MOA/Kinetics Flashcards
Biguanides
Decreases hepatic gluconeogenesis
Enhances muscle insulin sensitivity
Reduces intestinal glucose absorption in S.I.
*does NOT affect pancreas (this decreases chance of hypoglycemia)
It is eliminated renally
SGLT2 Inhibitors
Sugar is excreted rather than reabsorbed in the kidneys (“Peeing out Sugar)
Metabolized in the liver, excreted in the kidneys
Long half life
GLP-1 Agonists
Acts like GLP-1
- increases secretion of insulin from B-cells
- suppresses glucagon release after meals
DPP-IV Inhibitors
Prevents degradation / prolongs half life of GLP-1
Sulfonylureas
Insulin secretagogues - helps pancreatic B cells squeeze out more insulin
Drug loses efficacy once B cells stop fnxing
*Glimepiride - has a longer half life; protein bound; excreted in urine and feces
Thiazolidinediones (TZD)
Primary: increases insulin sensitivity in peripheral tissues (fat, muscles, liver)
Secondary: decreased hepatic function
TZD is dependent on endogenous insulin
Alpha-Glucosidase Inhibitors
Delays the breakdown and absorption of complex carbs and sucrose
-this decreases ppBG
Amylin Analog
Works with insulin to suppress ppBG secretion
-slows gastric emptying (liver and glucagon)
Long-Acting (basal) insulins
Forms a precipitate in SubQ tissues - delays absorption
Relatively constant
*Detemir - binds to albumin; not as long of effect as glargine
Ultra Long-Acting Insulin
Longer duration of the insulin
Rapid-Acting Insulins
Lowers ppBG
Onset: 5-15 min
Peak: 30-90 min
Duration: 3-5 hours
Short-Acting Insulins
Non-disease-producing E.Coli synthesizes human insulin
Prandial/constant infusion inpatient
Peak: 2-3 hours
Duration: 4-8 hours
Intermediate-Acting Insulins
Synthesized by E.coli strain
*Protamine - delays absorption
Premixed Insulins
Mimics how pancreas would act normally
