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Flashcards in Endocrine Deck (33):
1

cushings disease =

hyperadrenocorticism

2

addison's disease =

hypoadrenocorticism

3

what causes hyperadrenocorticism?

excess glucocorticoid production by the adrenals

4

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

pheocromocytoma (remember phenooxybenzamine is the drug of choice!)

5

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

ACTH

6

what are the three targets for drug therapy of hyperadrenocorticism?

-adrenal gland tissue (i.e. surgical adrenalectomy)
-production of glucocorticoids
-production of ACTH

7

how does mitotane target adrenal gland tissue?

cytotoxic to cells of the fasciculata

8

T/F: mitotane has a narrow therapeutic index

TRUE

9

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

-high dose (induction)
-lower dose (maintenance)

10

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

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

11

how do you monitor adrenal function?

ACTH stimulation test

12

what is an adverse effect of using mitotane?

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

13

what drugs used for hyperadrenocorticism should be monitored?

mitotane and trilostane

14

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

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

15

what drug is most commonly used to treat cushings?

triolostane

16

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

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

17

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

FALSE, opposite

18

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

TRUE

19

what are possible adverse effects of ketoconazole?

-potential for hepatotoxicity
-POTENT hepatic microsomal enzyme inhibitor

20

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

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

21

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

pergolide

22

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

cushings

23

what is selegiline labeled to treat in dogs?

cognitive dysfunction

24

what is the MOA of selegiline?

inhibits MAO-B which results in increased dopamine

25

why does dr. boots think selegiline is useless?

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

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

glucocorticoids +/- mineralcorticoids

27

what is the primary cause of hypoadrenocorticism?

chronic destruction of the adrenal gland (typical and atypical)

28

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

FALSE, dopamine is an inhibitor (gives negative feedback)

29

what corticosteroids would be insufficient in iatrogenic adrenal insufficiency?

glucocorticoids, treat with prednisone

30

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

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

31

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)?

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

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

inhibits enzymes in the steroid synthesis pathway

33

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

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