Diabetes and Insulin Flashcards
Insulin concentration
100U/ml
very rapid acting insulin
lisper, insulin aspart, glulisine
rapid acting insulin
regular
intermediate acting insulin
NPH
long acting insulin
detemir, glargine
ultra long acting
degludec
lispro
onset within 15 minutes, peak of action 45-75 minutes, duration 2-4h.
insulin aspart and glulisine
onset 10-15 minutes, peak 45-75 minutes, duration 2-4h
aspart (fiasp)
vitamin B3 added which may increase speed of absorption. onset 15-20 minutes, time to peak plasma concentration 1 hour, DOA 5-7h
regular insulin
onset 30 minutes, peak 2-4h after SQ injection because of insulin hexamers. duration 6-8h. periop single dose 1-5U or infusion .5-2U/h
Five Main SE:
- hypoglycemia
- allergic reactions
- lipodystrophy
- insulin resistance
- drug interactions
Oral Antidiabetic Drugs
- secretagogues
- biguanides
- thiazolidinediones or glitazones
- alpha glucosidase inhibitors
Metformin drug class and contraindications
oral biguanide, can be used in combination with insulin and sulfonylureas. contraindications: lactic acidosis, AKI, GI intolerance, acute hepatic disease
Metformin MOA
blood glucose lowering effect is not mediated through stimulation of endogenous insulin secretion
Metformin and Lactic Acidosis
- possible SE of metformin therapy
- discontinue 48h before elective surgery
- monitor for lactic acidosis, ABG, lactate, RFP
- anaerobic metabolism results in pyruvate–>reduced to lactate
- do not administer in patients with hepatic metabolism, renal insufficiency (creatinine >1.5mg/dL), IV contrast dye, acute MI, CHF, arterial hypoxemia, sepsis
- treatment: hemodialysis, bicarbonate administration
Sulfonylureas
- can lower glucose levels to hypoglycemic levels
- improved BG control, decreased hepatic production of very low density lipoproteins, improved hypertriglyceridemia
- up to 20% of patients do not have adequate hypoglycemic response to maximal doses (primary failures), and another 10-15% of patients who initially respond will fail to respond to therapy each year (secondary failure).
- successful treatment requires beta cell function
- do not administer to patients with sulfa allergy
Sulfonylureas MOA
act on sulfonylurea receptors on pancreatic and cardiac cells: inhibit adenosine triphosphate sensitive K channels on pancreatic beta cells resulting in calcium influx and stimulation of insulin release
How does sulfonylurea affect cardiovascular mortality
close potassium-ATPase channels and inhibit ischemic preconditioning aka the cardioprotective mechanism
Glyburide MOA
stimulates insulin secretion over 24 hour period. increases insulin sensitivity and inhibits liver production of glucose
glipizide MOA
increases glucose uptake and suppresses liver glucose output- effects persist for prolonged periods without tolerance. rapid plasma clearance minimizes risk for hypoglycemia
glimepiride MOA
decreases blood glucose by stimulating release of insulin from pancreas and may decrease hepatic glucose production. combined with insulin therapy when sulfonylureas are not effective
metglinide
exert effects on beta cells (similar to sulfonylureas). repaglinide, nateglinide.
repaglinide
stimulates release of insulin from beta islet cells of pancreas
nateglinide
lowers blood glucose by stimulating release of insulin from pancreas. accumulation of active metabolites may cause hypoglycemia
