2
Q

addison’s disease =

A

hypoadrenocorticism

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3
Q

what causes hyperadrenocorticism?

A

excess glucocorticoid production by the adrenals

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4
Q

what do you call a functional mass of the adrenal medulla?

A

pheocromocytoma (remember phenooxybenzamine is the drug of choice!)

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5
Q

what does a functional pituitary mass or pituitary dependent hyperadrenocorticism (PDH) produce?

A

ACTH

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6
Q

what are the three targets for drug therapy of hyperadrenocorticism?

A
  • adrenal gland tissue (i.e. surgical adrenalectomy)
  • production of glucocorticoids
  • production of ACTH
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7
Q

how does mitotane target adrenal gland tissue?

A

cytotoxic to cells of the fasciculata

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8
Q

T/F: mitotane has a narrow therapeutic index

A

TRUE

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9
Q

what are the two types of doses you give with mitotane?

A
  • high dose (induction)

- lower dose (maintenance)

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10
Q

what might you worry about with sending client home with mitotane?

A

potentially immunogenic, can be dangerous for client! (esp. pregnant women), USE GLOVES!!

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11
Q

how do you monitor adrenal function?

A

ACTH stimulation test

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12
Q

what is an adverse effect of using mitotane?

A

oversuppression of adrenal function (can lead to adrenal collapse where lose glucocorticoids AND mineralcorticoids)

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13
Q

what drugs used for hyperadrenocorticism should be monitored?

A

mitotane and trilostane

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14
Q

how does trilostane target the production of glucocorticoids in the adrenal?

A

inhibits the enzyme (3B-hydroxysteroid dehydrogenase) in the cortisol production pathway blocking the cells ability to produce the end product

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15
Q

what drug is most commonly used to treat cushings?

A

triolostane

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16
Q

T/F: trilostane has a wider TI making it safer to use than mitotane

A

FALSE, triolostane also has a narrow TI but is easier to use safely than mitotane

17
Q

T/F: mitotane is started with a low dose and then increased to a high dose where trilostane is started with a high dose and then decreased to a low dose

A

FALSE, opposite

18
Q

T/F: ketoconazole’s clinical efficacy has been questioned

A

TRUE

19
Q

what are possible adverse effects of ketoconazole?

A
  • potential for hepatotoxicity

- POTENT hepatic microsomal enzyme inhibitor

20
Q

how does pergolide target the production of ACTH by the pituitary?

A

=dopamine agonist, suppresses production of ACTH thus reducing cortisol production

21
Q

what drug is used to treat pituitary pars intermedia dysfunction in horses?

A

pergolide

22
Q

pituitary pars intermedia dysfunction is equivalent to what disease in canines?

A

cushings

23
Q

what is selegiline labeled to treat in dogs?

A

cognitive dysfunction

24
Q

what is the MOA of selegiline?

A

inhibits MAO-B which results in increased dopamine

25
Q

why does dr. boots think selegiline is useless?

A

methamphetamine is a byproduct, when given to an old dog with cushings it perks up and helps alleviate symptoms but the actual output of # of hormones don’t actually improve

26
Q

deficient production of what causes hypoadrenocorticism (addison’s)?

A

glucocorticoids +/- mineralcorticoids

27
Q

what is the primary cause of hypoadrenocorticism?

A

chronic destruction of the adrenal gland (typical and atypical)

28
Q

T/F: dopamine stimulates the anterior pituitary gland, therefore stimulating the adrenal gland to produce glucocorticoids

A

FALSE, dopamine is an inhibitor (gives negative feedback)

29
Q

what corticosteroids would be insufficient in iatrogenic adrenal insufficiency?

A

glucocorticoids, treat with prednisone

30
Q

T/F: iatrogenic adrenal insufficiency occurs when exogenous glucocorticoids are used chronically then stopped abruptly or adrenal glands are damaged through excessive action of drugs used to treat hyperadrenocorticism

A

TRUE, patient suffers insufficient adrenal output (chronic negative feedback) or adrenal glands were over suppressed

31
Q

between mitotane or trilostane which drug would result more rapid improvement if you needed to withdrawal the drug because of over suppressing the adrenal glands (over treating)?

A

trilostane, inhibits the enzyme whereas mitotane works on the cells of the fasciculata which means the body would need more time to regenerate the cells

32
Q

how does ketoconazole target the production of glucocorticoids in the adrenal?

A

inhibits enzymes in the steroid synthesis pathway

33
Q

is ketoconazole a hepatic microsomal enzyme inducer or inhibitor, and what effect might it have on other drugs?

A

INHIBITOR, might INCREASE half-life of other drugs bioinactivated through the P450 system

Pharm Final (7 decks)

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