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Cardiovascular Pharmacology- Part 4
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1.A patient with an acute coronary syndrome i s given a variety of cardiovascular drugs as he i s being readied for transport to the “cath lab” for possible placement of a One of the meds i s abciximab. What best describes the mechanism of action of this drug?
- Blocks thrombin receptors selectively
- Blocks ADP receptors
- Blocks glycoprotein IIb/IIIa receptors
- Inhibits cyclooxygenase
- Inhibits prostacyclin production
2. A patient presents in the emergency department with acute hypotension that requires Hypovolemia i s ruled-out as a cause or contributor, and information gathered from the patient and family indicates that the cause i s overdose of an antihypertensive drug.
One approach to treatment i s to administer a pharmacologic (ordinarily effective) dose of phenylephrine, an α-adrenergic agonist. You do just that, and blood pressure fails to ri se at all—and a second dose doesn’t work either. On which antihypertensive drug did the patient most l ikely overdose?
- Captopril or another ACE inhibitor
- Thiazide diuretic (eg, hydrochlorothiazide)
3. An elderly man who has just been referred to your practice has been taking a drug for symptomatic relief of benign prostatic In addition to i ts effects on smooth muscles of the prostate and urethra, this drug can lower blood pressure in such a way that i t reflexly triggers tachycardia, positive inotropy, and increased AV nodal conduction. The drug neither dilates nor constricts the bronchi. It causes the pupils of the eyes to constrict and interferes with mydriasis in dim l ight. Initial oral dosages of this drug have been associated with a high incidence of syncope.
Which prototype i s most s imilar to this unnamed drug in terms of the pharmacologic profile?
- Hydrochlorothiazide (prototype thiazide diuretic)
- Nifedipine Prazosin
4. You are contemplating starting ACE inhibitor therapy for a patient with essential Which one of the following patient-related condition(s) contraindicates use of any ACE inhibitor and so should be ruled out before you prescribe this drug?
- Heart failure
- Hyperlipidemia, coronary artery disease
- Is a woman who i s pregnant or may become pregnant
5. A patient develops s inus Heart rate i s dangerously low, and an effective and safe drug needs to be given right away. Which drug would be the best choice for normalizing heart rate without initiating any other arrhythmias?
6. A patient presents in the emergency department (ED) with severe angina pectoris, and acute myocardial i schemia i s confirmed by electrocardiographic and other cl inical Unknown to the ED team i s the fact that the i schemia i s due to coronary vasospasm, not to coronary occlusion with thrombi. Given this etiology, which drug, administered in usually effective doses, may actually make the vasospasm, and the resulting i schemia, worse?
- Alteplase (t-PA)
7. Many cl inical studies have investigated the benefits of daily aspirin use in the primary prevention of coronary heart disease and sudden death in The results have been somewhat inconsistent, in part because different dosages were studied, and there were important differences in the populations that were studied. Nonetheless, many (i f not most) of the studies have revealed that for some patients aspirin increased the incidence of a particularly unwanted adverse response, even when dosages were kept within the range typically recommended for cardioprotection (eg, 81-162 mg/day). What i s the most l ikely adverse response associated with aspirin prophylaxis, particularly in patients who have a low ri sk of an acute coronary syndrome or cardiovascular disease in general?
- Centrolobular hepatic necrosis
- Hemorrhagic stroke
- Tachycardia and hypotension leading to acute myocardial i schemia
- Vasospastic angina
8. A patient with essential hypertension has been treated with a fi xed-dose combination product that contains hydrochlorothiazide and Blood pressure and electrolyte profiles have been kept within acceptable l imits for the last 18 months. Now, however, blood pressure has ri sen to the point where the physician wants to add another antihypertensive drug. The drug i s started; after several weeks blood pressure falls into an acceptable range, but the patient has become hyperkalemic. What drug was added and was most l ikely responsible for the desired
blood pressure fall and the unwanted ri se of potassium levels.
9. A patient has a supraventricular We inject a drug and heart rate falls to a normal (or at least more acceptable) level. Although this drug caused the desired response, i t did so without any direct effect in or on the heart. Which drug was most l ikely used?
