Drugs Used in Diabetes Flashcards
Pathology behind Type 1 DM?
loss of pancreatic B cells > absolute dependence on insulin
Pathology behind Type 2 diabetes?
decreased response to insulin
Which type of diabetes is ketoacidosis prone?
Type 1 DM
Name some basal insulin forms.
glargine, determir, degludac
Name some meal time insulin medications.
lispro, regular, aspart, glulisine
What are some factors/drugs that can increase insulin release?
increased by glucose, sulfonylureas, M-agonists, B2 agonists
What are some factors that can decrease insulin release?
a2 agonists
What are the symptoms associated with diabetic ketoacidosis?
polyuria, polydipsia, nausea, fatigue, dehydration, Kussmaul breathing, “fruity” breath
What is the best treatment for diabetic ketoacidosis?
regular insulin IV, fluid and electrolyte replacement
Do most basal forms of insulin have a peak?
no
MOA of glargine.
insulin binds to the transmembrane receptors which activate tyrosine kinase to phosphorylate tissue-specific substrates
What is the DOC for Type II diabetes?
metformin
Does metformin cause hypoglycemia or weight gain?
no
MOA metformin.
may involve inc. tissue sensitivity to insulin and/or dec hepatic gluconeogenesis
Indications for metformin.
mono therapy or combinations for treatment of Type II DM
S/E metformin use?
possible lactic acidosis, GI distress
Name a drug class that metformin has synergistic activity with?
sulfonylureas
Acarbose MOA.
inhibits a-glucosidase in brush borders of SI > dec formation of absorbable carbs > dec postprandial glucose > dec demand for insulin
What are the S/E of acarbose?
GI discomfort, flatulence, diarrhea; recent concern over potential hepatotoxicity
What is a way to tell if diabetic medication has potential to cause hypoglycemia vs if it doesn’t?
If the target in the diabetes medication is glucose > there is not a risk of hypoglycemia;
If the target in the diabetes medication is insulin; then it has potential to cause hypoglycemia
What is the MOA of sulfonylureas? How do they affect glucagon release?
- Normally K+ efflux in pancreatic B cells maintains hyper-polarization of membranes; insulin is release only when depolarization occurs
- Acute action of sulfonylureas is to block K+ channels> depolarization > insulin release
*dec glucagon release
*inc. insulin receptor sensitivity