أسئلة الـ 11  فارما PPPM (قبل التعديل)
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Questions and Answers

How do beta-blockers reduce blood pressure via cardiovascular mechanisms?

  • By stimulating renin release from the kidneys, leading to increased angiotensin II production.
  • By increasing norepinephrine release from presynaptic terminals enhancing sympathetic activity.
  • By decreasing cardiac output via negative inotropic and chronotropic effects and reducing renin release. (correct)
  • By increasing cardiac output through positive inotropic and chronotropic effects.

A patient with essential tremors and mild hypertension is prescribed a beta-blocker. What is the most likely mechanism by which the beta-blocker reduces tremors?

  • Blocking beta-2 receptors in skeletal muscles. (correct)
  • Enhancing norepinephrine (NE) release, leading to muscle relaxation.
  • Blocking beta-1 receptors in the heart, thus reducing sympathetic drive.
  • Increasing aqueous humor secretion, leading to reduced muscle tension.

Why should beta-blockers be used with caution in patients with renal failure?

  • They can increase plasma sodium levels.
  • They can increase plasma potassium levels. (correct)
  • They can decrease plasma sodium levels.
  • They can decrease plasma potassium levels.

A patient with type 1 diabetes is prescribed a non-selective beta-blocker for hypertension. What potential metabolic side effect should the physician be aware of?

<p>Inhibition of glycogenolysis in the liver, potentially aggravating hypoglycemia. (A)</p> Signup and view all the answers

Which of the following is a primary therapeutic use of topical beta-blockers like timolol and betaxolol?

<p>Management of open-angle glaucoma by reducing aqueous humor secretion. (B)</p> Signup and view all the answers

A patient with a history of asthma and peripheral vascular disease requires treatment for hypertension. Which beta-blocker would be the MOST contraindicated?

<p>Propranolol (D)</p> Signup and view all the answers

A patient with diabetes is prescribed a beta-blocker for hypertension. What potential adverse effect should the patient be MOST aware of?

<p>Masking of hypoglycemia symptoms (D)</p> Signup and view all the answers

Why is tapering the dose of a beta-blocker recommended when discontinuing long-term use?

<p>To avoid receptor upregulation and excessive cardiovascular effects (D)</p> Signup and view all the answers

Which beta-blocker is LEAST likely to cause prolonged bradycardia due to its mechanism of action and half-life?

<p>Esmolol (A)</p> Signup and view all the answers

A patient taking a beta-blocker reports experiencing vivid dreams and nightmares. Which of the following is the MOST appropriate initial course of action?

<p>Evaluate the appropriateness of continuing the beta-blocker (D)</p> Signup and view all the answers

Which of the following is a characteristic of lipophilic beta-blockers like propranolol compared to hydrophilic beta-blockers like atenolol?

<p>Shorter duration of action (B)</p> Signup and view all the answers

A patient with a history of asthma is prescribed a beta-blocker. Which characteristic of beta-blockers is most concerning in this case?

<p>Non-selective beta blockade (C)</p> Signup and view all the answers

Which of the following is the primary reason propranolol has low bioavailability after oral administration?

<p>Extensive first-pass metabolism in the liver (C)</p> Signup and view all the answers

A patient is taking a beta-blocker that undergoes extensive hepatic metabolism. What is a potential consequence of liver dysfunction in this patient?

<p>Decreased drug clearance and increased risk of toxicity (B)</p> Signup and view all the answers

A doctor wants to prescribe a beta-blocker with a longer duration of action. Which of the following beta-blockers would be most suitable?

<p>Atenolol (D)</p> Signup and view all the answers

A patient is experiencing unwanted beta-2 blockade effects from a non-selective beta-blocker. Which of the following symptoms is the patient MOST likely to be experiencing?

<p>Vasoconstriction (A)</p> Signup and view all the answers

Why might a physician choose a cardioselective beta-blocker over a non-selective beta-blocker for a patient with peripheral artery disease?

<p>Cardioselective blockers are less likely to worsen intermittent claudication. (D)</p> Signup and view all the answers

A patient with anxiety and tremors is prescribed propranolol. What additional action of propranolol, besides beta-blockade, might contribute to reducing these symptoms?