10. A 69-year-old man presents with NYHA Stage II (“mild”) heart His symptoms failed to improve adequately in response to captopril and carvedilol so the physician stops the carvedilol and adds usual therapeutic doses of digoxin and furosemide. At a follow-up exam 3 months later we find good symptomatic relief of the heart failure. Blood electrolytes and all other lab tests are within normal l imits. At this time, which electrocardiographic change would you expect to see in response to the digoxin, compared with a baseline (pretreatment) ECG?
- P waves widened, amplitude increased
- PR intervals prolonged
- QRS complexes widened
- RR intervals shortened
- ST segments elevated
11. A patient presents with a blood pressure of 220/120 and a heart rate of 90 beats per minute despite usually effective antihypertensive drug Further work-up indicates the patient has a rare cause of these and other s igns and symptoms: pheochromocytoma. You realize that β- adrenergic blockers are useful as antihypertensive drugs, and for helping to normalize heart rate in patients with supraventricular tachycardia. As a result of the diagnosis, and your knowledge, you administer a usually effective dose of propranolol. What i s the most l ikely outcome of doing this?
- Blood pressure falls promptly, followed by reflex tachycardia
- Epinephrine release from the tumor i s suppressed, hemodynamics normalize
- Heart rate and cardiac function ri se quickly because the β-blocker has triggered additional epinephrine release from the tumor.
- Left ventricular afterload i s decreased, cardiac output ri ses via increases of both left ventricular stroke volume and heart rate.
- Total peripheral resistance ri ses, cardiac output falls, the patient goes into cardiogenic shock
12. A 59-year-old man presents in the emergency department with crushing chest An ECG indicates a small transmural left ventricular infarction, and prompt cardiac catheterization and assessment of prior lab results indicate s ignificant hypercholesterolemia. The patient i s given all the drugs l i sted below, for both immediate management of the i schemia and i ts symptoms and for long-term prevention of a subsequent, and potentially fatal, MI. Which drug would provide immediate relief of the consequences of myocardial i schemia, but has no long-term effects to reduce the ri sk of sudden death or ventricular dysfunction from another MI?
13. A 65-year-old woman i s transferred to the thoracic surgery ICU after cardiac She has diffuse rales bilaterally, a pulse of 90/min, an elevated central venous pressure, and a blood pressure of 160/98 mm Hg. The surgery resident wants to inject an otherwise-correct dose of an IV drug to control heart rate and blood pressure, but grabs a syringe that contains another drug. The patient’s heart rate increases to 150/min and her blood pressure ri ses to 180/106. Which drug did this patient most l ikely receive in error?
14. A patient with chronic-stable (“effort-induced”) angina begins taking metoprolol, and once blood levels approach the therapeutic range the frequency and severity of angina attacks, and the need for sublingual nitroglycerin, were Which of the following states the direct pharmacologic action by which the β-blocker provided the desired effects?
- Decreased myocardial oxygen demand
- Dilated the coronary vasculature
- Directly inhibited angiotensin II synthesis
- Reduced total peripheral resistance
- Slowed AV nodal conduction velocity
15. A 50-year-old man i s aware of the benefits of aspirin in terms of reducing the ri sk of death from an acute myocardial infarction, mainly because he has seen many of the ads and internet posts about this. He notices that the usual recommended dose of aspirin for cardioprotection i s 81 mg/day, but reasons that the bigger the dose, the bigger and better the protective He has taken “at least” 1,000 mg of aspirin (3 “regular strength” aspirin tablets) twice a day for the last 6 months. While he i s fortunate in terms of having no apparent gastrointestinal adverse effects that are associated with long-term, high-dose aspirin use, he suffers an MI. Autopsy results show considerable platelet occlusion of several coronary vessels. What explains the most l ikely mechanism by which high dose aspirin use these adverse events?
- Inhibited thromboxane A2 synthesis in platelets
- Favored adhesion of platelets to the vascular (coronary) endothelium
- Ruptured atherosclerotic plaque in the coronaries, exposing platelets to collagen
- Suppressed hepatic synthesis of vi tamin K-dependent clotting factors
- Triggered excessive activation of platelets by ADP
16. In cl inic you meet a 55-year-old man who i s described by the attending as having “metabolic syndrome,” including high LDL and low HDL cholesterol levels, essential hypertension, type 2 diabetes mellitus, and anginal attacks upon stress about once every 2 He currently has asymptomatic hyperuricemia, but has a gout attack about once a year. The patient i s obese (92 kg), 6 feet tall, and has a body mass index (kg/square meter of body surface area) of 40 (normal or desirable no more than 24.9 kg/m2). He has a 20 year history of smoking a half pack of cigarettes a day, and both parents died in their late 50s—the father from an acute MI, the mother from hemorrhagic stroke. The gentleman i s taking medications deemed appropriate for each of the conditions noted above. One i s colesevelam. What i s the probably reason why the colesevelam was given?
