32 drugs with mechanisms, doses, pearls, and NBRC high-yield facts.
ProAir, Proventil, Ventolin, AccuNeb
Selective beta-2 adrenergic agonist. Activates adenylyl cyclase → increases cAMP → smooth muscle relaxation and bronchodilation. Also stabilizes mast cells.
Xopenex
Pure R-enantiomer of racemic albuterol. Binds beta-2 receptors with greater affinity than the S-isomer. S-isomer (in racemic albuterol) may contribute to some adverse effects. Bronchodilation via cAMP-mediated smooth muscle relaxation.
Atrovent
Quaternary ammonium anticholinergic (antimuscarinic). Blocks muscarinic M3 receptors in airway smooth muscle → prevents acetylcholine-mediated bronchoconstriction. Also reduces mucus secretion.
Spiriva
Long-acting muscarinic antagonist (LAMA). Dissociates very slowly from M1 and M3 receptors, providing prolonged bronchodilation. Blocks parasympathetic bronchoconstriction and reduces mucus hypersecretion.
Serevent Diskus
Long-acting selective beta-2 adrenergic agonist. Long lipophilic side chain anchors it to cell membrane near receptor, allowing sustained receptor activation. Increases cAMP → bronchial smooth muscle relaxation.
Foradil, Perforomist, Symbicort (with budesonide)
Long-acting selective beta-2 agonist. Faster onset than salmeterol due to partial hydrophilicity. Activates adenylyl cyclase → cAMP → airway smooth muscle relaxation.
DuoNeb, Combivent Respimat
Combination of beta-2 agonist (albuterol) and anticholinergic (ipratropium). Dual bronchodilation via complementary mechanisms: albuterol relaxes smooth muscle via cAMP; ipratropium blocks muscarinic bronchoconstriction.
Pulmicort, Rhinocort, Symbicort (with formoterol), QVAR (beclomethasone — different)
Synthetic glucocorticoid. Binds intracellular glucocorticoid receptors → nuclear translocation → reduces transcription of inflammatory genes (cytokines, chemokines). Decreases airway eosinophilia, mast cell activity, and mucus production.
Flovent, Flonase, Advair (with salmeterol), Breo (with vilanterol)
High-potency synthetic glucocorticoid. High receptor binding affinity (approximately 3× beclomethasone). Reduces airway inflammation via glucocorticoid receptor-mediated gene regulation.
Solu-Medrol, Medrol (oral)
Synthetic glucocorticoid. Binds cytoplasmic glucocorticoid receptors → nuclear translocation → modifies transcription. Anti-inflammatory: reduces cytokine production, leukocyte migration, vascular permeability. Relative potency: 5× cortisol.
Deltasone, Rayos
Oral glucocorticoid prodrug, converted to active prednisolone in liver. Same mechanism as methylprednisolone. Potency: 4× cortisol.
Decadron, Dexasone
Potent synthetic glucocorticoid with no mineralocorticoid activity. 25–30× potency of cortisol. Penetrates CNS well. Long duration of action. Reduces inflammation and edema.
Mucomyst, Acetadote (IV)
Free thiol group cleaves disulfide bonds in mucus glycoproteins → reduces mucus viscosity. As antidote: replenishes glutathione stores → prevents hepatotoxicity from NAPQI (acetaminophen toxic metabolite).
Pulmozyme
Recombinant human DNase I enzyme. Cleaves extracellular DNA (from neutrophil breakdown) that contributes to the viscosity of CF sputum. Reduces sputum viscoelasticity without affecting mucin or disulfide bonds.
HyperSal, MucoClear
Osmotic agent. Draws water into airway lumen → rehydrates periciliary liquid layer → restores mucociliary clearance. Also reduces sodium absorption and may reduce airway surface liquid depletion.
Survanta
Natural bovine lung surfactant extract. Contains phospholipids (primarily DPPC), neutral lipids, fatty acids, and surfactant proteins SP-B and SP-C. Reduces alveolar surface tension → prevents alveolar collapse at end-expiration.
Infasurf
Natural bovine lung surfactant extract. Contains phospholipids and surfactant proteins SP-B and SP-C. Reduces alveolar surface tension to near-zero during expiration, preventing end-expiratory alveolar collapse.
Curosurf
Natural porcine surfactant extract. Highest phospholipid concentration of available surfactants (~80 mg/mL). Contains SP-B and SP-C. Reduces surface tension at the alveolar air-liquid interface.
