Br Pharmacology: Corticosteroids And Antagonists

Front 1

Describe the mechanism of glucocorticoid action!

Back 1

released in plasma from corticosteroid binding protein. cortisol enters cytoplasm and binds an intracellular receptor that is bound to Hsp90. Hsp90 dissociates and the cortisol receptor complex moves to the nucleus where it activates glucocorticoid response elements

Front 2

What effect do glucocorticoids have on blood sugar and insulin?

Back 2

increase gluconeogensis and blood sugar and thus increase insulin

Front 3

What effect do glucocorticoids have on skeletal muscle? What about lipids?

Back 3

1) protein catabolism
2) increased lipogenesis and lipolysis

Front 4

What happens to children taking glucocorticoids?

Back 4

reduced growth

Front 5

glucocorticoids have catabolic effects on multiple tissues. What tissues?

Back 5

muscle, fat, skin, lymph, connective tissue, and bone

Front 6

Why might a postmenopausal woman develop kyphosis when supplemented with glucocorticoids?

Back 6

increased rate of osteoporosis

Front 7

Why are glucocorticoids used in hematologic cancers?

Back 7

they are actively lymphotoxic and in particular impair cell-mediated immunity

Front 8

What is Addisons disease?

Back 8

partial or complete loss of glucocorticoid and mineralcorticoid function

Front 9

What leukocytes are not inhibited but actually increase with glucocorticoids?

Back 9

neutrophils, all the others decrease

Front 10

How does leukocyte migration and suppression of leukocytes actually take place with glucocorticoids?

Back 10

increased synthesis of phospholipase A2, decreased COX2, IL2, IL3 and PAF

IL-3 stimulates the differentiation of multipotent hematopoietic stem cells

Front 11

In large doses what can glucocorticoids induce?

Back 11

behavioral changes and increased gastric acid secretion

Front 12

Why would steroid use be contraindicated in someone with H. pylori infection?

Back 12

gastric acid production is increased and ulcer resistance is lost from reduced blood flow to the gastric epithelium

Front 13

When does ACTH peak throughout the day?

Back 13

ACTH is on a circadian rhythm and is released more in the morning and at midnight

Front 14

Cortisol in general is not able to diffuse across skin. Why is it given topically?

Back 14

it can move across inflamed skin and mucus membranes

Front 15

What are synthetic glucocorticoids?

Back 15

prednisone, prednisolone, dexamethasone, triamcinolone

Front 16

What steroids are available for asthma?

Back 16

beclomethasone and budesonide

Front 17

What are a few unusual conditions glucocorticoids are given in?

Back 17

mountain sickness, hypercalcemia, chemotherapy-induced vomiting

Front 18

What is unique about betamethasone and for this reason it can be given to mothers in premature labor to hasten maturation of fetal lungs?

Back 18

it has low plama binding protein capacity and is therefore quickly taken up

Front 19

Given the effects of glucocorticoids why might they not be given to someone with metabolic syndrome?

Back 19

they can elicit diabetes in someone by creating insulin sensitivity

Front 20

How is adrenal insufficiency avoided in someone taking longterm glucocorticoids?

Back 20

lower the dosage slowly over several months and taper them off

Front 21

Does aldosterone have a short or long half life? What is needed for its release?

Back 21

1) short
2) ACTH and angiotensin

Front 22

What are mineralocorticoids?

Back 22

deoxycorticosterone, aldsoterone, FLUDROCORTISONE

Front 23

What is unique about fludrocorticosterone?

Back 23

it has both mineralcorticoid and a lot of glucocorticoid activity

Front 24

What drug is favored in adrenal insufficiency to replace mineralcorticoid activity? Why?

Back 24

fludrocortisone because it has a long half life

Front 25

What are aldosterone antagonists?

Back 25

spirolactone and eplerenone

Front 26

Mifepristone is also known as what? What is its MOA? What can it be used for?

Back 26

RU-486 is a competitive inhibitor of progesterone receptors and is used to induce abortion or in the treatment of CUSHINGS SYNDROME

Front 27

What are drugs that inhibit synthesis of mineralcorticoids and glucocortiods?

Back 27

aminoglutehtimide, metyrapone and ketoconazole

Front 28

When is ketoconazole given?

Back 28

adrenal carcinoma, hirsutism, breast and prostate cancer, dermatophytes and candiasis

Front 29

What drug blocks the conversion of cholesterol to pregnenolone?

Back 29

aminoglutethimide inhibits desmolase

Front 30

Which drug inhibits normal synthesis of cortisol but not its precursors?

Back 30

metyrapone inhibits 11-hydroxylase

Front 31

3 zones of adrenal cortex and their products

Back 31

Glomerulosa (mineralocorticoids), fasciculata (glucocorticoid=GC), and reticularis (adrenal androgens)

Front 32

Used for Addison's disease, Congenital Adrenal Hyperplasia (CAH), inflammation, allergies, and asthma (as a local inhalation)

Back 32

Glucocorticoids

Front 33

Pneumonic for 3 zones of adrenal cortex

Back 33

GFR

Front 34

Short acting glucocorticoids

Back 34

Cortisone and hydrocortisone (equivalent to cortisol)

Front 35

Intermediate acting glucocorticoids

Back 35

Prednisone, methylprednisolone, prednisolone, and triamcinolone

Front 36

Long acting glucocorticoids

Back 36

Betamethasone and dexamethasone

Front 37

Some side effects of corticosteroids

Back 37

Osteopenia, impaired wound healing, inc. risk of infection, inc. appetite, HTN, edema, PUD, euphoria, psychosis, stria, thinning of skin

Front 38

Period of time of therapy after which GC therapy will need to be tapered

Back 38

5-7 days

Front 39

Used for Cushing's syndrome (increased corticosteroid)

Back 39

Dexamethasone suppression test

Front 40

Antiprogestin used as potent antagonist of GC receptor

Back 40

Mifepristone

Front 41

Common SE of spironolactone

Back 41

Gynecomastia and hyperkalemia