CCR Pharm

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CCR Pharm
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  1. What is the major site of action of the carbonic acid inhibitors?
    Proximal Tubule
  2. What is the major site of action of the loop diuretics?
    Thick Ascending Limb of the Loop of Henle
  3. What is the major site of action of the Thiazides?
    Distal Convoluted Tubule
  4. What is the major site of action of the Aldosterone and ADH inhibitors?
    Collecting Duct
  5. What is the major site of action of the osmotic diuretics?
    The Water Absorbing Segments of the Nephron
  6. What is the main osmotic diuretic?
    Mannitol
  7. What is the mechanism of action of osmotic diuretics?
    Supply an impermeable molecule to the renal tubules that cannot be reabsorbed. By increasing the osmolarity of the fluid within renal tubules, the osmotic effect of the molecule retards the reabsorption of water
  8. What are three unique things about Mannitol?
    • Does not affect a water transport system -- retards water reabsorption instead
    • Must be given IV bc causes an osmotic diarrhea when taken orally
    • Is not secreted -- is freely filtered across the glomerulus
  9. What are the main adverse effects of Mannitol?
    • Pseudohyponatremia: its osmotic effect reduces water in cells, thereby expanding the extracellular volume and producing this befoer diuresis occurs. May affect heart failure and cause pulmonary edema
    • Dehydration, Hyperkalemia, and Hypernatremia: may reduce water excessively, leading to these
  10. What is the main Carbonic Anhydrase Inhibitor?
    Acetazolamide
  11. What is the main adverse effect of Carbonic Anhydrase Inhibitors (Acetazolamide)?
    Hyperchloremic Metabolic Acidosis
  12. What is the mechanism of action of Loop Diuretics?
    Block the Na-K-2Cl Symporter
  13. What are the two main Loop Diuretics?
    • Furosemide
    • Torsemide
  14. What are the major adverse effects of the Loop Diuretics and Thiazides?
    • Excessive excretion of Na, Cl, K, H, Mg, & Ca, thereby producing volume depletion and acid-base abnormalities
    • Compete with other drugs that use the same secretory system as them, thereby reducing their (the other drugs') excretion
  15. What is the mechanism of action of Thiazides?
    Block the Na-Cl symporter in the distal tubule
  16. What are the three main Thiazides?
    • Chlorothiazide
    • Hydrochlorothiazide
    • Chlorthalidone
  17. What are the four main K-Sparing Diuretics? Which two are aldosterone inhibitors?
    • Spironolactone & Eplerenone: Aldosterone Inhibitors
    • Amiloride & Triamterene: block Na transport through the luminal ion channels
  18. What is the main adverse effect of the K-Sparing Diuretics/ Aldosterone Antagonists?
    Hyperkalemia
  19. What are the two main ADH Antagonists?
    • Conivaptan: IV only
    • Tolvaptan: Oral
  20. What are the two main adverse effects of the ADH antagonists?
    • Hypernatremia
    • Nephrogenic Diabetes Insipidus
  21. What is the difference between a diuretic and a natriuretic?
    • Diuretic: drug that enhances urine volume
    • Natriuretic: drug that enhances Na, and thus water, excretion
  22. What are the four classifications for the Antiarrhythmic Drugs (Vaughn Williams Classifications)?
    • Na Channel Blockers (local anesthetics)
    • Sympatholytic Agents (beta-blockers)
    • Prolonged Repolarization (potassium channel blockers)
    • Calcium Channel Blockers
  23. What is the mechanism of action of type I antiarrhythmic drugs?
    Block Na conduction through voltage-gated Na channels. These are in the class of local anesthetics
  24. The type I local anesthetics have high affinity for the _________ sodium channel and _________ channel, but low affinity for the ________ channel.
    • Open
    • Inactive
    • Closed
  25. Local anesthetics (Type I Na channel antiarrhythmics) enter the sodium channel from what side?
    Cytoplasmic
  26. The local anesthetics (Na channel blockers) are subdivided into groups depending on their affinity for the Na channel and their ability to dissociate from the channel. What is the effect of drugs with a low affinity on normal and high heart rates?
