Endocrine Flashcards
Lispro
1) Type I DM, Type II DM, gestational DM, life-threatening hyperkalemia, stress-induced hyperglycemia
2) Insulin/Bind insulin receptor (tyrosine kinase activity) -Liver: increase glucose stored as glycogen-Muscle: increase glycogen and protien synthesis and K+ uptake-Fat: aids in TG storage3)Hypoglycemia, very rarely hypersensitivy rxns4)Rapid-acting
Aspart
1)Type I DM, Type II DM, gestational DM, life-threatening hyperkalemia, stress-induced hyperglycemia2)Insulin/Bind insulin receptor (tyrosine kinase activity) -Liver: increase glucose stored as glycogen-Muscle: increase glycogen and protien synthesis and K+ uptake-Fat: aids in TG storage3)Hypoglycemia, very rarely hypersensitivy rxns4)Rapid-acting
Glulisine
1)Type I DM, Type II DM, gestational DM, life-threatening hyperkalemia, stress-induced hyperglycemia2)Insulin/Bind insulin receptor (tyrosine kinase activity) -Liver: increase glucose stored as glycogen-Muscle: increase glycogen and protien synthesis and K+ uptake-Fat: aids in TG storage3)Hypoglycemia, very rarely hypersensitivy rxns4)Rapid-acting
Regular
1)Type I DM, Type II DM, gestational DM, life-threatening hyperkalemia, stress-induced hyperglycemia2)Insulin/Bind insulin receptor (tyrosine kinase activity) -Liver: increase glucose stored as glycogen-Muscle: increase glycogen and protien synthesis and K+ uptake-Fat: aids in TG storage3)Hypoglycemia, very rarely hypersensitivy rxns4)Short-acting
NPH
1)Type I DM, Type II DM, gestational DM, life-threatening hyperkalemia, stress-induced hyperglycemia2)Insulin/Bind insulin receptor (tyrosine kinase activity) -Liver: increase glucose stored as glycogen-Muscle: increase glycogen and protien synthesis and K+ uptake-Fat: aids in TG storage3)Hypoglycemia, very rarely hypersensitivy rxns4)Intermediate
Glargine
1)Type I DM, Type II DM, gestational DM, life-threatening hyperkalemia, stress-induced hyperglycemia2)Insulin/Bind insulin receptor (tyrosine kinase activity) -Liver: increase glucose stored as glycogen-Muscle: increase glycogen and protien synthesis and K+ uptake-Fat: aids in TG storage3)Hypoglycemia, very rarely hypersensitivy rxns4)Long-acting
Detemir
1)Type I DM, Type II DM, gestational DM, life-threatening hyperkalemia, stress-induced hyperglycemia2)Insulin/Bind insulin receptor (tyrosine kinase activity) -Liver: increase glucose stored as glycogen-Muscle: increase glycogen and protien synthesis and K+ uptake-Fat: aids in TG storage3)Hypoglycemia, very rarely hypersensitivy rxns4)Long-acting
Metformin
1)First-line therapy in Type II DM, can be used in pts w/o islet function2)Biguanide/ Exact MOA unknown –> decreases gluconeogenesis, increases glycolysis, increases peripheral glucose uptake (insulin sensitivity)3)GI upset, lactic acidosis (most serious)4)Contraindicated in renal failure
Tolbutamide
1)Type II DM –stimulate endogenous insulin release2)Sulfonylureas (1st generation)/Close K+ channel in beta cell membrane so cell depolarizes –> triggers insulin release via Ca2+ influx3)Disulfiram-like effects4)Useless in Type I DM b/c requires some islet cell function
Chlorpropamide
1)Type II DM –stimulate endogenous insulin release2)Sulfonylureas (1st generation)/Close K+ channel in beta cell membrane so cell depolarizes –> triggers insulin release via Ca2+ influx3)Disulfiram-like effects4)Useless in Type I DM b/c requires some islet cell function
Glyburide
1)Type II DM – stimulates endogenous insulin release2)Sulfonylureas (2nd generation)/Close K+ channel in beta cell membrane so cell depolarizes –> triggers insulin release via Ca2+ influx3)Hypoglycemia4)Useless in Type I DM b/c requires some islet cell funciton
Glimepiride
1)Type II DM – stimulates endogenous insulin release2)Sulfonylureas (2nd generation)/Close K+ channel in beta cell membrane so cell depolarizes –> triggers insulin release via Ca2+ influx3)Hypoglycemia4)Useless in Type I DM b/c requires some islet cell funciton
Glipizide
1)Type II DM – stimulates endogenous insulin release2)Sulfonylureas (2nd generation)/Close K+ channel in beta cell membrane so cell depolarizes –> triggers insulin release via Ca2+ influx3)Hypoglycemia4)Useless in Type I DM b/c requires some islet cell funciton
Pioglitazone
1)Monotherapy in Type II DM or in combination therapy2)Glitazone/Thiazolidinedione: Incraeses insulin sensitivity in peripheral tissue; binds PPAR-gamma nuclear transcription regulator –> incr Adiponectin expression3)Weight gain, edema, hepatoxicity, heart failure
Rosiglitazone
1)Monotherapy in Type II DM or in combination therapy2)Glitazone/Thiazolidinedione: Incraeses insulin sensitivity in peripheral tissue;, binds PPAR-gamma nuclear transcription regulator –> incr Adiponecti expression3)Weight gain, edema, hepatoxicity, heart failure