Endocrine Drugs Flashcards
What are the rapid acting Insulin drugs?
How do they work?
Lispro
Aspart
Glulisine
MOA: Bind Insulin Receptor (tyr kinase activity)
Liver–>Make Glucose into Glycogen
Sk Muscle–>Incr Glycogen, protein synthesis, K+ uptake
Adipose–>Make TGs
Basically all the things that insulin does
Can use this to control postprandial glucose bc it peaks in like 45-75 mins
What are the short acting Insulin Drugs?
Just called Regular
Can use this for all types of diabetics including DKA & for hyperkalemia. ONLY ONE FOR DKA
starts working in 30 mins but PEAKS in 2-4 hours so not good bc its after postprandial tide.
Takes long bc of dimer/hexamer formation
What is the Intermediate acting Insulin?
NPH. Works like all the other insulins…tyrosine kinase and same effects on liver, sk muscle and adipose
What are the long acting Insulins?
Glargine, Detemir, Ultralente
MOA is same
This is for basal control of insulin
They stick around for a long time bc they attach to albumin, esp Detemir, it has a FA that attaches to Lysine residue on Albumin
What are the biguanides and how do they work?
Which diabetic is this for?
SE…there’s a serious one
Metformin
Works by preventing the liver from performing GLUCONEOGENESIS
Increases glycolysis, and increases peripheral insulin sensitivity
Mostly for Type II
SE: LACTIC ACIDOSIS!!! So cannot use in a renal failure patient
Since it blocks gluconeogenesis, lactate can’t be used in that cycle so has to be excreted and thats too much for a diseased kidney
What are the sulfonylureas?
MOA?
SE?
Two Generations
First: Tolbutamide, Chlorpropramide
Second: Gs…Glyburide, Glimepiride, Glipizide
Close the K+ channel in pancreatic B cell–>depolarization–>Ca+ channel opens–>Ca+ enters cell–>Insulin release
Obviously need some islet function for these to work so cant use in type I
SEs:
First Gen: Disulfiram like effects
Second Gen: Hypoglycemia
What are the glitazones/thiazolidinediones?
MOA
SEs
Pioglitazone, Rosiglitazone
Bind to PPARy which is a nuclear transcriptor regulator
Increases peripheral insulin sensitivity, increases adiponectin levels which is low in type II. Adiponectin also incr FA transport, increase insulin receptors, incr Glut-4 receptors
For Type II
SEs: Heart Failure and Hepatotoxic (check for Liver Function)
What are the a-glucosidase inhibitors?
MOA?
SEs?
Acarbose
Miglitol
Inhibits Intestinal brush border a-glucosidases–>delayed sugar hydrolysis amd glucose absorption–>lowers postprand hyperglycemia
Type II
SEs: GI Disturbances, so dont use in:
IBD, malabsorption, colonic ulcers, obstructions
also causes lactose intolerance like symptopms ie flatulence, bloating
What are the amylin analogs?
MOA?
SEs?
Pramlintide
Decreases gastric emptying, glucagon
For type I & II
SEs: Hypoglycemia, n/v diarrhea
What are the GLP-1 analogs?
MOA?
SEs?
Exenatide, Liraglutide
Increase Insulin, Decrease glucagon
Stands for glucagon like peptide
For type II
SEs: PANCREATITIS, n/v
How does GLP-1 work in the body?
Potent antihyperglycemic that simultanously INCREASES insulin and DECREASES glucagon ONLY IN THE PRESENCE OF GLUCOSE!!
w/o glucose it doesnt work so no hypoglycemia
GLP is blocked by DPP (dipeptidyl peptidase)
What are the DPP Inhibitors?
MOA?
SEs?
The Gliptins:
Linagliptin, Saxagliptin, Sitagliptin
Increase Insulin, Decrease glucagon
for Type II
DDP degrades GLP-1
