Comprehensive Pharmacology: Pharmacokinetics, Pharmacodynamics, and Clinical Therapeutics

High-yield vocabulary flashcards detailing core pharmacology concepts: pharmacokinetics (LADME), pharmacodynamics (receptor mechanisms, dose-response relationships), toxicology, autonomic and neuromuscular neurotransmission, and systemic therapeutics (cardiovascular, respiratory, gastrointestinal, and hematologic pharmacology).

Pharmacology (Farmacología)

The study of the effects of chemical substances (drugs) on the biological functions of living organisms.

Clinical Pharmacology (Farmacología clínica)

The branch of pharmacology that evaluates the practical application of drugs in patients to prevent, diagnose, or treat diseases and unwanted physiological processes.

Drug (Fármaco)

Any chemical substance that, upon interacting with an organism, elicits a biological response.

Medicinal Product (Medicamento)

A chemical preparation composed of active pharmaceutical ingredients (API / Principio Activo) plus excipients, formulated for administration to produce a therapeutic effect.

Type A Adverse Drug Reaction

Dose-dependent, predictable pharmacological effects resulting from augmented drug activity (e.g., hypoglycemia induced by insulin, constipation from opioids, or bleeding from anticoagulants).

Type B Adverse Drug Reaction

Dose-independent, unpredictable (bizarre) idiosyncratic or allergic reactions requiring prior sensitization (e.g., penicillin anaphylaxis, metamizole/Nolotil-induced agranulocytosis).

Secondary Effect (Efecto secundario)

An unintended consequence that arises naturally as an indirect outcome of the primary mechanism of action of a drug (e.g., hypokalemia developing from diuretic-induced ion wasting).

Pharmacokinetics (Farmacocinética)

The study of what the organism does to the drug, tracing the time course of drug and metabolite concentrations in biological fluids, tissues, and excreta across the LADME processes (Liberación, Absorción, Distribución, Metabolismo, Excreción).

Pharmacodynamics (Farmacodinamia)

The study of what the drug does to the organism, analyzing how medications act, the intensity with which they produce actions (potency), and their therapeutic or adverse consequences (effects).

Bioavailability ($F$)

The fraction of an administered drug dose that reaches systemic circulation unchanged, and the rate at which this occurs, evaluated on a scale from $0$ to $1$ relative to intravenous administration.

First-Pass Effect (Efecto de primer paso)

The pre-systemic metabolic degradation and elimination of an orally administered drug within the intestinal mucosa and liver via the portal vein before reaching the systemic circulation (e.g., extensive biotransformation of oral nitroglycerin).

Apparent Volume of Distribution ($V_d$)

The theoretical volume of fluid into which the administered drug dose would need to be dissolved to achieve the observed plasma concentration ($V_d = \frac{\text{Amount of drug in body}}{\text{Plasma concentration}}$).

P-glycoprotein (ABCB1)

An ATP-dependent cellular efflux pump that actively extrudes substrates across cell membranes back into the extracellular space, acting as an important resistance mechanism and limiting intracellular drug accumulation.

Plasma Concentration-Time Profile

The pharmacokinetic curve delineating maximum concentration ($\text{C}_{\text{max}}$), time to peak ($\text{T}_{\text{max}}$), area under the curve ($\text{AUC}$, representing total absorbed drug), minimum effective concentration ($\text{MEC/CME}$), minimum toxic concentration ($\text{MTC/CMT}$), latency period, and the therapeutic window.

Linear / First-Order Elimination Kinetics

A kinetic process where the rate of drug elimination is directly proportional to the plasma drug concentration; a constant percentage of drug is cleared per unit time.

Saturable / Zero-Order Elimination Kinetics

A non-linear kinetic process where clearance mechanisms are saturated, causing a constant amount of drug to be eliminated per unit time ($V = \text{constant}$) regardless of concentration (e.g., phenytoin).

Phase I Metabolic Reactions

Non-synthetic enzymatic transformations (oxidation primarily catalyzed by CYP450, reduction, and hydrolysis) that introduce or unmask reactive polar functional groups.

Phase II Metabolic Reactions

Synthetic enzymatic conjugation reactions (such as glucuronidation, acetylation, or sulfation) that covalently attach endogenous hydrophilic moieties to non-polar metabolites to facilitate excretion.

