Review Questions
1. A patient with edema is being treated with a drug that inhibits the absorption of bicarbonate ions from the glomerular filtrate. The effectiveness of this drug for long-term therapy is limited by drug-induced acidosis, which appears within the first weeks of therapy. With which of the following drugs is the patient being treated?
A. Metolazone
B. Ethacrynic acid
C. Amiloride
D. Acetazolamide
E. Spironolactone
2. Which of the following produces an acute increase in the urinary excretion of 20 to 30% of the filtered load of calcium and is therefore useful in treating symptomatic hypercalcemia, provided the plasma volume is maintained?
A. Furosemide
B. Chlorthalidone
C. Hydrochlorothiazide
D. Desmopressin
E. Mannitol
3. Which of the following may acutely reduce the glomerular filtration rate (GFR)?
A. Triamterene
B. Hydrochlorothiazide
C. Furosemide
D. Spironolactone
E. Mannitol
4. A 49-year-old man with high blood pressure tried to lower his blood pressure through diet and exercise. After 1 year, his blood pressure is slightly decreased, but it remains at 150/100 mm Hg. In the past year, he has been to your office once with a red, tender, and swollen first metatarsophalangeal joint at the base of the big toe. Which of the following drugs would have to be prescribed with caution in this patient?
A. Nifedipine
B. Labetalol
C. Prazosin
D. Chlorothiazide
E. Spironolactone
5. A 72-year-old man is being treated for congestive heart failure with a thiazide diuretic, an angiotensin-converting enzyme inhibitor, and a β-adrenergic receptor blocking agent. During a routine examination, serum electrolyte values were found to be the following: Na+ = 135 mEq/L, Cl− = 105 mEq/L, K+ = 2.8 mEq/L, HCO3− = 24 mEq/L. The electrolyte values could be balanced by which of the following drugs?
A. Acetazolamide
B. Amiloride
C. Furosemide
D. Hydrochlorothiazide
E. Aldosterone
6. Which of the following is useful in the treatment of diabetes insipidus of pituitary origin?
A. Triamterene
B. Amiloride
C. Ethacrynic acid
D. Desmopressin
E. Furosemide
7. Which of the following is useful in the treatment of nephrogenic diabetes insipidus?
A. Triamterene
B. Hydrochlorothiazide
C. Furosemide
D. Desmopressin
E. Mannitol
8. A 70-year-old Caucasian woman is brought to the emergency room with heart palpitations and an erratic, irregular pulse. She is admitted to the hospital and diagnosed with hypertension complicated by paroxysmal atrial fibrillation. She had been taking a blood pressure medication but ran out of pills 1 week before the incident. Which of the following antihypertensive agents was she most likely taking?
A. Propranolol
B. Enalapril
C. Hydrochlorothiazide
D. Losartan
E. Clonidine
9. Which of the following antihypertensive drugs is contraindicated in patients with asthma?
A. Reserpine
B. Hydrochlorothiazide
C. Nifedipine
D. Verapamil
E. Propranolol
10. Which of the following antihypertensive drugs is less effective as monotherapy for African American patients?
A. Clonidine
B. Enalapril
C. Labetalol
D. Nifedipine
E. Prazosin
11. A 62-year-old woman is being treated for hypertension with captopril and hydrochlorothiazide. She has had a cough for the last 6 months that started ~2 months after she began antihypertensive therapy. Her blood pressure is well controlled. Chest radiograph (Xray) and spirometry are normal. The cough is most likely a result of which of the following?
A. Pneumonia
B. The common cold
C. Poorly controlled blood pressure
D. A side effect of hydrochlorothiazide
E. A side effect of captopril
12. Given that the patient in question 11 has shown a favorable response to decreasing the function of angiotensin II, you decide to replace the drug with a drug that blocks the binding of angiotensin II to the angiotensin I–type angiotensin receptor. Which of the following drugs is prescribed?
