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Cardiovascular Pharmacology- Part 1
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1.;Your patient i s a 50-year-old man with Type 1 (insulin-requiring) diabetes, normal renal function, and no Although his HbA1c levels are acceptable, because of his l i festyle and eating habits he has experienced more than a few episodes of symptomatic hypoglycemia following insulin injections. He currently has asymptomatic hyperuricemia, but he has had several attacks of acute gout over the last 5 years. Today you diagnose hypertension that must be treated. Which antihypertensive drug would be the most rational fi rst choice for starting his antihypertensive therapy?
- Angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker
- β-adrenergic blocker
- Thiazide diuretic
- Verapamil or diltiazem
2. A patient i s hospitalized and waiting for coronary His history includes angina pectoris that i s brought on by “modest” exercise, and i s accompanied by transient electrocardiographic changes consistent with myocardial i schemia. There i s no evidence of coronary vasospasm. In the hospital, he i s receiving nitroglycerin and morphine (both by s low IV infusion), plus oxygen via nasal cannula.
He suddenly develops episodes of chest discomfort. Heart rate during these episodes ri ses to 170 to 190 beats/min; blood pressure reaches 180 to 200/110 to 120 mm Hg, and prominent findings on the ECG are runs of ventricular ectopic beats that terminate spontaneously, plus ST-segment elevation.
Although there are several things that need to be done for immediate care, what drug would you administer to remedy (at least temporarily) the majority of these s igns and symptoms and pose the lowest ri sk of doing further harm?
- Labetalol. Lidocaine
- Nitroglycerin (increased dose as a bolus)
3. A 55-year-old woman has just been diagnosed with Stage 2 essential/primary hypertension, and you conclude that i t i s time to start drug therapy for i t. She also tends to be Notes written by her ophthalmologist indicate that she has chronic open-angle glaucoma. Which one of the following drugs would be the most rational choice for this woman, given only the information presented in this question, because i t might help control both the hypertension and the increased intraocular pressure?
4. Nebivolol i s a fairly new and rather selective β1-adrenergic blocker that i s indicated for managing essential The drug allegedly causes fewer s ide effects than most other β-blockers, and orthostatic hypotension does not occur even with full therapeutic doses. The drug has no effects on changes of total peripheral resistance induced by infusion of phenylephrine or administration an amphetamine. Nebivolol’s antihypertensive mechanism of action clearly involves those common to all β-blockers, but another mechanism contributes to the overall effect. Given your general knowledge of blood pressure control and of auto-nomic/cardiovascular pharmacology, which one of the following i s the other most l ikely mechanism by which nebivolol helps lower TPR and blood pressure?
- Competitively blocks postsynaptic (α1) adrenergic receptors
- Competitively blocks presynaptic (α2) adrenergic receptors
- Increases nitric oxide formation
- Increases synthesis of thromboxane A2
- Inhibits catechol O-methyltransferase (COMT)
5. A 44-year-old woman i s transported to the emergency department after consuming what might be a lethal dose of a β-adrenergic blocker that has no intrinsic vasodilator Despite administration of large doses of i soproterenol to overcome the blockade, her cardiac output i s dangerously low because heart rate and stroke volume are profoundly depressed. Which one of the following approaches i s most l ikely to prove beneficial, i f not l i fesaving?
- Administer glucagon
- Administer phenylephrine
- Administer phentolamine
- Switch from i soproterenol to ephedrine
- Switch from i soproterenol to epinephrine
6. At high (but not necessarily toxic) blood levels, a cardiovascular drug causes many s igns and symptoms that resemble what you see with “low- grade” aspirin toxicity (salicylism): l ight-headedness, tinnitus, and visual disturbances such as What drug most l ikely caused these responses?
7. A patient has periodic episodes of paroxysmal supraventricular tachycardia (PSVT). What drug would be most suitable for outpatient prophylaxis of these worrisome electrophysiologic events?
8. You and a colleague are discussing which α-blocker to use, adjunctively, to control blood pressure in a pheochromocytoma patient before surgery for an adrenalectomy can be Your colleague correctly states that phenoxybenzamine i s the “preferred” drug. You state that prazosin would be a better choice. Which statement about prazosin i s correct in comparison with phenoxybenzamine, and might actually support your proposal that i t would be a better choice?
