The quizzes about Cardiovascular Pharmacology - Part 2

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Cardiovascular Pharmacology- Part 2

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Question 1

A woman has received a cardiovascular drug that i s absolutely contraindicated (category X) in pregnancy, but in the absence of pregnancy would have been deemed beneficial because of a particular cardiovascular disorder she Unfortunately, neither she nor her physician (whom she rarely vis i ted) knew she was pregnant until she had just started the second trimester. The drug i s stopped (and a suitable and safer alternative i s started), but i t i s too late. Her baby i s delivered prematurely, and sti l lborn. It i s obvious from examination of the baby that there i s a nasal deformity: the nose i s flattened into the face, with no apparent bridge. Standard x-rays reveal stippling of all the epiphyses. These responses are characteristic of which drug?

A	Clonidine
B	Heparin, low molecular weight (eg, enoxaparin)
C	Hydrochlorothiazide
D	Nitroglycerin
E	Warfarin

Question 1 Explanation:

The scenario describes the classic findings with “warfarin embryopathy”: nasal deformities (mainly a flattening of the nose) and stippling (based on standard x-ray images) at the epiphyses of the long bones. The drug is, as noted, absolutely contraindicated during pregnancy. The fetal risks are greatest if warfarin is taken at any time during the first 12 or so weeks of gestation, but adverse fetal effects can occur later. They are irreversible, sometimes fatal; there is no drug or vitamin (eg, vitamin K, folate) therapy that will be of benefit. All the other drugs listed pose some pregnancy-related risks (but lower and with less supporting data than with warfarin), and they do not share the characteristics of warfarin embryopathy. Clonidine (a) is in pregnancy category C. Its antihypertensive mechanism is largely identical to that of methyldopa, which is in category B and usually is a preferred drug for hypertension during pregnancy. Low molecular weight heparin (b) is also in pregnancy category B. If anticoagulation is required during pregnancy, it is the drug that most likely will be used. Hydrochlorothiazide (or thiazide diuretics in general) has no known human teratogenic effects (category B). Nitroglycerin is not contraindicated because of teratogenesis (category C). Note: I’ll kindly ask you to review the answers and explanations for Question 194, and recall that even though a cardiovascular drug may not be teratogenic nor absolutely contraindicated in pregnancy, it can cause adverse (potentially fatal) fetal effects if, for example, it causes hypotension and/or hypovolemia, which can significantly reduce placental blood flow. Recall that warfarin, ACE inhibitors, and angiotensin receptor blockers are contraindicated in pregnancy

Question 2

A patient who has been taking an oral antihypertensive drug for about a year develops a positive Coombs’ test, and now you are worried about the possibility (although low) that hemolytic anemia may develop i f the drug i s Which drug was the most l ikely cause?

A	Captopril
B	Clonidine
C	Labetalol
D	Methyldopa
E	Prazosin

Question 2 Explanation:

Among all the common oral antihypertensives, a Coombs-positive test is associated only with methyldopa. It occurs in up to about 20% of patients taking this drug long term. It may progress to hemolytic anemia, but that seldom occurs. The probable cause is an immune reaction (IgG antibodies) directed against and potentially lysing the red cell membrane. Other drugs with the potential to cause an immunohemolytic anemia are penicillins, quinidine, procainamide, and sulfonamides.

Question 3

A patient presents with severe hypertension and Blood chemistry results, radiologic studies, and the overall cl inical presentation point to pheochromocytoma. The tumor appears operable, but the patient will have to wait a couple of weeks for the adrenalectomy. We prescribe phenoxybenzamine in the interim, with the goal of suppressing some of the major s igns and symptoms caused by the tumor and the massive amounts of epinephrine i t i s releasing. Which of the following best summarizes what phenoxybenzamine does, or how i t acts?

A	Controls blood pressure by blocking α-adrenergic receptors in the peripheral vasculature
B	Controls heart rate by selectively blocking β1-adrenergic receptors
C	Inhibits catecholamine synthesis in the adrenal (suprarenal) medulla
D	Lowers blood pressure by inhibiting angiotensin converting enzyme
E	Stimulates catechol-O-methyltransferase, thereby facilitating epinephrine’s metabolic inactivation

Question 3 Explanation:

Phenoxybenzamine is a long-acting and noncompetitive α-adrenergic blocker. It works by alkylating (rather than merely occupying and “blocking”) α-adrenergic receptors, thereby rendering them incapable of interacting with α-adrenergic agonists such as epinephrine (which is being released in abundance by the pheochromocytoma). The drug has no ability to block β-adrenergic receptors (b), inhibit catecholamine synthesis (c), inhibit angiotensin converting enzyme (d), or affect any of the major enzymes involved in catecholamine degradation (COMT, answer e; or MAO).

Question 4

A 30-year-old man who has a history of asthma has just been diagnosed Stage 1 essential He regularly uses an inhaled corticosteroid, which seems to work well as a control medication, but also needs to use an albuterol inhaler about once every 3 weeks for suppression of asthma attacks (rescue therapy). Which antihypertensive drug or drug class poses the greatest ri sk of exacerbating the patient’s asthma and counteracting the desired pulmonary effects of the albuterol, even though i t might control his blood pressure well?

A	Diltiazem
B	Hydrochlorothiazide
C	Labetalol
D	Ramipril
E	Verapamil

Question 4 Explanation:

