Pharm5 - antilipemics

  1. name the fat soluble vitamins
    • a
    • d
    • e
    • k
  2. describe action of bile acid sequestants
    • they bind to bile acids (made of cholesterol) form large, insoluble complexes that can't be reabsorbed from small intestine to go back to liver, and are excreted instead.
    • loss of these bile acids makes liver synthesis more bile acids --> cycle continues and cholesterol continues to be excreted
  3. what cycle/circulation do bile acid sequestrants interrupt?
    • enterohepatic
    • normally bile is secreted by liver to emulsify fats in small intestine, then reabsorbed in ileum to return to liver and become part of bile; cholesterol in bile acids is recycled and only small amts leave body in feces.
  4. how do bile acid sequestrants interact with lipid soluble drugs and vitamins?
    they are not absorbed b/c bile acids are needed to break them down for absorption.

    • -can lead to vitamin deficiencies of a, d, e, k
    • -digoxin and coumadin: binds to these drugs and decreases their absorption
    • -(book says coumadin can become increasingly effective, not less so, because of vit K deficiency)
  5. bile acid sequestrant SFX
    GI only because never enters systemic circulation

    • -constipation, heartburn, nausea, belching, bloating, flatulence
    • -decrease over time
  6. bile acid sequestrant pregnancy category. why?
    • B.
    • relatively safe because never enters blood circulation, stays in GI tract
  7. bile acid sequestrant that is used to tx pruritis r/t partial biliary obstruction
    cholestyramine [Questran]
  8. name the bile acid sequestrants
    • cholesyramine [Questran]
    • colestipol [Colestid]
    • colesevelam [Welchol]
  9. describe the esophageal risk of taking a bile acid sequestrant. how can this be prevented?
    drug can expand in esophagus before getting to stomach/small intestine and cause esophageal blockage.

    avoided by taking med with lots of water, other non-carb beverage, applesauce, or crushed pineapple
  10. suffix used for all HMG-CoA reductase inhibitor drugs
  11. antilipemic drug type that lowers LDL most effectively

    (aka cholesterol synthesis inhibitors)
  12. type of lipid most effected by statins
  13. 6 HMG-CoA reductase inhibitors
    • lovastatin [ Mevacor]
    • pravastatin [Pravachol]
    • atorvastatin [Lipitor]
    • fluvastatin [Lescol]
    • rosuvastatin [Crestor]
    • simvastatin [Zocor]
  14. 2 ways statins decrease LDL levels
    • -decrease cholestrol synthesis
    • -increase # of LDL receptors in liver, leading to more LDL being removed from blood
  15. where cholesterol is made
  16. statin SFX
    • normally well-tolerated w/ few SFX
    • -GI: mild and decrease over time
    • -rash
    • -HA
    • -rhabdomyolosis, myopathy
    • -elevations in liver enzymes (which may or may not be indicative of liver damage)
    • -prolonged QT interval
  17. rhabdomyolosis
    breakdown of muscle fibers, usually d/t trauma or ischemia, but also as a potential SE of statins. contents of muscle cells spills into systemic circulation and can lead to acute renal failure
  18. statin pregnacy category
    X - teratogenic
  19. how grapefruit juice interacts with statins
    inhibits drug metabolism, leading to dangerously high serum drug levels
  20. important labs to monitor for statins and why
    • -liver enzymes: high levels could indicate liver failure
    • -creatine kinase (not same as creatinine): enzyme released during muscle injury --> high levels could indicate rhabdomyolysis or myopathy
  21. drugs that interact with statins
    • erythromycin (antibiotic)
    • gemfibrozil (antilipemic - fibric acid)
    • niacin (antilipemic - nicotinic acid)
  22. antihyperlipidemic with almost no effect on LDL (and no decrease in mortality r/t cardiovascular disease)? what is it used for?
    fibric acid aka fibrate

    used to tx hypertriglyceridemia, esp in combination with statins
  23. 2 fibric acid drugs and frequency of administration
    • -gemfibrozil [Lopid] = 2x/day
    • -fenofibrate [Antara, Tricor] = 1x/day
  24. fibric acid SFX
    • -GI: n/v/d
    • -neuro: HA, peripheral neuropathy, decreased libido
    • -allerigc rxns
    • -gallstones (contraindicated in pts with gallbladder disease)
  25. how fibrate works
    (according to Saarman; book says mechanism unknown)
    • -activates lipoprotein lipase, which breaks down cholesterol
    • -suppresses release of FFA (free fatty acids) from adipose tissue
    • -inhibits synthesis of triglycerides
    • -increases secretion of cholesterol in bile
  26. why wouldn't you give fibric acid to an immunocompromised pt?
    causes decrease in WBC (and H&H)
  27. fibric acid effect on liver enzymes
    increases liver enzymes - b/c functions in the liver
  28. vit B3 is the same thing as which antihyperlipidemic? how do doses compare?
    b3 = niacin (aka nicotinic acid)

    lipid-lowering doses are much higher than vitamin doses (~100x greater)
  29. how does niacin work (according to Saarman; book says mechanism unknown)
    • -increases activity of lipase, which breaks down lipids
    • -reduces metabolism/catabolism of cholesterol and triglycerides
  30. niacin SFX
    • -flushing, hot flashes in almost all pts, but can decrease this with ASA or other NSAID
    • -pruritis
    • -GI distress
    • -hyperglycemia (contraindicated in DM pts)
    • -hyperuricemia (contraindicated in pts with hx of gout)
  31. niacin interaction with statin or bile acid sequestrant

    --> usually combined with one of these drugs and then used in lower doses to avoid adverse FX
  32. Simcor is a combination of which two antihyperlipidemic classes
    niacin + statin (simvastatin)
Card Set
Pharm5 - antilipemics