Hepatic Enzyme Inducers

Compounds that accelerate CYP450 enzyme synthesis and metabolic rates, decreasing the circulating concentration and efficacy of co-administered drugs (e.g., phenytoin, phenobarbital, carbamazepine, rifampicin, St. John's wort).

Hepatic Enzyme Inhibitors

Compounds that decrease CYP450 catalytic activity, elevating plasma concentrations and toxicity risk of substrate drugs (e.g., cimetidine, ketoconazole, fluconazole, ritonavir, clarithromycin, fluoxetine).

CYP2C19 Polymorphism & Clopidogrel

A pharmacogenetic variation affecting clopidogrel bioactivation; poor metabolizers generate less active antiplatelet metabolite, creating a significantly elevated risk of thrombosis.

CYP2D6 Polymorphism & Codeine

A pharmacogenetic variation affecting the conversion of codeine to morphine; ultrarapid metabolizers risk life-threatening respiratory depression, while poor metabolizers obtain negligible analgesic relief.

Intrinsic Activity (Actividad intrínseca)

The relative ability of a drug-receptor complex to produce a maximal functional biological response ($1$ for full agonists, between $0$ and $1$ for partial agonists, and $0$ for competitive antagonists).

Drug Potency (Potencia)

The dose or concentration of a drug required to produce an effect of given intensity, quantified inversely by the effective concentration $50\,\%$ ($\text{EC}_{50}$).

Drug Efficacy (Eficacia)

The maximum achievable biological or clinical response ($\text{E}_{\text{max}}$) produced by a drug when all available receptors are occupied.

Competitive Reversible Antagonism

A blockade where the antagonist binds reversibly to the agonist receptor site; increasing the concentration of agonist surmounts the inhibition, retaining $\text{E}_{\text{max}}$ and shifting the concentration-response curve parallelly to the right.

Nicotinic Acetylcholine Receptor Complex

A pentameric ligand-gated ion channel composed of four distinct subunit types ($2\alpha, \beta, \gamma, \delta$) surrounding a central aqueous pore ($\sim 0.7\,\text{nm}$); binding of acetylcholine to the two $\alpha$ subunits triggers rapid $\text{Na}^+$ influx and membrane depolarization.

G-Protein-Coupled Receptor Structure (GPCR)

A transmembrane receptor architecture consisting of seven hydrophobic membrane-spanning $\alpha$-helices, an extracellular $N$-terminal ligand-binding domain, and an intracellular $C$-terminus that couples to heterotrimeric G proteins.

Heterotrimeric G-Protein Activation Cycle

A molecular cycle in which agonist binding stimulates GDP exchange for GTP on the $\alpha$ subunit, causing dissociation of $\alpha\text{-GTP}$ and $\beta\gamma$ complexes to activate downstream effectors until intrinsic GTPase hydrolyzes GTP to GDP, reforming the inactive trimer.

Receptor Tyrosine Kinase (RTK) Signaling

Transmembrane receptors that undergo ligand-induced dimerization followed by intracellular tyrosine autophosphorylation, recruitment of SH2-domain adaptors (such as Grb2), and cascade activation of the Ras/Raf/MEK/MAP kinase pathway.

JAK/STAT Cytokine Receptor Pathway

A signaling mechanism where cytokine binding induces receptor conformational changes that stimulate Janus kinase (JAK) autophosphorylation, phosphorylating receptor docking sites and activating STAT transcription factors that dimerize and translocate to the nucleus.

Voltage-Gated Ion Channel Subunit Architecture

A tetrameric pore structure assembled from four $\alpha$ subunits, each containing six transmembrane domains ($\text{S}_1\text{--S}_6$), in which the positively charged $\text{S}_4$ segment serves as the voltage sensor.

FDA Pregnancy Risk Category X

A classification where animal or human studies have confirmed clear evidence of fetal abnormalities, and where maternal risk distinctly outweighs any potential clinical benefit, rendering the drug absolutely contraindicated during pregnancy.

Noradrenergic Varicosity Signaling Targets

Pharmacological checkpoints at adrenergic terminals, including synthesis inhibition ($\alpha$-methyltyrosine), vesicular storage blockade (reserpine at VMAT), metabolic breakdown (MAO, COMT), reuptake inhibition (NET, EMT), and autoinhibitory presynaptic feedback ($\alpha_2$ receptors).

