Pharm2:adrenal Steroids

Front 1

Desribe the storage and synthesis of adrenal steroids

Back 1

not stored, synthesized when needed.
Z. golmerulosa makes aldosterone, a mineralcorticoid,
Z. faciculata makes cortisol, a glucocorticoid
Z. reticularis makes androgens
"the deeper you go, the sweeter it gets"
sugar makes you fasiculate
alsoterone affects the kidney where the golmerulus is

Front 2

what controls the synthesis of cortisol

Back 2

ACTH

Front 3

what controls the synthesis of aldosterone

Back 3

angiotensin II and plasma potassium

Front 4

Glucocorticoids (Cortisol) mediate CHO and protein metablism. Explain their effects

Back 4

Goal=maintain adequate blood sugar. Enhance GNG, stimulate AA mobilization, increase plasma gluose and liver glycogen increase uruinary N excretion, reduce periphearl glucose usage

Front 5

Why might a pt on steroids apperar diabetic

Back 5

Steroids with gluccorticoid effects increase plasma glucose by increasing its synthesis and reducing peripheral glucose utilization

Front 6

describe the effect of glucocorticoids on lipid metabolism

Back 6

redistrubution of body fat (expalins cushing's syndromes of moon face and buffalo hump), stimulate the release of FA from adipose

Front 7

Cortisol and aldosterone both bind the mineralocorticoid receptor yet cortisol does not trigger action at this receptor. HOw is this possible

Back 7

11B hydroxysteroid dehydrognease converts cortisol wot cortisone which does not bind the mineralocorticoid receptor leaving only aldosterone left to bind. This is an example of a receptor independent mechanism for confering specificty of the mineralocorticoid receptor to aldosterone

Front 8

What is the resposne to activation of the mineralocorticoid receptor by aldosterone

Back 8

increase Na reabs (make and insert more ENaC channels), increase K and H excretion, leads to an increase in fluid retention

Front 9

what is the effect of glucocorticoids on cell traffic/ accumlation

Back 9

glucocorticoids reduce access of cells to target tissue. They induce lympho and monocytopenia by causing redistrubution ot of the vascular space (no lysis. sequestered in spleen and bone marrow). They also prevent neutrophil adhesion to the endothelium and inhibit the action of chemotactic factors

Front 10

Glucocorticoids inhibit the fxn of marcophages. How?

Back 10

inhibit antigen processing, inhibing binding to Fc receptor, inhibit syntheiss and release of IL-1

Front 11

Glucocorticoids interfere with T cell fxn. How

Back 11

interefece with macropahge antigen processing, prevent action of IL-2 and other lymphokines, inhibition of macrophage IL-1 produciton prevents T cell activation, reduces IL-2 synthesis

Front 12

list 4 mechanisms by which glucocorticoids action as anti-inflammatory/immnosupressive drusg

Back 12

1. Inhibit cell trafficing and fxn 2. inhibit arachidonic acid release=no prostaglandins, leukotrienes 3. Inhibits the induction of COX2 (no prostaglandins) 4. decrease capillary permeabilty

Front 13

How specifically do glucocorticoids prevent the actions of immune stimulateors like TNF

Back 13

normally when TNF binds its receptor, IkBa is destroyed which frees NF-kB allowing NF-kB to move to the nucleus and mediate transcrption of inflammatory cytokines. When glucocorticoids are present they, stimulate the production of IkBa and keep NF-kB inactive which decreases cytokine synthesis

I kan't Believe my inflammation is gone! Let's celebrate with sugar

Front 14

how speciically do steroids block the release of  arachidonic acid thus inhibiting eicosanoid synthesis

Back 14

glucocorticoids stimulate the production of lipocortin (annexin) which inhibits PLA2. This prevents relase of arachidonic acid from the membrane phospholipids which decreases eicosanoid synthesis

Front 15

t/f use of adrenalsteroids to treat disease is usually etiological and curative

Back 15

false, steroids provide pallaitive or symptomatic theapy only. they usually do not treat the underlying cause of the disease

Front 16

Why is necessary to taper down treatment after long term therapy with adrenalsteroids

Back 16

Exogenous steroids (large doeses >2wks) supress pituitary function via negative feedback so there are very low levels of ACTH. THis leads to adrenal cortical atrophy and "shut down" of the endogenous system. Abrut discontinuation of exogenous steroids leads to  acute  secondary adrenal insufficiency which is characterized by salt wasting and CV collapse. The dosage must be reduced slowy as it can take up to 12 mo. to regain endogenous fxn.