No β-blocker ordinarily should be administered to patients with asthma, because of a great risk of severe and potentially fatal bronchoconstriction or bronchospasm (unless the β-blocker is being given for a medical emergency that requires β-blockade, and likely benefits outweigh likely risks). This applies to all classes of β-blockers: nonselective, like propranolol; β1 “selective,” that is, atenolol or metoprolol; those with intrinsic sympathomimetic/partial agonist activity, such as pindolol; and those that also have α-blocking activity, that is, labetalol and carvedilol. The contraindication applies to all administration routes, including topical (ophthalmic); there are clinical reports of fatal bronchospasm induced by topical ophthalmic administration of “just one drop” of β- blockers. The reason? Airways of persons with asthma are exquisitely sensitive to a host of bronchoconstrictor stimuli and exquisitely dependent on the bronchodilator effects of circulating epinephrine (β2-receptors). Block those β-receptors, and that sets the stage for bronchoconstriction or bronchospasm. Another important factor is that this patient needs albuterol for occasional relief of bronchospasm. The drug works, of course, byactivating β2 adrenergic receptors in the airways. Any or all of the available β-blockers will antagonize albuterol’s desired effects, the so-called cardioselective agents included, because their selectivity for β1-receptors is only relative, not absolute; and it is highly dose-dependent. Diltiazem (a) and particularly verapamil (e), both nondihydropyridine calcium channel blockers, might be a good choice for this patient. They not only lower blood pressure by blocking calcium influx into vascular smooth muscle, but also (theoretically, at least) do the same in airway smooth muscle, thereby preventing or at least reducing bronchoconstriction. Hydrochlorothiazide possibly could exacerbate the problems by causing excessive fluid loss (which could favor bronchoconstriction), but the chances of this are low. (Loop diuretics such as furosemide would be of more concern, owing to their greater efficacy in terms of causing loss of circulating fluid volume). There are no specific concerns with using ramipril, an angiotensin converting enzyme inhibitor. (Remember: Drugs with generic names ending in “-pril” are ACE inhibitors, so even if you learned about only captopril as an ACE inhibitor, you should have realized that ramipril is in the same class.) Note: It’s fair to say that the “Big 4” classes of antihypertensive drugs can be summarized as A, B, C, D: ACE inhibitors or angiotensin receptor blockers; Beta-blockers; Calcium channel blockers; and Diuretics (thiazides or thiazide-like agents such as metolazone). Which is “best” for a particular patient depends on a host of patient-related factors that may weigh in favor of selecting a drug from a particular class (A, B, C, D) or weigh against a particular class. There has been a resurgence in the use and recommendation of thiazides or thiazide-like drugs for initiating anti-hypertensive therapy. Likewise, much more recently, and for a variety of reasons, some experts are stating that β-blockers should be dropped from the Big 4 list for most patients.

Question 5

Digoxin affects a host of cardiac electrophysiologic Some of i ts effects are caused directly by the drug. Others are indirect: they may involve increasing “vagal tone” to the heart or other compensations that arise when cardiac output i s improved in a patient with heart failure. For some parameters the direct and indirect effects may be qualitatively (but not quantitatively) opposing, but one will predominate over the other. What i s an expected and usually predominant effect of the drug?

A	Increased rate of SA nodal depolarization
B	Reduced atrial automaticity
C	Reduced ventricular automaticity
D	Slowed AV nodal conduction velocity
E	Slowed conduction velocity through the atrial myocardium and His-Purkinje system

Question 5 Explanation:

Of the effects listed here, you would expect to find slowed AV nodal conduction velocity in response to digoxin. This is a common and, in many situations useful, effect. For example, when we give the drug as part of the pharmacologic management of atrial fibrillation or flutter, the main desired response is not suppression of the arrhythmia per se, but rather to “block down” the AV node so that as atrial rates fall (but are still high), the AV node will be unable to transmit the same frequency of impulses to the ventricles. That is, we “protect” the ventricles from excessive acceleration by inducing a degree of AV block. In terms of more specific effects on the AV node, digoxin slows conduction velocity and increases AV nodal refractory periods. Other “predominant” effects on the heart—all concentration-dependent—include increases of both atrial and ventricular automaticity and of conduction velocity through those structures and the His-Purkinje system.

Question 6

A patient has Stage 2 essential hypertension and heart After evaluating the responses to many other antihypertensive drugs, alone and in combination, the physician concludes that i t would be reasonable to try hydralazine. Which drug(s) i s/are l ikely to be needed, as add-ons (adjuncts), to manage the expected and unwanted cardiovascular and renal s ide effects of the hydralazine?

A	Captopril plus nifedipine
B	Digoxin plus spironolactone
C	Digoxin plus vi tamin K
D	Hydrochlorothiazide and a β-blocker
E	Nitroglycerin
F	Triamterene plus amiloride

Question 6 Explanation:

Hydralazine predominately dilates arterioles, with negligible effects on venous capacitance. It typically lowers blood pressure “so well” and quickly that it can trigger two unwanted cardiovascular responses that usually need to be dealt with: 1. Reflex cardiac stimulation (involving the baroreceptor reflex) is common, and it is typically managed with a β-adrenergic blocker (unless it is contraindicated). An alternative approach would be to use either verapamil or diltiazem (but not a dihydropyridine-type calcium channel blocker such as nifedipine, which would not suppress—and, in fact might aggravate—the reflex cardiac stimulation). 2. Activation of the renin-angiotensin-aldosterone system to compensate for what the body believes is an excessive and unwanted fall of blood pressure. One consequence of this unwanted response is increased renal sodium retention that would expand circulating fluid volume and counteract hydralazine’s pressure-lowering effects. This is typically managed with a diuretic. A thiazide may be sufficient to combat the sodium retention, but a more efficacious diuretic (loop diuretic) may be necessary and is usually selected. Captopril (or another ACE inhibitor, or an angiotensin receptor blocker such as losartan) might be a suitable add-on (it would cause synergistic antihypertensive effects and prevent aldosterone-mediated renal effects). However, combining it with nifedipine (dihydropyridine calcium channel blocker) is irrational. As noted above, given the “pure” vasodilator actions of nifedipine and the lack of cardiac-depressing activity (as occurs with verapamil), the net effect on heart rate would be either no suppression of the tachycardia or a worsening of it. Digoxin, alone or with virtually any other drug (c), is not rational because it would not meet the goals of blunting reflex cardiac stimulation and efficiently counteracting the consequences of renin-angiotensin-aldosterone system activation. There is no indication that there is need for inotropic support in this patient. Spironolactone, alone or with digoxin, would be of little benefit. One could argue that by virtue of the spironolactone’s ability to induce diuresis by blocking aldosterone’s renal tubular effects, it would counteract hydralazine’s ability to lead to renal sodium retention. That may be true, but spironolactone (with or without digoxin) will do nothing desirable to blunt the unwanted reflex cardiac activation. Nitroglycerin (e) would add to hydralazine’s antihypertensive effects, but it would probably aggravate (and certainly not counteract) the reflex cardiac stimulation, and may also increase the unwanted renal response (via a hemodynamic mechanism). Both triamterene and amiloride are potassium-sparing diuretics. The combination of two diuretics in this class is almost always irrational (it can lead to hyperkalemia). Either might beneficially combat a propensity for renal sodium retention in response to hydralazine. But, as with any diuretic alone, either or both would do little if anything to control the unwanted cardiac response. Vitamin K (included in answer c) was included as a foil. If you are associating hydralazine with some vitamin-related problem, you should be thinking of vitamin B6 (pyridoxine): hydralazine can interfere with B6 metabolism, causing such symptoms as peripheral neuritis, and so prophylactic B6 supplementation is often used along with long-term hydralazine therapy. Hydralazine is also known to cause a lupus-like syndrome. While prophylaxis with pyridoxine helps with the potential neuritis it does nothing for the lupus-like syndrome. Note: Nowadays many physicians consider hydralazine to be (at best) a fifth or sixth line agent for chronic hypertension. Regardless, the drug is not a “go to” drug unless, essentially, all other reasonable options have been tried and shown to be ineffective.

