Pharm.3

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cseubs24
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44882
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Pharm.3
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2010-10-26 00:38:47
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Pharm
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Pharmacology drugs for test 3
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  1. Hydrochlorothiazide
    • – Inhibit sodium reabsorption from distal tubule; 10% Na+
    • – Usually used for the long-term outpatient management of hypertension
    • - deplete potassium = HYPOKALEMIA
    • - inhibit uric acid elimination = promote gout
    • - increase LDL levels
  2. Chlorthalidone
    • – Inhibit sodium reabsorption from distal tubule; 10% Na+
    • – Usually used for the long-term outpatient management of hypertension
    • - deplete potassium = HYPOKALEMIA
    • - inhibit uric acid elimination = promote gout
    • - increase LDL levels
  3. Furosemide
    • – Loop Diuretic: 35% filtered Na+
    • -`Usually used for short-term management of more severe hypertension (morepowerful, high efficacy, shorter acting)
    • – Inhibit sodium, reabsorption from the loop of Henle
    • - deplete potassium = HYPOKALEMIA
    • - inhibit uric acid elimination = promote gout
  4. Ethacrynic acid
    • – Loop Diuretic; 35% Na+
    • -Usually used for short-term management of more severe hypertension (morepowerful, high efficacy, shorter acting)
    • – Inhibit sodium, reabsorption from the loop of Henle
    • - deplete potassium = HYPOKALEMIA
    • - inhibit uric acid elimination = promote gout
  5. Spironolactone
    • - Potassium sparing diuretic; 5% Na+
    • - Antagonist at mineralocorticoid receptor for aldosterone
    • – Reduced Na+/K+ exchange in distal tubule and collecting duct results inreduced Na+ re-absorption and K+ retention
    • – Commonly too weak to be used alone but counteract hypokalemia associated with other diuretics in high-risk patients
    • - All diuretics have dehydration as a potential side effect
  6. Triamterine
    • - Potassium sparing diuretic; 5% Na+
    • - Blocker of Na channel
    • – Reduced Na+/K+ exchange in distal tubule and collecting duct results inreduced Na+ re-absorption and K+ retention
    • – Commonly too weak to be used alone but counteract hypokalemia associated with other diuretics in high-risk patients
    • - All diuretics have dehydration as a potential side effect
  7. Amiloride
    • - Potassium sparing diuretic; 5% Na+
    • - Blocker of Na+ channel on apical membrane
    • – Reduced Na+/K+ exchange in distal tubule and collecting duct results inreduced Na+ re-absorption and K+ retention
    • – Commonly too weak to be used alone but counteract hypokalemia associated with other diuretics in high-risk patients
    • - All diuretics have dehydration as a potential side effect
  8. clonidine
    • - sympatholytic indirect acting
    • - a2 receptor agonist
    • - cns acting to reduce symp n.s. activity
    • - act at N. Tractus Solitarius
  9. reserpine
    • - VMAT inhibitor
    • - indirect acting sympatholytic
  10. propranolol
    • - Non-selective B Blocker
    • - decrease CO
    • - B2 Activation...lungs, liver, skeletal vasculature
  11. atenolol
    • - B1 Selective blocker
    • - dec CO
  12. nadolol
    • - Non-selective B Blocker
    • - decrease CO
    • - B2 Activation...lungs, liver, skeletal vasculature
  13. prazosin
    • SYMPATHOLYTIC DRUGS
    • Block sympathetic n.s. induced contraction of arterial smooth muscle a1 adrenergic receptor antagonists
    • -OSIN
  14. terazosin
    • SYMPATHOLYTIC DRUGS
    • Block sympathetic n.s. induced contraction of arterial smooth muscle a1 adrenergic receptor antagonists
    • -OSIN
  15. hydralazine
    • - direct vasodilator
    • - oral drug: used for outpatient treatment of hypertension
    • - selective arterial dilator
  16. Calcium Channel Blockers
    • - direct vasodilator
    • - oral drug: used for outpatient treatment of hypertension
    • - block voltage dep calcium channels (L-type) on vascular smooth muscle
    • - tx for stable/classic angina when b blockers or nitrates unuseful
    • - first choice for variant angina esp cardioactive ccb's
    • -short acting should not be used w/ unstable angina or hx of MI
  17. minoxidil
    • - direct vasodilator
    • - oral drug: used for outpatient treatment of hypertension
    • - highly effective with lots of side effects (fyi: hypertrichosis); reserved for severehypertension that does not respond to other drugs
    • - inc hair growth = rogaine
