Cardiovascular Therapeutics Midterm
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Cardiovascular Therapeutics Midterm

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Questions and Answers

What does MAP stand for in the context of cardiovascular health?

  • Muscle Activation Pattern
  • Mean Arterial Pressure (correct)
  • Metabolic Activity Potential
  • Myocardial Action Potential

    • What physiological role does cAMP play in the heart muscle contraction?

  • Facilitates calcium release (correct)
  • Stimulates adenylyl cyclase
  • Inhibits contractility
  • Promotes breakdown of ATP

    • Which of the following conditions is a cardiac indication for the use of B-blockers?

  • Essential tremor
  • Elevated intraocular pressure
  • Heart failure with reduced ejection fraction (correct)
  • Migraine prophylaxis

    • Which B-blocker is noted for its mild agonist activity?

    <p>Pindolol</p> Signup and view all the answers

    What is the main consequence of atrial fibrillation?

    <p>Chaotic electrical signals in the atria</p> Signup and view all the answers

    Which B-blocker is heavily dependent on renal function?

    <p>Nadolol</p> Signup and view all the answers

    What is the primary physiological effect of B-receptor agonism?

    <p>Increased heart rate</p> Signup and view all the answers

    In which condition is propranolol indicated as a treatment?

    <p>Migraine prophylaxis</p> Signup and view all the answers

    What is the recommended way to take carvedilol to enhance its bioavailability?

    <p>With meals</p> Signup and view all the answers

    Which beta-blocker is administered exclusively via intravenous (IV) route?

    <p>Esmolol</p> Signup and view all the answers

    What is the half-life of esmolol compared to most other beta-blockers?

    <p>Approximately 10 minutes</p> Signup and view all the answers

    What is a key adverse drug reaction associated with lipophilic beta-blockers like propranolol?

    <p>Sleep disturbances</p> Signup and view all the answers

    Which beta-blocker is most dependent on renal function for clearance?

    <p>Atenolol</p> Signup and view all the answers

    What condition may be masked by the use of beta-blockers?

    <p>Hypoglycemia</p> Signup and view all the answers

    Which of the following beta-blockers is known to be hepatically cleared?

    <p>Propranolol</p> Signup and view all the answers

    What is a potential adverse effect of withdrawing beta-blockers too suddenly?

    <p>Rebound tachycardia</p> Signup and view all the answers

    What effect do calcium channel blockers (CCBs) have on the myocardium?

    <p>Decrease contractility</p> Signup and view all the answers

    Which of the following conditions is NOT indicated for the use of non-dihydropyridine (non-DHP) CCBs?

    <p>Heart failure</p> Signup and view all the answers

    What role do L-type calcium channels play during the action potential in cardiac muscle cells?

    <p>They allow calcium influx</p> Signup and view all the answers

    How do non-DHP CCBs affect electrical conduction in the heart?

    <p>They decrease conduction velocity</p> Signup and view all the answers

    What is the primary difference between dihydropyridine (DHP) and non-DHP CCBs?

    <p>DHPs bind to different locations on L-type channels</p> Signup and view all the answers

    What does automaticity refer to in the context of cardiac cells?

    <p>The ability to generate electrical impulses spontaneously</p> Signup and view all the answers

    Which type of calcium channel is primarily responsible for relaxation of vascular smooth muscle?

    <p>L-type channels</p> Signup and view all the answers

    Which suffix indicates 'blood' in medical terminology, often used in the context of ischemic conditions?

    <p>-emia</p> Signup and view all the answers

    What is a common adverse effect associated with calcium channel blockers?

    <p>Peripheral edema</p> Signup and view all the answers

    Which calcium channel blocker is associated with the shortest half-life?

    <p>Clevidipine</p> Signup and view all the answers

    What is the mechanism of action of ACE inhibitors?

    <p>Block the activity of ACE</p> Signup and view all the answers

    Which drug class is likely to cause bradycardia more frequently?

    <p>Non-dihydropyridine (Non-DHP) CCBs</p> Signup and view all the answers

    Amlodipine is characterized by which pharmacokinetic feature?

    <p>Long half-life and duration of action</p> Signup and view all the answers

    What condition is NOT commonly indicated for the use of ACE inhibitors or ARBs?

    <p>Hepatic insufficiency</p> Signup and view all the answers

    Which interaction is specifically noted for Verapamil?

    <p>Interacts with digoxin</p> Signup and view all the answers

    What is true regarding neprilysin inhibitors?

