Complete Pharmacology Guide for CRNA School Interviews

Comprehensive vocabulary flashcards covering general pharmacology concepts, receptor subtypes, vasoactive drugs, antihypertensives, anti-arrhythmics, paralytics, sedatives, opioids, and anticoagulants designed for CRNA school interview preparation.

Ligand

A molecule (e.g., a drug) that binds to a specific receptor, initiating a response.

Agonist

A drug that binds and activates a receptor, mimicking the action of an endogenous ligand (such as a neurotransmitter or hormone) to produce a response.

Antagonist

A drug that binds to a receptor and prevents other molecules (i.e., agonists) from binding, thereby preventing an endogenous chemical response and producing a physiologic consequence.

Endogenous Substance

A substance that is naturally produced within the body, such as the neurotransmitter GABA or catecholamines like norepinephrine.

Exogenous Substance

A substance introduced into the body from an external source, such as a synthetic or administered drug like Levophed.

Selective Agonist

An agent that activates a single receptor type (e.g., phenylephrine is a selective $\alpha_1$-adrenergic agonist).

Non-Selective Agonist

An agent that activates multiple receptor types (e.g., norepinephrine activates both $\alpha_1$ and $\beta_1$ receptors).

Chronotropy

An increase in heart rate.

Inotropy

An increase in the strength or force of myocardial contraction (contractility).

Lusitropy

The ability of the heart to relax after contraction (diastolic relaxation).

Dromotropy

The rate at which impulses are conducted through the heart's conduction system, specifically through the AV node.

Sympathomimetic

Drugs that mimic the effects of the sympathetic nervous system by stimulating adrenergic receptors or increasing endogenous catecholamines (e.g., epinephrine, norepinephrine, phenylephrine, dopamine).

Vasopressor

Drugs that increase blood pressure primarily by increasing systemic vascular resistance (SVR) through vasoconstriction.

Inotrope

Drugs that increase myocardial contractility, thereby increasing cardiac output (CO).

Ligand-Gated Ion Channels

Integral membrane proteins that serve as ion channels; ligand binding induces a conformational change that opens or closes the channel to allow ions ($\text{Na}^+$, $\text{K}^+$, $\text{Cl}^-$) to flow across the membrane, altering membrane potential (e.g., $\text{GABA}_A$ receptor).

G-Protein Coupled Receptors (GPCR)

A large family of cell surface receptors composed of seven transmembrane domains associated with a G-protein; ligand binding activates the G-protein and triggers intracellular cascades involving second messengers such as $\text{cAMP}$ (e.g., $\alpha_1$ receptor).

Enzyme-Linked Receptors

Receptors possessing both a ligand-binding domain and an enzymatic activity domain; binding activates the enzymatic domain to initiate intracellular signaling cascades (e.g., receptor tyrosine kinases binding insulin).

Intracellular (Nuclear) Receptors

Receptors located within the cell nucleus activated by lipophilic ligands (e.g., steroid hormones like testosterone) that cross the cell membrane and regulate gene expression by binding DNA sequences.

$\alpha_1$ Adrenergic Receptor

A G-protein coupled receptor located on vascular smooth muscle; agonism increases $\text{DAG}$ and $\text{IP}_3$, elevating intracellular $\text{Ca}^{2+}$ to increase smooth muscle tone, causing vasoconstriction, increased SVR, and elevated blood pressure.

$\alpha_2$ Adrenergic Receptor

A G-protein coupled receptor located on pre- and postsynaptic neurons; presynaptic stimulation decreases norepinephrine release (causing sedation and analgesia), while postsynaptic stimulation reduces sympathetic outflow from the CNS (causing decreased blood pressure and bradycardia).

$\beta_1$ Adrenergic Receptor

A G-protein coupled receptor located in the heart; agonism activates adenylate cyclase, increasing $\text{cAMP}$ and intracellular $\text{Ca}^{2+}$, leading to increased inotropy, chronotropy, dromotropy, and lusitropy.

$\beta_2$ Adrenergic Receptor

A G-protein coupled receptor located in the lungs and vasculature; agonism activates adenylate cyclase, increasing $\text{cAMP}$ which decreases intracellular $\text{Ca}^{2+}$, resulting in smooth muscle relaxation, bronchodilation, and vasodilation.