    Do not alter Na conduction at normal heart rate, only at high heart rate. This is because at a normal heart rate they dissociate from the channel before the next action potential. At high rates of channel opening, they are still bound to the channel when the next action potential is initiated and block Na conduction.
  27. The local anesthetics (Na channel blockers) are subdivided into groups depending on their affinity for the Na channel and their ability to dissociate from the channel.What is the effect of drugs with a high affinity on heart rate?
    Drugs with high affinity inhibit Na conduction at both normal and high heart rates and will affect both normal and abnormal tissues
  28. What are the subclasses of Type I antiarrhythmic drugs?
    • Type Ia: Medium Affinity -- Procainamide
    • Type Ib: Low Affinity -- Lidocaine, Mexiletine
    • Type Ic: High Affinity -- Flecainide, Propafenone
  29. What drug, used for short-term antiarrhythmic therapy, directly inhibits the automaticity of the SA and AV nodes and ectopic pacemakers? It has little vagolytic effects compared to the other drugs in its class.
    Procainamide
  30. What is the main side effect of Procainamide?
    Approximately 1/3 of patients receiving long term procainamide develop symptoms similar to lupus erythematosus with athralgia and arthritis
  31. What is the main use for Procainamide?
    Short term antiarrhythmic therapy -- supraventricular and ventricular arrhythmias, atrial fibrillation, and flutter
  32. What are the Type Ib, low affinity, antiarrhythmic drugs?
    • Lidocaine
    • Mexiletine
  33. What local anesthetic is the agent of choice for termination of ventricular tachycardia and prevention of ventricular fibrillation after cardioversion in the setting of acute ischemia? How is it administered?
    • Lidocaine
    • IV only
  34. What are the side effects associated with Lidocaine?
    • Paresthesias
    • Tremor
    • Nausea of Central Origin
    • Lightheadedness
    • Tinnitus
    • Slurred Speech
    • Convulsions
  35. What drug is an orally active analog of Lidocaine that has been modified to reduce first-pass hepatic metabolism? Its pharmacological effects and side effects are similar to those of Lidocaine. This drug is used in the treatment of ventricular arrhythmias.
    Mexiletine
  36. What is the use of Mexiletine?
    Ventricular Arrhythmias
  37. What are the two Type Ic, high affinity, antiarrhythmic drugs?
    • Flecainide
    • Propafenone
  38. What two drugs have proarrhythmic effects in damaged heart tissue and should not be used in patients with heart disease such as congestive heart failure or myocardial ischemia?
    • Flecainide
    • Propafenone
  39. What drug is currently used for patients with otherwise normal hearts who have supraventricular arrhythmias? It is also effective in preventing premature ventricular contractions (PVCs). It has no antimuscarinic effects. It can exacerbate congestive heart failure in patients with depressed left ventricular performance.
    Flecainide
  40. What is the most serious adverse effect of Flecainide?
    Provocation or exacerbation of potentially lethal arrhythmias
  41. What drug is used to maintain sinus rhythm in patients with supraventricular tachycardias, including atrial fibrillation; like other Na channel blockers, it also can be used in ventricular arrhythmias, but with only modest efficacy. This drug has weak beta-blocking activity.
    Propafenone
  42. What are the three Type II, beta-adrenergic receptor antagonists?
    • Propanolol
    • Metoprolol
    • Esmolol
  43. What class of drugs have acute antiarrhythmic effects, primarily due to the inhibition of abnormal automaticity of the SA and AV nodes or are a portion of a reentry loop. They also help to inhibit ventricular response to atrial tachycardia by decreasing conduction through the AV node. These drugs can also reduce ventricular ectopic beats, particularly if the ectopic activity has been precipitated by catecholamines. They are also useful in suppressing exercise-induced tachycardias. They are useful in chronic antiarrhythmic therapy, and decrease the likelihood of sudden cardiac death after myocardial infarction. These drugs can also decrase blood pressure by suppressing the renin aldosterone, angiotensin axis.