Question 7

A healthy adult subject participating in a cl inical trial i s given an intravenous injection of a test Both blood pressure and total peripheral resistance ri se promptly. This i s followed immediately by a reduction of heart rate. In repeated experiments we find that the vasopressor response i s not affected by pretreatment with prazosin. However, pretreatment with atropine prevents the cardiac chronotropic response. The test drug was most l ikely which of the following?

A	Angiotensin II
B	Dobutamine
C	Isoproterenol
D	Norepinephrine
E	Phenylephrine

Question 7 Explanation:

The bradycardia caused by the unknown drug is reflex-mediated by baroreceptor activation in response to the rise of blood pressure. Angiotensin II, by activating vascular A-II receptors, raises blood pressure and peripheral resistance, and that response would not be inhibited by pretreatment with prazosin (selective α1-adrenergic antagonist), nor any other adrenergic blocker (antagonist) for that matter. The bradycardia, of course, involves reflex parasympathetic activation (and relative and simultaneous withdrawal of sympathetic tone to the heart), release of ACh from the vagus and activation of muscarinic receptors on the SA node. Atropine pretreatment indeed prevents that response, as described in the question—and regardless of whether the original pressor response was caused by A-II, or any other vasopressor drug for that matter. Dobutamine (b) doesn’t fit the bill; it is largely a selective β1 agonist. For all practical purposes it causes no vasoconstriction (an α1 response if we limit things to adrenergic drugs), and via the β1 activation will directly increase heart rate, contractility, automaticity, and electrical impulse conduction (eg, through the AV node). No α-activation occurs (rises of blood pressure, if they occur in response to dobutamine, are due to the positive inotropic effect), and so prazosin would have no direct effect on responses to dobutamine. Isoproterenol (c) can be ruled-out for largelysimilar reasons; it activates both β1 and β2 receptors; and lacks vasoconstrictor activity, whether due to activation of α-adrenergic receptors or by other mechanisms. Could norepinephrine (d) be a reasonable answer? It certainly causes a vasopressor response and reflex bradycardia (at usual doses). However, the question stated that the unknown drug’s pressor response is not inhibited by α-blockade. Since a major element of NE’s pressor effect depends on α activation, it’s not a reasonable choice. The same applies to phenylephrine (e): this nonselective α-agonist also causes a pressor response that would be reduced or blocked altogether by prazosin pretreatment.

Question 8

We are administering nitroprusside intravenously for control of severe hypertension during The dose has gotten too high, and the drug has been administered too long. Refractoriness to the antihypertensive effects has occurred. Blood pressure i s ri s ing, and other s igns and symptoms of potentially severe toxicity develop. What nitroprusside metabolite accounts for or at least contributes to these problems?

A	A highly efficacious α-adrenergic agonist
B	An extraordinarily potent and i rreversible Na-K-ATPase inhibitor
C	An i rreversible antagonist for angiotensin at the A-II receptors
D	Cyanide
E	Nitric oxide

Question 8 Explanation:

Cyanide is the ultimate toxic metabolite of nitroprusside sodium. The drug is initially metabolically reduced to nitric oxide, which is responsible for the arteriolar and venular dilation. However, it is another metabolite, CN– (and to a lesser extent the next metabolite, thiocyanate) that is the main cause of or contributor to toxicity. When CN– accumulates to sufficiently high levels (as from excessive or excessively prolonged administration of the drug), the vasculature develops what amounts to a tolerance to the drug’s vasodilator effects, and so blood pressure usually starts to rise despite the presence of high drug levels. Toxic cyanide accumulation can also lead to severe lactic acidosis: the CN– reacts with Fe3+ in mitochondrial cytochrome oxidase, inhibiting oxidative phosphorylation. Other characteristic signs and symptoms of the toxic syndrome include a cherry red skin (because mitochondrial oxygen consumption is blocked, venous blood remains oxygenated and as “bright red” as normal arterial blood), hypoxia, and, ultimately, hypoxic seizures and ventilatory arrest. Note: Nitroglycerin and other similar nitrovasodilators are not metabolized to CN– and so manifestations of CN– poisoning are not elements of their toxicity profile.

Question 9

A 66-year-old man who l ives in a small rural town, and who has been treated by his family doctor for decades, presents at your medical He has coronary atherosclerosis and “mild” heart failure that has been treated for the last 10 years with digoxin and several other drugs. His chief complaints are nausea, vomiting, and diarrhea, which have not resolved despite a recommendation from his physician to take prescription medications for those conditions. His ECG reveals a bigeminal rhythm and second-degree heart block. A drug-drug interaction i s suspected. What coadministered drug most l ikely provoked the problem?

A	Captopril
B	Cholestyramine
C	Furosemide
D	Lovastatin
E	Nitroglycerin

Question 9 Explanation:

Hypokalemia due to the effects of potassium-wasting diuretics such as furosemide increase susceptibility to digoxin toxicity, and they are probably the most common cause of it. How does this occur? Digoxin binds to a K+-binding site on the sodium pump (ATPase). That is, there is competition between digoxin molecules and K+ for the same binding sites. When potassium levels are low (as can occur with any potassium-wasting diuretic, ie, a loop, thiazide, or thiazide-like diuretic), more digoxin molecules are able to bind to the ATPase—even though the actual digoxin concentration in the bloodstream hasn’t changed. More binding leads to greater ATPase inhibition: an intensified digoxin effect that, quite often, can lead to adverse responses rather than better therapeutic effects. Captopril (a) has no direct effects on digoxin’s actions. (We might add that an ACE inhibitor such as captopril, along with a β-blocker and a diuretic—not digoxin—are now considered the preferred therapy for most patients with recent onset and mild heart failure.) Cholestyramine (b), a cholesterol-binding resin, interacts with concomitantly administered (oral) digoxin to reduce digoxin absorption. It would not increase the risk of digoxin toxicity; quite the opposite, it would reduce digoxin’s therapeutic effectiveness. Lovastatin (d; an HMG-Co-A reductase inhibitor/“statin”) and nitroglycerin (e) are not likely to cause the observed toxicity either.

Question 10

We have a patient who i s diagnosed with variant (vasospastic) Which drug would be most appropriate, and generally regarded as most effective, for long-term therapy aimed at reducing the incidence or severity of the coronary vasospasm?

