Pharmacology Exam II

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Rx2013
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65969
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Pharmacology Exam II
Updated:
2011-02-12 23:22:00
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Lipid Lowering Agents
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Lipid lowering agents
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  1. HMG CoA reductase
    • converts HMG CoA to mevalonic acid
    • rate limiting step in cholesterol biosynthesis
  2. Low cholesterol may be a marker for
    cancer presence
  3. Lipoproteins consist of
    • Triglycerides
    • esterified cholesterol
  4. Apolipoproteins
    • characterized by weight
    • solubilizors
    • receptor recognition
    • enzyme co-factors
  5. Apo B's are in volved in transport of
    • chylomicrons
    • VLDL
    • IDL
    • LDL
  6. Apo (a)
    • transport
    • inhibits thrombolysis
  7. VLDL
    carries TGs to peripheral cells from the liver
  8. LDL
    • bad cholesterol
    • primary cholesterol carrying particle
  9. HDL
    removes cholesterol from cells
  10. LP (a)
    potential to obstruct endogenous anti-platelet enzymes
  11. Triglycerides synthesized in the liver leave through
    LDL
  12. lipoprotein lipase acts on LDL particles to make them
    smaller
  13. Carry cholesterol back to the liver
    • HDL
    • IDL
    • LDL
  14. Elevated homocysteine levels
    • cytotoxic to endothelium (inhibit NO production)
    • promote prothrombic activity
    • increase LDL oxidation resulting in increased risk of stroke, CAD and PVD
  15. Used to reduce homocysteine levels
    • folic acid
    • does not prevent elevation
  16. C Reactive protein
    • measured to asses CV risk
    • accute phase reactant released in inflammatory situations
    • increased when inflamation to vessel walls is present
  17. Increased c-reactive protein levels are reduced by
    • aspirin
    • HMG-CoA reductase inhibitors
  18. Measurements of CV risk
    • homocysteine levels
    • C-reactive protein levels
    • walking speed
  19. Secondary causes of dislipidemias
    • hypotheyroidism
    • protenuria
    • DM
    • liver disease
    • alcohol
  20. Drugs that can cause dislipidemias
    • androgens
    • beta blockers
    • thiazides
  21. Beta-blocker effect on lipid profiles
    • inhibit lipoprotein lipase disrupting cholesterol cycle
    • increases triglycerides
    • increases total cholesterol
  22. Alcohol effects on lipid profiles
    • alcohol increases VLDL secretion from the liver
    • results in higher triglyceride levels
  23. NCEP screening guidelines say screening should be completed every
    5 years for adults >20
  24. Desired total cholesterol level
    < 200 mg/dl
  25. High total cholesterol
    > 240 mg/dl
  26. Optimal LDL cholesterol
    < 100 mg/dl
  27. Borderline high LDL
    130 - 159 mg/dl
  28. Very high LDL
    > 190 mg/dl
  29. Low HDL level
    • < 40 mg/dl for men
    • < 50 mg/dl for women
  30. High HDL level
    >60 mg/dl
  31. Calculation of LDL cholesterol
    TC- [HDL + (TG/5)]
  32. High triglycerides can contribute to
    pancreatitis
  33. calculation of non-HDL cholesterol and its use
    • TC - HDL
    • best used to asses risk in pt with hypertriglyceridemia
  34. Low risk non-HDL level
    <160 mg/dl
  35. Moderate risk non-HDL level
    190-219 mg/dl
  36. high risk non-HDL level
    > 220 mg/dl
  37. Another good ratio to look at to asses CV risk
    ApoB/ApoAI
  38. Risk factors for CHD other than LDL
    • Age
    • Family history
    • Smoking
    • Hypertension
    • HDL < 40 mg/dl
    • DM
  39. Male age at risk for CHD
    > 45
  40. Female age at risk for CHD
    • > 55
    • or premature menopause w/o estrogen replacement
  41. Negative risk factors for CHD
    • HDL > 60 mg/dl
    • if present, subtract one risk factor (except smoking)
  42. Small LDL particle vs Large LDL particles
    Large LDL particles are better
  43. Small HDL particles vs Large HDL particles