<p>Membrane stabilizing effect (D)</p> Signup and view all the answers

Why does increased plasma potassium in renal failure patients occur as a result of beta-blocker administration?

<p>Beta-2 receptor blockade impairs the ability of insulin to drive potassium into cells, exacerbating hyperkalemia in renal failure. (C)</p> Signup and view all the answers

How do beta-blockers contribute to a reduction in intraocular pressure (IOP) in the treatment of glaucoma?

<p>By decreasing the production of aqueous humor via beta-receptor blockade in the ciliary epithelium. (B)</p> Signup and view all the answers

What is the most likely mechanism by which beta-blockers can induce vivid dreams, nightmares, and depression?

<p>CNS penetration and beta-receptor blockade (C)</p> Signup and view all the answers

Which mechanism primarily explains the anti-anxiety effect of beta-blockers in treating situational anxiety?

<p>Decreased sympathetic activity, reducing the physical symptoms of anxiety, such as palpitations and tremors. (D)</p> Signup and view all the answers

How do beta-blockers potentially increase the hypoglycemic effect of insulin?

<p>Beta-blockers inhibit glycogenolysis in the liver (mediated by beta-2 receptors), impairing glucose release and prolonging hypoglycemia. (B)</p> Signup and view all the answers

Why is tapering the dose of beta-blockers crucial when discontinuing long-term use, especially in patients with conditions like hypertension or angina?

<p>To minimize the risk of rebound effects from upregulated beta-receptors. (B)</p> Signup and view all the answers

In a patient with diabetes mellitus who is taking beta-blockers, what is the potential risk related to hypoglycemia, and how should it be managed?

<p>Beta-blockers can mask the typical adrenergic warning signs of hypoglycemia, such as tremor and tachycardia. Patients should be educated to recognize other symptoms like sweating and be advised to monitor their blood glucose levels more frequently. (C)</p> Signup and view all the answers

Why are non-selective beta-blockers contraindicated in patients with bronchial asthma?

<p>They can block beta-2 receptors in the bronchial smooth muscle, causing bronchoconstriction. (B)</p> Signup and view all the answers

A patient with a history of heart block is prescribed a non-selective beta-blocker for hypertension. What is the most critical concern in this scenario?

<p>The beta-blocker will exacerbate the heart block potentially leading to a complete heart block and severe bradycardia. (A)</p> Signup and view all the answers

How does carvedilol, with its combined alpha-1 and beta-blocking activity, offer a theoretical advantage over traditional beta-blockers in managing hypertension?

<p>It causes vasodilation by blocking alpha-1 receptors, which reduces peripheral vascular resistance, complementing the beta-blocking effect. (D)</p> Signup and view all the answers

A researcher is comparing the effects of propranolol and atenolol on cerebral blood flow in animal models. Which of the following statements BEST describes the expected difference, considering their pharmacokinetic properties?

<p>Propranolol would be expected to have a greater effect on cerebral blood flow compared to atenolol due to its higher lipophilicity and ability to cross the blood-brain barrier more readily. (C)</p> Signup and view all the answers

A patient with moderate hepatic impairment requires a beta-blocker. Considering the pharmacokinetic properties of propranolol and atenolol, which of the following adjustments is MOST appropriate?

<p>Administer propranolol at a lower dose due to its extensive hepatic metabolism. (A)</p> Signup and view all the answers

An investigator is studying the duration of action of different beta-blockers. Which statement accurately compares the expected durations of propranolol and atenolol after a single oral dose?

<p>Atenolol is expected to have a longer duration of action than propranolol because it is primarily excreted by the kidneys and has less extensive metabolism. (A)</p> Signup and view all the answers

A researcher aims to minimize beta-2 blockade effects in a study participant. Knowing the properties of beta-blockers, which agent would be MOST suitable if beta-blockade is still required?

<p>Acebutolol, due to its intrinsic sympathomimetic activity and beta-1 selectivity. (C)</p> Signup and view all the answers

A patient who is a chronic smoker has hypertension and requires beta-blocker therapy. Considering the impact of smoking on drug metabolism, which beta-blocker's dosage might need adjustment, and in which direction?