A	Aspirin
B	Atorvastatin
C	Diltiazem
D	Nitroglycerin
E	Propranolol

Question 10 Explanation:

The etiology involves coronary vasospasm, and that can be blocked well with a calcium channel blocker (CCB): diltiazem, verapamil, or dihydropyridines (eg, nifedipine, for which slow-/extended-acting oral formulations are used). The CCBs block coronary vascular smooth muscle influx of calcium, which is a critical process in triggering vasospasm. Nitroglycerin seems to be marginally effective in terms of long-term symptom relief, although it may be the only rapidly acting drug that will be efficacious for acute angina and self-medication. Aspirin, through its antiplatelet aggregatory effects, would be beneficial, prophylactically, if coronary thrombosis were part of the etiology of variant angina, but thrombosis is not the main problem with coronary vasospasm. Atorvastatin (or other statins) are useful for primary prevention of coronary heart disease, but coronaries that undergo spasm may be remarkably free of atherosclerotic plaque, and the statins have no antispasmodic effects per se. The β-blockers, which are important drugs for many patients with ischemic heart disease, can do more harm than good in vasospastic angina. In essence, β-receptor activation in the coronaries tends to cause vasodilation, an effect that to a degree counteracts simultaneous α-mediated constriction. Block only the β-receptors and the α-mediated constrictor effects—vasospasm-favoring effects—are left unopposed. Variant angina, then, is likely to be made worse, not better, with β-blockers. (You might ask whether a combined α-/β-blocker like labetalol or carvedilol might be better than a nonselective or cardioselective β-blocker. Perhaps in theory, but not in practice. Remember that the α-blocking effects of these drugs are comparatively weak; their β-blocking, spasm-favoring effects will predominate.)

Question 11

A 56-year-old man has heart His family doctor, who has been treating him s ince he was a young lad, has been treating him with digoxin, furosemide, and triamterene for several years. The patient now develops atrial fibrillation, and so his doctor starts quinidine and clopidogrel. What i s the most l ikely outcome of adding the quinidine?

A	Development of s igns and symptoms of quinidine toxicity (cinchonism)
B	Hyponatremia due to quinidine’s ability to enhance diuretic-induced sodium loss
C	Onset of s igns and symptoms of digoxin toxicity
D	Precipitous development of hypokalemia
E	Prompt suppression of cardiac contractility, onset of acute heart failure

Question 11 Explanation:

Digoxin toxicity is likely to occur within 24 to 48 hours unless the digoxin dose is adjusted down. The reason is that quinidine will reduce the renal excretion of digoxin (digoxin’s main elimination route). This is probably due to some mechanism by which quinidine inhibits P-glycoprotein transport of digoxin in the kidneys. (See the answer for question 10, on page 28, for a short table listing some drugs that are substrates, inducers, and inhibitors of P-glycoprotein.) There is no “reverse interaction”—that is, an ability of digoxin to cause signs and symptoms of quinidine toxicity (a). Quinidine has no significant impact on the renal actions of any diuretics, whether these actions are expressed in terms of urine output (volume or concentration) or renal handling of sodium or potassium or other electrolytes or solutes (b, d). Quinidine-induced digoxin toxicity may suppress cardiac contractility, but that would not necessarily be a direct effect of an interaction on the inotropic state of the myocardium. Rather, it would be secondary to potential digoxin-induced arrhythmias, and it would not occur “promptly.” Quinidine does cause some drug-drug interactions by pharmacokinetic mechanisms. It is a potent inhibitor of CYP2D6, and can (for example) inhibit the analgesic effects of codeine by inhibiting its metabolism to morphine. However, this mechanism does not apply to the quinidinedigoxin interaction; digoxin is eliminated completely by the kidneys, with no prior metabolism

Question 12

Flecainide and propafenone are in Vaughan-Williams (antiarrhythmic) Class I-C. What i s the cl inically relevant “take home” message about this class of drugs?

A	Are only given for arrhythmias during acute myocardial infarction
B	Are particularly suited for patients with low ejection fractions or cardiac output
C	Are preferred drugs (drugs of choice) for relatively innocuous ventricular arrhythmias
D	Cause pulmonary fibrosis and a hypothyroid-like syndrome when given long term
E	Have a s ignificant pro-arrhythmic effect (induction of lethal arrhythmias)

Question 12 Explanation:

The class I-C antiarrhythmics are associated with a higher incidence of severe proarrhythmic events than virtually any other antiarrhythmics in other classes. This risk partially explains why, when these drugs were first approved, they were indicated only for life-threatening ventricular arrhythmias that failed to respond to all other reasonable (and safer) alternatives. (This risk also contributed to why another I-C agent, encainide, was withdrawn from the market.) Nowadays, these I-C agents are still used for serious (life-threatening) and refractory ventricular arrhythmias, their efficacy arising from significant sodium channel blockade. However, they also block some potassium channels, which accounts for modestly growing interest in and use of these drugs for some atrial arrhythmias. Regardless of whether the use is for an atrial or ventricular arrhythmia, the proarrhythmic effects should be of concern. Pulmonary fibrosis and alterations of thyroid hormone status (typically, a hypothyroid-like state) are uniquely associated with amiodarone (among all the antiarrhythmics), and amiodarone was not one of the answer choices. Note: I’ll opine that memorizing which antiarrhythmic agents are in which Vaughn-Williams class may not be profitable (except for answering nit-picky and clinically irrelevant exam questions). Among the reasons why (1) this classification is based largely on electrophysiologic effects of the drugs in largely normal, isolated cardiac cells, not in diseased intact human hearts; (2) some antiarrhythmic drugs haveelectrophysiologic/ionic mechanisms of action that would reasonably place them in more than one Vaughn-Williams class (eg, amiodarone); (3) belonging to a particular Vaughn-Williams class does not necessarily predict clinical use of the antiarrhythmic; and (4) side effects profiles and toxicities of drugs in the same Vaughn-Williams class—both cardiac and extracardiac—can differ substantially.

Question 13

You want to compare and contrast the cardiac and hemodynamic profiles of immediate-acting dihydropyridine-type calcium channel blockers (CCBs) and the nondihydropyridine, verapamil (or diltiazem). Which of the following best summarizes how, in general, a nondihydropyridine CCB differs from nifedipine?