    • large HDL good
    • small HDL bad
  44. High risk patient (# of risk factors, goal LDL, when to start lifestyle change, when to start drug therapy)
    • pt has CHD or risk equivalents
    • goal LDL < 100 mg/dl
    • lifestyle change >100
    • start drugs at > 100
  45. Moderately high risk patient
    • pt has two or more risk factors
    • Goal LDL < 130 mg/dl
    • start lifstyle change at >130
    • start drugs at >130
  46. Moderate risk patient
    • two or more risk factors
    • goal LDL < 130
    • start lifestyle change >130
    • start drugs at >160
  47. Low risk patient
    • < one risk factor
    • Goal LDL <160 mg/dl
    • start lifestyle change at > 160
    • Start drugs at >190
  48. Diet and exercise will lower LDL by
    15 to 20%
  49. Normal triglyceride levels
    < 150 mg/dl
  50. High triglyceride levels
    200-499 mg/dl
  51. Why LDL is bad
    • attaches to walls of blood vessels and becomes oxidized releasing cholesterol
    • macrophages & WBC are attracted to the area
    • Foam cells form which lead to fatty streaks which leades to plaque
  52. % of 20 y/o that have fatty streak formation
    33%
  53. Complications of untreated hyperlipidemia
    • Coronary heart disease
    • Peripheral vascular disease
    • Carotid artery disease
  54. Treatment options for hyperlipidemia
    • diet therapy
    • exercise
    • drugs that reduce cholesterol absorption/reabsorption
  55. Diet therapy
    • diet and exercise should be tried for 6 mo
    • may drop cholesterol up to 14%
  56. Diet has the most effect on decreaseing
    • LDL
    • triglycerides
  57. Exercise
    • 3 sessions per week for 20 min each have an impact
    • duration is better than intensity
  58. Exercise changes triglycerides by
    • raising HDL up to 1%
    • drops VLDL
    • drops triglycerides
  59. Drug therapies for reducing cholesterol absorption/reabsorption
    • bile acid binding resins
    • cholesterol absorption inhibitors
    • inhibitors of dietary fat absorption
    • niacin
  60. Bile acid resins usually decrease ____ & ____.
    __, __, ___ may increase.
    • decrease LDL by 15-20%
    • decrease total cholesterol
    • VLDLD, TG and HDL my increase
  61. Bile acid resin agents
    • cholestyramine
    • colestipol
    • colesevelam
  62. Bile acid binding resins are indicated for
    • familial hypercholesterolemia with normal TGs
    • rarely used as mono therapy
    • usually combined with reductase inhibitors
  63. Mechanism of action for bile acid resins
    • bind bile salts in the GI tract inhibiting them to be reabsorbed to hepatic circulation
    • Hepatic LDL receptors upregulated
    • cholesterol 7a hydroxylase upregulated
    • HMG CoA reductase upregulated
    • phosphatidit acid phosphatase upregulated
  64. Adverse reactions with bile acid resins
    • GI problems as drug is not absorbed
    • Constipation (fecal impaction) 39% elderly
    • Bloating and gas
    • abdominal pain
    • nausea
    • vitamin deficiency?
  65. Drug interactions with bile acid resins
    • drug binds anions, cations and neutral compounds
    • (warfarin, thyroid hormone, digoxin, niacin)
  66. Bile acid resin that does not interfere with absorption of warfarin, digoxin or statins
    colesevelam
  67. cholesterol absorption inhibitors
    ezetimibe
  68. cholesterol absorption inhibitors (ezetimibe) are indicated for
    • familial hypercholesterolemia + statin
    • combined hyperlipidemia (cautiously with statins or fenofibrates)
    • sitosterolemia + diet
  69. ezetimibe drops GI cholesterol absorption by ___%, and drops total cholesterol by ___%
    • 50%, however only 25% of cholesterol comes from diet
    • 10%
  70. Statins + ezetimibe
    • synergistic
    • lowers LDL
    • no difference in carotid intima thickness
  71. mechanism of action for ezetimibe
    • inhibits abs. of cholesterol from the small intestine at ABCG5
    • upregulation of LDL receptors on the liver occurs
    • inhibition of NPC1L1 (increases cholesterol elimination through the bile acid mech.)
