Advanced Pharmacodynamics Flashcards
(20 cards)
What is the pharmacodynamic explanation for fatigue and bradycardia in a patient on atenolol?
Atenolol blocks β1-adrenergic receptors in the heart, reducing heart rate and contractility, causing fatigue and bradycardia.
Why is salbutamol preferred in asthma management?
It is a β2-agonist that causes bronchodilation by relaxing bronchial smooth muscle – high receptor selectivity reduces cardiac side effects.
Why must warfarin levels be closely monitored?
Warfarin has a narrow therapeutic index. Small changes in plasma levels can lead to bleeding (toxicity) or clotting (subtherapeutic effect).
What’s the pharmacodynamic rationale for combining levodopa with carbidopa in Parkinson’s disease?
Carbidopa inhibits peripheral breakdown of levodopa, allowing more to reach the brain and reducing peripheral side effects.
How do NSAIDs cause gastric irritation pharmacodynamically?
They inhibit COX-1, reducing protective gastric prostaglandins, leading to mucosal damage and increased risk of ulcers.
What’s the role of receptor upregulation and downregulation in prescribing?
Chronic agonist use may cause downregulation (tolerance). Chronic antagonist use may cause upregulation (hypersensitivity).
Why is naloxone used in opioid overdose?
It is a competitive opioid receptor antagonist that displaces opioids from μ-receptors, reversing respiratory depression.
How does drug selectivity affect side effect profiles?
More selective drugs (e.g., β1 vs β2 blockers) tend to have fewer off-target side effects.
What is the pharmacodynamic consequence of combining benzodiazepines with alcohol?
Both enhance GABAergic activity, leading to additive CNS depression and increased risk of respiratory failure.
Why is it important to understand receptor saturation?
Once all receptors are occupied, increasing the dose won’t increase effect but may increase side effects.
Why is aspirin contraindicated in children with viral infections?
Aspirin can trigger Reye’s syndrome due to effects on mitochondrial function during viral illness.
How do calcium channel blockers like amlodipine reduce blood pressure?
They block L-type calcium channels in vascular smooth muscle, causing vasodilation and decreased systemic vascular resistance.
How does pharmacodynamics differ from pharmacokinetics in prescribing?
Pharmacodynamics = What the drug does to the body (effects, receptors). Pharmacokinetics = What the body does to the drug (ADME).
What are the pharmacodynamic concerns related to prescribing propranolol in a patient with COPD?
Propranolol is a non-selective beta-blocker that blocks both β1 and β2 receptors, which can cause bronchoconstriction and worsen respiratory function.
What alternative might be more appropriate than propranolol for a patient with COPD?
A more appropriate choice would be a cardioselective beta-blocker like bisoprolol, which primarily affects β1 receptors and is less likely to impact pulmonary function.
What is the pharmacodynamic risk of NSAIDs in chronic kidney disease (CKD)?
NSAIDs inhibit COX enzymes, reducing prostaglandin synthesis, which can lead to vasoconstriction of renal afferent arterioles and decrease renal perfusion, increasing the risk of AKI.
Why are topical NSAIDs preferred in elderly patients with CKD?
They provide localized pain relief with minimal systemic absorption, reducing the risk of renal and gastrointestinal side effects.
What is the pharmacodynamic rationale for using PPIs with NSAIDs?
PPIs reduce gastric acid secretion, protecting the mucosa from NSAID-induced inhibition of protective prostaglandins and reducing ulcer risk.
Why is paracetamol considered safe in CKD?
Paracetamol is metabolized in the liver and has minimal renal impact, making it a safer analgesic option in CKD patients.
What are key monitoring parameters when prescribing NSAIDs to patients with impaired renal function?
Renal function (eGFR, creatinine), signs of GI bleeding, blood pressure, and hydration status.
