Endocrine Pharmacology Flashcards
Name the 3 rapid acting insulins, and their peak time.
Lispro
Aspart
Glusine
What is the MOA of insulin in Liver, Muscle, Fat, and Cell Membranes.
Bind insulin receptor (tyrosine kinase activity).
Liver: Increase glucose stored as glycogen.
Muscle: increase glycogen, protein synthesis.
Fat: increase triglyceride storage.
Cell membrane: increase K+ uptake
Name the short acting insulin, and its peak time.
Regular - peak time 2-3hrs
Name the intermediate acting insulin, and it’s peak time.
NPH - 4-10hrs peak time
Name the 3 long acting insulins, and their peak times.
Detemir (Levemir) - 24hrs
Glargine (Lantis/Toujeo) - 20-24hrs
Degludec (Tresiba) - 42hrs
MOA: Normally secreted with insulin (made also in beta cells)- Decrease glucagon release, decrease gastric emptying, and increase satiety. Used in Px taking insulin but either type 1 or type 2. What class of drug is at hand, and what is its name?
Amylin analogs - Pramlintide
MOA: Decrease glucagon release, decrease gastric emptying, and increase glucose dependent insulin release, with increased satiety. What class of drugs are at hand, and what are their names. Side effects are nausea, vomiting, pancreatitis, and promotion of weight loss.
GLP-1 analogs: Exenatide, Liraglutide, Dulaglutide
MOA: Inhibit mGPD —> inhibition of hepatic gluconeogenesis and the action of glucagon. Increase glycolysis, peripheral glucose uptake (increase insulin sensitivity). SE: GI upset, B12 deficiency. Promotes weight loss. Name the class and medication.
Biguanides - Metformin
MOA: close K+ channel in pancreatic beta cell membrane —> cell depolarizes —> insulin release via increased Ca2+ influx. SE: Hypoglycemia (increased risk with renal failure), weight gain. Name the class of drug, and the first generation and second generations + their SEs.
Sulfonylureas:
1st Gen: Clorpropamide, Tolbutamide. SE: Disulfiram-like reactions/effects.
2nd Gen: Glimepiride, Glipizide, Glybiride. SE: hypoglycemia
MOA: close K+ channel in pancreatic beta cell membrane —> cell depolarizes —> insulin release via increased Ca2+ influx. SE: Hypoglycemia (increased risk with renal insufficiency), weight gain. Name the drug class plus medications.
Meglitinides - Nateglinide, Repaglinide
*Differs from Sulfonylureas because occurs at different binding site).
MOA: inhibits DPP-4 enzyme that deactivates GLP-1. Decrease glucagon release, gastric emptying. Increase glucose-dependent insulin release, satiety. SE: mild urinary or respiratory infections, weight neutral. Name the drug category and the 3 associated drugs.
DPP-4 Inhibitors.
Names: Linagliptin, saxagliptin, sitagliptin.
MOA: This drug binds to PPAR-gamma nuclear transcription regulator —> increasing insulin sensitivity and levels of adiponectin (in peripheral tissue of adipose and skeletal tissue)—> regulation of glucose metabolism and fatty acid storage. SE: weight gain, edema, HF, increased risk of fractures and hepatically excreted (CI in liver failure). Delayed onset of action (several weeks). Name the drug class and it’s associated drugs.
Glitazones/ Thiazolidinediones:
Pioglitazone (risk of bladder CA and osteoporosis) and Rosiglotazone (incr. MI and cardiovascular death)
MOA: Block the re absorption of glucose in proximal convoluted tubule. What is the drug class and associated drug?
Sodium-glucose-cotransporter 2 (SGLT2): Canagliflozin, dapagliflozin, empagliflozin
MOA: Inhibit intestinal brush-border alpha-glucosidases —> delayed carbohydrate hydrolysis and glucose absorption—> decreased postprandial hyperglycemia. SE: osmotic diarrhea, and CI in patients with impaired kidney function. What is the drug class and drug?
Alpha-glucosidase inhibitors: Acarbose and miglitol.
What if the MOA of Propylthioiracil and Methimazole.
Block conversion of T4 to T3.