- Counteracts hypokalemia caused by a thiazide diuretic
- Lowers LDL-cholesterol levels
- Lowers plasma urate levels, prophylaxis of gout
- Prevents myocardial i schemia, angina, by reducing myocardial oxygen demand
- Provides antihypertensive and natriuretic effects
17.A man has an aneurysm in the aortic root, a consequence of Marfan He experiences a hypertensive cris i s that requires prompt blood pressure control. Nitroprusside will be infused for i ts immediate antihypertensive effects. What drug would we administer along with the nitroprusside to minimize the ri sk of aneurysm rupture due to increases of left ventricular dP/dt (ΔP/Δt; change in pressure/change in time) as blood pressure falls?
18. Nicotinic acid (niacin), in the relatively large doses that are used to treat certain and common hyperlipidemias, often causes a cutaneous flush and These can be accompanied by widely distributed and sharp “pins and needles” or burning sensation on the skin. The response can be attenuated by several means, one of which involves pretreatment with aspirin. What mechanism or action most l ikely contributes to the vasodilatory response and the flushing?
- Activation of α-adrenergic receptors on vascular smooth muscle
- Calcium channel blockade in vascular smooth muscle
- Local production of prostaglandins
- Release of angiotensin II
- Release of histamine
19. The figure below shows typical cardiovascular responses to the s low IV injection of four adrenergic drugs into a normal, resting Assume the doses of each are sufficient to cause the effects seen here, but not so high that toxic effects occur. No other drugs are present, and sufficient time has been allowed to enable complete dissipation of the effects of any prior drugs. The dashed l ine between the systolic and diastolic pressure traces approximates mean arterial pressure.
Abbreviations used, and answer choices, are EPI, epinephrine ISO, i soproterenol NE, norepinephrine PHE, phenylephrine PHN, phentolamine PRO, propranolol
Select the letter that indicates the drugs that are ordered in the sequence shown (1, 2, 3, 4). EPI, NE, PHE, ISO
- ISO, EPI, NE, PHE
- ISO, PHE, EPI, NE
- NE, ISO, PHE, EPI. PHE, EPI, NE, PRO
- PHE, ISO, NE, EPI
- PRO, PHN, PHE, ISO
Look at the ECG below and answer the following three questions.
Here you see a continuous (uninterrupted) tracing of lead V1, before and after carotid s inus massage (at arrow).
20. What i s the mechanism by which carotid massage exerted i ts effect?
- Activated what i s tantamount to the baroreceptor reflex, increasing vagal tone and acetylcholine release considerably
- Caused catecholamine release
- Induced atrial fibrillation (atrial rate >> 300/min)
- Occluded venous return to the heart, thereby interfering with fi l l ing and contraction of all heart chambers “downstream” of the right atrium
21. Based on the outcome of carotid s inus massage, what can you say about the origin of the aberrant electrical activity that leads to the tachycardia you see before the massage?
- Bundle of Kent (ie, anomalous or accessory pathway for AV conduction) with retrograde and antegrade conduction
- Left bundle branch
- Multiple ectopic ventricular foci
22. What drug, given as an intravenous bolus, might be used as an alternative to carotid massage, causing essentially the same outcome and, therefore, the same interpretation of the origin of the ventricular tachycardia?
23. A 23-year-old nonpregnant woman has been using a preparation of oral ergotamine to manage her frequent migraine She consumes an excessive dose of the drug while trying to abort a particularly severe and refractory attack. What adverse cardiac or cardiovascular consequences are most l ikely to occur as a result of the ergot overdose?
- Myocardial and peripheral (eg, l imb) i schemia due to intense vasoconstriction
- Renal failure secondary to rhabdomyolysis
- Spontaneous bleeding due to direct inhibition of platelet activation/aggregation
- Syncope secondary to acute hypotension
- Tachycardia, tachyarrhythmias from β-1 adrenergic receptor activation