Hyperlipidemia Davis Flashcards
Major risk factors for CHD?
- prior chd
- diabetes
- age
- high LDLC low HDLC
- family history
- current smoker
- obesity
What is the MOA of STATINS
HMG-CoA reductase inhibitor
inhibits cholesterol biosynthesis, upregulation of LDL-R
What are the “other” potential benefits of statins (besides increasing LDLR!)
improved endothelial cell fxn! (vascular tone)
improved plaque stability
potential cancer treatment
MILD side effect profile of statins include
myopathy, rhabdomyolysis, diabetes risk, cognitive problems
What are the two Bile acid binding resins?
Cholestyramine and colestipol
What is the MOA of BABR?
Resins Reside in intestine, tightly bind to bile acids, eliminated in the feces. This directs more cholesterol to bile synthesis (and reduces LDL C)
Can a bile acid binding resin be used monotherapy?
noooooo.depletion of levels compensated by upregulation! SO use with statin! cholesterol syn blocked
What are the lipid modifying effects of Niacin?
B3! Lowers LDL-C, raises HDL-C, lowers triglycerides
How does Niacin exert its beneficial effects on lipids??
ACTIVATES a GPR in adipose tissue, decreases the release of Free Fatty Acids from stored triglycerides.
What class of drugs work through activation of PPARalpha?
Fibrates: gemfibrozil, ciprofibrate, fenofibrate
dec trig, inc hdlC
What are three possible glucose toxicity mechanisms?
Covalent addition of glucose to protein, increased glucose metabolism leading to increased formation of oxidants, osmotic effects of high glucose.
What makes T2DM treatment distinct from T1DM?
T2DM relies on patient’s residual capactiy for insulin secretion. drugs act to enhance insulin production or enhance actions
What are the two fastest acting insulin preparations?
Lispro and aspart insulin
Which form of insulin is the longest acting?
glargine
MOA lowers blood glucose levels HOW?
Activates AMPKinase which leads to reduced gluconeogenesis, enhanced insulin action on peripheral tissues
what is the difference between 1st generation and 2nd generation sulfonyureas?
2nd generation are 100x more potent
Tulbutamide
first generation sulfonyurea
bind to ATP sensitive K channel to reduce conductance, turns on the normal regulation of insulin secretion.
Chlorpropamide (sulfonyurea) main difference from tolbutamide is?
WAYY longer half life
second generation sulfonyurea?
glyburide and glipizide
Glitinides have a similar MOA to sulfonyreas. What are two examples of drugs and what is the MOA?
Replaglinide and nateglinide!!
CLOSE atp sensitive K channel…. these have a rapid onset and a short duration
What drug classs is an agonist of PPAR gamma?
Thiazolidiniediones! Rosiglitazone and pioglitazone
What is the MOA of the glitazones?
through agonist at ppar gamma, potentiation of insulin action on peripheral tissue
What is the philosophy behind incretin analogs?
oral glucose provokes higher insulin release because induces release of gut hormones (GLP) that act upon Beta cells to amplify insulin release. no real risk of hypoglycemia because need high bg to function
Exenatide MOA
A reptilian GLP that is resistant to DPP-4 so remains in circulation longer. induces insulin release, depresses glucagon release