A. Clonidine
B. Enalapril
C. Labetalol
D. Nifedipine
E. Losartan
13. A 48-year-old African American man has had a blood pressure of 160/90 mm Hg, 170/95 mm Hg, and 165/95 mm Hg on three monthly visits. The patient's hypertension is treated with nifedipine. How does this drug reduce hypertension?
A. By blocking α2-adrenergic receptors
B. By inhibiting angiotensin-converting enzyme
C. By blocking β-adrenergic receptors
D. By blocking L-type calcium channels
E. By inhibiting sodium reabsorption in the loop of Henle
14. Abrupt cessation of antihypertensive therapy may cause a serious rebound hypertension with which of the following drugs?
A. Prazosin
B. Clonidine
C. Guanethidine
D. Enalapril
E. Reserpine
15. A 68-year-old man with asthma, long-standing hypertension, and diabetes mellitus who is receiving digoxin, hydrochlorothiazide, and 35 units of Neutral Protamine Hagedorn (NPH) insulin gradually develops congestive heart failure. Why would the addition of captopril to the patient's medication be potentially harmful?
A. It results in hypokalemia.
B. It blocks the subjective warning signs of hypoglycemia.
C. It aggravates the patient's asthmatic condition.
D. It may cause severe hypotension.
E. It activates the cytochrome P-450 enzymes that metabolize digoxin.
16. A 58-year old man is being treated for heart failure with a diuretic, an angiotensin-converting enzyme (ACE) inhibitor, and a β-adrenergic receptor blocking agent. He continues to experience dyspnea on exertion. The patient may benefit from the addition of a drug that inhibits which of the following proteins on the membrane of cardiac myocytes?
A. α2-adrenergic receptors
B. Glucose transporter 1 (GLUT1)
C. Na+−K+−ATPase
D. L-type Ca2+ channels
E. Delayed rectifier K+ channels
17. Digoxin is a cardiac glycoside used for the treatment of heart failure. The drug has a low therapeutic index, in part because it may affect the intracellular K+ concentration of cardiac myocytes. What would be the expected effect of digoxin on intracellular K+ levels?
A. It would lead to membrane hyperpolarization.
B. It would lead to membrane depolarization.
C. It would lead to no change in membrane potential.
D. It would decrease automaticity.
E. It would decrease contractility.
18. An elderly man comes to the emergency room with an acute myocardial infarction. He is in cardiogenic shock in which the cardiac output is very low, and there is a reflex vasoconstriction. He has tachycardia. Which of the following drugs would be most appropriate to administer?
A. Dobutamine
B. Isoproterenol
C. Bethanecol
D. Propranolol
19. Relief of pulmonary congestion after administration of nitroglycerin to a patient in congestive heart failure (CHF) is primarily due to
A. arteriolar dilation.
B. inotropic stimulation.
C. increased cardiac output.
D. increased venous capacitance.
20. A 62-year-old patient is experiencing chest pain on exertion. Effort-induced angina is diagnosed, and treatment is begun. Nitroglycerin and isosorbide dinitrate are given sublingually and are rapidly absorbed through the oral mucosa. Once in the bloodstream, they increase the level of which signaling molecule in smooth muscle?
A. Inositol triphosphate
B. Phospholipase Cß
C. RAF kinase
D. Cyclic guanosine monophosphate (cGMP)
E. Cyclooxygenase-3 (COX-3)
21. The patient in question 20 is prescribed another drug to take daily to prevent the effort-induced angina attacks. This drug is most likely which of the following?
A. Diltiazem
B. Nitroglycerin
C. Metoprolol
D. Isosorbide dinitrate
E. Verapamil
22. Organic nitrates may relieve angina by which of the following mechanisms?
A. Reduction of the heart rate
B. Reduction of myocardial contractility
C. Increase in the left ventricular residual volume
D. Reduction of ventricular wall stress
E. Increase in venous pressure
23. A common property of all class I antiarrhythmic drugs is
A. reduction of membrane responsiveness.
B. prolongation of the effective refractory period.
C. hyperpolarization of the membrane.
D. atropine-like effect.
24. A 58-year-old female patient with recurrent ventricular tachycardia requires treatment with an antiarrhythmic drug. She has a previous history of systemic lupus erythematosus (SLE). Which of the following drugs would be contraindicated in this patient?