- Causes not only peripheral α-blockade but also suppresses adrenal epinephrine release
- Has a longer duration of action, which enables less frequent dosing
- Has good intrinsic β-blocking activity, phenoxybenzamine does not
- Overdoses, and the hypotension i t may cause, are easier to manage pharmacologically
- Will not cause orthostatic hypotension, which i s a common consequence of phenoxybenzamine
9. A patient with a history of atrial fibrillation develops acute coronary syndrome and i s admitted to the hospital’s coronary care As of today, he has been receiving otherwise “proper” doses of a drug for 5 days straight. Dosing was done correctly, starting with usual maintenance doses; no loading dose strategy was used. Then, and rather precipitously, the patient develops s igns and symptoms of widespread thrombotic events, and platelet counts decline s ignificantly concomitant with the thrombosis. The patient dies within 24 hours of the onset of s igns and symptoms. What drug most l ikely caused these ultimately fatal responses?
- Heparin (unfractionated)
10. A 65-year-old man with heart failure i s unable to cl imb a fl ight of stairs without experiencing After several years of therapy with carvedilol, captopril, low doses of labetalol, and furosemide, the therapeutic plan probably needs to change now. You empirically add digoxin to improve cardiac muscle contractility. Within 4 weeks, he has a marked improvement in his symptoms. What best describes the main cellular action of digoxin that accounts for i ts ability to improve his cardiovascular function and overall hemodynamic status?
- Activates β1-adrenergic receptors
- Facilitates GTP binding to specific G proteins
- Increases mitochondrial calcium (Ca 2+) release
- Inhibits sarcolemmal Na+-K+-ATPase
- Stimulates cyclic adenosine 5′-monophosphate (cAMP) synthesis
11. A patient with newly diagnosed essential (primary) hypertension starts treatment with a commonly used antihypertensive drug at a dose that i s considered to be therapeutic for the vast majority of Soon after starting therapy the patient experiences crushing chest discomfort. ECG changes show myocardial i schemia. Studies in the cardiac cath lab show episodes of coronary vasospasm, and i t i s l ikely the antihypertensive drug provoked the vasospasm. Which antihypertensive drug or drug class most l ikely caused the i schemia and the angina?
12. A patient with chronic-stable (“effort-induced”) angina i s on prophylactic β-blocker (propranolol) therapy, with sublingual nitroglycerin (NTG) used as needed for managing acute One day he experiences particularly severe angina and takes the usually recommended dose of sublingual NTG. His discomfort i s not reduced at all. Seeking relief, he repeats the usual recommended NTG dose frequently over a period of about 10 minutes, and now has taken far too much of the nitrovasodilator. An electrocardiogram taken by the paramedics, who were called for the patient’s emergency, shows changes consistent with severe myocardial i schemia. The patient goes into cardiac arrest and cannot be resuscitated. What i s the most l ikely cause of or contributing factor to the patient’s responses to the excessive dosage of NTG?
- Cyanide, a toxic metabolite of NTG, accumulated
- Nitroglycerin directly induced coronary vasoconstriction
- The NTG lowered arterial pressure excessively
- The patient has vasospastic (variant or Prinzmetal) angina, not chronic-stable The β-blocker’s intrinsic vasodilator activity potentiated that of the NTG
13. A 50-year-old man has a long history of asymptomatic hyperuricemia (elevated uric acid levels), and you are about to start therapy for newly diagnosed essential hypertension (BP 136/90 mm Hg, based on repeated measurements with the patient supine and at rest). Which antihypertensive drug i s most l ikely to increase his uric acid levels further, and in doing so, be most l ikely to cause the most common cl inical presentation of the hyperuricemia—gout?
14. We conduct an experiment to assess the effects of other drugs on the anti-platelet aggregatory effects of In each case we sample venous blood from an otherwise healthy patient, centrifuge the blood to obtain a platelet-rich fraction, and put samples of the platelets into an instrument that accurately measures platelet aggregation in vitro. We then activate the platelets by adding ADP (or collagen; makes no difference). Results are graphed below.
The control (top l ine) condition reflects results from the patients who has been taking no drugs at all. The bottom trace shows aggregation of platelets i solated from the patient after they have taken aspirin (ASA; 81 mg/day) for 14 days in a row. We stop aspirin for 2 weeks to ensure that the patient has no aspirin in their blood. Then we restart 81 mg/day aspirin plus an unknown drug taken with each aspirin tablet for final 2 weeks. The platelets taken at the end of the 14 days show only s l ight inhibition of platelet aggregation—results not s ignificantly from control.
The results are shown here:
Which drug was taken with the aspirin and inhibited i ts aggregatory effects in response to ADP or collagen?
