Pharm- DM Flashcards
(12 cards)
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