  18. diazoxide
    • - PARENTERAL DRUGS: used for emergency situations (hypertension crises)Too efficacious for outpatient use: too many side effects for outpatient use
    • - highly effective and long-acting = not a first choice-drug
  19. sodium nitroprusside
    • - PARENTERAL DRUGS: used for emergency situations (hypertension crises)Too efficacious for outpatient use: too many side effects for outpatient use
    • - nitrate drug
    • - dinitrated to NO = vasodilator
  20. verapamil
    - CARDIOACTIVE CCBs: relax vascular smooth muscle andreduce cardiac output (decrease heart rate, AVconduction, and force of contraction)
  21. dihydropyridines
    • - DIPINE
    • - NON-CARDIOACTIVE CCBs: relax vascular smooth muscle but have little effect on cardiac output
    • - long-acting orsustained releaseformulations
  22. amlodipine
    - long-acting dihydropuridine
  23. nifedipine
    - Short-acting dihydropyridines CCBs = increased risk ofmyocardial infarction relative to patient taking diuretics or beta blockers
  24. Vasodilator Side Effects
    • Postural hypotension
    • flushing, sweating
    • headache
    • reflex tachycardia: prevented w/ coadmin B Blocker
    • reflex fluid ret: coadmin w/ diuretic
    • - Vasodilators are almost always coadmin w/ either to prevent reflexes
  25. Carvedilol
    • - mixed beta-1 and alpha-1antagonist
    • - B Blocker/Vasodilator
    • - dec both CO and TPR
  26. Nebivolol
    • - beta blocker that promotes nitric oxide (NO) production
    • - dec both CO and TPR
    • - B blocker/vasodilator
  27. captopril
    • - ACE Inhibitors: inhibit conversion of angiotensin to angiotensin II by angiotensin converting enzyme (ACE)
    • - PRIL
    • - no metabolism necessary
  28. enalapril
    • - ACE Inhibitors: inhibit conversion of angiotensin to angiotensin II byangiotensin converting enzyme (ACE)
    • - PRIL
    • - pro-drug
  29. losartan
    • - Angiotensin Receptor Blockers (ARBs) inhibit binding of angiotensin IIto the AT1 receptor
    • - ARTAN
  30. valsartan
    • - Angiotensin Receptor Blockers (ARBs) inhibit binding of angiotensin IIto the AT1 receptor
    • - ARTAN
  31. aliskiren
    - Renin Inhibitors: inhibit conversion of angiotensinogen to angiotensin I by the enzyme renin
  32. Angiotensin related Agents
    • Block effects of the renin-angiotensin system, thereby reducing blood pressure primarily by inhibiting angiotensin II induced…
    • • Vasoconstriction
    • • Increases in aldosterone production
    • • Increases in vasopressin release
    • • No reflex sympathetic activation (resetting of baroreceptors?)
  33. ACE Inhibitor Side Effects
    • SIDE EFFECTS:
    • • Dry cough (bradykinin effect due to ACE inhibition)
    • • Angioedema (rapid non-allergic swelling of skin and mucosa; also dueto bradykinin)
    • • Hyperkalemia (reduced sodium potassium exchange in kidney)
    • • Reduced kidney function (use with caution if kidney function is alreadyimpaired)
    • • TERATOGENIC: DO NOT USE DURING PREGNANCY
  34. Enoxaparin
    • - Low molecular weight HEPARIN = less activity
    • - anticoagulant
    • - less risk for bleeding
  35. Heparins
    • - parenteral anticoagulants
    • - Binds to and stimulates ANTITHROMBIN III, an endogenousinhibitor of clotting factors.
    • • Given as mixture of different sizemolecules purified from animal sources biological units)
    • • Molecular weight determines activity
    • - Polysaccharide = very hydrophilic & susceptible to digestion so must be given IV or SC
    • - reversed by PROTAMINE
  36. Unfractionated Heparin
    - combination of low and high molecular weights = more activity = more bleeding
  37. Lepirudin
    - Direct Thrombin Inhibitors (DTI’s) Analogs of Hirudin – purifiedfrom medicinal leeches (Hirudo medicinalis); directly inhibit thrombin
  38. Warfarin
    • ORAL ANTICOAGULANT
    • • PREVENTS VITAMIN K RE-ACTIVATION by inhibiting Vit K epoxidereductase
    • • Active Vitamin K is required for synthesis of clotting factors in both theintrinsic and extrinsic systems
    • • Delayed onset of action
    • • Teratogenic: avoid during pregnancy; Has many drug interactions
    • - • Genetic variation in CYP2C9 reduceswarfarin metabolism = increased bleedingrisk
    • • variation in the VKORC1 subunit reduces warfarin sensitivity = increased clotting risk
  39. Alteplase
    - recombinant T-PA
  40. T-PA
    • - tissue plasminogen activator drugs
    • - destroy blood clots after they have formed
    • - digests fibrin and breaks down fibrin-rich clots (red-thrombi)
  41. Streptokinase
    - T-PA purified from bacteria
  42. Aspirin
    • - acetylates and inhibits COX-1 to reduce TXA2 sythesis
