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Cardiovascular Pharmacology- Part 3
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1.A patient in the coronary care unit develops episodes of paroxysmal AV nodal reentrant tachycardia (PSVT). What drug would generally be considered fi rst-l ine for promptly stopping the arrhythmia?
2. A 60-year-old man, hospitalized for an acute myocardial infarction, i s treated with warfarin (among other drugs). What i s the main mechanism by which warfarin i s causing the effects for which i t i s given?
- Increase in the plasma level of Factor IX
- Inhibition of thrombin and early coagulation steps
- Inhibition of synthesis/activation of prothrombin and Factors VII, IX, and X
- Inhibition of platelet aggregation Activation of plasminogen
- Binding of Ca 2+ ion cofactor in some coagulation steps
3. A 42-year-old man with an acute MI i s treated with alteplase, and electrocardiographic and hemodynamic status improve By what mechanism did the alteplase cause i ts beneficial effects?
- Blocked platelet ADP receptors
- Inhibited platelet thromboxane production
- Inhibited synthesis of vi tamin K-dependent coagulation factors
- Prevented aggregation of adjacent platelets by blocking glycoprotein IIb/IIIa receptors .
- Promoted conversion of plasminogen to plasmin
4. A patient with atrial fibrillation i s placed on long-term arrhythmia control with In addition to “standard” monitoring, what should be assessed periodically in order to detect adverse effects that are rather unique to this drug among vi rtually all the antiarrhythmics?
- Blood glucose, triglyceride, cholesterol, and sodium concentrations
- Hearing thresholds (audiometry) and plasma albumin concentration
- Prothrombin time and antinuclear antibody (ANA) ti ters
- Pulmonary function and thyroid hormone status
- White cell counts and blood urate concentration
5. A 64-year-old woman has had several episodes of transient i schemic attacks (TIAs). Aspirin would be a preferred treatment for prevention of thrombosis, but she has a history of severe “aspirin sensitivity” manifest as intense bronchoconstriction and What would you consider to be the best alternative to the aspirin?
- Aminocaproic acid
6. A patient who has excessively s low AV nodal conduction rates, that unfortunately haven’t been recognized, i s started on a As soon as blood levels cl imb toward the usual therapeutic range the patient goes into complete heart block. Which drug most l ikely provoked this further prolongation of the P-R interval, ultimately leading to the cessation of all AV nodal conduction?
7. A patient with heart failure, Stage 1 essential hypertension, and hyperlipidemia (elevated LDL cholesterol and abnormally low HDL-C) i s taking furosemide, captopril, atenolol, and s imvastatin (an HMG-CoA reductase inhibitor).
During a scheduled physical exam, about a month after starting all the above drugs, the patient reports a severe, hacking, and relentless cough. Other vi tal s igns, and the overall physical assessment, are consistent with good control of both the heart failure and blood pressure and indicate no other underlying disease or abnormalities. Results of blood tests are not yet available.
Which of the following i s the most l ikely cause of the cough?
- An expected s ide effect of the captopril
- An allergic reaction to the statin
- Dyspnea due to captopril’s known and powerful bronchoconstrictor action
- Excessive doses of the bumetanide, which led to hypovolemia
- Hyperkalemia caused by an interaction between bumetanide and captopril
- Pulmonary edema from the bumetanide
8. A patient with a history of hypertension, heart failure, and peripheral vascular disease has been on oral therapy, with drugs suitable for each, for about 3 He runs out of the medication and plans to have the prescriptions refilled in a week or so.
Within a day or two after stopping his medications he experiences an episode of severe tachycardia accompanied by tachyarrhythmias, and an abrupt ri se of blood pressure to 240/140 mm Hg—well above pretreatment levels. He complains of chest pain, anxiety, and a pounding headache. Soon thereafter he suffers a hemorrhagic stroke.
Which drug or drug group that the man was taking and stopped taking suddenly most l ikely caused these responses?