$V_1$ Receptor

A G-protein coupled receptor located on vascular smooth muscle targeted by vasopressin, causing vasoconstriction and increased blood pressure.

$V_2$ Receptor

A G-protein coupled receptor located in renal collecting ducts; activation causes insertion of aquaporin-2 ($\text{AQP2}$) channels into the apical membrane, promoting water reabsorption.

$D_1$ Receptor

A dopamine receptor subtype located in renal, mesenteric, and coronary vasculature; low doses of dopamine stimulate this receptor to produce vasodilation, increasing renal blood flow, GFR, $\text{Na}^+$ excretion, and urine output.

Phenylephrine (Neo-Synephrine)

A pure $\alpha_1$-adrenergic agonist vasopressor administered as a $50\text{--}200\,\text{mcg}$ bolus or $20\text{--}200\,\text{mcg/min}$ infusion for hypotension and distributive shock; notable for causing reflex bradycardia.

Norepinephrine (Levophed)

A mixed $\alpha_1 > \beta_1$ adrenergic agonist infused at $0.05\text{--}0.5\,\text{mcg/kg/min}$; the first-line vasopressor for septic shock when $\text{MAP} < 65\,\text{mmHg}$ despite fluid resuscitation.

Epinephrine

A potent mixed adrenergic agonist with dose-dependent receptor affinity ($\le 0.05\,\text{mcg/kg/min}$: $\beta_1 > \beta_2 > \alpha_1$; $> 0.05\,\text{mcg/kg/min}$: $\alpha_1 > \beta_1 > \beta_2$); used in anaphylaxis, cardiac arrest, and distributive shock.

Dopamine

An inotrope/vasopressor with dose-dependent receptor activity: low dose ($0.5\text{--}2\,\text{mcg/kg/min}$) acts on $D_1$ receptors; intermediate dose ($5\text{--}10\,\text{mcg/kg/min}$) acts on $\beta_1$; high dose ($> 10\,\text{mcg/kg/min}$) acts on $\alpha_1$.

Dobutamine

A predominantly $\beta_1 > \beta_2$ adrenergic agonist inotrope administered at $2\text{--}20\,\text{mcg/kg/min}$ for cardiogenic shock and decompensated heart failure; increases cardiac output while decreasing SVR and PVR.

Milrinone

A phosphodiesterase-3 (PDE-3) inhibitor inodilator that prevents the breakdown of $\text{cAMP}$; increases myocardial contractility while decreasing SVR, afterload, and PVR without increasing myocardial oxygen demand directly.

Isoproterenol

A pure $\beta_1$ and $\beta_2$ adrenergic agonist administered at $0.01\text{--}0.2\,\text{mcg/kg/min}$ for refractory bradycardia and AV block; increases heart rate and contractility while decreasing SVR.

Selective $\alpha_1$ Blockers

Sympatholytic antihypertensives (e.g., prazosin, doxazosin, terazosin) that inhibit norepinephrine binding on vascular smooth muscle, decreasing intracellular $\text{Ca}^{2+}$ and causing vasodilation; carry a risk of first-dose syncope and reflex tachycardia.

Non-Selective $\alpha$ Blockers

Agents including phenoxybenzamine (irreversible) and phentolamine (reversible) that block both $\alpha_1$ and presynaptic $\alpha_2$ receptors; the $\alpha_2$ blockade increases norepinephrine release, exacerbating reflex tachycardia; indicated for pheochromocytoma.

Selective $\beta_1$ Blockers

Cardioselective agents (e.g., metoprolol, esmolol, atenolol) that block cardiac $\beta_1$ receptors to reduce $\text{cAMP}$ and $\text{Ca}^{2+}$ influx, leading to negative chronotropy, inotropy, and dromotropy while sparing bronchial $\beta_2$ receptors.

Non-Selective $\beta$ Blockers

Agents (e.g., propranolol) that block both $\beta_1$ and $\beta_2$ receptors; blocking $\beta_2$ receptors can trigger bronchoconstriction (contraindicated in severe asthma/COPD) and mask hypoglycemic symptoms in diabetics.