Presynaptic $\alpha_2$-Adrenergic Autoreceptor

A $G_i$-coupled presynaptic receptor that inhibits adenylyl cyclase and reduces intracellular $\text{Ca}^{2+}$, mediating negative feedback inhibition of norepinephrine exocytosis.

Anticholinergic Syndrome

A toxic clinical syndrome resulting from muscarinic receptor antagonism characterized by dry mouth, mydriasis, hyperthermia, flushed skin, urinary retention, sinus tachycardia, confusion, and delirium, managed centrally with physostigmine.

Suxamethonium (Succinylcholine)

A short-acting depolarizing neuromuscular blocking agent that stimulates nicotinic receptors to cause persistent end-plate depolarization and desensitization, whose paralysis is prolonged by cholinesterase inhibitors.

Sugammadex

A selective cyclodextrin-binding agent designed to encapsulate aminosteroid non-depolarizing neuromuscular blockers (rocuronium, vecuronium) in plasma to rapidly reverse paralysis.

Short-Acting Beta-2 Agonists (SABA)

Inhaled bronchodilators with a duration of $4\text{--}8\,\text{h}$ (e.g., salbutamol, terbutaline) that stimulate adenylyl cyclase, increase intracellular $\text{cAMP}$, and relax bronchial smooth muscle during acute asthma attacks.

Long-Acting Muscarinic Antagonists (LAMA)

Bronchodilators that produce sustained competitive blockade of pulmonary $M_3$ receptors to reduce vagal bronchoconstrictor tone and mucus hypersecretion in COPD and advanced asthma (e.g., tiotropium, aclidinium, glycopyrronium).

CFTR Modulators (Ivacaftor & Lumacaftor)

Targeted therapies for cystic fibrosis; ivacaftor acts as a potentiator to increase CFTR channel gating and chloride transport, while lumacaftor acts as a corrector that improves conformational folding and trafficking of F508del-CFTR proteins to the cell surface.

Pirfenidone

An antifibrotic and anti-inflammatory immunosuppressant that inhibits fibroblast proliferation and profibrogenic cytokine production, used to attenuate the decline of forced vital capacity (FVC) in idiopathic pulmonary fibrosis.

Nintedanib

A triple angiokinase and receptor tyrosine kinase inhibitor that blocks PDGF, FGF, and VEGF receptors, indicated to reduce disease progression and acute exacerbations in idiopathic pulmonary fibrosis.

Proton Pump Inhibitors (IBP)

Lipophilic weak base prodrugs (omeprazole, pantoprazole) that accumulate in parietal cell canaliculi, undergo acid-catalyzed conversion into active sulfonamides, and form irreversible disulfide bonds with the active $\text{H}^+/\text{K}^+\text{-ATPase}$.

Metoclopramide (Primperan)

A prokinetic and antiemetic benzamide that blocks central and peripheral $D_2$ dopamine receptors, stimulates $5\text{-HT}_4$ receptors to facilitate myenteric acetylcholine release, and antagonizes $5\text{-HT}_3$ receptors, carrying risks of extrapyramidal side effects and hyperprolactinemia.

Domperidone

A peripheral dopamine $D_2$ antagonist with prokinetic and antiemetic properties that acts on the area postrema / chemoreceptor trigger zone without crossing the blood-brain barrier, preventing central extrapyramidal motor reactions.

Aprepitant

A selective neurokinin-1 ($\text{NK}_1$) receptor antagonist that blocks substance P binding in the central nervous system, used in combination with dexamethasone and $5\text{-HT}_3$ antagonists to prevent delayed chemotherapy-induced emesis.

Loperamide (Fortasec)

A synthetic peripheral $\mu$-opioid receptor agonist that does not cross the blood-brain barrier, slowing intestinal peristalsis, extending fecal transit time, and increasing water reabsorption to control diarrhea.

N-Acetylcysteine (Toxicology)

The specific antidote for paracetamol poisoning that replenishes hepatic glutathione ($\text{GSH}$) stores to detoxify the hepatotoxic reactive metabolite NAPQI.

Naloxone

A pure competitive opioid receptor antagonist devoid of intrinsic activity, administered intravenously to rapidly reverse opioid-induced central nervous system and respiratory depression.

Flumazenil

A competitive antagonist at the central benzodiazepine recognition site on the $\text{GABA}_A$ receptor complex, utilized for the acute reversal of benzodiazepine-induced sedation and overdose.