  72. Ezetimibe effects on cholesterol levels
    • decrease in total cholesterol
    • LDL, apo B and TG decreased
    • small increase in HDL
    • does not decrease small LDL as much
  73. Adverse drug reactions with ezetimibe
    • very low incidence of:
    • diarrhea
    • arthralgia
    • respiratory issues
  74. Drug interactions with ezetimibe
    • Eze levels decreased by bile acid resins
    • fibric acids increase Eze level = not recommended may lead to cholelithiasis
    • cyclosporin can increase eze levels
  75. Any drugs that effect cholesterol should be avoided in
    moderate-severe hepatic dysfunction
  76. Inhibitors of dietary fat absorption
    orlistat (alli)
  77. Use of orlistat
    • not used for hypercholesterolemia
    • used with statins or eze (synergistic) to drop TC, LDL and increase HDL
    • primarily used for obesity
    • OTC
  78. Mechanism of action for orlistat
    • reversible lipase inhibitor
    • decreases absorption of fats by 30%
    • forms bond with pancreatic lipase to inactivate
    • decreases TC hydrolysis in stomach and Sm. I.
    • no effects on serum lipases
  79. ADRs with orlistat
    • GI issues (diarrhea do to fat in bowels)
    • increased urinary oxalate = kidney stones
    • DM pt may need to decrease dosage of insulin or hypoglycemics
    • abuse potential: no additive effects above 120mg tid
  80. Drug interactions with orlistat
    • fat soluble vitamins 2hr before or after orlistat
    • insulin (may need to decrease)
    • cyclosporin
    • warfarin (vit K levels may decrease)
  81. orlistat + fenofibrate
    reduced clotting risk
  82. Niacin is indicated for
    all lipid disorders
  83. Niacin administration results in
    • decreased VLDL, LDL, TG, Lp(a), apo B, TC
    • increases HDL
  84. Niacin is the only drug to
    • decrease LP(a)
    • increase HDL as much
  85. Niacin can result in ____% increase in HDL
    14-39%
  86. Mechanism of action for niacin in the liver
    • Decreased TG synthesis
    • Decreased APO B formation
    • Decreased VLDL secretion
    • Decreased LPa
  87. Mechanism of action for niacin in the systemic circulation
    • decreased serum VLDL results in reduced lipolysis to LDL
    • decreased serum LDL and ApoB
    • increased HDL and Apo A-1
    • decreased mobilization of fats from tissues
    • increased reverse cholesterol transport
  88. Key receptor for the action of niacin
    GPR109a which mediates VLDL formation and secretion
  89. Niacin kinetics
    • well absorbed
    • rapidly metabolized
    • usually dosed in ER dosage forms
  90. _____ causes the problem that leads to flushing and adverse effects associated with niacin.
    nicotinuric acid
  91. conversion of niacin to nicotinuric acid is
    high capacity low affinity
  92. ER tablets convert niacin to nicotinamide which results in
    • low capacity, high affinity reactions
    • some hepatotoxicity
  93. Adverse reactions wtih niacin
    • skin flushing 90% of pt experience
    • pruritis
    • abdominal pain
    • activation of peptic ulcer
    • increased liver enzymes
    • hyperuricemia (caution in gout)
    • glucose intolerance (DM pt can still take)
    • myopathy
  94. Mechanisms to avoid flushing with niacin
    • gradual dose increase
    • use prostaglandin inhibitor 30-60 min before dose (nsaids)
    • take ER pills at bedtime
    • tolerance will build up over time
    • D2 antagonist laropiprant
  95. Drug interactions with niacin
    • vasodilators => postural hypotension
    • HMG-CoA reductase inhibitors => increased risk of myopathy
    • Anticoagulatns => decreased platelet count and increased prothrombin times
  96. Niacin receptor agonists
    • adiponectin
    • increases leptin levels which has an anorexic effect

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