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Pharmacology: Anti hyperlipidemic drugs flashcards

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Excellent study aid for medical students, nursing students, pharmacology students, and university or college students.

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Pharmacology: Anti hyperlipidemic drugs flashcards

  1. 1. ANTI-HYPERLIPIDEMIC DRUGS
  2. 2. HMG-COA INHIBITORS Lovastatin; Atarvostatin  Analogs of HMG (3-hydroxy-3 methylglutaryl-CoA)  HMG-CoA reductase catalyzes synthesis of mevalonic acid from HMG-CoA and is the rate limiting step in cholesterol biosynthesis  Leads to up-regulation of LDL receptors in liver  ACTIONS  Decrease LDL by 20 – 55%  Decrease TG by 10 – 35%  Slight increase in HDL 
  3. 3. HMG-COA INHIBITORS  Adverse Hepatotoxicity (check ALT and AST, if >3x normal...stop drug)  Myopathy (w/ rhabodmyolysis) and may cause myoglobinuria which may lead to urine obstruction (measure CPK levels)     Increased chances when mixed with fibric acid derivatives (gemfibrizol), niacin, or P450 3A4 inhibitors CATEGORY X in pregnancy Therapeutic Uses Great for all hyperlipidemias involving increased levels of LDL or cholesterol  Atherosclerosis; stroke prevention  Primary prevention of CAD 
  4. 4. BILE ACID RESIN Cholestyramine  Anion-exchange resin – binds bile acids in intestinal lumen preventing enterohepatic circulation (this increases excretion of bile which is made from cholesterol)  this causes an up-regulation of hepatic LDL receptors and increased production of cholesterol  Action: decreases LDL by 10 – 35%  Not absorbed at all 
  5. 5. BILE ACID RESIN  Adverse       Constipation, flatulence, dyspepsia Hypertriglyceridemia Hyperchloremic acidosis (since they exchange Cl) Bind many things (drugs, vitamins, toxins, anything fat soluble) which limits their absorption Prexisting coagulopathy is a contraindication since they prevent absorption of vit K Uses Hyperlipidemias involving ISOLATED INCREASES OF LDL  Diarrhea from excess fecal bile resins 
  6. 6. VLDL SECRETION INHIBITORS NIACIN (vit B3)  MoA: inhibition of VLDL production by hepatocyte  decreases TG synthesis in liver; inhibition of Hormone sensitive lipase in adipose; stimulation of LPL which causes hydrolysis of VLDL  Actions  Decreases LDL by 15-25%  Decreases VLDL by 40%  Decreases TG by 30 – 50%  Increases HDL by 15-30% (niacin is MOST EFFECTIVE in increasing HDL levels!!) 
  7. 7. VLDL SECRETION INHIBITORS  Adverse         Cutaneous flush (prevented with NSAID) Stimulates histamine release  pruritis, rash, nausea, etc Decreased glucose tolerance (contra in DM pts) Hyperuricemia (inhibits tubular secretion of uric acid) Lowers fibrinogen (good for AS; bad for coag disorders) Hepatotoxicity (check AST, ALT levels) Rhabdomyolysis (especially when given with Statins) Uses Hyperlipidemias with very high VLDL and LDL  Pts with very low HDL (despite risk factors you should give niacin) 
  8. 8. FIBRIC ACID DERIVATIVES Gemfibrozil  MoA: activation of nuclear transcription receptor to increase LPL synthesis (removes TGs from lipoproteins); enhanced removal of VLDL from plasma  Actions  Decreases TG by 30-60%  Decreases VLDL by 30%  Increases HDL by 5 – 10% 
  9. 9. FIBRIC ACID DERIVATIVES  Adverse Myopathy (rhabdomyolysis) when combined with statins  Cholesterol levels may actually increase  Cholethiasis due to increased biliary excretion of cholesterol   Therapeutic Uses DOC fro type III lipoproteinemia (familial dysbetalipoproteinemia)  Hypertriglyceridemias 
  10. 10. INTESTINAL STEROL ABSORPTION INHIBITOR Ezetimibe  Localizes at the brush border, selectively inhibits intestinal absorption of cholesterol and related sterols (only blocks exogenous sterol intake)  Actions  Decreases LDL by 15-20%  Decreases TG by 5-8%  THIS DRUG IS WEAK ALONE 
  11. 11. INTESTINAL STEROL ABSORPTION INHIBITOR  Adverse Hypersensitivity reactions  Severe hepatic disease prolongs drug life   Uses  Combined with statins for hyperlipidemias
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