    Beta-blockers (Type II drugs)
  44. Which beta-blocker is a non-selective beta-antagonist. It crosses the blood brain barrier and has been associated with changes in affect of patients.
    Propanolol
  45. What beta-blocker is a selective beta-1-antagonist
    Metoprolol
  46. What beta-blocker is a short-acting, selective beta-1-antagonist and is only administered IV. This is used in urgent situations when rapid blockade is needed.
    Esmolol
  47. What are the 5 Type III delayed rectifier K channel blockers?
    • Amiodarone
    • Dronetarone
    • Sotalol
    • Dofetilide
    • Ibutilide
  48. What type of antiarrhythmic drugs include those agents that specifically prolong refractoriness in atrial and ventricular tissue? This class includes very diferent drugs; they share the common effect of delaying repolarization by blocking the rapidly activating delayed rectifier potassium channels (IKr) responsible for phase 2 and phase 3 repolarization. Most drugs in this class prolong the QT interval.
    • Type III, Delayed Rectifier K Channel Blockers
    • (Amiodarone, Dronetarone, Sotalol, Dofetilide, Ibutilide)
  49. What are the common side effects of all type III agents?
    They may cause proarrhythmia in the form of provoking EADs by blocking potassium channels and delaying repolarization
  50. What is the most widely perscribed antiarrhythmic drug?
    Amiodarone
  51. What drug markedly prolongs the action potential duration (and the QT interval on the ECG) by blockade of delayed rectifier K channel? The action potential duration is prolonged uniformly over a wide range of heart rates. The drug has broad spectrum antiarrhythmic action, and is very extensively used for a wide variety of arrhythmias. It is used to treat serious ventricular arrhythmias. It is also highly effective for the treatment of supraventricular arrhythmias such as atrial fibrillation.
    Amiodarone
  52. What are the side effects of Amiodarone?
    • Peripheral vasodilation and hypotension and depressed myocardial performance when administered IV.
    • Most serious adverse effect is pulmonary fibrosis
    • Photodermatitis and a gray-blue skin discoloration
    • Corneal Microdeposits
    • Hyper or Hypothyroidism
  53. What drug has a black box warning and is contraindicated in patients with severe or decompensated heart failure?
    Dronedarone
  54. What new antiarrythmic drug is an analog of Amiodarone that lacks the thyroid side effects? It is approved for use of atrial fibrillation. Not as effective at treating arrhythmias as Amiodarone.
    Dronedarone
  55. What drug inhibits the delayed rectifier K channels and is also a non-selective beta-adrenergic receptor antagonist? It prolongs action potential duration throughout the heart and QT interval on the ECG. It decreases automaticity, slows AV nodal conduction, and prolongs AV refractoriness by blocking both K channels and beta-adrenergic receptors. It is used to treat patients with both ventricular tachyarrhythmias and atrial fibrillation or flutter.
    Sotalol
  56. What side effects are associated with Sotalol?
    Causes EADs and triggered activity in vitro and can cause torsades de pointes with overdose
  57. What drug is a potent and pure blocker of rapidly activating delayed rectifier K channels, with no effects on the Na channel? This drug prolongs the duration of the action potential. It is used to maintain normal sinus rhythm in patients with atrial fibrillation and to restore normal sinus rhythm in patients with atrial fibrillation.
    Dofetilide
  58. What drug blcoks the rapidly activating delayed rectifier K channel and also activates the voltage-gated Na channel. It is administered IV to convert atrial flutter and atrial fibrillation to normal sinus rhythm.
    Ibutilide
  59. What side effect is associated with Ibutilide?
    Excessive QT interval prolongation and torsades de pointes
  60. What are the two Type IV, L-type Ca Channel Blockers?
    • Verapamil
    • Diltiazem
  61. What drug class has its primary site of action in the slow response action potentials in the SA and AV nodes? These agents are effective in automatic or reentrant tachycardias, which arise from or use the SA nodes. They will slow ventricular response during atrial fibrillation by slowing AV conduction. This class is also effective in exercise-triggered tachycardias or tachycardias triggered by automaticity
    • Type IV, L-type Ca Channel Blockers
    • (Verapamil, Diltiazem)
  62. What drug blocks both open and inactivated L-type calcium channels? Its effect is more marked in tissue that fire frequently, those that are less completely polarized at rest, and those in which activation depends exclusively on the Ca current, such as the SA and AV nodes.