- ACE inhibitor
- Nifedipine (a long-acting formulation)
9. Your class just completed a minireview of the physiology and pathophysiology of blood pressure control and finally dawned on a classmate: bradykinin, an endogenous vasodilator, contributes to keeping blood pressure low; and i ts metabolite, formed by an enzyme cleverly called brady- kininase, lacks vasodilator A colleague says “wouldn’t i t be great i f we had a drug that could inhibit bradykinin’s metabolic inactivation? We could probably use i t as an antihypertensive drug!” You reply that we already have a drug—several, in fact—that does that very thing. What drug or drug group would that be?
- Atenolol or metoprolol
- Captopril or other “prils”
- Hydrochlorothiazide or s imilar diuretic-antihypertensives
- Labetalol or carvedilol
- Losartan or other “sartans”
10. A 70-year-old woman i s treated with sublingual nitroglycerin for occasional bouts of effort-induced What best describes part of the mechanisms by which nitroglycerin causes i ts desired antianginal effects?
- Blocks α-adrenergic receptors
- Forms cyanide, much l ike the metabolism of nitroprusside does
- Increases local synthesis and release of adenosine
- Raises intracellular cGMP levels
- Selectively dilates/relaxes coronary arteries
11. Your patient has bipolar i l lness, hypercholesterolemia, chronic-stable angina, and Stage 1 essential He has been taking l i thium and an SSRI for the bipolar i l lness. Cardiovascular drugs include atorvastatin, diltiazem, sublingual nitroglycerin, captopril, and hydrochlorothiazide. What outcome, due to interactions involving these drugs, should you most l ikely expect?
- Development of acute psychosis from an ACE inhibitor-antipsychotic interaction
- Development of a hypomanic state from antagonism of l i thium’s action by the nitroglycerin
- Li thium toxicity because of hyponatremia caused by the hydrochlorothiazide
- Loss of cholesterol control from antagonism of the HMG Co-A reductase inhibitor by the antipsychotic Worsening of angina because the antipsychotic counteracts the effects of the calcium channel blocker
- Worsening of angina because the l i thium antagonizes the effects of the nitroglycerin
12. A fi rst-year house officer notices that a patient i s experiencing s ignificant and rapidly ri s ing blood pressure (currently 180/120 mm Hg). One of the medications the patient had been taking i s immediate-acting nifedipine oral There i s a dose of this nifedipine formulation at the bedside, so the physician pricks the capsule open and squirts the contents into the patient’s mouth. This technique avoids “fi rst-pass” metabolism of the drug and causes rapid absorption and all the effects associated with this calcium channel blocker. What i s the most l ikely outcome of giving nifedipine as described here?
- AV nodal block
- Further ri se of heart rate, worsening of the ventricular arrhythmia
- Hypotension and bradycardia
- Normalization of blood pressure and heart rate
- Return of blood pressure toward normal, no s ignificant effect on heart rate or the ECG
13. A 55-year-old patient with multiple cardiovascular diseases i s being treated with digoxin, furosemide, triamterene, atorvastatin, and nitroglycerin—all prescribed by the family physician he’s had for The patient now experiences nausea, vomiting, and anorexia, and describes a “yellowish-greenish tint” to white objects and bright l ights. These s igns and symptoms are most characteristic of toxicity due to which drug?
14. A 28-year-old female patient has Stage 1 essential hypertension (resting BP 144/98), tachycardia, and occasional palpitations (ventricular ectopic beats). Normally we might consider prescribing a β-blocker to control the blood pressure and cardiac responses, but our patient also has asthma, and she i s trying to get Which drug would be the best alternative to the β-blocker in terms of l ikely efficacy on pressure and heart rate, and in terms of relative safety?
15. A patient presents with The underlying cause—a pheochromocytoma—is not looked-for or detected in the initial work-up. An oral antihypertensive drug i s prescribed. We soon find that the patient’s blood pressure has ri sen to levels above pretreatment levels—so much so that we are worried about imminently dangerous effects from the drug-induced worsening of hypertension—in response to a drug. Concomitant with the drug-induced ri se of blood pressure the patient develops s igns and symptoms of heart failure. Which drug was most l ikely administered?