Mixed $\alpha$ and $\beta$ Blockers

Antihypertensive agents (e.g., labetalol, carvedilol) that provide non-selective $\beta$-blockade along with selective $\alpha_1$-blockade, lowering blood pressure via vasodilation while attenuating reflex tachycardia.

Dihydropyridine Calcium Channel Blockers

Calcium channel blockers ending in '-dipine' (e.g., nicardipine, amlodipine) that selectively block L-type voltage-gated $\text{Ca}^{2+}$ channels in arterial smooth muscle, causing peripheral vasodilation and decreased SVR.

Non-Dihydropyridine Calcium Channel Blockers

Agents (verapamil, diltiazem) that primary target L-type $\text{Ca}^{2+}$ channels in cardiac myocytes, the SA node, and the AV node, resulting in decreased heart rate, slowed conduction velocity, and reduced contractility.

Hydralazine

A direct-acting arteriolar vasodilator that inhibits $\text{IP}_3$-mediated $\text{Ca}^{2+}$ release from the sarcoplasmic reticulum in smooth muscle, reducing afterload and SVR without significantly dilating veins.

Nitroglycerin

A potent venodilator that is converted to nitric oxide ($\text{NO}$) in vascular smooth muscle, stimulating guanylyl cyclase to increase $\text{cGMP}$ and reduce intracellular $\text{Ca}^{2+}$, primarily lowering cardiac preload.

Sodium Nitroprusside

A balanced mixed arterial and venous dilator that spontaneously releases $\text{NO}$ in the blood to increase $\text{cGMP}$, reducing both preload and afterload; prolonged or high-dose infusions carry a risk of cyanide toxicity.

ACE Inhibitors

Antihypertensives ending in '-pril' (e.g., lisinopril, enalapril) that block the conversion of angiotensin I to angiotensin II, reducing vasoconstriction and aldosterone release; associated with hyperkalemia, angioedema, and a dry cough from bradykinin accumulation.

Angiotensin II Receptor Blockers (ARBs)

Antihypertensives ending in '-sartan' (e.g., losartan, valsartan) that selectively block angiotensin II type 1 ($\text{AT}_1$) receptors, preventing vasoconstriction and aldosterone release without inhibiting bradykinin breakdown.

Cardiac Myocyte Action Potential

An electrical cycle consisting of Phase 0 (rapid $\text{Na}^+$ influx depolarization), Phase 1 (initial $\text{K}^+$ efflux repolarization), Phase 2 (plateau via $\text{Ca}^{2+}$ influx balanced by $\text{K}^+$ efflux), Phase 3 ($\text{K}^+$ efflux repolarization), and Phase 4 (resting membrane potential).

Class 1 Anti-Arrhythmics

Fast sodium ($\text{Na}^+$) channel blockers (e.g., lidocaine, procainamide, quinidine) that depress the Phase 0 upstroke velocity in ventricular myocytes and Purkinje fibers, decreasing conduction velocity.

Class 3 Anti-Arrhythmics

Potassium ($\text{K}^+$) channel blockers (e.g., amiodarone) that prolong Phase 3 repolarization, thereby increasing action potential duration, the effective refractory period, and the QT interval.

Lidocaine

A Class 1b anti-arrhythmic that blocks fast $\text{Na}^+$ channels to suppress ventricular arrhythmias (VT/PVCs); CNS toxicities (tinnitus, perioral numbness, seizures) typically precede signs of cardiac toxicity.

Amiodarone

A Class 3 anti-arrhythmic with multi-class properties (blocks $\text{Na}^+$, $\beta$-receptors, $\text{K}^+$, and $\text{Ca}^{2+}$ channels); effective for ventricular and supraventricular arrhythmias, but associated with pulmonary fibrosis, thyroid dysfunction, and hepatotoxicity.

Adenosine

An endogenous nucleoside that stimulates $A_1$ receptors in the AV node, enhancing $\text{K}^+$ efflux and reducing $\text{Ca}^{2+}$ influx to produce transient AV block; administered as a $6\,\text{mg}$ rapid IV push (followed by $12\,\text{mg}$ if needed) for stable narrow-complex SVT.