    Verapamil
  63. What is the primary use of Verapamil? What is its main side effect?
    • Treatment of supraventricular tachycardia
    • Peripheral Vasodilation
  64. What drug is administered as an acute IV bolus for treatment of reentrant supraventricular arrhythmias? It binds to specific receptors and activates the acetylcholine-sensitive K channel in the atrium, SA, and AV nodes. This causes a shortening of the action potential duration, hyperpolarization and slowing of automaticity.
    Adenosine
  65. What is the primary use of Adenosine?
    Administered as an acute IV bolus for treatment of reentrant supraventricular arrhythmias
  66. What drug, in addition to its inotropic effects, also has vagotonic effects? It causes an inhibition of Ca currents in the AV node and activation of acetylcholine-sensitive K currents in the atrium. This results in hyperpolarization, shortening of atrial action potentials, and increase in the refractory period of the AV node. It is used in patients with reentry arrhythmias in the AV node and atrial fibrillation.
    Digitalis
  67. What is the primary use of Digitalis?
    Reentry arrhythmias in the AV node and atrial fibrillation
  68. What is the biggest compensatory response that vasodilators must overcome, and what is a likely response of this response? What is the short-term compensatory response? Long term?
    • Sympathetic Nervous System
    • Arrythmias
    • Baroreceptor Reflex
    • Salt and Water Retention
  69. What is the mechanism of action of Calcium Channel Antagonists?
    Block L-type Ca channels, leading to vasodilation (no Ca = cells cant contract)
  70. What are the Ca Channel Antagonists (6)?
    • Dihydropyridines: Nifedipine, Nicardipine, Amlodipine, Felodipine
    • Verapamil
    • Diltiazem
  71. What are the main adverse effects of the Ca Channel Antagonists?
    • Hypotension
    • Headache
    • Peripheral or Pulmonary Edema
  72. Verapamil and Diltiazem should not be administered if a patient is taking what other drug type?
    Beta Blockers
  73. What class of drugs block the conversion of angiotensin I to angiotensin II by antagonizing angiotensin converting enzyme? This reduces vasoconstriction, reduces the secretion of aldosterone, and retards Na and water retention.
    Angiotensin Converting Enzyme (ACE) Inhibitors
  74. The primary action of ACE inhibitors to block the degradation of __________ may be the primary beneficial effect of these drugs on the peripheral vasculature.
    Bradykinin
  75. What are the three ACE inhibitors?
    • Captopril
    • Enalapril
    • Benazepril
  76. What are the adverse effects of the ACE inhibitors? What drug interactions are seen with these drugs?
    • Hypotension
    • Hyperkalemia
    • Dry Cough
    • Angioedema
    • Drug Interaction: NSAIDS
  77. Angiotensin II acts on two types of receptors, AT1 and AT2. What class of drugs antagonize the AT1 receptor?
    Angiotensin Receptor Blockers
  78. What are the Angiotensin Receptor Blockers?
    • Losartan
    • Candesartan
    • Valsartan
  79. What are the adverse effects associated with Angiotensin Receptor Blockers?
    • Hypotension
    • Hyperkalemia
    • Angioedema
  80. What is the ultimate result of the renin inhibitor?
    • A reduction in Angiotensin II synthesis
    • The advantage of blocking renin is that the blockade reduces the compensatory response to reduction of angiotensin II. With chronic use of ACE inhibitors or angiotensin receptor blockers, production of renin increases to compensate; blocking renin mitigates this compensatory response
