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15 Cards in this Set

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activating receptor for steroids is called?
GRalpha
Inhibitory receptor for steroids is called?
GRbeta (made from the same GR transcript but alternatively spliced).

Increase in GRbeta/GRalpha may be responsible for steroid-resistant asthma.
At physiological conc., what keeps the mineralocorticoid activity of glucocorticoids minimum/low in mineralocorticoid target tissue?
Done by 11beta-hydroxysteroid dehydrogenase (HSD11B2), which inactivates cortisol in those tissues, because cortisol has a 1:1 GC and MC activity otherwise.

At pharmacologic conc., this enzyme is insufficient to inactivate all MC activity of cortisol, and unwanted side effects result.
List drugs with more GC activity than MC activity?
Prednisone (not active until metabolized), Prednisolone, Dexamethasone, Betamethasone.

Last 2 has zero MC acitivty
List drugs with more MC acitivity than GC activity?
Aldosterone, corticosterone, Fludrocortisone
Availability and Metabolism of steroids?
unlike the natural occuring cortisol, synthetic analogues do not bind CBG in plasma so more are availabe. Also, most synthetic i.e. dexamethasone are excluded from CNS by mdr1a p glycoprotein.

Metabolic modifications can lead to increase or decreased acitivty. Fluticasone and budesonide are extensive metabolized during first pass hepatic metabolism.
Some disorders?
Addison's Dz: Adrenal insufficiency

Apparent MC excess: mutation in HSD11B2 in kidney resulting in decreased conversion of cortisol to cortisone

CAH: enzyme defect causing low cortisol and aldosterone and increased androgens (21-hydroxylase)

Conn's: hyeraldosteronism

Cushing's: hypercortisolism
Dosing regiment: Some different stratergies?
Replacement such as in addison's: give a 5mg prednisone in the morning.

Divided dose in AM and PM given to keep ACTH low and repress Adrenal function and reduce adrenal androgens such as in CAH.

Daily dose given to supress inflammatory disorders.

Alternate Day therapy: given to pts in remission to avoid/minimize immunosupressive side effects while maintaining inflammation supression.
Adr Steroid Antagonists: mifepristone
aka RU 486, Antiprogestin (induction of early term abortion) and anti-glucocorticoid (in Cushing's).
Adr Steroid Antagonists: Spironolactone
Competitive Inhibitor of Aldosterone binding to MC receptors. Used in HTN, effective in severe CHF.

side effects: hyperkalemia, gynecomastia and impostence
Adre Steroid Antagonists: Eplerenone
selective MC receptor antagonist (fewer side effects), for HTN, CHF
Adr Steroid Biosynthesis Inhibitors: Dexamethasone
This and other glucocorticoids feedback inhibit ACTH andhence endogenous corticosteroid production
Adr Steroid Biosynthesis Inhibitors: metyrapone
inhibits 11beta-hydroxylation, so no corticosterone and hence aldosterone

and Cortisol can be synthesized
Adr Steroid Biosynthesis Inhibitors: aminoglutethimide
Inhibits first comitted step from Cholesterol to Pregnenolone;

ALSO inhibits aromatase
Adr Steroid Biosynthesis Inhibitors: ketoconazole
an antifungal, inhibits side chain cleavage, and 11beta-hydroxylase (just like metyrapone).