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38 Cards in this Set

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  • Back
Dopamine agonist treatment for prolactinoma
Bromocriptine (D2/D1) and Cabergoline (D2)
Side effects of Cabergoline
Headache, nausea, orthostatis HTN; discontinue for psychosis
Treatment for Acromegaly: Octreotide
Somatostatin analogue (cholesterol gallstones common)
Treatment for Acromegaly: Bromocriptine
Dopamine agonist (20% see improvement)
Treatment for Acromegaly: Pegvisomant
Competitive GH-receptor antagonist
Dexamethasone testing for HPA differentiation on cortisol
Adrenal/ectopic ACTH-production cortisol levels NOT suppressed by negative feedback
Metyrapone testing
If ACTH rises, but cortisol precursors don't, signals adrenal insufficency. If neither ACTH or precursors rise, impaired HPA axis. (MOA: blocks conversion of precursors to cortisol)
Vasopressin receptors
V1- vasoconstrictor (IP3,Low affinity); V2- antidiuretic (cAMP, high); V3- ACTH stimulation from pituitary
Desmopressin receptor selectivity
V2- antidiuretic
Desmopressin in DI treatment
Central (eliminates thirst/fluid intake), Dipsogenic (eliminates urination, not thirst/intake)
Water deprivation test
Central/polydipsia respond as normal. Central responds with Desmopressin. Nephrogenic never responds.
Treatment for SIADH
Cautious infusion of hypertonic saline / furosemide (diuretic) (not too quickly, avoid demyelination); fluid restriction if not severe, V2 receptor antagonists (Aquaretics)
Somatropin MOA
Recombinant human GH
Mecasermin MOA
Agonist directly at IGF-1 receptor in target tissues if somatropin fails
Desmopressin MOA
Selective V2 receptor agonist in kidney (antidiuretic)
Cellular response to Desmopressin
Activates G protein in V2 receptor; activation of kinases to receptor coupled aquaporin; increases transport of H2O to reverse hyperosmolality; dilutes concentration of sodium
Vasopressin
Non-selective V1/V2 receptor; corrects low bp; may lead to HTN / CNS toxicity
Octreocide MOA
Somatostatin receptor to inhibit GH release; injection; gallstones, GI, hyperglycemia, hypoinsulinemia
Pegvisomant MOA
Liver GH receptor antagonist; blocks IGF-1 production
Conivaptan MOA
Non-seletive vasopressin V1/V2 receptor antagonist (SIADH), reduces hyponatremia
Tolvaptan MOA
Oral V2 antagonist (SIADH)
Common side-effects of dopamine receptor agonists
Bromocriptine/Cabergoline- orthostatic HTN, ergot-related (burning), CV risk (arrythmia), CNS (delusions, hallucinations, psychosis)
Mineralocorticoid MOA
Alters transcription to increase Na+/K+ ATPase expression (inc. blood vol.)
Glucocorticoid MOA
Dislodged heat shock protein (HSP), activates receptor, activates glucocorticoid response element (GRE)
Anti-inflammatory MOA of glucocorticoids
Cortisol binds GRE, prevents transcription of cytokines and increases anti-inflammatory transcription (PLA2 inhibitor)
Adrenal steroid agonist with 1:1 ratio
Hydrocortisone (gluco:mineralo)
Short-acting, low selectivity corticosteroids
Prednisone (oral), prednisolone, methyprednisolone
Intermediate-acting low selectivity corticosteroids
Triamcinolone
Long-acting, highly selective corticosteroids
Betamethasone, dexamethasone, beclomethasone (antiinflammatory effect)
MOA for corticosteroids
Increase transcription of lipocortin-1 (inhibits PLA2)
Long-term effects of corticosteroids
Catabolic (growth suppression, muscle loss), osteoporosis, cataracts/glaucoma, neurological (hypomania, psychosis, insomnia, anxiety)
Why must pt ween off of corticosteroids?
Adrenal suppression
Tx for Addison's
Hydrocortisone, androgens, fludrocortisone (selective mineralocorticoid receptor agonist)
Reason for iatrogenic Cushing's in pt on Ritonavir
Ritonavir is a CYP3A4 inhibitor, required for corticosteroid metabolism
Ketoconazole MOA
Inhibits 17a-hydroxylase and 11B-hydroxylase
Aminoglutethimide MOA
Inhibits Cholesterol desmolase and aromatase; nausea, dizziness (decreased T4 -> T3 conversion)
Major ketoconazole effect
CYP3A4 inhibitor (drug interactions), hepatotoxicity
Metyrapone MOA in Cushing's Tx
11B-hydroxylase inhibitor, causes HTN (precursor build-up), androgenic