16. A patient on long-term warfarin therapy has an INR that i s excessive (4.5; normal, not anticoagulated i s 1.0; the target for this patient was 5). She reports episodes of epistaxis over the last 2 days and now there i s a great ri sk of serious bleeding episodes. In addition to stopping warfarin administration for a day or more, which drug would you want to administer to counteract warfarin’s excessive effects that led to spontaneous bleeding?
- Aminocaproic acid
- Epoetin alfa
- Ferrous sulfate
- Phytonadione (vi tamin K
- Protamine sulfate
17. A patient with hypertension and heart failure has been treated for 2 years with carvedilol and l i s He has just had hip replacement surgery, but because he i s not ambulating he i s started on unfractionated heparin, postoperatively, for prophylaxis of deep venous thrombosis. Oral antacids and esomeprazole (gastric parietal cell proton pump inhibitor) have been added for prophylaxis of acute stress ulcers. Five days postop, he experiences sudden onset dyspnea and electrocardiographic and other indications of an acute MI. The patient’s platelet counts are dangerously low. What i s the most l ikely underlying problem?
- Accidental substitution of low-molecular-weight heparins (LMWH) for unfractionated heparin
- Accidental/inadvertent aspirin administration
- Hemolytic anemia from a carvedilol-ACE inhibitor interaction
- Heparin-induced thrombocytopenia
- Reduced heparin effects by increased metabolic clearance (caused by ranitidine)
18. A patient with angina pectoris i s started on a nitroglycerin transdermal delivery system (“skin patch”) for prophylaxis of his He wears the patch 24 hours a day, 7 days a week, except for the few minutes when he showers each day. What i s the main concern with “around-the-clock” administration of this or other long-acting formulations of nitrovasodilators?
- Cyanide poisoning
- Development of tolerance to their vasodilator actions
- Gradual development of reflex bradycardia in response to successive doses
- Onset of delayed, characteristic adverse responses including thrombosis and thrombocytopenia
- Paradoxical vasoconstriction leading to hypertension
19. For many hypertensive patients we can prescribe either l i s inopril (or an alternative in the same class) or What statement correctly summarizes how losartan differs from l i s inopril other l i s inopril-like drugs?
- Lis inopril competitively blocks catecholamine-mediated vasoconstriction, losartan does not
- Lis inopril effectively inhibits synthesis of angiotensin II, losartan does not
- Losartan causes a higher incidence of bronchospasm and hyperuricemia
- Losartan i s preferred for managing hypertension during pregnancy, whereas captopril i s contraindicated
- Losartan i s suitable for administration to patients with heart failure, whereas captopril and related drugs should be avoided.
20. A 46-year-old man has Stage 1 essential hypertension (resting BP 150/98), primary hypercholesterolemia, and modestly elevated fasting glucose levels (130 mg/dL) measured on several His cholesterol levels (total, HDL, LDL) have not been acceptably modified by dietary changes and daily use of a “statin.” The physician adds ezetimibe to the regimen. Which statement summarizes ezetimibe’s actions, or what would be expected in response to i ts use?
- Exerts profound cardiac negative inotropic effects that poses a ri sk of heart block
- Frequently causes orthostatic hypotension that in turn triggers reflex cardiac stimulation
- More l ikely than other drugs to increase the ri sk of severe statin-induced myopathy
- Reduces intestinal cholesterol uptake, has no direct hepatic effect to inhibit cholesterol synthesis
- Significantly increases ri sk of atherosclerotic plaque rupture
21. A 58-year-old man presents in the emergency department with his fi rst episode of acute coronary syndrome (ACS) and all evidence points to a myocardial Angioplasty and stenting are not possible because the cardiac cath lab i s busy with other higher-priority patients, so administration of a thrombolytic drug i s the only option. What i s the most important determinant, overall, of the success of thrombolytic therapy in terms of salvaging viable cardiac muscle (or other i schemic ti ssues)?
- Choosing a “human” (cloned) plasminogen activator (eg, t-PA), rather than one that i s bacterial-derived (eg, streptokinase)
- Infarct location (ie, anterior wall of left ventricular vs another s i te/wall)
- Presence of collateral blood vessels to the infarct-related coronary artery
- Systolic blood pressure at the time the MI i s diagnosed
- Time from onset of infarction to administration of the thrombolytic agent