Offline Medication Study Lab · Top 300 of 2024

Medication Mastery

300 ranked outpatient drugs, pharmacology review cards, mechanisms, warnings, recall practice and a deeper physiology lens. Includes selected emergency/critical-care teaching where appropriate.

Study tool, not a prescribing reference. Doses shown are examples for selected medications, not instructions for an actual patient. Most cards explicitly defer drug-specific dose/route verification. Formulation, indication, renal/hepatic function, allergies and local policy change decisions. Some cards are class overviews or unverified placeholders; see each card's review status. This is not a 300-drug clinical monograph set.

300 medicines

Flashcard 1

What is its class, mechanism and major safety warning?

Flashcards use the available content of each card. They are not validated NCLEX test items.

Deep physiology primers

Receptor signaling: α1, β1, β2

α1 is Gq-coupled: PLC → IP3/DAG → Ca²⁺-dependent smooth-muscle contraction. β1 is Gs-coupled: cAMP/PKA increases nodal pacemaking and myocyte calcium handling. β2 is Gs-coupled: cAMP/PKA suppresses myosin light-chain kinase activity in smooth muscle, promoting bronchodilation and selected vascular relaxation. The same cAMP signal produces different effects because the downstream machinery differs by tissue.

Hemodynamics: preload, afterload, contractility

MAP roughly depends on cardiac output × systemic vascular resistance; cardiac output is heart rate × stroke volume. Venodilators mainly reduce preload, arteriolar dilators mainly reduce afterload, and inotropes change contractility. Reflexes, ventilation, right ventricular function and disease state can alter the response dramatically. Hemodynamic numbers must be interpreted with perfusion, not alone.

Pharmacokinetics in advanced practice

Separate bioavailability, volume of distribution, clearance, elimination half-life and context-sensitive decrement time. The same drug can behave differently when given as one bolus versus a long infusion, in shock, obesity, liver failure or kidney dysfunction. Protein binding, active metabolites and transporters matter. Receptor affinity does not by itself predict clinical effect or safety.

Ion channels and action potentials

Fast cardiac myocytes: phase 0 mostly Na⁺ entry, phase 2 Ca²⁺ plateau and phase 3 K⁺ repolarization. SA/AV nodal phase 0 is Ca²⁺-dependent. Class I antiarrhythmics affect Na⁺ channels, class III prolong repolarization largely through K⁺ currents, class IV nondihydropyridine calcium blockers slow nodal conduction. Blockade may be state- and rate-dependent.