A. Flecainide
B. Procainamide
C. Quinidine
D. Amiodarone
E. Verapamil
25. A 69-year-old man is taking mexiletine for prevention of ventricular arrhythmia. He has experienced some ataxia, paresthesias, and tremor 2 to 3 hours after taking the medicine. These effects result from mexiletine acting as which of the following?
A. Calcium channel blocker
B. β-blocker to decrease blood flow
C. Local anesthetic to affect neuronal conduction
D. Alcohol dehydrogenase inhibitor
E. Benzodiazepine receptor agonist
26. Following an acute myocardial infarction, a patient is given an anti arrhythmic drug to prevent supraventricular and ventricular a rrhythmias. Administration of this drug will be continued for 2 to 3 years. Which of the following drugs was the patient given?
A. Phenylephrine
B. Isoproterenol
C. Norepinephrine
D. Nitroglycerin
E. Propranolol
27. A hospitalized patient is receiving heparin for prevention of deep vein thrombosis. One of the drugs the patient received during the procedure was eptifibatide. What is the action of this drug?
A. To inhibit platelet aggregation by reversibly binding to the platelet receptor glycoprotein IIb/IIIa
B. To block the glycoprotein IIb/IIIa receptor in human platelets
C. To inhibit the release of adenosine diphosphate (ADP) by increasing cyclic adenosine monophosphate (cAMP) levels
D. To acetylate platelet cyclooxygenase
E. To inhibit ADP-induced platelet fibrinogen binding
For questions 28–30.
A 44-year-old man has swelling and pain in his right leg, ankle, and foot. At first he thought he had a cramp, but then he noticed his calf had become red and warm. The swelling has not decreased after 3 days. He has chest pain but no shortness of breath. Blood pressure is 145/85 mm Hg, heart rate is 105 beats/min, and respiration is 30 breaths/min. Auscultation reveals a loud pulmonary heart sound. Arterial partial pressure of oxygen (pO2) is slightly decreased. Pulmonary embolism is suspected, and the patient is admitted to the hospital. Heparin therapy is initiated. Two days later, the patient's activated partial thromboplastin time (aPTT) is found to be excessively prolonged.
28. Which of the following drugs could be used to restore the patient's aPTT to within an acceptable range?
A. Protamine sulfate
B. Warfarin
C. Vitamin K
D. Enoxaparin
E. Bivalirudin
29. In addition to monitoring aPTT, what other parameter should be monitored for patients receiving heparin?
A. Platelet count
B. Bone density
C. Vitamin K levels
D. Cytokine levels
E. Vitamin C levels
30. A transition from heparin to warfarin anticoagulant therapy is initiated while the patient is in the hospital. After discharge of the patient from the hospital, warfarin anticoagulant therapy is continued. Following discharge, the patient decides to institute lifestyle changes, including diet and exercise. His dietary plan is to dramatically decrease his in-take of meat to try to become a vegetarian. How would an increased consumption of green leafy vegetables (which contain vitamin K) be expected to alter the patient's International Normalized Ratio (INR)?
A. It would be increased.
B. It would be decreased.
C. It would be unchanged.
D. It would be doubled.
E. It would be halved.
31. Which of the following decreases cholesterol synthesis by inhibition of 3-hydroxy-3-methylglutaryl (HMG) coenzyme A (CoA) reductase?
A. Lovastatin
B. Cholestyramine
C. Nicotinic acid
D. Clofibrate
32. A 56-year-old man has a total cholesterol of 245 mg/dL, low-d ensity lipoprotein (LDL) = 160 mg/dL, high-density lipoprotein (HDL) = 60 mg/dL, and triglycerides = 107 mg/dL. He is 69 inches (5 ft 9 in, 175 cm) tall and weighs 160 lb (72.5 kg). His father had a heart attack at age 45, and his older brother has had coronary angioplasty. He was started on the initial recommended dose of lovastatin 6 months ago. The National Cholesterol Education Program goal for this patient is to reduce his LDL cholesterol to < 130 mg/dL. Which of the following would be most optimal for further lowering the patient's cholesterol?