    • - anti-thrombotic
    • -75-81 mg (one baby aspirin/day) is sufficient to protect against acute MI in moderate tohigh risk individuals
    • -At time of heart attack: four baby aspirin (325 mg; chewed) to protect against re-occlusionand subsequent heart attack
    • -Maintain on higher-dose (325 mg) aspirin after acute MI to protect against another heartattac
  43. Clopidogrel
    • - anti-thrombotic
    • - Prodrug activated by the CYP system
    • - prevent ADP from binding to platelet purinergic receptors
    • - Higher-risk individuals for MI; post-MI; post PCI surgery
  44. Ticlopidine
    • - ADP receptor blocker
    • - anti-thrombotic
    • - More side effects than clopidogrel : GI effects, greater bleeding risk
    • - Higher-risk individuals for MI; post-MI; post PCI surgery
  45. Abciximab
    • PLATELET RECEPTOR ANTAGONISTS
    • • Antagonize receptors on platelet cell membranes to prevent physicalinteraction of platelets with fibinogen and therefore platelet aggregation
    • • Administered parenterally for Percutaneous Coronary Interventions (PCIs;new term for angioplasty) to prevent reocclusion of coronary vessel
    • - anti-GPIIb/IIIa antibody
    • - given during PCI surgery
  46. Tirofiban
    • PLATELET RECEPTOR ANTAGONISTS
    • • Antagonize receptors on platelet cell membranes to prevent physicalinteraction of platelets with fibinogen and therefore platelet aggregation
    • • Administered parenterally for Percutaneous Coronary Interventions (PCIs;new term for angioplasty) to prevent reocclusion of coronary vessel
    • - GPIIb/IIa Antagonists
    • - given during PCI surgery
  47. Niacin
    • - TREATMENT OF HYPERTRIGLYCERIDEMIA INVOLVES DECREASINGCIRCULATING VLDL LEVELS
    • - increases HDL levels
    • - does have net dec in LDL due to mainly acting on dec vldl syn in liver
  48. Gemfibrozil
    • - TREATMENT OF HYPERTRIGLYCERIDEMIA INVOLVES DECREASINGCIRCULATING VLDL LEVELS
    • - no change in LDL
  49. Colestipol
    • - tx hypercholestolemia hyperlipidemia
    • - bile acid-binding resin
    • - less bile available for reabsorption
    • - dec liver bile, lower live cholesterol, increase in ldl receptors, inc ldl uptake into liver
  50. Cholestyramine
    • - tx hypercholestolemia hyperlipidemia
    • - bile acid-binding resin
    • - less bile available for reabsorption
    • - dec liver bile, lower live cholesterol, increase in ldl receptors, inc ldl uptake into liver
  51. Statins
    • HMG-CoA Reductase Inhibitors
    • – HMG-CoA reductase is a key liver enzyme for the synthesis of cholesterol
    • – By inhibiting cholesterol synthesis in the liver, cellular concentrations are reduced andLDL receptors are up-regulated resulting in increased removal of LDL from the blood.
    • - Also produce modest increases in HDL (less than niacin) and decreases in VLDL (lessthan niacin/fibric acid drugs)
  52. atorvastatin
    • - Lipitor; most prescribed statin drug
    • - High efficacy
    • - no available generically
  53. fluvastatin
    - statin drug
  54. lovastatin
    - statin drug
  55. pravastatin
    - low efficacy statin
  56. rosuvastatin
    • - high efficacy statin
    • - Crestor
    • - not available generically
  57. simvastatin
    • - Zocor
    • - medium efficacy
    • - available generically
  58. Ezetimibe
    • Binds to protein on GI epithelial cells that promotes cholesterol absorption in the small intestine.
    • • Inhibits of intestinal absorption of dietary cholesterol
    • • Reduces LDL levels (tx. hypercholestolemia)
    • • GI side effects
  59. Vytorin
    • Ezetimibe (Zetia) + simvastatin
    • •ENHANCE study (fyi: Merck and Schering-Plough): although Vytorin produced greaterreductions in LDL than simvastatin alone,coronary atherosclerotic plaque formationwas no different
    • Implications:
    • 1. Vytorin is no more protective against coronary heart disease than statinmonotherapy; potentially questions the effectiveness of ezetimibe
    • 2. Suggests that effectiveness of statins versus coronary heart diseasemay not only involve reductions in LDL; potential anti-inflammatoryeffects
  60. Nitroglycerin
    • - inactivated through first pass metabolism and therefore are usually given sublingually as a tablet or spray or transdermally
    • - organic nitrate
    • - classic and variant angina
  61. isosorbide di-/mono-nitrate
    • - organic nitrate
    • - admin orally
    • - classic and variant angina
  62. diltiazem
    • -CCB
    • - cardioactive: Block channels in vascular smooth muscle AND in the heart
    • – Vasodilators AND cardiac inhibitors

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