drugs-corticosteroids, DM, thyroid Flashcards
(51 cards)
corticosteroids are used to establish the endocrine disorder dx of ___
cushings syndrome
mifepristone is a _____ receptor antagonists
glucocorticoid
prednisone is a ____ agonist, fludrocortisone is a a ___ agonist
glucocorticoids
mineralocorticoids
aldosterone and cortisol bind with ___ affinity to the ___ receptor
equal affinity to the MR receptor
what enzyme converts cortisol from active to inactive back to active form? and what is the inert steroid name?
active: cortisol (corticosterone, prednisolone)
- — [11 B-HSD2] —> inactive: cortisone, 11-dehydrocortisone, prednisone—-[11 B-HSD1]—> active form
- 11 B-HSD2 = 11 B-dehydrogenase
- 11-B HSD1 = 11-ketoreductase
therapeutic effects of corticosteroids
immunosupression (transplants, cancer, autoimmune dz)
anti-inflammatory
anti-allergy
pain relief (secondary)
side effects of glucocorticoids
infections osteoporosis hyperglycemia weight gain "cushingoid" appearance HPA insufficiency (adrenal atrophy) HTN neuropsychiatric DO cataracts/glaucoma myopathies skin thinning
factors of corticosteroids that influence therapeutic and adverse affects
- potency
- pharmokinetics
- daily dose
- timing of dose
- difference of metabolism in individuals
- duration of tx
what is the criteria for initiating therapy with corticosteroids
- medical emergencies (high doses for ONLY a few days)
2. chronic therapy (must be evidence foe use)
T/F corticosteroids cannot be given chronically without the risk of adverse affects
true
tx of addisons dz (primary adrenal insufficiency) and CAH
both: hydrocortisone and fludrocortisone
effects of corticosteroids on the immune system
decrease: Prostaglandins , leukotrienes, immune cells, cytokines and receptors, neutrophil and MO migration, cell adhesion molecules
= 1. decreased inflammation and mainfestations
- immune suppression
- decreased allergic and hypersensitivity reactions
corticosteroids affect of carbohydrate metabolism
increase gluconeogenisis increase glucose output increase glycogen synthesis decrease glucose uptake =HYPERGLYCEMIA
what causes inhibition of 11 B HSD2 ? what is the effect/
inhibitors: glycyrrhizin (licorice)
-excessive activation of MR receptor mediated by cortisol [ increase NA and H2O retention, increase K+ loss—>increase BP]
= HTN
corticosteroids drug dosing rules
- lowest dose for shortest time (use short/intermediate acting > long acting)
- reduce distribution (use topical/inhaled vs systemic)
- single daily AM doses or alternate days with pulse tx
- dose-tapering for HPA recovery
____ can tx cancer of the adrenal gland (adrenal cortical carcinoma)
mitotane
“mighty tank”
name short, intermediate and long acting corticosteroids and the duration of action
short: 8-12 hours
- hydrocortisone (cortisol)
- cortisone acetate
intermediate: 12-36 hrs
- prednisone / prednisolone / methylprednisolone
- triamcinolone
long: 36-72 hrs
- dexamethasone
- bethamethosone
*dexamethasone suppression test use to dx cause of Cushings syndrome
pharmokinetics and toxicities of prednisolone
(intermediate acting: 12-36hr ; glucocorticoid agonist)
pharmokinectics: duration of activity is longer than pharmokinectic T 1/2 of drug owing to gene transcription effects
- SE: adrenal suppression
___ is used in dx of adrenal insufficiency (addisons) and occasionally in tx of Cushings (hypercortisolism)
metyrapone
mifepristone MOA, clinical use and SE
- glucocortcoid and progesterone antagonist
- use: medical abortion
- se: vaginal bleeding
two mineralocorticoid receptor antagonists, clinical use, pharmokinetics, and SE
- spironolactone
- tx aldosteronism, hypokalemia from diuretic use, post MI
- kinectics: slow onset and offset (lasts 24-48hrs)
- SE: hyperkalemia, gynecomastia, interaction with other K+ retaining drugs - eplerenone
- tx HTN
- kinectics: cleared by CYP 450 {FYI}
- SE: hyperkalemia, no gynecomastia
ketoconazole MOA, use, SE
MOA: corticosteroids synthesis inhibitor
use: inhibits mammalian steroid hormone synthesis and FUNGAL ERGOSTEROL SYNTHESIS (tx fungal infections)
SE: many drug-drug CYP 450 interactions
what anti-thyroid medication takes weeks for the effects to start ? what is its MOA? and used for tx of? and SE?
radioactive idodine 131 sodium
-MOA: taken up by thyroid, collects in colloid, and creates permanent destruction and damage to thryoid
- tx: graves (hyperthyroidism) ; multi nodular goiter
- SE: AVOID IN PREGANCY ; worsens graves opthalmopathy, will need thyroid replacement following tx
2 types of thioamides? MOA, SE, and tx use
- MOA: decrease TH production/ inhibit hormone synthesis by INHIBITING TPO –> inhibit iodide oxidation organification and coupling
- SE: maculopapular pruritic rash (MC) , lupus like syndrome, agranulocytosis (most dangerous , increases risk of infection) , worsens graves opthalmopathy, hypothyroidism
- PTU (propylthiouracil)
- also inhibits T4–> T3 peripheral conversion by blocking 5 deiodinase
- tx: thyroid storms , used first trimester of pregnancy
- SE: hepatotoxic - methimazole
- perferred thioamide
- used in 2 and 3 trimesters in pregnancy