<p>Propranolol dosage may need to be increased due to induced hepatic metabolism. (B)</p> Signup and view all the answers

In a clinical trial comparing beta-blockers, researchers note variations in patient responses. Which factor explains why some patients might not respond as expected to propranolol, despite adequate dosing?

<p>Genetic polymorphisms affecting CYP2D6 enzyme activity, which alters propranolol metabolism. (C)</p> Signup and view all the answers

A patient with anxiety and migraine is prescribed propranolol. What is the MOST likely mechanism by which propranolol prevents migraines?

<p>Prevention of cortical spreading depression through membrane stabilization and beta-adrenergic blockade. (C)</p> Signup and view all the answers

A cardiologist is selecting a beta-blocker for a patient with hypertension and a history of frequent hypoglycemic episodes. Which agent is LEAST suitable?

<p>Propranolol, a non-selective beta-blocker. (D)</p> Signup and view all the answers

Flashcards

How do Beta-blockers affect Blood Pressure?

Beta-blockers lower blood pressure by reducing cardiac output, renin release, and norepinephrine release.

CNS Side Effects of Beta-Blockers?

Beta-blockers can cause nightmares, vivid dreams, depression, and impact sexual function.

Beta-blockers and Tremors?

Beta-blockers decrease tremors by blocking beta-2 receptors in skeletal muscles.

Beta-blockers and Glaucoma?

Beta-blockers, especially timolol, reduce aqueous humor secretion, decreasing intraocular pressure.

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Therapeutic Uses of Beta-Blockers?

Beta-blockers can manage hypertension, arrhythmias, prevent angina/migraine, reduce anxiety, treat thyrotoxicosis & glaucoma.

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Beta-blocker adverse effects

Tiredness, hypotension, bradycardia, heart failure/block, bronchospasm, vivid dreams, masking hypoglycemia, allergic reactions.

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Absolute Contraindications of Beta-blockers

Any heart block, acute/severe heart failure, bronchial asthma, sudden withdrawal after long-term use.

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Relative Contraindications of Beta-blockers

Peripheral vascular disease, athletes, diabetes mellitus.

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Propranolol's Additional Property

Has membrane-stabilizing action.

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Chronic Beta-Blocker Use & Withdrawal

Receptor upregulation occurs. Taper dose to avoid rebound effects of endogenous amines.

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Non-selective β-blockers

Block both β1 and β2 receptors. Examples: Propranolol, Timolol, Indolol.

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Cardio-selective β-blockers

Primarily block β1 receptors in the heart. Examples: Metoprolol, Atenolol.

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β-blockers with VD action

β-blockers with additional vasodilation action. Examples: Carvedilol, Labetalol.

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Propranolol

A non-selective β-blocker with low bioavailability due to first-pass metabolism.

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Pharmacokinetics

The process by which a drug is absorbed, distributed, metabolized, and excreted by the body.

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Lipophilic β-blockers

Better absorbed, reach the CNS more, undergo extensive hepatic metabolism, shorter duration, excreted by the liver.

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Hydrophilic β-blockers

Less absorbed, reach CNS less, undergo less hepatic metabolism, longer duration, excreted by the kidney.

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β1-blockade effects

Blocking β1 receptors leads to a decrease in all cardiac properties.

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Beta-blockers: Cardiac Effects

Decreases cardiac output by negative inotropic and chronotropic effects via β1 receptor blockade.

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Beta-blockers: Bronchospasm Risk

Bronchospasm can occur even with β1-selective blockers at high doses due to loss of selectivity.

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Beta-blockers & Hypoglycemia

Beta-blockers can exacerbate hypoglycemia by inhibiting glycogenolysis in the liver via β2 receptor blockade.

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Timolol: Glaucoma Treatment

Treats open-angle glaucoma by decreasing aqueous humor secretion.

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Beta-blockers & Potassium

Can increase plasma potassium levels in patients with renal failure.

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Esmolol's Key Feature

An ultrashort-acting beta-blocker.

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Labetalol's Action

Blocks both alpha and beta receptors.

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Carvedilol's Unique Effect

Has alpha-1 receptor blocking actions.

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Beta-blocker Withdrawal

Taper the dose to prevent excessive cardiovascular effects.

