Flashcards in 173 DM drugs Deck (18):
insulin receptor type and mechanism of action once bound
receptor tyrosine kinase --> tyrosine phosphorylation activates...
1) phophoinositide-3 kinase pathway --> glycogen synthesis AND GLUT4 into membrane
2) Ras/MAP kinase pathway --> cell growth and differentiation
is insulin anabolic or catabolic? what transporter is insulin dependent? what tissue has it?
anabolic in liver, muscle, fat
muscle and adipose
what happens to glycogen, triglycerides, and proteins with an insulin deficiency?
broken down to provide fuel --> hyperglycemia --> osmotic diuresis, dehydration --> low cerebral bloodf low --> coma and death
also get ketone bodies --> metabolic acidosis
short acting insulins names? Difference?
regular + "LAG"
the bottom 3 are faster onset - take before meal and last while meal is digested
asapart and gluilisine are used for CSII
longer acting insulin
NPH (neutral protamine hagedorn) - protamine slows absorption
Glargine - acidic so can't mix
detemir - binds albumin
1-2 x day w/ short acting insulin
basal/bolus - long acting at night or morning w/ premeal short acting insulin
split-mixed - pre breakfast and pre dinner injections - combo of short and long acting
hyperglycemia responds more rapidly than acidosis
insulin-induced hypoglycemia rx
#1 glucose - oral,iv
glucagon - sc, im, iv --> GPCR --> cAMP --> increases hepatic glucose production
diazoxide - opens K channel, decreases insulin
blocks K channel --> depol --> insulin release
DM2 (requires islet fxn)
hypoglycemia (esp old with bad liver/kidney)
--I serine protease dpp-4 which stops it from blocking GLP-1 (thus allows GLP-1 to fxn) --> increases Insulin AND lowers glucagon
UTI, respiratory infections
AMP kinase --> decreases gluconeogenesis, increases glucose uptake
monotherapy, 1st line for DM2 (can be used in those without islet fxn)
GI upset, lactic acidosis (careful in those w/ renal failure)
__tide (NOT _lintide) - exenatide, liraglutide
GPCR --> cAMP --> PKA --> Ca --> insulin release AND lowers glucagon release
nausea, vomiting, pancreatitis
binds PPAR --> promotes transcription of insulin sensitive genes in liver, muscle, adipose --> increases insulin sensitivity
weight gain, edema, hepatotoxicity, heart failure
--I glucosidase at brush border --> decreased glucose absorption
mimics amylin in hindbrain --> slows gastric emptying --> decreases glucose concentrations after meals AND decreases glucagon
DM1 and 2
hypoglycemia, nausea, diarrhea
what increases glucose excretion?
SGLT2 inhibitor - canagliflozin