Pharm- DM Flashcards
What are the drug classes for DM that can be injected?
Insulins
Amylin Analogs
GLP1 Analogs
What are the different Insulins (classes and peak activity time)
Rapid Acting- (no LAG)- lispro, aspart, glulisine (1 hr)
Short Acting- regular insulin (use for DKA and hyperkalemia) (2-3hr)
Intermediate Acting- NPH (4-10 hr)
Long Acting- detemir and glargine (no peak activity)
What are the actions and AE of insulins?
Actions- inc glycogen and protein synthesis and inc K uptake
AE- hypoglycemia (confusion and LOC)
What is the amylin analog? What is its MOA? What are its AE?
Pramlintide
MOA- dec glucagon and gastric emptying, inc insulin sensitivity and fullness
AE- hypoglycemia and nausea
What are the GLP1 analogs? What is its MOA? What are its AE?
Exenatide and Liraglutide
MOA- dec glucagon and gastric emptying, inc glucose dependent insulin secretion and fullness
AE- NV, pancreatitis, and wt loss
What are the oral drug classes used for DM?
Biguanides, K-ATP blockers (sulfonylureas or glunides), DDP4 inhibitors, glitazones, SGLT2 inhibitors, and a-glucosidase inhibitors
What is the biguanide? What is its MOA? What is its AE and CI?
Metformin
MOA- activates AMPK- inc glucagon, glycolysis, and insulin sensitivity
AE- lactic acidosis, b12 deficiency, and GI problems
CI- RF, HF, COPD, and alcoholism
What are the K-ATP inhibitors? What are their MOA? What are their AE?
1st gen sulfonylureas- “amides”- AE- wt gain and alcohol induced flushing
2nd gen sulfonylureas- “gli-ides”- AE- wt gain and hypoglycemia
Glinides- AE- wt gain and hypoglycemia
MOA- block K-ATP channel -> release insulin
What are the DDP4 inhibitors? What is the MOA? What are their AE?
“Gliptins”
MOA- DDP4 typically degrades GLP1; same actions as GLP1 analogs; dec glucagon and gastric empyting, inc glucose dependent insulin secretion and fullness
AE- urinary and respiratory infections
What are the Glitazones MOA and AE?
Glitazones
MOA- activate PPARgamma- inc adoponectin which inc tissue sensitivity to insulin by stim FA oxidation; move NEFAs into fat deposits
AE- wt gain, edema, HF, and osteoporosis
What are the SGLT2 inhibitors? What are their MOA? What are their AE?
“Gliflozins”
MOA- block glucose reabsorption in PCT
AE- glucosuria, dehydration, hypotension, and UTI
What are the a-glucosidase inhibitors? What are their MOA? What are their AE?
Acarbose and miglitol
MOA- inhibit brush border a-glucosidase to dec GI absorption of glucose and prevent post-meal hyperglycemia
AE- diarrhea