A. Increase the dose of lovastatin.
B. Add a bile acid sequestrant.
C. Add niacin.
D. Add clofibrate.
E. Lose more weight.
33. The main side effect of which of the following drugs is flushing of the skin?
A. Lovastatin
B. Cholestyramine
C. Nicotinic acid
D. Probucol
34. A 58-year-old Caucasian female patient has a total cholesterol of 299 mg/dL, low-density lipoprotein (LDL) = 240, high-density lipoprotein (HDL) = 30, and triglycerides = 928 mg/dL. She is 62 inches (5 ft 2 in, 157 cm) tall and weighs 220 lb (~100 kg). Which of the following drugs would be most effective for this patient?
A. Nonselective β-blocker
B. β1 selective adrenergic receptor blocker
C. Ezetimibe
D. Gemfibrozil
E. Verapamil
Answers and Explanations
1. D Acetazolamide is a carbonic anhydrase inhibitor that acts in the proximal convoluted tubule to reduce the absorption of bicarbonate ions from the glomerular filtrate. The effectiveness of its diuretic action decreases as plasma bicarbonate is depleted. This causes a metabolic acidosis (p. 185).
A Metolazone is a thiazide-like diuretic.
B Ethacrynic acid is a loop diuretic that inhibits the Na+–K+–2Cl− cotransporter in the thick ascending loop of Henle.
C Amiloride is a potassium-sparing diuretic used that directly interferes with sodium transport in the distal convoluted tubule.
E Spironolactone is a competitive antagonist to aldosterone and so inhibits the synthesis of Na+ channel proteins and Na+–K+-ATPases which promotes the reabsorption of Na+, Cl−, and water.
2. A Furosemide and the loop (or high-ceiling) diuretics increase calcium ion excretion into the urine and are therefore useful in treating symptomatic hypercalcemia (p. 185–187).
B, C Thiazide diuretics, such as chlorthalidone and hydrochlorothiazide, decrease calcium excretion.
D Desmopressin is the synthetic replacement for antidiuretic hormone (ADH), the hormone that reduces urine production.
E Mannitol is an osmotic diuretic that increases the solute load (solutes cannot be absorbed but bind to water), causing increased urine production.
3. B Thiazide diuretics, such as hydrochlorothiazide, may decrease the GFR in some patients. Thus, they may worsen existing mild renal failure (p. 187).
A, C–E The other drugs do not decrease the GFR.
4. D The foot inflammation in a male patient of this age indicates a gout attack. Thiazide diuretics, such as chlorothiazide, produce hyperuricemia (elevated blood uric acid level), which may precipitate further attacks (p. 187).
5. B The patient has hypokalemia (normal range 3.5–5.0 mEq/L). Amiloride is a potassium-sparing diuretic that is useful when given along with a thiazide to prevent potassium depletion (p. 188).
A Acetazolamide is a carbonic anhydrase inhibitor that will increase the excretion of bicarbonate.
C Furosemide is a loop diuretic that may worsen the hypokalemia.
D The patient is already taking hydrochlorothiazide, a thiazide diuretic.
E Aldosterone is an endogenous mineralocorticoid hormone that increases sodium reabsorption and potassium excretion.
6. D Diabetes insipidus of pituitary origin is the most common type of diabetes insipidus and is caused by a deficiency of arginine vasopressin (AVP). Desmopressin (1-deamino-8-d-arginine vasopressin) is a synthetic analogue of AVP used as replacement therapy for AVP (p. 190).
A, B Triamterene and amiloride are potassium-sparing diuretics used in combination with a thiazide diuretic to treat hypertension.
C, E Ethacrynic acid and furosemide are loop diuretics used to treat chronic heart failure, pulmonary edema due to left ventricular failure, hypertension, acute oliguria, and hypercalcemia.