  81. What is the renin inhibitor?
    Aliskiren
  82. What are the adverse effects of Aliskiren?
    • Hypotension
    • Hyperkalemia
    • Angioedema
  83. What is the mechanism of action of the Nitrates?
    The nitrates relax all types of smooth muscle. Smooth muscle cells enzymatically convert nitrates to nitric oxide, which relaxes the cells through the guanylyl cyclase system
  84. What are the 4 Nitrates?
    • Nitroglycerin
    • Isosorbide dinitrate
    • Isosorbide mononitrate
    • Sodium nitroprusside
  85. Which two nitrates are given sublingually? What is their duration of action?
    • Nitroglycerin & Isosorbide Dinitrate
    • About an hour
  86. Which nitrate can be administered orally? What is its duration of action?
    • Isosorbide Mononitrate
    • 6-10 hours
  87. Which nitrate can be given transdermally? What is its duration of action?
    • Nitroglycerin
    • Up to 10 hours
  88. Which Nitrate can only be given IV? What is its duration of action?
    • Sodium Nitroprusside
    • 1-10 minutes
  89. What are the adverse effects of the nitrates? What are they contraindicated for?
    • Hypotension
    • Orthostatic Hypotension
    • Contraindication: phosphodiesterase 5 inhibitor such as sildenafil (Viagra) due to the risk of a large decrease in arterial pressure
    • Tolerance to these develop quickly
  90. What is the mechanism of action of Hydralazine?
    Releases NO from endothelium, dilating via the cGMP pathway. Dilates arterioles but not veins
  91. What are the adverse effects of Hydralazine?
    • Compensatory salt and water retention
    • Angina
    • Arrhythmias
    • Tachyphylaxis
  92. What is the mechanism of action of Minoxidil?
    Opens K channels in vascular smooth muscle membranes. This effect maintains the cells in a more hyperpolarized state, reducin gthe ability to contract. Just dilates arterioles
  93. What are the adverse effects of Minoxidil?
    • Salt and Water Retention
    • Increase in Sympathetic Outflow
    • Tachycardia
    • Angina
    • Palpitations
    • Edema
    • Hypertrichosis (hair growth)
  94. What is the mechanism of action of Diazoxide? How is it administered?
    • Opens K channels in vascular smooth muscle
    • Given parenterally for treating hypertension; given orally to treat hyperinsulinism
  95. What are the adverse effects associated with Diazoxide?
    • Excessive hypotension resulting in stroke or MI
    • Angina
    • Cardiac Ischemia
    • Cardiac Failure in people with ischemic heart disease
  96. What is the mechanism of action of Fenoldopam? How is it administered
    • Stimulates dopamine D1 receptors which produces arteriolar dilation, and also produces natriuresis
    • IV (half-life is ten minutes)
  97. What are the adverse effects associated with Fenoldopam?
    • Reflex Tachycardia
    • Increased Intraocular Pressure -- should not be used in people with glaucoma
  98. What two things are Ca Channel Antagonists used to treat?
    • Hypertension
    • Angina
  99. What 3 things are ACE Inhibitors and Angiotensin Receptor Blockers used to treat?
    • Hypertension
    • Congestive Heart Failure
    • Slowing the advancement of Diabetic Nephropathy
  100. What are Nitroglycerin, Isosorbide Dinitrate, and Isosorbide Mononitrate used to treat?
    Angina
  101. What is Sodium Nitroprusside used to treat?
    Hypertensive Emergencies
  102. What is Hydralazine used to treat?
    Refractory Hypertension
  103. What is Minoxidil used to treat?
    Hypertension in people who do not respond well to hydralazine or in people with renal failure
  104. What is Diazoxide used to treat?
    Hypertensive Emergencies and Hyperinsulinism
  105. What is Fenoldopam used to treat?
    Hypertensive Emergencies and Postoperative Hypertension
  106. At low doses, what is the effect of Nitrates on venous smooth muscle?
    Venous capacitance is increased, resulting in lower venous return and thus preload. This reduces wall tension, which reduces myocardial oxygen demand (to reduce angina)
  107. At low doses, nitrates primarily affect what type of smooth muscle? At high doses, it relaxes _________ smooth muscle as well.