    <p>Decrease breakdown of bradykinin and natriuretic peptides</p> Signup and view all the answers

    Study Notes

    Mean Arterial Pressure (MAP) Calculation

    • MAP formula: ( \text{MAP} = \frac{(2 \times DBP) + SBP}{3} )

    Introduction to Cardiovascular Medications

    Beta-Adrenergic Agonists and Antagonists (Beta Blockers)

    • Beta receptors are G-protein coupled, activating adenylyl cyclase for ATP to cAMP conversion.
    • Vital for myocardium contractility and conduction velocity in heart function.
    • Post-synaptic B-receptors lead to tissue-specific physiological responses.
    • Beta blockers function by competitively inhibiting beta receptors.
    Key Physiological Effects of Beta Agonism
    • Mild agonism from acebutolol, penbutolol, and pindolol.
    • Bisoprolol and nadolol require renal function considerations.
    Clinical Indications for Beta Blockers
    • Cardiac:
      • Angina prevention
      • Treatment of arrhythmias, including atrial fibrillation
      • Management of heart failure with reduced ejection fraction (EF)
      • Post-myocardial infarction care
    • Non-cardiac:
      • Management of elevated intraocular pressure (timolol)
      • Treatment for essential tremor (propranolol)
      • Prophylaxis for migraines (propranolol, timolol)
    Pharmacokinetics of Beta Blockers
    • Generally well absorbed, peak peak levels within 1-3 hours after oral administration.
    • Some, like carvedilol, require concurrent food intake to enhance bioavailability.
    • Different formulations (IV solutions for metoprolol and propranolol; esmolol is IV only).
    • Distinct lipophilicity: propranolol is highly lipophilic; atenolol is hydrophilic and renally dependent.
    • Varying half-lives: esmolol (~10 minutes), others 3-30 hours depending on the specific beta blocker.
    Class-Wide Adverse Drug Reactions
    • Bradyarrhythmias (decreased heart rate)
    • Drug-dose dependent bronchospasm
    • Side effects like fatigue and sleep disturbances, especially common with lipophilic options.
    • Risk of hypotension and potential masking of hypoglycemia symptoms.
    • Metabolic effects include hypercholesterolemia and hypertriglyceridemia.
    • Withdrawal effects can include rebound tachycardia and hypertensive crises.
    Precautions and Contraindications
    • Notably affected by CYP2D6 metabolism (e.g., carvedilol, metoprolol, propranolol).

    Calcium Channel Blockers (CCBs)

    Mechanism of Action
    • Target L-type channels in myocardium, SA/AV nodes, and vascular smooth muscle for calcium influx management.
    • CCBs decrease myocardial contractility and produce vasodilation.
    Indications for CCBs
    • Non-DHP:
      • Hypertension management
      • Ischemic heart disease treatment
      • Supraventricular tachyarrhythmias
    • DHP: Primarily used for hypertension and ischemic heart disease.
    Pharmacokinetics of CCBs
    • Rapid onset for IV formulations (e.g., verapamil, diltiazem).
    • Different half-lives observed (e.g., clevidipine ~15 minutes, amlodipine has longer duration).
    Adverse Drug Reactions (ADRs)
    • Gastrointestinal issues (constipation due to decreased GI motility)
    • Peripheral edema from arterial vasodilation.
    • Non-DHP versions more likely to induce bradycardia.
    Drug-Drug Interactions (DDIs)
    • Noteworthy interactions with anticoagulants and statins, especially involving CYP enzymes.

    ACE Inhibitors, ARBs, and ARNI

    Mechanism of Action
    • ACE inhibitors block angiotensin-converting enzyme, preventing the breakdown of bradykinin.
    • ARBs inhibit angiotensin II Type 1 receptors.
    • Neprilysin inhibitors decrease the breakdown of bradykinin and natriuretic peptides, promoting vasodilation.
    Indications
    • ACEi/ARBs:
      • Used in acute coronary syndrome and heart failure with reduced EF.
      • Effective for hypertension and proteinuric chronic kidney disease.
    • ARNI: Beneficial in both reduced and preserved EF heart failure.
    Pharmacokinetics
    • Specific pharmacokinetic profiles not provided; important for understanding drug actions and interactions.

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    Description

    Test your knowledge on cardiovascular medications with this midterm quiz. The quiz covers essential topics such as B-adrenergic agonists and antagonists, their mechanisms, and their effects on heart function. Prepare to deepen your understanding of how these medications influence cardiovascular health.

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