7. B Nephrogenic diabetes insipidus is caused by a defect in the tubules of the kidney, leading to an improper response to anti-diuretic hormone (ADH) and overproduction of dilute urine. Thiazide diuretics, such as hydrochlorothiazide, exert a paradoxical effect to decrease the urine output of patients with nephrogenic diabetes insipidus (p. 189).
A Triamterene is a potassium-sparing diuretic used in combination with a thiazide diuretic to treat hypertension.
C Furosemide is a loop diuretic used to treat chronic heart failure, pulmonary edema due to left ventricular failure, hypertension, acute oliguria, and hypercalcemia.
D Desmopressin is the synthetic replacement for antidiuretic hormone (ADH), the hormone that reduces urine production.
E Mannitol is an osmotic diuretic that increases the solute load (solutes cannot be absorbed but bind to water), causing increased urine production.
8. A The patient's symptoms suggest that the antihypertensive drug she was taking may also have been preventing the atrial fibrillation.
A Propranolol, a nonselective β-blocker, has both antihypertensive and antiarrhythmic effects (p. 195).
B Enalapril is an angiotensin converting enzyme (ACE) inhibitor that has antihypertensive but no antiarrhythmic effects.
C Hydrochlorothiazide is a thiazide diuretic that has antihypertensive but no antiarrhythmic effects.
D Losartan is an angiotensin II receptor antagonist that has antihypertensive but no antiarrhythmic effects.
E. Clonidine is an α2-adrenergic receptor agonist that has antihypertensive but no antiarrhythmic effects.
9. E The nonselective β-adrenergic receptor blocking agents, such as propranolol, may worsen asthma by blocking the bronchodilation produced via β2-adrenergic receptor activation (p. 196).
A Reserpine is an adrenergic neuron blocker that reduces blood pressure by depleting norepinephrine stores and by preventing its reuptake and storage. It will have no effect on asthma.
B Hydrochlorothiazide is a thiazide diuretic. It will have no effect on asthma.
C, D Nifedipine and verapamil are calcium-channel blockers. Nifedipine acts predominantly on vascular smooth muscle causing vasodilation and so reduces blood pressure. Verapamil also causes vasodilation of vascular smooth muscle but it also acts on cardiac muscle cells to reduce heart rate, force of contraction, and velocity of contraction. It is therefore also useful in the treatment of angina and some arrhythmias. Both nifedipine and verapamil have no effect on asthma.
10. B Angiotensin-converting enzyme (ACE) inhibitors, such as enalapril, are less effective in African American patients than in other patient groups unless combined with a thiazide diuretic (p. 194).
A, C–E The other drugs listed are not associated with this reduced effectiveness.
11. E The test results are negative for other causes for her cough, and cough is a common side effect of angiotensin-converting enzyme (ACE) inhibitors, such as captopril (p. 194).
12. E Losartan blocks the binding of angiotensin II to the angiotensin I–type angiotensin receptor. Its side effects are similar to those of captopril, but it does not produce a cough (p. 194).
A–D The other drugs do not affect the angiotensin system directly.
13. D Nifedipine is a dihydropyridine calcium channel antagonist that acts by blocking L-type (long-lasting) calcium channels. This causes vasodilation of vascular smooth muscle and a reduction in blood pressure (p. 196).
14. B Clonidine stimulates α2-adrenergic receptors in the medulla, which in turn decreases sympathetic tone and blood pressure. Persistent activation of α2-adrenergic receptors leads to their downregulation. Upon cessation of clonidine, this decrease in α2-adrenergic receptor function leads to a rebound in blood pressure that may last a day or two until the normal level of α2-adrenergic receptors is restored (p. 200).
A Prazosin is an α1-adrenergic receptor antagonist that reduces blood pressure by vasodilation of vascular smooth muscle. Ortho-static hypotension is common after the first dose.
C Guanethidine is an adrenergic neuron blocker that reduces blood pressure by preventing norepinephrine release, depleting norepinephrine stores, and blocking its reuptake.