Obidoxime & Pralidoxime

Cholinesterase-reactivating oximes that chemically break covalent organophosphate-enzyme bonds, restoring functional acetylcholinesterase activity during organophosphate poisoning.

Angiotensin-Converting Enzyme Inhibitors (IECA)

Antihypertensive agents (captopril, enalapril) that block the conversion of angiotensin I to angiotensin II and inhibit bradykinin breakdown, frequently resulting in a persistent dry cough and rare angioedema.

Angiotensin II Receptor Blockers (ARA-II)

Antihypertensive drugs (losartan, valsartan) that selectively block $\text{AT}_1$ receptors to inhibit angiotensin II-induced vasoconstriction and aldosterone release without increasing bradykinin levels.

Sacubitril/Valsartan (ARNI)

A dual-acting heart failure therapeutic that combines a neprilysin inhibitor (sacubitril, protecting natriuretic peptides from degradation) with an $\text{AT}_1$ blocker (valsartan), proven to decrease cardiovascular death and hospitalizations in HFrEF.

Digoxin (Mechanism in Heart Failure)

A cardiac glycoside that inhibits myocardial $\text{Na}^+/\text{K}^+\text{-ATPase}$, increasing intracellular $\text{Na}^+$ and secondary $\text{Ca}^{2+}$ accumulation via the $\text{Na}^+/\text{Ca}^{2+}$ exchanger to exert positive inotropic and vagomimetic negative chronotropic actions.

Finerenone

A non-steroidal selective mineralocorticoid receptor antagonist that blocks inflammation and fibrosis in the heart, kidneys, and vasculature, indicated to reduce heart failure hospitalizations and renal damage in patients with type 2 diabetes and chronic kidney disease.

Amiodarone

A broad-spectrum Class III antiarrhythmic that blocks voltage-dependent $\text{K}^+$ channels to prolong action potential duration and refractory periods, known for high lipophilicity, a prolonged elimination half-life ($10\text{--}100\,\text{days}$), and risks of pulmonary fibrosis, corneal deposits, and thyroid dysfunction.

Acetylsalicylic Acid (Antiplatelet Mechanism)

An antiplatelet agent that irreversibly acetylates and inactivates platelet cyclooxygenase-1 (COX-1), permanently suppressing the synthesis of prothrombotic thromboxane $A_2$ ($\text{TXA}_2$) throughout the lifespan of the platelet.

Direct Oral Anticoagulants (DOACs)

Anticoagulants that directly target specific coagulation enzymes, including direct thrombin inhibitors (dabigatran) and direct Factor Xa inhibitors (rivaroxaban, apixaban, edoxaban), producing predictable anticoagulation without requiring INR monitoring.

Protamine Sulfate

A positively charged polycationic peptide that forms a stable, inactive chemical chelate with negatively charged unfractionated heparin molecules, acting as a rapid intravenous reversal agent.

HMG-CoA Reductase Inhibitors (Statins)

Lipid-lowering agents (atorvastatin, rosuvastatin) that competitively inhibit 3-hydroxy-3-methylglutaryl-coenzyme A reductase, upregulating hepatic LDL receptors and demonstrating pleiotropic plaque-stabilizing and anti-inflammatory vascular actions.

Alirocumab (PCSK9 Inhibitor)

A monoclonal antibody that binds proprotein convertase subtilisin/kexin type 9 (PCSK9), preventing the degradation of hepatic LDL receptors and significantly enhancing clearance of circulating LDL cholesterol.

Pharmacokinetics (Farmacocinética)

The study of what the body does to the drug ('lo que el organismo hace al fármaco'), examining the time course of drug and metabolite concentrations in biological fluids, tissues, and excreta via the LADME processes (Liberation, Absorption, Distribution, Metabolism, and Excretion).

Pharmacodynamics (Farmacodinamia)

The study of what the drug does to the body ('lo que el fármaco hace al organismo'), investigating biochemical and physiological mechanisms of action, dose-response relationships, potency, and pharmacological effects.

First-Pass Effect (Efecto de Primer Paso)

The enzymatic degradation or hepatic biotransformation of an orally administered drug that occurs in the gut wall or liver via the portal circulation before reaching systemic circulation, resulting in decreased bioavailability.

Volume of Distribution ($V_d$)

A theoretical, non-physiological apparent volume of fluid required to contain the total dose of administered drug at the same concentration measured in blood plasma ($V_d = \frac{\text{Dose}}{\text{Plasma Concentration}}$).