A	Causes a much higher incidence of reflex tachycardia
B	Causes s ignificant dose-dependent s lowing of AV nodal conduction velocity
C	Causes s ignificant venodilation, leading to profound orthostatic hypotension
D	Has s ignificant and direct positive inotropic effects
E	Is best used in conjunction with a β-blocker or digoxin

Question 13 Explanation:

In a nutshell, this question summarizes some of the main and important differences between the dihydropyridine CCBs (eg, nifedipine, and especially in immediate-release formulations, plus many others) and the nondihydropyridines (particularly verapamil, less so with diltiazem). The dihydropyridines are quite “selective” for their vascular effects. They cause significant arteriolar dilation, which usually activates the baroreceptor reflex that increases sympathetic influences on the heart: positive inotropy, positive chronotropy (reflex tachycardia can be severe), and increased automaticity and conduction velocity (dromotropic effects). In contrast, and importantly, verapamil and diltiazem cause not only arteriolar dilation (via calcium channel blockade in vascular smooth muscle), but also direct cardiac depressant effects (due to calcium channel blockade in cardiac tissues). These cardiac effects oppose, or blunt, reflex sympathetic cardiac activation that otherwise would occur in response to only peripheral vasodilation: such problems as reflex tachycardia and positive inotropy are much less—often nonexistent—with the nondihydropyridines. In fact, when reflex cardiac stimulation caused by other drugs (eg, nitroglycerin) is problematic and must be controlled, either vera-pamil (probably preferred) or diltiazem may be a reasonable alternative to the traditional agents for blocking the unwanted cardiac responses: the β-adrenergic blockers. Moreover, a nondihydropyridine CCB is usually the drug of choice for controlling cardiac stimulatory responses when a β-blocker is contraindicated (eg, in asthma). Be aware that combined use of diltiazem or verapamil with a β-blocker is risky due to possibility of additive or greater inhibitory effects on the cardiac rate, contractility, and especially AV nodal function. And, whether used alone or in combination, β-blockers and the nondihydropyridine CCBs (verapamil, diltiazem) should not be administered to patients with severe heart failure due to the added risks from further suppression of cardiac output. Notes: The vasodilator effects of verapamil are weaker than those of diltiazem, but the peripheral vascular (vasodilating) effects of either are still far weaker than those of a dihydropyridine. Diltiazem is classified, chemically, as a benzothiazepine (similar to but not to be confused with benzodiazepines—diazepam, midazolam, and many other drugs used for their CNS effects.) Verapamil is, chemically, a phenylalkylamine. However, memorizing the names of these chemical groups is probably a waste of your time: these drugs are almost always referred to simply as nondihydropyridines.

Question 14

A patient has received excessive doses of nitroprusside, and toxic manifestations are developing in response to a Which of the following drugs or drug groups would be most effective in l imiting and ultimately counteracting the effects of the toxic product?

A	Aminocaproic acid
B	Hydroxycobalamin
C	Protamine sulfate
D	Thrombin
E	Vitamin K

Question 14 Explanation:

Nitroprusside’s main toxic metabolite is cyanide. Nowadays, a preferred and effective approach to managing cyanide toxicity from nitroprus-side overdose is to administer hydroxycobalamin. It reacts with cyanide, forming cyanocobalamin, which is largely nontoxic (and is considered a form of vitamin B12). A more traditional (older) approach to managing cyanide toxicity—one that is still occasionally used, is based on the fact that cyanide normally is metabolized to the less toxic and more readily excreted thiocyanate by an enzymatic process (rhodanese is the key enzyme) that uses thiosulfate as a cofactor. Endogenous thiosulfate stores are rather limited, and with more serious degrees of cyanide (or nitroprusside) toxicity the thiosulfate is readily depleted. Other endogenous sulfur-containing substrates are depleted too. This traditional treatment plan, therefore, involves administering sodium thiosulfate to restore thiocyanate production. Nitrites (amyl and sodium nitrites) are administered to induce methemoglobinemia. The methemoglobin then binds free cyanide, forming less toxic cyan(o) methemoglobin. None of the other drugs listed play a role in the management of cyanide poisoning, whether from nitroprusside excess or from other causes (eg, suicide attempts, environmental exposure to cyanide). Aminocaproic acid (a) is an antithrombolytic (antifibrinolytic) drug used, for example, when such drugs as alteplase (t-PA; plasminogen activators) cause excessive thrombolysis that needs to be counteracted pharmacologically. The drug inhibits the actions of not only therapeutic plasminogen activators, but also those of endogenous activators. It also weakly inhibits plasmin activity. Protamine sulfate (c) should be remembered as the antidote for excessive anticoagulation caused by heparin (which occurs mainly with unfractionated, rather than low molecular weight, heparin). Thrombin (d) is a prothrombotic agent that plays no role in nitroprusside (or cyanide) toxicity. Vitamin K (e) is used to antagonize excessive effects of warfarin.

Question 15

A patient with Stage 2 essential hypertension i s treated with usually effective doses of an ACE After a suitable period of time, blood pressure has not been lowered satisfactorily. The patient has been compliant with drug therapy and other recommendations (eg, weight reduction, exercise). A thiazide i s added to the ACE inhibitor regimen. What i s the most l ikely and earliest (and probably transient) untoward outcome of this drug add-on, for which you should monitor closely?

A	Fall of blood pressure sufficient to cause syncope
B	Hypokalemia due to synergistic effects of the ACE inhibitor and the thiazide on renal potassium excretion
C	Onset of acute heart failure from depression of ventricular contractility
D	Paradoxical hypertensive cris i s
E	Sudden prolongation of the P-R interval and increasing degrees of heart block

Question 15 Explanation:

Although combined use of an ACE inhibitor (or angiotensin receptor blocker [ARB], eg, losartan) and a diuretic is quite common, great care must be taken when adding one of the drugs to therapy that has been started with the other. The reason is that some patients develop a sudden fall of blood pressure that may be sufficient to cause syncope or other complications. Volume and sodium depletion seem to be among several probable causative factors. Answer b is incorrect. The effects of ACE inhibitors (or ARBs) and thiazides on renal handling of potassium are the opposite of one another, not synergistic. ACE inhibitors tend to elevate potassium levels (in part, by lowering aldosterone levels); the thiazides (and loop diuretics, eg, furosemide) are potassium-wasting. There is no evidence that adding one of these drugs to therapy with the other can cause acute (or chronic) heart failure (c); indeed, such a combination is often an essential component in managing chronic heart failure. Blood pressure will fall, not rise, and certainly not cause hypertensive crisis (d); and slowed AV nodal conduction rates (e) due to this drug combination do not occur.

Question 16

A 45-year-old man postmyocardial infarction (MI) i s being treated with several drugs, including intravenous unfractionated Stool guaiac on admission was negative, but i s now 4+, and he has had an episode of hematemesis. What would be the best drug to administer to counteract the effects of excessive heparin remaining in the ci rculation?

