Endocrine Rx Flashcards
1) uses 2) class/ MOA 3) ADE 4)Fun fact/note
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 storage
3) Hypoglycemia, very rarely hypersensitivy rxns
4) Rapid-acting
1) uses 2) class/ MOA 3) ADE 4)Fun fact/note
Aspart
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 storage
3) Hypoglycemia, very rarely hypersensitivy rxns
4) Rapid-acting
1) uses 2) class/ MOA 3) ADE 4)Fun fact/note
Glulisine
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 storage
3) Hypoglycemia, very rarely hypersensitivy rxns
4) Rapid-acting
1) uses 2) class/ MOA 3) ADE 4)Fun fact/note
Regular
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 storage
3) Hypoglycemia, very rarely hypersensitivy rxns
4) Short-acting
1) uses 2) class/ MOA 3) ADE 4)Fun fact/note
NPH
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 storage
3) Hypoglycemia, very rarely hypersensitivy rxns
4) Intermediate
1) uses 2) class/ MOA 3) ADE 4)Fun fact/note
Glargine
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 storage
3) Hypoglycemia, very rarely hypersensitivy rxns
4) Long-acting
1) uses 2) class/ MOA 3) ADE 4)Fun fact/note
Detemir
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 storage
3) Hypoglycemia, very rarely hypersensitivy rxns
4) Long-acting
1) uses 2) class/ MOA 3) ADE 4)Fun fact/note
Metformin
1) First-line therapy in Type II DM, can be used in pts w/o islet function
2) 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
1) uses 2) class/ MOA 3) ADE 4)Fun fact/note
Tolbutamide
1) Type II DM –stimulate endogenous insulin release
2) Sulfonylureas (1st generation)/Close K+ channel in beta cell membrane so cell depolarizes –> triggers insulin release via Ca2+ influx
3) Disulfiram-like effects
4) Useless in Type I DM b/c requires some islet cell function
1) uses 2) class/ MOA 3) ADE 4)Fun fact/note
Chlorpropamide
1) Type II DM –stimulate endogenous insulin release
2) Sulfonylureas (1st generation)/Close K+ channel in beta cell membrane so cell depolarizes –> triggers insulin release via Ca2+ influx
3) Disulfiram-like effects
4) Useless in Type I DM b/c requires some islet cell function
1) uses 2) class/ MOA 3) ADE 4)Fun fact/note
Glyburide
1) Type II DM – stimulates endogenous insulin release
2) Sulfonylureas (2nd generation)/Close K+ channel in beta cell membrane so cell depolarizes –> triggers insulin release via Ca2+ influx
3) Hypoglycemia
4) Useless in Type I DM b/c requires some islet cell funciton
1) uses 2) class/ MOA 3) ADE 4)Fun fact/note
Glimepiride
1) Type II DM – stimulates endogenous insulin release
2) Sulfonylureas (2nd generation)/Close K+ channel in beta cell membrane so cell depolarizes –> triggers insulin release via Ca2+ influx
3) Hypoglycemia
4) Useless in Type I DM b/c requires some islet cell funciton
1) uses 2) class/ MOA 3) ADE 4)Fun fact/note
Glipizide
1) Type II DM – stimulates endogenous insulin release
2) Sulfonylureas (2nd generation)/Close K+ channel in beta cell membrane so cell depolarizes –> triggers insulin release via Ca2+ influx
3) Hypoglycemia
4) Useless in Type I DM b/c requires some islet cell funciton
1) uses 2) class/ MOA 3) ADE 4)Fun fact/note
Pioglitazone
1) Monotherapy in Type II DM or in combination therapy
2) Glitazone/Thiazolidinedione: Incraeses insulin sensitivity in peripheral tissue;, binds PPAR-gamma nuclear transcription regulator
3) Weight gain, edema, hepatoxicity, heart failure
1) uses 2) class/ MOA 3) ADE 4)Fun fact/note
Rosiglitazone
1) Monotherapy in Type II DM or in combination therapy
2) Glitazone/Thiazolidinedione: Incraeses insulin sensitivity in peripheral tissue;, binds PPAR-gamma nuclear transcription regulator
3) Weight gain, edema, hepatoxicity, heart failure
1) uses 2) class/ MOA 3) ADE 4)Fun fact/note
Acarbose
1) Monotherapy in Type II DM, or in combination therapy
2) Alpha-glucosidase Inhibitor/ Inhibits intestinal brush-border alpha-glucosidases –> get delayed sugar hydrolysis and glucose absorption
- decreases postprandial hyperglycemia
3) GI disturbances
1) uses 2) class/ MOA 3) ADE 4)Fun fact/note
Miglitol
1) Monotherapy in Type II DM, or in combination therapy
2) Alpha-glucosidase Inhibitor/ Inhibits intestinal brush-border alpha-glucosidases –> get delayed sugar hydrolysis and glucose absorption
- decreases postprandial hyperglycemia
3) GI disturbances
1) uses 2) class/ MOA 3) ADE 4)Fun fact/note
Pramlinitide
1) Type I and II DM
2) Amylin Analog/ Decreases glucagon
3) Hypoglycemia, nausea, diarrhea
1) uses 2) class/ MOA 3) ADE 4)Fun fact/note
Exenatide
1) Type II DM
2) GLP-1 Analog/ Increase insulin and decrease glucagon release
3) Nausea, vomiting, pancreatitis
1) uses 2) class/ MOA 3) ADE 4)Fun fact/note
Liraglutide
1) Type II DM
2) GLP-1 Analog/ Increase insulin and decrease glucagon release
3) Nausea, vomiting, pancreatitis
1) uses 2) class/ MOA 3) ADE 4)Fun fact/note
Linagliptin
1) Type II DM
2) DPP-4 Inhibitors/ Increase insulin and decrease glucagon release
3) Mild urinary or respiratory infections
1) uses 2) class/ MOA 3) ADE 4)Fun fact/note
Saxagliptin
1) Type II DM
2) DPP-4 Inhibitors/ Increase insulin and decrease glucagon release
3) Mild urinary or respiratory infections
1) uses 2) class/ MOA 3) ADE 4)Fun fact/note
Sitagliptin
1) Type II DM
2) DPP-4 Inhibitors/ Increase insulin and decrease glucagon release
3) Mild urinary or respiratory infections
1) uses 2) class/ MOA 3) ADE 4)Fun fact/note
Propylthiouracil
1) Hyperthyroidism
2) Block peroxidase inhibiting organificatoin of iodide anda coupling of thyroid hormone synthesis
- also blocks 5’-deiodinase –> decreases peripheral conversion of T4 to T5
3) Skin rash, agranulocytosis (rare), aplastic anemia, hepatotoxicity