Pharmacology and Pharmacotherapeutics
Core concepts
Anchor your study on receptors and signal transduction: agonists vs antagonists, partial agonists, inverse agonists, competitive vs non-competitive antagonism, and dose–response relationships (potency vs efficacy, ED50, therapeutic index). Understand pharmacokinetics: absorption, distribution (protein binding, volume of distribution), metabolism (phase I and II, CYP450, induction/inhibition) and excretion, plus half-life and steady-state principles.
Major drug classes and mechanisms
Know the mechanism and key adverse effects of first-line agents in hypertension, diabetes, asthma, heart failure, infection and anticoagulation. Link autonomic pharmacology (muscarinic, adrenergic receptors) to clinical effects and antidotes.
Traps in questions
- Confusing potency (dose needed) with efficacy (maximal effect).
- Assuming a CYP inhibitor speeds elimination - it slows it, raising toxicity risk.
- Forgetting prodrugs require activation (e.g., clopidogrel via CYP2C19).
- Applying adult doses to renal or hepatic impairment without adjustment.
Rule of thumb
When asked for the most likely adverse effect, reason from the receptor: beta-blockade causes bradycardia and bronchospasm; ACE inhibition raises bradykinin, causing cough and angioedema.
Worked example
A patient on simvastatin develops muscle pain after starting a strong CYP3A4 inhibitor. The mechanism: reduced statin metabolism raises plasma levels, increasing rhabdomyolysis risk. Appropriate action: assess CK, stop or switch the statin, and review the interacting drug.