A	Aminocaproic acid
B	Dipyridamole
C	Factor IX
D	Protamine sulfate
E	Vitamin K

Question 16 Explanation:

Administration of protamine sulfate will quickly reverse the bleeding caused by excessive effects of heparin. Protamine binds to heparin, forming a stable complex that abolishes heparin’s anticoagulant activity. It may also have its own anticoagulant effect by binding with platelets and fibrinogen. Aminocaproic acid (a) binds avidly to plasmin and plasminogen, and so is an effective inhibitor of fibrinolysis and an antagonist of fibrinolytic/thrombolytic drugs. Dipyridamole weakly blocks platelet ADP receptors, and has a long but uninspiring history as an antiplatelet drug. Factor IX will not reverse the excessive effects of heparin. Vitamin K is used as an antidote for excessive effects of such drugs as warfarin, and does nothing for heparin overdoses.

Question 17

A 45-year-old man asks his physician for a prescription for s i ldenafil to improve his sexual Because of ri sks from a serious drug interaction, this drug should not be prescribed, and the patient should be urged not to try to obtain i t from other sources, i f he i s also taking which of the following drugs?

A	Angiotensin-converting enzyme inhibitor
B	β-Adrenergic blocker
C	Nitrovasodilator (eg, nitroglycerin)
D	Statin-type antihypercholesterolemic drug.
E	Thiazide or loop diuretic

Question 17 Explanation:

Nitroglycerin causes its vasodilator effects via a nitric oxide (NO)- and cyclic GMP-dependent mechanism. The NO activates guanylyl cyclase which forms cGMP from GMP. The cGMP, in turn, dephosphorylates myosin light chains, leading to reduced actin-myosin interactions and relaxation of the smooth muscle cells. Normally, this vascular effect is modulated by cGMP degradation (to GMP) by cGMP-specific phosphodiesterases (PDEs). Sildenafil (and the related drugs tadalafil and vardenafil) inhibit the activity of those PDEs, thereby maintaining cGMP levels and potentiating the vasodilator effects. This interaction may lead to severe excessive effects, including lifethreatening hypotension and myocardial and cerebral ischemia. Sildenafil and related drugs also increase the risk of symptomatic hypotension if taken by people who are also being treated with α-adrenergic blockers, including those that selectively block α1 receptors (eg, prazosin and doxazosin) and are used for managing hypertension. Note the important mechanistic links between vasodilation/hypotension, sexual intercourse, and potentially fatal cardiac responses. Sexual arousal—and, especially orgasm—causes a massive activation of the sympathetic nervous system. One consequence of that, α-mediated vasoconstriction that tends to keep blood pressure up, is too feeble to overcome the hypotensive effects of the sildenafil-nitroglycerincombination. Along with a fall of blood pressure is a fall of coronary perfusion pressure (diastolic blood pressure), that is, reduced myocardial blood flow/oxygen supply. Yet the sympathetic activation concomitantly causes significant increases of cardiac rate and contractility, that is, increased myocardial oxygen demand. Oxygen demand rises, supply falls, and the stage is set for acute myocardial ischemia. A final point to consider. It is reasonable to assume that if the patient is taking any or even several of the drugs listed in the question, he has underlying cardiac disease. However, and in contrast with what some students have suggested, underlying cardiac disease per se does not automatically contraindicate or even excessively increase the risks from sexual intercourse and orgasm. (How severe is the patient’s cardiovascular disease? It is well controlled? What are the specific diseases and risks he has?) Similarly, none of the drugs listed other than the nitrovasodilators (and some α-blockers mentioned in the previous paragraph) contraindicate the use of any of the ED drugs.

Question 18

A physician i s preparing to administer a drug for which there i s a label warning: “do not administer this drug to patients with second-degree or greater heart block, or give with other drugs that may cause heart ” Which finding would be specifically indicative of heart block, and second-degree heart block in particular?

A	Auscultation of the precordium reveals an i rregular rhythm
B	Blood pressure i s low
C	Heart rate i s abnormally low (bradycardia), but there i s normal s inus rhythm
D	ECG reveals ventricular ectopic beats
E	ECG shows an excessively prolonged PR interval, and some P waves are not followed by a normal QRS complex
F	ECG shows abnormally widened QRS complexes

Question 18 Explanation:

Although you may not consider this question a pharmacology question, being able to answer it correctly is important to the rational and safe use of many drugs. In general, heart block refers to excessively slowed AV nodal conduction, which you assess by measuring the PR interval on the ECG. Recall that this interval gives information on how long it takes for electrical impulses that originate with SA nodal depolarization to pass through the atrial myocardia and the AV node, ultimately leading to ventricular activation (manifest as the QRS complex). Impulse conduction through the atria is normally quick; it is the AV node that has the slowest intrinsic impulse conduction rate anywhere in the heart, and it is arguably the structure that is most susceptible to drug- (or disease-) induced changes of supraventricular conduction that lead to the diagnosis of AV block. In first-degree heart block, the main manifestation is a prolonged PR interval, but each P wave is followed by a normally generated QRS complex. In second-degree heart block, the PR interval is prolonged and some P waves are not conducted through the AV node, and so are not followed by a QRS triggered by the prior atrial activation (eg, 2:1 block). In third-degree (complete) heart block, no P waves are conducted normally through the AV node, and ventricular activation is solely dependent on intrinsic automaticity of the ventricles (or conducting tissue therein). Auscultation of the heart, the presence of blood pressures that are above or below what is generally regarded as normal, or the presence of a slow sinus rhythm, are not reliable indicators of heart block.

Question 19

A 52-year-old woman with essential hypertension, hypercholesterolemia, and chronic-stable angina develops severe It i s attributed to one of her medications. What was the most l ikely cause?

A	Atorvastatin
B	Captopril
C	Labetalol
D	Nitroglycerin
E	Verapamil

Question 19 Explanation:

Constipation is a fairly common, sometimes very bothersome, and occasionally dangerous response to verapamil (more so than with any other calcium channel blocker). It is a widely used drug. The mechanism underlying this side effect isn’t known for sure, but probably lies in vera-pamil’s rather unique ability to block calcium channels on longitudinal and sphincter smooth muscle cells in the GI tract. Regardless of whether we know the mechanism for sure, it is important to know that verapamil tends to cause constipation in more than a handful of patients. Statins (a), ACE inhibitors (b), β-blockers of any class or organic nitrovasodilators such as nitroglycerin (d) do not cause constipation as a side effect.

Question 20

We use standard invasive hemodynamic techniques to measure or calculate the effects of various drugs on such parameters as arterial pressure, total peripheral resistance, and central venous (right atrial) Our goal i s to evaluate whether the drug primarily causes arteriolar or venular dilation, or affects both s ides of the ci rculation. Which drug exerts vasodilator effects only in the arterial s ide of the ci rculation?