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Propranolol Absorption

Orally absorbed, but with low bioavailability due to extensive first-pass metabolism.

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Lipophilic β-blocker traits

Better absorption, more CNS penetration, hepatic metabolism, shorter duration, liver excretion.

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Hydrophilic β-blocker traits

Less absorption, less CNS penetration, less hepatic metabolism, longer duration, kidney excretion.

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Propranolol type

Non-selective β adrenergic blocker.

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β1-blockade

Decreases all cardiac properties.

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β2-blockade

Blocks β2-mediated vasodilation, potentially causing ischemia.

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Study Notes

Types of Beta-Adrenergic Blocking Drugs

  • Non-selective Beta-blockers: Include Propranolol, Pindolol, and Timolol
  • Cardio-selective Beta1-blockers: Include Metoprolol, Atenolol, and Bisoprolol
  • Beta-blockers with additional vasodilation action: Include Carvedilol and Dilevalol

Propranolol

  • Prototype beta-blocker.

Pharmacokinetics: Absorption

  • Almost completely absorbed after oral administration.
  • Low bioavailability due to extensive first-pass metabolism.

Pharmacokinetics: Distribution, Metabolism, and Excretion

  • Lipophilic beta-blockers (e.g., Propranolol) have better absorption and reach the CNS more readily compared to hydrophilic beta-blockers (e.g., Atenolol).
  • Propranolol: Undergoes extensive hepatic metabolism and has a shorter duration of action.
  • Atenolol: Primarily excreted via the kidneys, resulting in a longer duration of action.

Dynamics

  • Non-selective beta-adrenergic blocker and membrane stabilizer.

Pharmacological Effects

  • Beta1-blockade: Reduces all cardiac properties.
  • Beta2-blockade: Blocks Beta2-mediated vasodilation, potentially leading to ischemia.
  • Decrease Blood Pressure: Achieved by reducing cardiac output (negative inotropic and chronotropic effects via Beta1 blockade), reducing renin release from the kidneys (Beta1 blockade), and reducing norepinephrine release (blocking presynaptic Beta2 receptors).
  • Has anti-anxiety action.
  • CNS Effects: Include nightmares, vivid dreams, and depression.
  • Can cause sexual dysfunction.
  • Skeletal Muscle: Reduces essential tremors by blocking Beta2 receptors.
  • Eye: Decreases aqueous humor secretion, reducing intraocular pressure (IOP); Timolol and Betaxolol are effective.
  • Respiratory: Can cause bronchospasm, even with Beta1-selective blockers at high doses, due to the loss of selectivity.
  • Metabolic: Can aggravate the hypoglycemic effect of insulin by inhibiting glycogenolysis in the liver (Beta2 blockade), and can increase plasma potassium levels in patients with renal failure

Therapeutic Uses

  • Heart conditions like hypertension, myocardial infarction, and cardiac arrhythmias.
  • Prophylaxis against angina and migraine attacks.
  • Used for anxiety by suppressing the physical manifestations of situational anxiety
  • Treatment of thyrotoxicosis.
  • Open-angle glaucoma treatment using topical Timolol, which decreases aqueous humor secretion.

Adverse Reactions

  • Common adverse reactions: tiredness, fatigue, hypotension, bradycardia, heart failure, heart block, and bronchospasm
  • Other adverse effects: vivid dreams, nightmares, hallucinations, withdrawal symptoms upon abrupt discontinuation, masking of hypoglycemia in diabetic patients, and allergic reactions.

Contraindications

  • Absolute: Include any degree of heart block, acute or severe heart failure, bronchial asthma, and sudden withdrawal after long-term use.
  • Relative: Include peripheral vascular disease, use in athletes, and diabetes mellitus.

Other Properties of Beta-Adrenergic Blockers

  • Propranolol: Has membrane-stabilizing action.
  • Esmolol: Is ultrashort-acting.
  • Labetalol: Has mixed alpha- and beta-blocking actions.
  • Carvedilol: Possesses alpha1 receptor blocking actions.

Clinical Considerations

  • Chronic beta-blocker use (e.g., in angina, hypertension): Leads to receptor upregulation.
  • During withdrawal, taper the dose to avoid excessive cardiovascular effects (rebound effects) from endogenous amines.

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