Front 17

describe the realtive mineranl/ gluco corticoid activity of cortisol

Back 17

both functions, equal potency (cortisol has all)

Front 18

describe the realtive mineranl/ gluco corticoid activity of prednisolone

Back 18

gluco>>mineral (ed was a diabed)

Front 19

describe the realtive mineranl/ gluco corticoid activity of dexamethasone

Back 19

glucocorticoid ONLY (x the meth~white powder~mineral)

Front 20

describe the realtive mineranl/ gluco corticoid activity of fludrocortisone

Back 20

Minearal>gluco (fluroid in your mineral water)

Front 21

what sxs would you expect with adrenal insufficiency caused by abrupt cessatino of adrenalsteroid therapy

Back 21

inadequate mineralocorticoid activity=hyperkalemia, nateuresis=>hypotension, CV collapse

Front 22

What is the cause of cushings sydrome? Clinical featues

Back 22

too much cortisol. Moon face and buffalo hump, thin extremeties (due to effects on lipid metabolism), poor wound healing (immunosupression), think skin, hypertension, striae

Front 23

class and mech of metyrapone

Back 23

adrenal steroid syntheis inhibitor. blocks 11 beta hyodroxylation

Front 24

Metyrapone can be used to diagnose pituitary dysfunction. HOw

Back 24

Metyrapone inhibits adrenal steroid synthesis by blocking 11 beta hydroxylation so synthesis is stopped at 11-deoxycortisol. 11-deoxycortisol does not inhibit ACTH (no ngeative feedback).   The patient is given metyrapone to block cortisol synthesis which would reduce the negative feedback cortisol is putting on the pituitary. IF the pituitary is working, you would expect an  increase in ACTH and 11-deoxycortisol. If there is no increase in ACTH or 11  you know there is a problem with the pituitary. IF there is ACTH but no 11-deoxy, you know there is a problem with the adrenal gland.

Front 25

mifepristone class and mech and use

Back 25

competitive antagonist and progesterone and glucocorticoid receptor.  Used fro termination of pregnancy and treatment of cushings disease
Hint: No suga baby

Front 26

what is the mechanism of action of  spironolactone and eplerenone

Back 26

aldoesterone antagonists at the AT1 receptor in the collecting duct, block the aldoesterone mediated insertion of Na channels into the CCD, increases excretion of Na, decreases K excretion

Front 27

drospirenone mech and class

Back 27

progesterone receptor agonist (supress ovulation, HRT), mineralocorticoid antagonist(diuretic, antagonize salt retaining effects of estrogen), androgen receptor antagonist

Old women can be DROS. Keep them womanly instead of rock hard Men. (up progresterone, down mineralocorticoid, down androgen)

Front 28

prednisolone mech and class

Back 28

steroid, glucocorticoid> mineralocorticoid ( Poor ED was a diabed)

Front 29

fludrocortisone mech and class

Back 29

steroid, mineral> gluco (fluoride in your mineral water)

Front 30

dexamethasone mech and class

Back 30

steroid, glucocorticoid only (x the meth, white poweder, mineral)

Front 31

This is a major contraindication to the use of steroid drugs

Back 31

existing infection particularly TB

Front 32

THis steroid drug would not be appropriate for treating adrenal insufficiency. These two drugs would be better choices

Back 32

Dexamethasone would not be apropriate because it only has glucocorticoid activity. To effectively treat adrenal insufficiency, the steroid must have both properties. Cortisol or prednisolone would be better choices.

Front 33

this drug can be used to treat cushings disease but would be absolutey contraindicated in pregnancy

Back 33

mifepristone. A competitve antagonist against protesterone and the glucocorticoid receptor

hint: no suga baby

Front 34

this drug is a progesterone receptor agonist, a mineralocorticoid antagonist and an androgen antagonist

Back 34

drospirenone

Front 35

this steriod drugs has minearl and glucocorticoid effects at equal potency

Back 35

cortisol

Front 36

This steriod has both mineal and glucocorticoid effects but the glucocorticoid effect is more potent

Back 36

prednisolone (ed was a diabed)

Front 37

THis steroid has both mineral and glucocorticoid effect but the mineralocorticoid effect is greater

Back 37

fludrocortisone (fluoride in your mineral water)

Front 38

This steroid has only glucocorticoid activity

Back 38

dexamethazone (x the meth, mineral)

Front 39

THis steroid drug would not be appropriate for treating adrenal insufficiency. These two drugs would be better choices

Back 39

Dexamethasone would not be apropriate because it only has glucocorticoid activity. To effectively treat adrenal insufficiency, the steroid must have both properties. Cortisol or prednisolone would be better choices.