D Enalapril is an angiotensin-converting enzyme inhibitor that reduces blood pressure by preventing the vasoconstrictive effects of angiotensin II on vascular smooth muscle.
E Reserpine is an adrenergic neuron blocker that reduces blood pressure by depleting norepinephrine stores and by preventing its reuptake and storage.
15. D Hypotension is a side effect of captopril, an angiotensin-converting enzyme inhibitor. This effect is amplified when it is combined with hydrochlorothiazide and is more frequently observed in patients with heart failure (p. 194).
A–C, E The other results are not normally associated with captopril.
16. C Because the patient is already being treated with a diuretic, an ACE inhibitor, and a β-blocker, a logical next choice would be digoxin. Both the therapeutic and toxic effects of digoxin are attributable to inhibition of Na+-K+–ATPase (the digitalis receptor) located on the outside of the myocardial cell membrane (p. 205).
A, B, D, E The other choices are not valid mechanisms for drugs that treat heart failure.
17. B As an inhibitor of Na+– K+–ATPase, which pumps Na+ out of the cell and K+ into the cell, digoxin would be expected to decrease the level of intracellular K+. According to the Nernst equation, membrane potential is proportional to the level of K inside the cell/K outside the cell. Decreasing the K inside the cell will decrease membrane potential (i.e., depolarize the cell) (p. 205).
A, C–E The other effects listed are not typical of digoxin.
18. A Dobutamine is used for short-term support in severe heart failure. It acts by stimulating cardiac β1 receptors to increase cardiac contractility. It is not used long term, as it may cause arrhythmias and increase oxygen consumption (p. 206).
B Isoproterenol is a nonselective β-adrenergic receptor agonist that increases heart rate and contractility. It is more likely than dobutamine to cause arrhythmias and increase oxygen consumption. It is used to improve cardiac output in patients with heart block.
C Bethanechol is a cholinergic muscarinic receptor agonist that would decrease, not improve, cardiac function.
D Propranolol is a nonselective β-adrenergic receptor blocker and would have a negative inotropic effect.
E Phenylephrine is an α adrenoceptor agonist that would produce vasoconstriction, but reflex vasoconstriction is already present.
19. D In CHF, the main therapeutic actions of nitroglycerin are due to dilation of large capacitance veins (p. 207).
A Nitroglycerin will cause some arteriolar dilation but this is not its primary effect.
B,C Nitroglycerin does not increase cardiac contractility (inotropism) or increase cardiac output.
20. D Organic nitrates are converted to nitric oxide, which activates guanylate cyclase, increases intracellular cGMP concentrations, and causes vasodilation of venous and arterial blood vessels (p. 209).
21. C Metoprolol is a β-adrenergic receptor antagonist. It is useful for the prophylaxis of effort-induced angina but is not effective for the acute termination of effort-induced angina or for the treatment of coronary artery spasm (p. 211).
A, E The calcium channel blockers diltiazem and verapamil are more appropriate for variant or unstable angina due to coronary vasospasm.
B, D Nitroglycerin and isosorbide dinatrate are indicated for acute relief of an angina pectoris attack. They are given sublingually and rapidly absorbed through the oral mucosa. Therapeutic effects are observed within 2 to 4 minutes but last for only 1 to 2 hours.
22. D Organic nitrates act like the endogenous compound nitric oxide. They activate guanylate cyclase to increase the level of cyclic guanosine monophosphate (cGMP) in smooth muscle. This leads to relaxation of vascular smooth muscle and both arterial and venous dilation. This results in a decrease in ventricular preload and a reduction of ventricular wall stress (p. 209).
A–C The vasodilation produced by the organic nitrates may result in reflex increases in heart rate and contractility and a decrease in left ventricular residual volume.
E Organic nitrates will cause a decrease in venous pressure.
23. A By definition, class I antiarrhythmic action is Na+ channel blockade, which reduces membrane excitability or responsiveness (p. 217).
24. B Acute lupus erythematosus has been observed with procainamide; thus, this drug is contraindicated in patients with a history of SLE (p. 217).
A, C–E None of the other drugs will precipitate lupus erythematosus.
