Drug cards

What it is for: Acute anxiety, seizures, severe alcohol withdrawal, and procedural sedation.

How it works: Binds an allosteric site on the GABA-A receptor and enhances the inhibitory effect of GABA, increasing chloride influx and calming neuronal firing.

First-line: First-line for acute seizures and severe alcohol withdrawal. Short-term anxiolysis and procedural sedation.

Note: Used for short, targeted windows because of dependence risk; never stop abruptly after chronic use.

What it is for: Hypertension, angina, heart failure (selected), arrhythmias, migraine prophylaxis.

How it works: Blocks beta-1 (and some beta-2) adrenergic receptors, blunting catecholamine effects on heart rate and contractility - slowing the heart and reducing oxygen demand.

First-line: First-line for stable angina and rate control in tachyarrhythmias; mainstay in heart failure (selected) and post-MI.

Note: Do not stop abruptly - rebound can provoke angina or acute coronary events.

What it is for: Asthma/exacerbations, autoimmune flares, allergic reactions, and cerebral edema.

How it works: Crosses the cell membrane, binds a cytoplasmic receptor, and alters gene transcription in the nucleus - broadly dampening inflammation and immune activity.

First-line: First-line for many acute inflammatory and allergic emergencies, and an empirical 'test' of inflammatory disease.

Note: Steroids treat inflammation, not the cause; taper after prolonged use to avoid adrenal crisis.

What it is for: Acute ischemic stroke, massive myocardial infarction, and massive pulmonary embolism.

How it works: Converts plasminogen to plasmin, which degrades the fibrin mesh of a clot, restoring blood flow through the occluded vessel.

First-line: Emergency reperfusion when done fast - time is brain and time is muscle. Used when benefit outweighs bleeding risk.

Note: Time-critical and risk-stratified; used after imaging rules out bleeding.

What it is for: Empiric coverage of suspected serious bacterial infection while cultures are pending.

How it works: Most target bacterial-specific structures or processes human cells lack - the cell wall, or bacterial enzymes/ribosomes - killing or stalling the bacteria.

First-line: Empiric for the most dangerous suspected pathogens, then narrowed once the organism is identified.

Note: The discipline is to narrow therapy as soon as cultures identify the organism to spare the microbiome and slow resistance.

What it is for: Autoimmune disease and transplant rejection - calming the immune system when it attacks the body.

How it works: Range from broad agents that blunt immune cells to targeted drugs (like B-cell depleting rituximab) that block specific steps in the inflammatory cascade.

First-line: Cyclophosphamide for severe vasculitis and lupus nephritis; mycophenolate for lupus and transplant rejection.

Note: Every immunosuppressant trades disease activity for infection vulnerability - patients are monitored closely.

What it is for: Influenza A prophylaxis/treatment (historical) and Parkinsonian symptoms.

How it works: Blocks viral M2 ion channel and enhances dopamine release/re-uptake blockade, improving motor symptoms.

First-line: Not generally first-line today; reserved for specific Parkinson or influenza settings.

Note: Has a narrow therapeutic margin - toxicity (including cardiac and neurologic effects) can be severe at high levels.

What it is for: Moderate to severe pain, cough suppression, and sedation. Hydrocodone is the fictional backbone of House's chronic pain (Vicodin).

How it works: Bind mu-opioid receptors in the brain and spinal cord, reducing pain signaling, slowing respiration, and producing euphoria. Tolerance develops because receptors down-regulate and adapt.

First-line: Mainstay for moderate-severe pain when used appropriately, but carries dependence and overdose risk.

Note: Naloxone is the opioid antidote and reverses respiratory depression. Chronic use causes tolerance, so escalating doses are needed for the same effect - the mechanism behind House's escalating Vicodin use.

What it is for: Anticoagulants prevent or limit thrombosis; thrombolytics actively dissolve an existing clot. Choice depends on the clinical goal and timing.

How it works: Heparin activates antithrombin to block clotting factors; warfarin blocks vitamin-K-dependent clotting-factor synthesis; DOACs directly inhibit factor Xa or thrombin. Thrombolytics (like tPA) convert plasminogen to plasmin to break down existing fibrin clots.

First-line: Anticoagulants for prevention/treatment of DVT, PE, AF, and after certain strokes; thrombolytics for acute STEMI (when PCI delayed), massive PE, and acute ischemic stroke within the time window.

Note: The key distinction: anticoagulants stop new clot from forming; thrombolytics dissolve clot that already exists. Anticoagulation and thrombolysis are different, and thrombolysis carries far higher bleeding risk.

What it is for: Specific antidotes for specific poisonings - used alongside supportive care.

How it works: Naloxone reverses opioid effects at mu receptors; flumazenil reverses benzodiazepine sedation at GABA-A; N-acetylcysteine replenishes glutathione to prevent hepatotoxicity in acetaminophen overdose; glucagon raises blood sugar and can reverse beta-blocker/calcium-channel-blocker poisoning.

First-line: Naloxone: opioid overdose (first-line); N-acetylcysteine: acetaminophen overdose; flumazenil is used selectively (can precipitate seizures in mixed/sedative-hypnotic or chronic benzodiazepine use).

Note: Antidotes are specific, time-sensitive tools embedded in supportive care - knowing which poison each reverses is core toxicology.