First Aid: Diabetes Drugs nccaffey

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insulin examples
lispro: rapid acting (post prandial)
aspart: rapid acting (post prandial)
regular: short acting (DKA)
NPH: intermediate (twice daily)
glargine: long acting (once daily)
detemir: long acting

insulin MOA
bind insulin receptor (tyrosine kinase activity)
liver: increase glucose stored as glucagon
muscle: increase glycogen and protein synthesis, K uptake
fat: aids TG storage

insulin clinical use
type I DM, type 2 DM, gestational diabetes, life-threatening hyperkalemia, and stress-induced hyperglycemia

insulin toxicities
hypoglycemia, hypersensitivity reaction (very rare)

sulfonylurea examples
1st gen: tolbutamide, chlorpropamide
2nd gen: glyburide, glimepiride, glipizide

sulfonylurea MOA
close K channel in beta-cell membrane, so cell depolarizes –> triggering of insulin release via increased Ca influx

sulfonylurea clinical use
stimulate release of endogenous insulin in type 2 DM. require some islet function, so useless in type 1 DM

sulfonylurea toxicities
1st gen: disulfiram-like effects
2nd gen: hypoglycemia

biguanide examples
metformin

biguanide MOA
exact mechanism unknown. decrease gluconeogenesis, increase glycolysis, increase peripheral glucose uptake (insulin sensitivity)

biguanide clinical use
oral. first line therapy in type 2 DM. can be used in patients without islet function

biguanide toxicities
most grave adverse effect is lactic acidosis (contraindicated in renal failure)

glitazones/thiazolidinedione examples
pioglitazone, rosiglitazone

glitazones/thiazolidinedione MOA
increase insulin sensitivity in peripheral tissue. binds to PPAR-gamma nuclear transcription regulator

glitazones/thiazolidinedione clinical use
used as monotherapy in type 2 DM or combined with above agents

glitazones/thiazolidinedione toxicities
weight gain, edema. hepatotoxicity, heart failure

alpha-glucosidase inhibitor examples
acarbose, miglitol

alpha-glucosidase inhibitor MOA
inhibit intestinal brush border alpha glucosidases. delayed sugar hydrolysis and glucose absorption –> decreased postprandial hyperglycemia

alpha-glucosidase inhibitor clinical use
used as monotherapy in type 2 DM or in combination with above agents

alpha-glucosidase inhibitor toxicities
GI disturbances

mimetic examples
pramlintide

mimetic MOA
decrease glucagon

mimetic clinical use
type 2 DM

mimetic toxicities
hypoglycemia, nausea, diarrhea

GLP-1 analog examples
exenatide

GLP-1 analog MOA
increase insulin, decrease glucagon release

GLP-1 analog clinical use
type 2 DM

GLP-1 analog toxicities
nausea, vomiting, pancreatitis

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We use cookies to give you the best experience possible. By continuing we’ll assume you’re on board with our cookie policy Diabetes mellitus characterized by sustained hyperglycemia Two Major Forms -Type I diabetes (formerly known as insulin-dependent diabetes mellitus or …

We use cookies to give you the best experience possible. By continuing we’ll assume you’re on board with our cookie policy type 2 diabetes occurs from: a combination of pancreatic beta cell impairment and cellular insulin resistance what are likely …

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We use cookies to give you the best experience possible. By continuing we’ll assume you’re on board with our cookie policy TERMINOLOGY … alpha glucosidase inhibitor type of oral anti diabetic agent that delays the absorption of carbohydrates in the …

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