Diabetes Final Study Flashcards
Metformin
MOA: activates AMPK
(increase AMPK in hepatocytes and SKM –> decrease ATP consumption while increase ATP production –> increase insulin sensitivity –> decrease glucose –> decrease insulin)
AEs:
GI (D/N, metallic taste, decreased B12 abs)
Lactic acidosis (risk factors: decrease kidney function, low O2, liver diseases/XS ETOH)
CI: Pregnancy
*Improves lipid profile
*decreases LDL, decreases, TG, increases HDL
Pioglitazone, Rosiglitazone
MOA: PPRA(gamma) agonist –> gene transcription
(increase good adipocytokines, decreases bad adipocytokines, inflammatory cytokines)
AEs: edema (Na/H2O rtn) –> weight gain
bone loss
hepatotoxiciy
CI: HF, bladder CA, bone fractures, liver disease
*Improves lipid profile (Pio)
*Slow onset effects (1-2wk onset, 2-3 months max effect)
Glimerpiride, Glipizide, Glyburide, Nateglinide, Repaglinide
MOA: inhibit K channels –> increase insulin secretion
(inhibit/close K channels –> depolarization –> open VG Ca2+ channels –> increase insulin secretion)
AEs:
Hypoglycemia (palpitations, sweating, tremor, anxiety, hunger, etc)
-risk factors: exercise/ skip meal, high drug dose, XS ETOH, impaired renal/liver function
Weight gain
CI: renal impairment
*does not work on T1DM pts
Glimerpiride, Glipizide, Glyburide, Nateglinide, Repaglinide
MOA: inhibit K channels –> increase insulin secretion
(inhibit/close K channels –> depolarization –> open VG Ca2+ channels –> increase insulin secretion)
AEs:
Hypoglycemia (palpitations, sweating, tremor, anxiety, hunger, etc)
-risk factors: exercise/ skip meal, high drug dose, XS ETOH, impaired renal/liver function
Weight gain
CI: renal impairment
*does not work on T1DM pts
Exenatide, Lixisenatide, Liraglutide, Dulaglutide, Semaglutide
MOA: stimulated glc-mediated insulin secretion (Gs coupled) (dependent on depolarization)
AEs:
GI: (N/V/D)
Weight loss (decrease appetite, decrease gastric emptying) (Lira)
CI: Medullary thyroid cancer, pancreatitis
*administer SC
*decrease CV risk (Lira)
Sitagliptin, Linagliptin, Saxagliptin, Alogliptin
MOA: inhibit DPP4 –> decrease breakdown of GLP1
AEs: increase upper respiratory infection
well tolerated
CI: HF
*doesn’t share AEs with GLP1 agonists
*breaks down many peptides
Canagliflozin, Dapagliflozin, Empagliflozin
SGLT2 Inhibitor
MOA: inhibits SGLT2 –> increase U(glc)V
AEs:
Amputations (Cana)(neuropathy, foot lesions, etc)
UTIs
Hypotension (acts as osm. diuretics)
AKI
euglycemic DKA
CI: severe renal impairment
*decrease CV risk
*weight loss
Insulin
MOA: increase glc uptake into adipose tissue and SKM –> decrease hepatic glc production
AEs:
hypoglycemia
weight gain