25. C Class IB antiarrhythmic agents, such as mexiletine, are Na+ channel blockers and act like local anesthetics, which is producing this patient's symptoms. The symptoms are most prominent as the drug levels peak at 2 to 3 hours after administration (p. 219).
26. E A β-adrenergic receptor antagonist, propranolol is a class II anti-arrhythmic agent that is used to prevent ventricular fibrillation during the first 2 years following myocardial infarction (p. 220).
A Phenylephrine is an α-adrenergic agonist.
B Isoproterenol is a nonselective β-adrenergic receptor agonist.
C Norepeinephrine is the endogenous postganglionic sympathetic neurotransmitter with both α and β agonist activity.
D Nitroglycerin is indicated for acute relief of an angina pectoris attack.
27. B Eptifibatide is a cyclic peptide that blocks the glycoprotein IIb/IIIa receptor to prevent platelet aggregation (p. 226).
28. A Protamine sulfate is an antidote for heparin and forms a 1:1 complex with the anticoagulant. Administration of this drug will return the patient's aPTT to a normal range (p. 227).
B–E The other drugs have no effect on aPTT.
29. A Thrombocytopenia is one of the adverse effects that may be observed following heparin administration. It may be mild and transient, but it may become severe if antiplatelet antibodies are formed. Platelet counts should be performed to monitor for thrombocytopenia (p. 226).
B–E None of these have any relevance in heparin therapy.
30. B Warfarin is an oral anticoagulant drug that antagonizes the hepatic synthesis of the vitamin K-dependent clotting factors II (prothrombin), VII, IX, and X. It increases a patient's INR. Green leafy vegetables are a good source of vitamin K. Vitamin K is a warfarin antagonist. Thus, the expected result would be a decreased INR (pp. 228 and 229).
31. A Lovastatin competitively inhibits HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis (p. 237).
B Cholestyramine is an insoluble resin that is not absorbed by the body, but binds bile acids in the gut, thus preventing bile acids from being absorbed. This necessitates an increase in the hepatic conversion of cholesterol to bile acids, thereby reducing the cholesterol available through the enterohepatic circulation for production of plasma lipids. This also lowers LDL and plasma cholesterol.
C Nicotinic acid (niacin) inhibits hepatocyte diacylglycerol acyltransferase-2, a key enzyme for triglyceride synthesis, decreasing the secretion of very low density lipoprotein (VLDL) and low density lipoprotein cholesterol (LDL-C). It also decreases the hepatic catabolism of apo A-I increases the half-life and concentrations of high density lipoprotein cholesterol (HDL-C).
D Clofibrate lowers very low density lipoproteins (VLDL) and plasma triglycerides by stimulating lipoprotein lipase. It also lowers cholesterol by inhibiting its synthesis and enhancing excretion in the bile.
32. A Because the patient was started on the initial recommended dose, the cholesterol-lowering response was not great enough, and adverse reactions to the drug were not reported, the next step should be to increase the dose (p. 237).
B Bile acid sequestrant may be added if the statin does not reach the desired goal, but an adequate dose of the statin should be tried first.
C Nicain is especially useful in patients with both hypertriglyceridemia and low HDL-C levels. This patient has normal triglycerides and borderline high HDL.
D Clofibrate is useful in hypertriglyceridemia and hypercholesterolemia.
E The patient's weight is near normal.
33. C Flushing of the skin is a side effect of nicotinic acid (niacin). It results from the stimulation of prostaglandins D2 and E2 from subcutaneous Langerhans cells by a G protein-coupled niacin receptor (p. 240).
A, B, D Flushing is not associated with lovastatin, cholestyramine, or probucol.
34. D Gemfibrozil is indicated for hypertriglyceridemia and hypercholesterolemia (p. 241).
A, B, E β-blockers and verapamil (a calcium channel blocker) do not lower cholesterol levels.
C Ezetimibe inhibits cholesterol absorption in the small intestine but it is not as effective at lowering cholesterol or triglyceride levels as gemfibrozil.