A	Hydralazine
B	Losartan
C	Nifedipine
D	Nitroglycerin
E	Prazosin

Question 20 Explanation:

Hydralazine’s primary vasodilator actions occur on arterioles, not on venules. The others have both arteriolar and venular dilator activity, thereby lowering both afterload and central venous pressure (venous capacitance; right atrial pressure). Hydralazine’s probable mechanism of action involves a nitric oxide (NO)-mediated process. (There is also some evidence that the drug opens voltage-gated potassium channels on vascular smooth muscle cells, causing muscle cell hyperpolarization and ultimate vasodilation.) The other drugs listed cause vascular smooth muscle relaxation on both arterioles and venules: losartan (b), by blocking angiotensin II receptors; nifedipine (c) via calcium channel blockade; nitroglycerin (d) by NO as an intermediate; and prazosin (e) by selective α1-adrenergic blockade. Here is a short table listing the main sites where various drugs or drug classes exert their main or sole vasodilator actions.

Question 21

A 20-year-old collegiate varsity hockey player i s referred to you by his The young athlete has excessive bruising after a very physical match 2 days before. His knee had been bothering him, so he took two 325 mg aspirin tablets several hours before the contest. He got checked hard into the boards many times during the game, but denies any excessive or unusual trauma. As you ponder the s i tuation you order several blood tests. Which test or finding do you most l ikely expect to be abnormal as a result of the prior aspirin use?

A	Activated partial thromboplastin time (APTT)
B	Bleeding time
C	INR (International Normalized Ratio)
D	Platelet count
E	Prothrombin time

Question 21 Explanation:

Aspirin inhibits cyclooxygenases I and II. In terms of clotting, the main effect will be inhibition of platelet aggregation by reduced formation of thromboxane A2. Bleeding time will be prolonged and will remain that way until sufficient numbers of new platelets have been synthesized and released into the bloodstream, because aggregation of those platelets already exposed to the drug will be inhibited for their lifetime. The APTT, which should not be affected by aspirin, is used to monitor effects and adjust the dose of unfractionated heparin (such monitoring is not required with low molecular weight heparin, eg, enoxaparin). The prothrombin time and its normalized value, the INR, are used with warfarin. Platelet counts, also not affected by aspirin, are used to assess for the development of thrombocytopenic purpura, which may rarely occur during therapy with, for example, the clopidogrel-like drug ticlopidine, or with heparin when thrombocytopenia is anticipated or suspected.

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1.A woman has received a cardiovascular drug that i s absolutely contraindicated (category X) in pregnancy, but in the absence of pregnancy would have been deemed beneficial because of a particular cardiovascular disorder she Unfortunately, neither she nor her physician (whom she rarely vis i ted) knew she was pregnant until she had just started the second trimester. The drug i s stopped (and a suitable and safer alternative i s started), but i t i s too late. Her baby i s delivered prematurely, and sti l lborn. It i s obvious from examination of the baby that there i s a nasal deformity: the nose i s flattened into the face, with no apparent bridge. Standard x-rays reveal stippling of all the epiphyses. These responses are characteristic of which drug?

Clonidine
Heparin, low molecular weight (eg, enoxaparin)
Hydrochlorothiazide
Nitroglycerin
Warfarin

2. A patient who has been taking an oral antihypertensive drug for about a year develops a positive Coombs’ test, and now you are worried about the possibility (although low) that hemolytic anemia may develop i f the drug i s Which drug was the most l ikely cause?

Captopril
Clonidine
Labetalol
Methyldopa
Prazosin

3. A patient presents with severe hypertension and Blood chemistry results, radiologic studies, and the overall cl inical presentation point to pheochromocytoma. The tumor appears operable, but the patient will have to wait a couple of weeks for the adrenalectomy. We prescribe phenoxybenzamine in the interim, with the goal of suppressing some of the major s igns and symptoms caused by the tumor and the massive amounts of epinephrine i t i s releasing. Which of the following best summarizes what phenoxybenzamine does, or how i t acts?

Controls blood pressure by blocking α-adrenergic receptors in the peripheral vasculature
Controls heart rate by selectively blocking β₁-adrenergic receptors
Inhibits catecholamine synthesis in the adrenal (suprarenal) medulla
Lowers blood pressure by inhibiting angiotensin converting enzyme
Stimulates catechol-O-methyltransferase, thereby facilitating epinephrine’s metabolic inactivation

4. A 30-year-old man who has a history of asthma has just been diagnosed Stage 1 essential He regularly uses an inhaled corticosteroid, which seems to work well as a control medication, but also needs to use an albuterol inhaler about once every 3 weeks for suppression of asthma attacks (rescue therapy). Which antihypertensive drug or drug class poses the greatest ri sk of exacerbating the patient’s asthma and counteracting the desired pulmonary effects of the albuterol, even though i t might control his blood pressure well?

Diltiazem
Hydrochlorothiazide
Labetalol
Ramipril
Verapamil

5. Digoxin affects a host of cardiac electrophysiologic Some of i ts effects are caused directly by the drug. Others are indirect: they may involve increasing “vagal tone” to the heart or other compensations that arise when cardiac output i s improved in a patient with heart failure. For some parameters the direct and indirect effects may be qualitatively (but not quantitatively) opposing, but one will predominate over the other. What i s an expected and usually predominant effect of the drug?

Increased rate of SA nodal depolarization
Reduced atrial automaticity
Reduced ventricular automaticity
Slowed AV nodal conduction velocity
Slowed conduction velocity through the atrial myocardium and His-Purkinje system

6. A patient has Stage 2 essential hypertension and heart After evaluating the responses to many other antihypertensive drugs, alone and in combination, the physician concludes that i t would be reasonable to try hydralazine. Which drug(s) i s/are l ikely to be needed, as add-ons (adjuncts), to manage the expected and unwanted cardiovascular and renal s ide effects of the hydralazine?

Captopril plus nifedipine
Digoxin plus spironolactone
Digoxin plus vi tamin K
Hydrochlorothiazide and a β-blocker Nitroglycerin
Triamterene plus amiloride

7. A healthy adult subject participating in a cl inical trial i s given an intravenous injection of a test Both blood pressure and total peripheral resistance ri se promptly. This i s followed immediately by a reduction of heart rate. In repeated experiments we find that the vasopressor response i s not affected by pretreatment with prazosin. However, pretreatment with atropine prevents the cardiac chronotropic response. The test drug was most l ikely which of the following?

Angiotensin II
Dobutamine
Isoproterenol
Norepinephrine
Phenylephrine

8. We are administering nitroprusside intravenously for control of severe hypertension during The dose has gotten too high, and the drug has been administered too long. Refractoriness to the antihypertensive effects has occurred. Blood pressure i s ri s ing, and other s igns and symptoms of potentially severe toxicity develop. What nitroprusside metabolite accounts for or at least contributes to these problems?