    • Venous Smooth Muscle
    • Arterial Smooth Muscle
  108. In general, what is the primary hemodynamic effect of nitrates to relieve angina?
    The increase in venous compliance results in a decrease in myocardial oxygen demand
  109. Does coronary blood flow decrease with nitrates?
    No
  110. What are the nitrates primarily used for?
    Quickly relieve the pain of angina
  111. What is the primary reason the Ca Channel Antagonists can be used to treat angina?
    They cause a reduction in afterload that produces a net decrease in myocardial oxygen demand
  112. What additional Ca Channel Antagonist has a similar profile to Verapamil, but its inhibition of the fast inward Na current is more effective than verapamil's? As a result, AV nodal refractory period is increased, and QTc interval is increase. This can lead to torsades de pointes, which limits the usage of the drug.
    Bepridil
  113. What types of angina are the Calcium Channel Antagonists useful for?
    • Stable & Variant (Prinzmetal)
    • Not useful for unstable, unless the instability is caused by a vasospasm
  114. What types of angina are beta-blockers useful for?
    • Stable -- though not used for acute bc nitrates work more quickly
    • Unstable -- reduce the likelihood it will occur, as well as the likelihood it will develop into MI if it does occur
    • Silent Ischemia
    • Not useful for Variant Angina bc have no effect on epicardial arteries
  115. What are two contraindications for the beta-blockers?
    • Asthma
    • Bronchospasm
  116. What combination of drugs is very useful for treating stable angina because each drug counteracts the other drug's limitations?
    Nitrates & Beta-Blockers -- the reflex sympathetic activity caused by nitrates is blocked by beta blockers, and the increase in end-diastolic volume caused by beta blockers is reduced by the increase in venous capacitance caused by nitrates
  117. What is the most effective combination of drugs for treating a patient's angina if it is often caused by vasospasm? What is a downside of this?
    • Calcium Channel Blockers and Nitrates
    • Excessive vasodilation may occur
  118. In erections, the parasympathetic system releases _____ from nerve terminals and also stimulates its release from endothelial cells; it then diffuses into the smooth muscle cells and activate the relaxation system.
    NO
  119. The most common drugs currently used to treat ED are inhibitors of _________. By reducing the breakdown of ________, these drugs enhance the magnitude and prolong the duration of smooth muscle relaxation.
    • PDE5
    • cGMP
  120. What is the main PDE5 drug used to treat ED?
    Sildenafil (Viagra)
  121. What are the contraindications for Sildenafil (Viagra) use?
    • Nitrate drugs: combination can produce excessive hypotension
    • Alpha-Adrenergic drugs: combination can produce excessive hypotension
  122. What drug is a PGE1 analog that is the most common drug used in men who do not respond to a PDE5 inhibitor for treatment of ED? This will result in erections in most of these men. It can be injected into the cavernosal tissue or placed in the urethra as a minisuppository.
    Alprostadil
  123. What is the drug treatment algorithm for treating congestive heart failure?
    • Loop Diuretic
    • ACE Inhibitor
    • Beta-blocker
    • Aldosterone Inhibitor
    • Angiotensin Receptor Blocker
    • Inotropic Agent
  124. What is the recommended first drug therapy for heart failure? Which of these is most effective and why?
    • Loop Diuretics (Furosemide and Torsemide)
    • Furosemide -- also increases venous capacitance, which reduces preload (pulmonary edema is eased quickly)
  125. What is the clinical use of K-sparing diuretics/aldosterone antagonists in treating CHF?
    The major influence is thought to be a reduction in remodeling of the heart, which is brought about by their aldosterone blocking ability.
  126. Which K-sparing agents are used in CHF?
    Only Aldosterone blockers -- Spironolactone & Eplerenone
  127. What is the mechanism of action of ACE Inhibitors for treatment of CHF?
    • Reduce vasoconstriction, thereby reducing afterload. Reduced venoconstriction reduces filling pressures and end-diastolic volumes in both ventricles
    • Reduce secretion of aldosterone, which retards Na and water retention
    • Reverse remodeling that has already occured
  128. What drugs can the first drugs of choice for treating heart failure, particularly in people who have no overt signs yet of heart failure? These reduce mortality from heart failure resulting from any cause
    ACE Inhibitors
  129. What drug type is recommended in mild to moderate heart failure, and reduces mortality from all causes by about 33%? These provide protection for people who have a myocardial infarction due to their antiarrhythmic effects, and reduce hospitalizations and the progression of heart failure.