Neuromuscular Junction (NMJ)

The specialized synapse between a motor neuron axon terminal and the motor end plate of a skeletal muscle fiber where acetylcholine release triggers muscle contraction.

Acetylcholinesterase

The enzyme located within the synaptic cleft that terminates the action of acetylcholine by rapidly hydrolyzing it into choline and acetate.

Succinylcholine

The only clinical depolarizing neuromuscular blocker; binds post-junctional nicotinic receptors causing persistent depolarization (initial fasciculations followed by flaccid paralysis); metabolized by pseudocholinesterase; triggers malignant hyperthermia and can elevate serum $\text{K}^+$ by $0.5\,\text{mEq/L}$.

Rocuronium

An aminosteroid non-depolarizing neuromuscular blocker that competitively antagonizes nicotinic receptors on the motor end plate; dosed at $1\text{--}1.2\,\text{mg/kg}$ for RSI; primarily eliminated unchanged in bile via the liver; rapidly reversed by sugammadex.

Cisatracurium (Nimbex)

A benzylisoquinolinium non-depolarizing neuromuscular blocker that undergoes organ-independent Hofmann elimination in plasma and tissue, making it ideal for patients with significant hepatic or renal impairment; degrades into laudanosine.

Propofol (Diprivan)

An IV hypnotic sedative that binds $\text{GABA}_A$ receptors to enhance chloride influx, hyperpolarizing neuronal membranes; causes profound vasodilation, decreases ICP and cerebral blood flow, and carries no analgesic efficacy.

Etomidate

A $\text{GABA}_A$ agonist hypnotic agent favored for induction in hemodynamically unstable patients due to minimal cardiovascular side effects; causes transient adrenocortical suppression, precluding continuous infusion use.

Ketamine

A non-competitive NMDA receptor antagonist that inhibits glutamate to induce dissociative anesthesia; preserves respiratory drive and bronchodilates while increasing heart rate, blood pressure, cardiac output, and intracranial pressure.

Dexmedetomidine (Precedex)

A selective $\alpha_2$-adrenergic agonist that produces sedation and hypnosis via the locus ceruleus and analgesia via the spinal cord; mimics natural physiologic sleep with minimal to no respiratory depression.

Flumazenil

A competitive antagonist at the benzodiazepine receptor site on $\text{GABA}_A$ complexes; administered at $0.2\,\text{mg}$ IV increments to reverse benzodiazepine-induced sedation, with a risk of precipitating acute withdrawal or rebound seizures.

Naloxone (Narcan)

A pure competitive opioid receptor antagonist used to reverse opioid-induced ventilatory depression; duration of action ($45\text{--}60\,\text{min}$) is often shorter than that of long-acting opioids, posing a risk of renarcotization.

Unfractionated Heparin (UFH)

An injectable anticoagulant that binds to and accelerates antithrombin III, thereby inactivating thrombin (Factor IIa) and Factor Xa; monitored using the aPTT and fully reversible with protamine sulfate.

Enoxaparin (Lovenox)

A low-molecular-weight heparin (LMWH) that binds antithrombin III to preferentially inhibit Factor Xa over Factor IIa; administered subcutaneously and does not require routine aPTT monitoring.

Warfarin

An oral anticoagulant that acts as a vitamin K antagonist, inhibiting the hepatic synthesis of vitamin K–dependent clotting factors (II, VII, IX, X) and proteins C and S; monitored via the PT/INR and reversed with vitamin K, FFP, or PCC.

Aspirin

An antiplatelet agent that irreversibly inhibits cyclooxygenase-1 (COX-1), blocking the production of thromboxane $A_2$ and thereby suppressing platelet aggregation for the lifespan of the platelet ($7\text{--}10\,\text{days}$).

Clopidogrel (Plavix)

An oral antiplatelet thienopyridine that irreversibly inhibits the platelet $P2Y_{12}$ ADP receptor, preventing ADP-mediated activation of the glycoprotein IIb/IIIa complex.

tPA (Alteplase)

A recombinant tissue plasminogen activator fibrinolytic that cleaves plasminogen into active plasmin, which directly degrades fibrin clots in acute ischemic stroke, massive PE, and STEMI.