Pharmacology & Therapeutics

Choose anticoagulation by indication, thrombotic risk, bleeding risk, renal function and patient preference; warfarin and direct oral anticoagulants have different monitoring, interactions and reversal pathways.

Digoxin inhibits the myocardial sodium-potassium pump, so in excess it both blocks conduction and provokes ectopic firing, giving bradycardia, heart block and ventricular arrhythmia.

Lithium is cleared by the kidney alongside sodium, so volume depletion, renal impairment or a drug that blocks its elimination turns an unchanged dose into rising concentrations and neurotoxicity.

Central dopamine blockade, or abrupt loss of dopaminergic therapy, disables thermoregulation and motor control together, so rigid muscle generates heat faster than the body can shed it.

Excess mu-opioid activation blunts the brainstem response to carbon dioxide, so ventilation fails first; naloxone displaces the opioid, but for less time than the opioid lasts.

Paracetamol overdose saturates conjugation and depletes hepatic glutathione, letting the reactive metabolite N-acetyl-p-benzoquinone imine (NAPQI) kill hepatocytes over 24 to 72 hours while the patient still feels well.

Excess central serotonergic activity produces neuromuscular excitation, autonomic instability and altered mental state within hours, and the muscle activity itself generates the hyperthermia that kills.