    Beta-Blockers
  130. What beta-blockers are used in CHF?
    • Carvedilol
    • Metoprolol succinate
  131. What drug type can be used in CHF patients who cannot tolerate ACE inhibitors? These reduce mortality from heart failure. The combination of these with an ACE inhibitor reduces hospitalizations due to heart failure.
    Angiotensin Receptor Blockers
  132. What Inotropic Agent is used for treatment of CHF? What patients is this drug perscribed for?
    • Digoxin
    • Patients with a high heart rate, and those that are not adequately treated with any of the other drugs
  133. For treatment of CHF, what is the mechanism of action for the beta agonists?
    Stimulate beta1 receptors in the heart which increases contractility
  134. When are beta agonists used?
    To treat CHF patients that are in a hospital bc of severe heart failure. Given IV for short periods of time.
  135. What are the beta agonists used in CHF?
    • Dopamine
    • Dobutamine
  136. What are the vasodilators used in CHF? When combined, these two drugs reduce both venous and arterial resistances. What is the trade name for this combination? In what population is this combination particularly effective in?
    • Isosorbide dinitrate & Hydralazine
    • Bidil
    • African American Males
  137. What drug is used to treat dyspnea caused by heart failure?
    Nesiritide (a recombinant version of BNP)
  138. What is the most effective class of drugs for treating dyslipidemia?
    Statins
  139. What is the mechanism of action of statins for treating dylipidemia?
    • Competitively inhibit the rate limiting step of cholesterol synthesis, HMG-CoA reductase, thereby reducing the synthesis of cholesterol
    • More LDLs are absorbed into the liver, thereby decreasing plasma LDLs
  140. What are the three major statins? Which one is unique in that it is metabolized differently, making it a useful alternative for a patient that has trouble tolerating the other statins?
    • Lovastatin, Simvastatin, Pravastatin
    • Pravastatin
  141. What are the major adverse effects associated with the statins?
    Myopathy and Rhabdomyolysis (muscle cells are destroyed)
  142. What are the safest antilipidemic drugs because they are not absorbed from the GI tract? What drug is included in this class?
    • Bile Acid Resins
    • Cholestyramine
  143. What is the mechanism of action of the Bile Acid Resins (Cholestyramine)?
    • They are positively charged, and bind the negatively charged bile acids. The bound acids cannot be reabsorbed, and are excreted in the feces.
    • Excretion causes bile acid synthesis to increase, which reduces cholesterol in the liver. The activity of HMG-CoA reductase and synthesis of LDLR both increase. The latter reduces plasma LDLs, an effect that is partially mitigated by the increase in cholesterol synthesis
  144. What is the mechanism of action of Niacin?
    • Inhibits the lipolysis of triglycerides in adipose tissue. In the liver, it inhibits the synthesis and esterification of fatty acids. Both of these effects prevent the liver from synthesizing VLDLs, which reduces LDLs.
    • Niacin also increases the activity of lipoprotein lipase
    • The clearance of ApoA-I is reduced, which increases HDLs and thus reverse cholesterol transport
  145. What is the major adverse effect of Niacin, which prevents it from being regularly used?
    Hepatotoxicity
  146. What is the mechanism of action of Ezetimibe?
    Blocks cholesterol absorption by interfering with the transport protein NPC1L1
  147. What drug class is the first choice for treating severe triglyceridemia? What drug is in this class?
    • Fibrate Derivatives: PPAR Activators
    • Clofibrate
  148. What is the mechanism of action of Clofibrate?
    Probably involves activation of peroxisom proliferator activated receptors (PPARs), which are regulators of gene transcription. Fatty acid oxidation and synthesis of LPL are facilitated when fibrates bind to PPAR. The ultimate result is a reduction of triglycerides in plasma

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