15. A 57-year-old patient complains of muscle aches, pain, and tenderness. These affect the legs and There i s no fever, bruising, or any recent history of muscle trauma or strains (as from excessive exercise). He has myoglobinuria, a cl inically s ignificant fall of creatinine clearance, and a ri se of plasma creatine kinase (CK) to levels nearly ten times the upper l imit of normal. Which drug i s the most l ikely cause of these findings?
- Aspirin (low dose) for i ts cardioprotective/antiplatelet effects
- Captopril for hypertension and heart failure
- Carvedilol for hypertension, heart failure, and angina prophylaxis
- Furosemide as adjunctive management of his heart failure
- Rosuvastatin to control his hypercholesterolemia and the associated ri sks
16. A coronary artery sample was removed from a healthy animal, put inside a suitable oxygenated salt and nutrient solution, and connected to a transducer that measured increases (contraction) or decreases (relaxation) of smooth muscle tension (force). ACh was then added to give the cumulative concentrations shown
As expected, in the control setting (left) ACh caused concentration-dependent vasorelaxation (equivalent to vasodilation in the intact animal).
The ACh was washed out several times, control conditions returned. The conditions were manipulated, and then the ACh dose-response experiment was repeated (right). Now the data show increased tension developed by the muscle sample (vasoconstriction in vivo) in response to ACh and incremental increases of i ts concentration.
Which one of the following summarizes what was most l ikely done to the vessel under the experimental conditions, before retesting the responses to added ACh? Assume that the vascular responses in this animal model are identical to those that would occur in a human.
- Endothelium was removed mechanically
- Isoproterenol was added right before ACh
- Muscarinic receptors were blocked with atropine
- Sample was pretreated with prazosin
- Tissue was pretreated with botulinum toxin
17. A 28-year-old woman i s receiving drug therapy for essential (primary) She subsequently becomes pregnant. You realize that the drug she’s been taking for her high blood pressure can have serious, i f not fatal, effects on the fetus (i t i s in pregnancy category X). As a result, you stop the current antihypertensive drug and substitute another that i s deemed to be equiefficacious in terms of her blood pressure, and safer for the fetus. Which drug was she most l ikely taking before she became pregnant?
18. We treat a patient with a drug that affects the clotting-thrombolytic systems for a time sufficient to let the drug’s effects and blood levels stabilize at a therapeutic We then i solate platelets from a blood sample and test their in vi tro aggregatory responses to ADP, collagen, PAF, and thromboxane A2. Aggregatory responses to ADP are inhibited; responses to the other platelet proaggregatory agonists are unaffected. Which drug exhibits these properties?
19. Your newly diagnosed hypertensive patient has vasospastic angina. Which drug or drug class would be the most rational for starting anti- hypertensive therapy because i t exerts not only antihypertensive effects, but also directly lowers myocardial oxygen demand and consumption and tends to inhibit cellular processes that otherwise favor coronary vaso-spasm? Assume there are no other specific contraindications to the drug you
- Angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker
- β-Adrenergic blocker
- Thiazide diuretic
- Verapamil (or diltiazem)
20. You are reviewing the medication history of a 59-year-old He has been taking ramipril and pravastatin for the last 5 years. Other medications include metformin for type 2 diabetes mellitus, and escitalopram to help manage his depression. At his last cl inic vis i t, a year ago, he was told to continue his current medications but he was also started on s low-release niacin because diet, exercise and other l i festyle modifications, and his current medications were not adequate. What was the most l ikely reason for adding the niacin?
- Counteract deficiencies of B-vitamin absorption caused by the antidepressant
- Counteract polyphagia, and over-eating, caused by the metformin.
- Lower HDL and triglyceride levels that did not respond adequately to the statin
- Prevent statin-induced neuropathy
- Slow the progression of diabetic nephropathy caused by the ACE inhibitor
21. Quinidine i s ordered for a patient with recurrent atrial fibrillation and who refuses any interventions other than drugs in an attempt to terminate and control the He has some pulmonary fibrosis and a thyroid disorder—both leading you to conclude that amiodarone therapy might not be the best approach. Which statement applies to the quinidine?
- Decreases SA nodal automaticity due to a strong anticholinergic/vagolytic effect
- Is l ikely to increase blood pressure via a direct vasoconstrictor effect
- Is contraindicated i f the patient also requires anticoagulant therapy
- Tends to increase electrical impulse conduction velocity through the AV node
- Will increase cardiac contractility (positive inotropic effect) independent of i ts antiarrhythmic effects