Drugs Flashcards
amphotericin B
antifungal.
MOA: binds ergosterol and drills pores into membrane
flucytosine
antifungal.
MOA: the fungal enzyme cytosine permease eats this yummy 5-FC –> inhibition of RNA and DNA synthesis
covers Crytpococcus (used with ampho B), candida
SE: bone marrow toxicity
azoles (fluconazole)
antifungal.
MOA: inhibits production of ergosterol, and CYP450 enzymes
SE: hepatotoxicity, GI upset
echocandins (caspofungin)
antifungal.
MOA: inhibits synthesis of B-1,3-glucan –> disruption of cell wall. for candida.
SE: GI, flushing. don’t give with cyclosporin (LFTs)
griseofulvin
oral antifungal. keratophilic (skin hair nails)
MOA: deposits in skin, binds keratin, protects skin/hair while new layers grow
SE: serum-sickness allergy, hep, interactions
terbinafine
oral antifungal. keratophilic
MOA: fungicidal - inhibits squalene epoxidase - buildup of squalene kill fungi. allyamines
SE: liver toxicity, GI, HA
nystatin
topical antifungal.
MOA; like ampho B, binds ergosterol and makes membrane holes
use: oral thrush, vulvovaginal candidiasis
metformin
1st line for type II diabetes. decreases gluconeogenesis. SEs: GI upset, LACTIC ACIDOSIS is a potential super bad effect
sulfonylureas
used in type II diabetes. close K+ channel so that depolarization of beta cells occurs. SEs: hypoglycemia, weight gain. require pancreatic function.
Thiazolidinediones (TZDs) - “glitazones”
increase insulin sensitivity by binding to PPAR-y. weight gain, edema, heart failure
DPP-4 inhibitors - “gliptins”
increases insulin, decreases glucagon
GLP-1 analogs - exenatide and liraglutide
increases insulin, decreases glucagon. mimics incretins, delays gastric emptying. SEs: N+V, pancreatitis. no hypoglycemia because this drug is glucose dependent yay!
Amylin analogs (pramlintide)
decrease gastric emptying, decrease glucagon
a-glucosidase inhibitors (acarbose, miglitol)
decrease postprandial hyperglycemia. SEs: GI, cirrhosis, bowel problems
