endocrine pharm Flashcards
aminoglutethimide: moa
blocks synthesis of all adrenal steroids
aminoglutethimide: I
temporary therapy to decrease cortisol production
reduce cortisol by 50%
does not affect underlying disease process
temporary, dont use longer than 3 mo, usually just waiting for sx or want to do radiation before sx
aminoglutethimide: SE
drowsy, n, anorexia, rash
ketoconazole: moa
antifungal drug that also inhibits glucocorticoid synthesis
ketoconazole: I
I: adjunct therapy to sx or radiation for cushing S
ketoconazole: SE
severe liver damage
dont take with OH or other drugs that harm liver
dont give pregnant (fetal thyroid damage)
phenoxybenzamine HCl
alpha blocker - non competitive receptor antagonist (receptor blocking is not reversible)
I: pheochromocytoma
phenoxybenzamine HCl: moa
long lasting irreversible blockage of alpha adrenergic receptors
lowers bp
phenoxybenzamine HCl: SE
orthostatic hypoT, reflex tachy, nasal congestion, sexual SE in men
demeclocycline
tetracycline broad spectrum abx
I: abx and chronic SIADH
demeclocycline: SE
photosensitivity
teeth staining
nephrotoxic
demeclocycline: moa
interferes with renal response to ADH, lowers response
desmopressin
DDAVP
treatment for neurogenic DI
nasal spray, PO, IV, SQ
desmopressin: moa
synthetic ADH replacement, antidiuretic effects
desmopressin: SE
small doses = none
nasal spray = nasal irritation
large doses = hypoNa, water intox
levothryroxine
replacement hormone therapy with
T4 synthetic thyroid hormone
drug 1/2 life = 7 days -> results ~1 mo, stay consistent with regimen
take for life
levothryroxine: moa
converted to T3 in body
levothryroxine: SE
rare, if dose too high or too low you can have hypoT or hyperT s
drug interactions (warfarin - increase risk of bleed) and food can reduce abs (empty stomach, 30 min before eating in morning)
PTU
antithyroid hormone med
blocks thyroid hormone synthesis, suppress conversion of T4 -> T3
hepatotox: BB!
can be used in 1st T with caution, change to different med in 2nd and 3rd bc hepatotox
Hydrocortisone
Prednisone (5-10 mg/day)
Dexamethasone (0.25 – 0.75 mg/day)
glucocorticoid
Some MCC action - hydro
Direct replacement of glucocorticoid
P: chronic disease states (COPD)
D: get idea of adrenal function
glucocorticoids: SE
Low dose = minimal to none
Large dose = toxic
Acute: increase intraocular pressure (eye diseases like glaucoma), fluid retention, htn, mood swings, weight gain (fat deposits in abdomen, face, back of neck – centralized), hunger, high BS
Long term (months to years): clouded eye lens, high BS, increased risk of infection (wbc depression), thinning bones and fractures, suppressed adrenal hormone gland production (fatigue, loss of appetite, n, muscle weakness), thin skin, bruising, slow wound healing
glucocorticoid: nc
Synthetic, identical to cortisol (can distinguish from endogenous, except dexamethasone)
Oral = 15-25 mg/day
Parenteral (50-100 mg IV q8hr
Don’t abruptly stop taking, steroid taper, deadly
Take at same time throughout day (esp with long term)
Wear medical alert bracelet with long term
Monitor weight and BS
fludrocortisone
mineralcorticoid
direct replacement
low mineralcorticoids
not as many SE
Only mineralcorticoid replacement, may be needed with GCC replacement to combat salt wasting (inability to maintain Na and K levels high despite adequate renal function)