Zero-Order Elimination Kinetics (Orden Cero)

A constant amount of drug eliminated per unit of time regardless of drug plasma concentration, characteristic of saturable, non-linear kinetics (e.g., Fenitoína).

First-Order Elimination Kinetics (Primer Orden)

A constant fraction of drug eliminated per unit of time, where the metabolic rate and rate of clearance are directly proportional to the plasma drug concentration (linear kinetics).

Phase I Reactions (Fase I)

Nonsynthetic enzymatic modifications (principally oxidation, reduction, and hydrolysis) largely mediated by hepatic Cytochrome P450 (CYP450) enzymes that create or expose polar functional groups.

Phase II Reactions (Fase II)

Synthetic conjugation reactions (such as glucuronidation and acetylation) that attach polar endogenous groups to lipophilic compounds or Phase I metabolites to facilitate renal or biliary elimination.

Enzyme Inducer (Fármaco Inductor)

A drug that accelerates hepatic enzymatic metabolism, leading to decreased plasma concentrations and reduced therapeutic effect of co-administered active drugs, or increased effects in the case of prodrugs (e.g., Fenitoina, fenobarbital, carbamacepina, Rifampicina, Hierba de San Juan).

Enzyme Inhibitor (Fármaco Inhibidor)

A substance that impairs CYP450 catalytic activity, leading to increased plasma concentrations and elevated toxicity risks for active substrates, or reduced efficacy for prodrugs (e.g., Cimetidina, Ketoconazol, Ritonavir, Eritromicina).

CYP2C19 Polymorphism

A pharmacogenetic variation affecting Clopidogrel activation; poor metabolizers produce less active antiplatelet metabolite resulting in increased thrombosis risk, whereas ultrarapid metabolizers experience elevated bleeding risk.

CYP2D6 Polymorphism

A genetic variation altering the metabolic conversion of Codeína into active morphine; ultrarapid metabolizers risk life-threatening respiratory depression, while poor metabolizers obtain minimal analgesia.

Therapeutic Window (Margen Terapéutico)

The concentration range between the Minimum Toxic Concentration ($\text{CMT}$) and the Minimum Effective Concentration ($\text{CME}$), requiring close therapeutic drug monitoring when narrow (e.g., Digoxina, litio, valproico, vancomicina).

Potency (Potencia)

A measure of drug concentration or dose required to produce a specified pharmacological response, inversely related to the half-maximal effective concentration ($\text{EC}_{50}$ or $\text{CE}_{50}$).

Efficacy (Eficacia)

The maximum functional therapeutic response ($E_{\max}$) attainable by a drug at receptor saturation, indicating its capacity to induce biological activity.

Competitive Reversible Antagonism

Receptor blockade where the antagonist reversibly competes with the agonist for the same binding site, shifting the concentration-response curve to the right without reducing the maximal achievable response ($E_{\max}$).

Non-Competitive / Irreversible Antagonism

Receptor blockade caused either by covalent binding to the active site or allosteric site binding, preventing receptor activation and depressing the maximal response ($E_{\max}$) regardless of agonist concentration.

Partial Agonist (Agonista Parcial)

A ligand that binds to a receptor but demonstrates lower intrinsic activity than a full agonist, eliciting only a submaximal response even at $100\%$ receptor occupancy (e.g., Buprenorfina).

Nicotinic Acetylcholine Receptor

A pentameric ionotropic receptor composed of $2\alpha, \beta, \gamma, \delta$ subunits surrounding a central pore ($\sim 0.7\,\text{nm}$ diameter); binding of two acetylcholine molecules to the N-terminal domains of the $\alpha$ subunits triggers rapid channel gating and $\text{Na}^+$ influx.

G-Protein Coupled Receptors (GPCR / Metabotrópicos)

Membrane receptors characterized by seven transmembrane $\alpha$-helices, an extracellular amino-terminal ligand-recognition domain, and an intracellular carboxyl-terminal domain coupled to heterotrimeric G-proteins ($\alpha, \beta, \gamma$).

Receptor Tyrosine Kinases (RTK / Tipo III)

Single-pass transmembrane receptors with an extracellular ligand-binding domain and an intracellular enzymatic catalytic domain; agonist binding induces receptor dimerization, tyrosine autophosphorylation, and recruitment of SH2-domain proteins like Grb2.

