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What is a significant effect of non-dihydropyridine calcium channel blockers, especially verapamil and diltiazem?
Which calcium channel blocker has the longest duration of action?
What is a common side effect of calcium channel blockers?
Which of the following is contraindicated when using calcium channel blockers?
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What is the mechanism of action common to all nitrates?
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Which calcium channel blocker exerts the least negative impact on heart rate?
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Which adverse effect is least commonly associated with nitrate usage?
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Which agent is considered a short-acting dihydropyridine calcium channel blocker?
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What is the primary mechanism through which calcium channel blockers reduce myocardial oxygen consumption?
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Which type of calcium channel blockers are preferred for use when beta blockers are contraindicated or not tolerated?
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How do dihydropyridine calcium channel blockers, such as amlodipine, primarily function in the cardiovascular system?
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What effect do calcium channel blockers generally have on the heart's conduction system?
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What is a potential side effect of dihydropyridine calcium channel blockers that can paradoxically increase myocardial oxygen demand?
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What is the primary symptom of ischemic heart disease?
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Which type of angina is characterized by chest pain that occurs predictably with physical exertion?
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What condition most often leads to unstable angina?
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Which of the following medications is primarily used for the immediate relief of anginal symptoms?
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What characterizes Prinzmetal’s Angina?
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How is the diagnosis of angina typically categorized?
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What signifies a critical condition in the context of unstable angina?
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What is the main difference between stable and unstable angina?
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What is one primary mechanism by which beta-blockers reduce myocardial oxygen consumption?
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Which of the following is NOT a common toxicity associated with beta-blockers?
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In what scenario would beta1 selective beta-blockers be preferred in clinical practice?
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What should be the target resting heart rate when titrating beta-blocker therapy?
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Which of the following beta-blockers is known for having ISA (Intrinsic Sympathomimetic Activity)?
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What is the recommended approach for discontinuing beta-blocker therapy to avoid withdrawal symptoms?
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Which condition is a contraindication for the use of beta-blockers?
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Which effect is a direct consequence of the blockade of beta2 receptors by beta-blockers?
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What characterizes silent ischemia in patients?
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Which treatment objective is specific to unstable angina?
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Which non-pharmacologic intervention is recommended for managing ischemic heart disease?
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Which of the following drug groups is NOT primarily used as an anti-ischemic agent?
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What is a common consequence of repetitive bouts of myocardial ischemia?
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Which of the following indicates a high-risk assessment for angina?
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What mechanism do main anti-ischemic agents target to provide relief?
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In stable angina management, which objective is essential?
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Study Notes
Pharmacology of Ischemic Heart Disease
- Ischemic heart disease is characterized by angina pectoris, caused by transient episodes of myocardial ischemia.
- Angina pectoris is chest pain due to myocardial ischemia (not infarction)
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Types of angina:
- Stable angina: Predictable chest pain related to exertion or stress, often chronic.
- Unstable angina: Caused by ruptured plaque and platelet aggregation, leading to decreased blood flow. Requires urgent management as part of acute coronary syndrome.
- Prinzmetal's angina (Variant angina): Unprovoked coronary artery spasm causing chest pain, often unpredictable and cyclical.
- Silent ischemia: Myocardial ischemia without chest pain or symptoms.
- Therapeutic objectives for stable angina: Improve exercise tolerance, decrease anginal symptoms, relieve chest pain, prevent ischemia, reduce risk of future events.
- Therapeutic objectives for unstable angina: Stabilize chest pain, decrease risk of infarction, prevent recurrence of ischemic events, decrease mortality.
- Pharmacologic management aims to affect either the demand or supply of oxygen to the heart.
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Beta-blockers: Blockade of beta1 and beta2 receptors on myocardial and smooth muscle cells.
- Decrease heart rate, force of contraction, and blood pressure.
- Reduce cardiac workload and myocardial oxygen consumption.
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Calcium channel blockers (CCBs): Block calcium entry into myocardial and smooth muscle cells.
- Dihydropyridines: Primarily dilate peripheral arterioles and coronary arteries, reducing afterload and increasing oxygen supply. Can cause reflex tachycardia.
- Non-dihydropyridines (Verapamil and Diltiazem): Inhibit sinus and atrioventricular nodes, reducing heart rate and contractility.
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Nitrates: Simple nitric and nitrous acid esters of polyalcohols.
- Reduce preload and afterload by dilating veins and arteries.
- Decrease myocardial oxygen demand and increase oxygen supply.
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Other anti-ischemic agents:
- Molsidomine: Vasodilator like nitrates.
- Ranolazine: Reduces myocardial oxygen demand.
- Ivabradine: Decreases heart rate.
- Nikorandil: Vasodilator.
- Trimetazidin: Improves myocardial energy metabolism.
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Antiplatelet agents:
- Aspirin (ASA): Inhibits platelet aggregation.
- ADP inhibitors: Inhibit adenosine diphosphate-mediated platelet aggregation.
- GP IIb/IIIa inhibitors: Prevent platelets from binding to fibrinogen.
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Anticoagulants:
- Heparins: Prevent blood clotting.
- Warfarin: Inhibits the synthesis of clotting factors.
- ACE inhibitors: Inhibit angiotensin-converting enzyme, lowering blood pressure and improving cardiac remodeling.
- HMG-CoA reductase inhibitors (Statins): Lower cholesterol levels, reducing cardiovascular risk.
Calcium Channel Blockers (CCBs)
- Potent vasodilators of peripheral and coronary arteries.
- Non-Dihydropyridines (Verapamil, Diltiazem): Less potent vasodilators, with negative chronotropic and inotropic actions.
- Dihydropyridines (Nifedipine, Nicardipine, etc.): Strong vasodilators.
- Administration: Oral (PO) or intravenous (IV).
- Indications: Chronic therapy when beta blockers or nitrates are ineffective or not tolerated.
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Pharmacologic issues:
- Short-acting dihydropyridines can cause conduction abnormalities.
- Negative inotropic properties can worsen heart failure.
- Drug interactions can occur.
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Toxicity:
- Depression of contractility, heart failure, AV nodal blockade, bradycardia, hypotension.
- Constipation, flushing, edema, dizziness, and nausea.
- Contraindications: Conduction abnormalities.
- Patient information: Side effects and drug interactions should be discussed with patients.
Nitrates
- Mechanism of action: Venodilation, reducing preload. Arteriodilation, reducing afterload.
- Reduce myocardial oxygen demand: By lowering heart rate and blood pressure.
- Increase myocardial oxygen supply: By improving coronary blood flow.
- Administration: Various forms (sublingual, oral, topical, intravenous).
- Uses: Treatment and prevention of angina pectoris, acute coronary syndromes, and heart failure.
- Toxicity: Headache, hypotension, flushing, reflex tachycardia, tolerance with prolonged use.
- Important Note:* This is a summary of the pharmacological information provided in the document. Always consult with a healthcare professional for specific medical advice and treatment options.
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Description
This quiz focuses on the pharmacological aspects of ischemic heart disease, including different types of angina such as stable, unstable, and Prinzmetal's angina. It covers the therapeutic objectives for managing both stable and unstable angina, aiming to improve patient outcomes. Test your knowledge on the causes, symptoms, and treatment strategies related to this condition.
