Copy of Endocrine Rx - Sheet1 Flashcards
Lispro, aspart, gluisine
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
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
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
Glargine, 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
Metformin
1) oral; 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
Tolbutamide, chloropropamide
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
Glyburide, glimepiride, 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
Pioglitazone, 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–> activates genes that reg fa storage and glucose met–> inc insulin sensitivity & adiponectin
3) Weight gain, edema, hepatoxicity, heart failure
Acarbose, 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
Pramlinitide
1) Type I and II DM
2) Amylin Analog/ Decreases glucagon
3) Hypoglycemia, nausea, diarrhea
Exenatide, liraglutide
1) Type II DM
2) GLP-1 Analog/ Increase insulin and decrease glucagon release
3) Nausea, vomiting, pancreatitis
Linagliptin, saxagliptin, sitagliptin
1) Type II DM
2) DPP-4 Inhibitors/ Increase insulin and decrease glucagon release
3) Mild urinary or respiratory infections
Propylthiouracil, methimazole
1) Hyperthyroidism
2) Block peroxidase inhibiting organificatoin of iodide and coupling of thyroid hormone synthesis
- propylthiouracil also blocks 5’-deiodinase –> decreases peripheral conversion of T4 to T3
3) Skin rash, agranulocytosis (rare), aplastic anemia, hepatotoxicity (propylthiouracil), Teratogen (methimazole)
Levothyroxine, triiodothyronine
1) Hypothyroidism, myxedema
2) THyroxine replacement
3) Tachycardia, heat intolerance, tremors, arrhythmias
GH
1)GH deficiency, Turner’s Syndrome