A highly efficacious α-adrenergic agonist
An extraordinarily potent and i rreversible Na-K-ATPase inhibitor
An i rreversible antagonist for angiotensin at the A-II receptors
Cyanide
Nitric oxide

9. A 66-year-old man who l ives in a small rural town, and who has been treated by his family doctor for decades, presents at your medical He has coronary atherosclerosis and “mild” heart failure that has been treated for the last 10 years with digoxin and several other drugs. His chief complaints are nausea, vomiting, and diarrhea, which have not resolved despite a recommendation from his physician to take prescription medications for those conditions. His ECG reveals a bigeminal rhythm and second-degree heart block. A drug-drug interaction i s suspected. What coadministered drug most l ikely provoked the problem?

Captopril
Cholestyramine
Furosemide
Lovastatin
Nitroglycerin

10. We have a patient who i s diagnosed with variant (vasospastic) Which drug would be most appropriate, and generally regarded as most effective, for long-term therapy aimed at reducing the incidence or severity of the coronary vasospasm?

Aspirin
Atorvastatin
Diltiazem
Nitroglycerin
Propranolol

11. A 56-year-old man has heart His family doctor, who has been treating him s ince he was a young lad, has been treating him with digoxin, furosemide, and triamterene for several years. The patient now develops atrial fibrillation, and so his doctor starts quinidine and clopidogrel. What i s the most l ikely outcome of adding the quinidine?

Development of s igns and symptoms of quinidine toxicity (cinchonism)
Hyponatremia due to quinidine’s ability to enhance diuretic-induced sodium loss
Onset of s igns and symptoms of digoxin toxicity
Precipitous development of hypokalemia
Prompt suppression of cardiac contractility, onset of acute heart failure

12. Flecainide and propafenone are in Vaughan-Williams (antiarrhythmic) Class I-C. What i s the cl inically relevant “take home” message about this class of drugs?

Are only given for arrhythmias during acute myocardial infarction
Are particularly suited for patients with low ejection fractions or cardiac output
Are preferred drugs (drugs of choice) for relatively innocuous ventricular arrhythmias
Cause pulmonary fibrosis and a hypothyroid-like syndrome when given long term
Have a s ignificant pro-arrhythmic effect (induction of lethal arrhythmias)

13. You want to compare and contrast the cardiac and hemodynamic profiles of immediate-acting dihydropyridine-type calcium channel blockers (CCBs) and the nondihydropyridine, verapamil (or diltiazem). Which of the following best summarizes how, in general, a nondihydropyridine CCB differs from nifedipine?

Causes a much higher incidence of reflex tachycardia
Causes s ignificant dose-dependent s lowing of AV nodal conduction velocity
Causes s ignificant venodilation, leading to profound orthostatic hypotension
Has s ignificant and direct positive inotropic effects
Is best used in conjunction with a β-blocker or digoxin

14. A patient has received excessive doses of nitroprusside, and toxic manifestations are developing in response to a Which of the following drugs or drug groups would be most effective in l imiting and ultimately counteracting the effects of the toxic product?

Aminocaproic acid
Hydroxycobalamin
Protamine sulfate
Thrombin
Vitamin K

15. A patient with Stage 2 essential hypertension i s treated with usually effective doses of an ACE After a suitable period of time, blood pressure has not been lowered satisfactorily. The patient has been compliant with drug therapy and other recommendations (eg, weight reduction, exercise). A thiazide i s added to the ACE inhibitor regimen. What i s the most l ikely and earliest (and probably transient) untoward outcome of this drug add-on, for which you should monitor closely?

Fall of blood pressure sufficient to cause syncope
Hypokalemia due to synergistic effects of the ACE inhibitor and the thiazide on renal potassium excretion
Onset of acute heart failure from depression of ventricular contractility
Paradoxical hypertensive cris i s
Sudden prolongation of the P-R interval and increasing degrees of heart block

16. A 45-year-old man postmyocardial infarction (MI) i s being treated with several drugs, including intravenous unfractionated Stool guaiac on admission was negative, but i s now 4+, and he has had an episode of hematemesis. What would be the best drug to administer to counteract the effects of excessive heparin remaining in the ci rculation?

Aminocaproic acid
Dipyridamole
Factor IX
Protamine sulfate
Vitamin K

17. A 45-year-old man asks his physician for a prescription for s i ldenafil to improve his sexual Because of ri sks from a serious drug interaction, this drug should not be prescribed, and the patient should be urged not to try to obtain i t from other sources, i f he i s also taking which of the following drugs?

Angiotensin-converting enzyme inhibitor
β-Adrenergic blocker
Nitrovasodilator (eg, nitroglycerin)
Statin-type antihypercholesterolemic drug.
Thiazide or loop diuretic

18. A physician i s preparing to administer a drug for which there i s a label warning: “do not administer this drug to patients with second-degree or greater heart block, or give with other drugs that may cause heart ” Which finding would be specifically indicative of heart block, and second-degree heart block in particular?

Auscultation of the precordium reveals an i rregular rhythm
Blood pressure i s low
Heart rate i s abnormally low (bradycardia), but there i s normal s inus rhythm
ECG reveals ventricular ectopic beats
ECG shows an excessively prolonged PR interval, and some P waves are not followed by a normal QRS complex
ECG shows abnormally widened QRS complexes

19. A 52-year-old woman with essential hypertension, hypercholesterolemia, and chronic-stable angina develops severe It i s attributed to one of her medications. What was the most l ikely cause?

Atorvastatin
Captopril
Labetalol
Nitroglycerin
Verapamil

20. We use standard invasive hemodynamic techniques to measure or calculate the effects of various drugs on such parameters as arterial pressure, total peripheral resistance, and central venous (right atrial) Our goal i s to evaluate whether the drug primarily causes arteriolar or venular dilation, or affects both s ides of the ci rculation. Which drug exerts vasodilator effects only in the arterial s ide of the ci rculation?

Hydralazine
Losartan
Nifedipine
Nitroglycerin
Prazosin

21. A 20-year-old collegiate varsity hockey player i s referred to you by his The young athlete has excessive bruising after a very physical match 2 days before. His knee had been bothering him, so he took two 325 mg aspirin tablets several hours before the contest. He got checked hard into the boards many times during the game, but denies any excessive or unusual trauma. As you ponder the s i tuation you order several blood tests. Which test or finding do you most l ikely expect to be abnormal as a result of the prior aspirin use?

Activated partial thromboplastin time (APTT)
Bleeding time
INR (International Normalized Ratio)
Platelet count
Prothrombin time

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