INOmax, Genosyl
Endogenous signaling molecule. Inhaled NO diffuses into pulmonary vascular smooth muscle → activates guanylyl cyclase → increases cGMP → vasodilation. Effect is selective to ventilated lung segments, improving V/Q matching.
Flolan, Veletri
Synthetic prostacyclin (PGI2). Binds prostacyclin receptors on pulmonary vascular smooth muscle → increases cAMP → vasodilation. Also inhibits platelet aggregation.
Revatio (PAH), Viagra (erectile dysfunction)
Phosphodiesterase-5 (PDE-5) inhibitor. PDE-5 degrades cGMP in smooth muscle. By inhibiting PDE-5 → increased cGMP → smooth muscle relaxation and vasodilation. Potentiates effect of nitric oxide in pulmonary vasculature.
Adrenalin, EpiPen, Auvi-Q
Endogenous catecholamine. Activates alpha-1 (vasoconstriction), beta-1 (increased HR and contractility), and beta-2 (bronchodilation) receptors. Dose-dependent effects: low doses primarily beta; high doses alpha-dominant.
Levophed
Endogenous catecholamine. Predominantly alpha-1 and alpha-2 agonist → peripheral vasoconstriction → increased MAP. Minimal beta-2 effects (no bronchodilation). Some beta-1 effects (inotropic) at high doses.
Intropin
Endogenous catecholamine precursor. Dose-dependent receptor activation: low doses (1–5 mcg/kg/min): dopaminergic D1 receptors → renal/mesenteric vasodilation. Moderate doses (5–10 mcg/kg/min): beta-1 → increased contractility and HR. High doses (>10 mcg/kg/min): alpha-1 → vasoconstriction.
Dobutrex
Synthetic catecholamine. Primarily beta-1 agonist (inotropic and chronotropic). Mild beta-2 effects (mild vasodilation). Negligible alpha effects — does NOT raise SVR.
Diprivan
General anesthetic/sedative. Potentiates GABA-A receptor activity → CNS depression. Mechanism not fully understood but primarily GABAergic. Provides sedation, hypnosis, and anticonvulsant properties. Has intrinsic bronchodilatory properties.
Versed
Benzodiazepine. Positive allosteric modulator of GABA-A receptors → enhances chloride influx → CNS depression. Provides anxiolysis, sedation, amnesia, and anticonvulsant effects. No analgesic properties.
Sublimaze (IV), Duragesic (patch), Actiq (lozenge)
Synthetic opioid. Binds mu-opioid receptors in CNS and periphery → analgesia via decreased pain signal transmission, altered pain perception. Also produces sedation, euphoria, respiratory depression, and GI effects.
Precedex
Selective alpha-2 adrenergic agonist. Activates central (locus coeruleus) alpha-2 receptors → decreased norepinephrine release → sedation and anxiolysis. Peripheral alpha-2 activation → decreased sympathetic outflow and pain signal transmission.
Anectine, Quelicin
Depolarizing neuromuscular blocking agent. Structurally mimics acetylcholine. Binds and persistently activates nicotinic receptors at neuromuscular junction → initial muscle fasciculations → sustained depolarization → flaccid paralysis (phase I block).
Zemuron
Non-depolarizing neuromuscular blocking agent. Competitive antagonist at nicotinic acetylcholine receptors at neuromuscular junction. Blocks ACh binding → prevents end-plate depolarization → flaccid paralysis. No fasciculations.
Norcuron
Non-depolarizing neuromuscular blocking agent. Competitive antagonist at nicotinic ACh receptors. Structurally similar to pancuronium but without vagolytic effects (no tachycardia).
Lasix
Loop diuretic. Inhibits Na+/K+/2Cl− cotransporter (NKCC2) in the thick ascending limb of Loop of Henle → blocks reabsorption of Na+, K+, and Cl− → profound diuresis. Also reduces preload via venodilation (acute effect).
Heliox
Mixture of helium (60–80%) and oxygen (20–40%). Helium is less dense than nitrogen. Lower gas density reduces turbulent flow (decreases Reynolds number) and resistance to flow in large airways. Enhances laminar flow through narrowed airways → reduces work of breathing.
Various
Divalent cation. Physiological calcium antagonist in smooth muscle → inhibits calcium-mediated bronchoconstriction → bronchodilation. Also inhibits mast cell and T-lymphocyte activation. Reduces neuromuscular transmission at high doses.
Cafcit
Methylxanthine. Competitively antagonizes adenosine receptors (A1 and A2A) in CNS → stimulates respiratory drive (chemoreceptor sensitivity to CO2). Also increases diaphragmatic contractility and reduces hypoxic depression of breathing.