Nuclear Receptors (Tipo IV / Intracelulares)

Soluble intracellular receptors (Class I in cytosol, Class II in nucleus) containing zinc-finger DNA-binding motifs that modulate gene transcription upon binding lipophilic ligands such as steroid hormones and vitamin D.

Type A Adverse Drug Reactions (Augmented)

Predictable, dose-dependent adverse drug reactions directly related to the known pharmacological action of the drug, exhibiting high incidence and low mortality (e.g., insulin-induced hypoglycemia, morphine constipation).

Type B Adverse Drug Reactions (Bizarre)

Unpredictable, dose-independent idiosyncratic or immunologic reactions unrelated to the drug's primary pharmacology, exhibiting low incidence and potentially high mortality (e.g., penicillin anaphylaxis, metamizole-induced agranulocytosis).

FDA Teratogenicity Category X

A regulatory classification for drugs whose animal or human studies demonstrate definite fetal abnormalities, where fetal risk clearly outweighs any possible maternal therapeutic benefit, making them strictly contraindicated in pregnancy.

Short-Acting Beta-2 Agonists (SABA)

Short-duration ($4\text{--}8\,\text{h}$) bronchodilators that stimulate adenylyl cyclase to elevate intracellular cAMP, lowering intracellular $\text{Ca}^{2+}$ and relaxing airway smooth muscle during acute bronchospasm (e.g., Salbutamol, Terbutalina).

Long-Acting Muscarinic Antagonists (LAMA)

Inhaled bronchodilators that provide extended ($\ge 24\,\text{h}$) blockade of pulmonary $M_3$ muscarinic receptors, inhibiting parasympathetic vagal bronchoconstriction and excessive mucus secretion (e.g., Tiotropio, Aclidinio, Glicopirronio).

Omalizumab

A humanized monoclonal antibody directed against circulating free $\text{IgE}$, blocking its binding to high-affinity receptors on mast cells and basophils; indicated in severe persistent allergic asthma.

CFTR Correctors (Correctores de CFTR)

Small molecules (e.g., Lumacaftor, Tezacaftor) that directly bind mutant CFTR proteins (such as F508del) to correct cellular folding, processing, and membrane trafficking, thereby increasing the number of functional channels on epithelial surfaces.

Pirfenidone

An antifibrotic and anti-inflammatory agent that inhibits fibroblast proliferation, collagen synthesis, and profibrogenic cytokines, used to slow forced vital capacity (FVC) decline in idiopathic pulmonary fibrosis.

Metoclopramide

A substituted benzamide prokinetic and antiemetic that acts as an antagonist at dopamine $D_2$ and serotonin $5\text{-HT}_3$ receptors and an agonist at $5\text{-HT}_4$ receptors, promoting upper GI motility; carries a risk of extrapyramidal adverse effects.

Ondansetron

A selective serotonin $5\text{-HT}_3$ receptor antagonist acting peripherally on vagal nerve terminals and centrally in the chemoreceptor trigger zone (CTZ), widely indicated for chemotherapy-induced and postoperative emesis.

Proton Pump Inhibitors (IBP / Omeprazol)

Prodrugs that concentrate in the acidic secretory canaliculi of gastric parietal cells, converting to active sulfonamide forms that irreversibly inhibit the $\text{H}^+/\text{K}^+\text{-ATPase}$ pump via disulfide bond formation.

Racecadotril

An oral peripheral enkephalinase inhibitor that protects endogenous enkephalins from degradation, activating intestinal $\delta$ opioid receptors to decrease electrolyte and water hypersecretion without slowing GI transit.

Bulk-Forming Laxatives (Incrementadores de la Masa)

Hydrophilic agents (e.g., Plantago ovata, metilcelulosa) that absorb intestinal water to expand fecal volume and stimulate peristalsis; first-line therapy for chronic constipation requiring adequate concurrent fluid intake.

N-Acetylcysteine (N-Acetilcisteína)

The specific antidote for paracetamol toxicity that supplies cysteine to replenish depleted hepatic glutathione ($\text{GSH}$) stores, neutralizing toxic reactive electrophilic metabolites.

Flumazenil

A competitive, pure benzodiazepine receptor antagonist that displaces benzodiazepines from the $\text{GABA}_A$ receptor complex, reversing sedative and CNS depressant effects.