Toxicology is the study of the adverse effects of chemical, physical, or biological agents on living organisms.
Overview and Clinical Importance
Toxicology is the study of the adverse effects of chemical, physical, or biological agents on living organisms. Understanding toxicology general principles is essential for veterinarians because poisoning cases are common in clinical practice and require rapid, evidence-based decision-making. The principles covered in this guide form the foundation for diagnosing and treating all toxicoses.
On the BCSE, toxicology questions frequently test your understanding of toxicokinetics (how the body handles toxicants), dose-response relationships, and decontamination protocols. These concepts integrate with pharmacology, pathology, and emergency medicine domains.
High-YieldDomain 2 (Pharmacology, Physiology, and Toxicology) accounts for 28-32 questions on the BCSE - approximately 14% of the exam. Toxicology principles frequently appear in clinical scenarios across multiple domains.
| Factor |
Clinical Significance |
| Lipid solubility |
Lipophilic compounds cross cell membranes more readily; many toxicants are lipid-soluble |
| Ionization state |
Non-ionized forms absorb better; pH affects ionization (weak acids absorb in acidic stomach, weak bases in alkaline intestine) |
| Molecular size |
Smaller molecules generally absorb more quickly |
| Concentration gradient |
Higher concentrations at absorption site increase rate of passive diffusion |
| Blood flow |
Greater perfusion increases absorption rate; shock decreases absorption |
| GI motility |
Increased motility may decrease absorption time; decreased motility prolongs exposure |
| Vd Value |
Interpretation |
Clinical Example |
| Low (less than 0.6 L/kg) |
Remains in plasma compartment; highly protein-bound |
Warfarin, aspirin - dialysis may be effective |
| Moderate (0.6-1 L/kg) |
Distributes to extracellular fluid |
Aminoglycosides, many antibiotics |
| High (greater than 1 L/kg) |
Extensive tissue binding; accumulates in fat or tissues |
Digoxin, ivermectin, lipophilic drugs - dialysis ineffective |
| Reaction Type |
Description |
Examples |
| Oxidation |
Addition of oxygen or removal of hydrogen; most common Phase I reaction |
Hydroxylation of phenobarbital; N-dealkylation of morphine |
| Reduction |
Addition of hydrogen or removal of oxygen |
Reduction of nitro groups, azo compounds |
| Hydrolysis |
Addition of water to cleave ester or amide bonds |
Procaine hydrolysis by esterases; organophosphate metabolism |
Toxicokinetics
Toxicokinetics describes what the body does to a toxicant - the processes of Absorption, Distribution, Metabolism, and Excretion (ADME). Understanding these processes is crucial for predicting the onset, severity, and duration of toxic effects, as well as guiding treatment decisions.
Memory Aid - ADME Mnemonic
"A Dog May Escape" - Absorption, Distribution, Metabolism, Excretion. This is the same sequence a toxicant follows through the body!
[Include Image: Figure 1. ADME pathway diagram showing absorption from GI tract, distribution to tissues, hepatic metabolism, and renal/biliary excretion]
Absorption
Absorption is the process by which a toxicant enters the systemic circulation from the site of exposure. The rate and extent of absorption depend on the physical and chemical properties of the substance, the route of exposure, and physiological factors.
Key Factors Affecting Absorption
High-YieldBioavailability (F) represents the fraction of toxicant that reaches systemic circulation. IV administration has 100% bioavailability. Oral bioavailability is reduced by first-pass hepatic metabolism.
Distribution
Distribution refers to the movement of a toxicant from the blood to various tissues and organs. The volume of distribution (Vd) describes the theoretical volume required to contain the total amount of drug at the same concentration as in plasma.
Volume of Distribution Interpretation
Memory Aid - Protein Binding
"Only the FREE can flee!" - Only unbound (free) drug is pharmacologically active, can cross membranes, and can be eliminated. Highly protein-bound toxicants have prolonged effects.
High-YieldToxicants with high volumes of distribution are NOT effectively removed by hemodialysis. For dialysis to work, the toxicant must have: low Vd, low protein binding, low molecular weight, and water solubility.
Metabolism (Biotransformation)
Biotransformation is the enzymatic conversion of xenobiotics (foreign substances) into more polar, water-soluble metabolites that can be excreted. The liver is the primary site of biotransformation, though other organs (kidney, lung, intestine) also contribute.
Phase I Reactions (Functionalization)
Phase I reactions introduce or expose a functional group (-OH, -NH2, -SH) through oxidation, reduction, or hydrolysis. These reactions are primarily catalyzed by the Cytochrome P450 (CYP450) enzyme system located in the smooth endoplasmic reticulum of hepatocytes.
[Include Image: Figure 2. Phase I and Phase II biotransformation pathway diagram showing CYP450 reactions and conjugation]
Phase II Reactions (Conjugation)
Phase II reactions involve conjugation of the parent compound or Phase I metabolite with an endogenous polar molecule. These reactions typically produce inactive, highly polar metabolites ready for excretion.
Memory Aid - Phase I vs Phase II
"Phase I: Function, Phase II: Fashion" - Phase I adds functional groups (makes it functional), Phase II adds fashionable accessories (conjugates) to dress it up for elimination!
High-YieldCATS LACK GLUCURONIDATION! Cats have deficient UDP-glucuronosyltransferase activity, making them highly susceptible to toxicity from drugs metabolized by this pathway (e.g., acetaminophen, aspirin, phenol-containing compounds, benzoic acid preservatives).
Bioactivation (Lethal Synthesis)
Some compounds become MORE toxic after metabolism - this is called bioactivation or lethal synthesis. Understanding this concept is crucial for treating specific toxicoses.
Memory Aid - Ethylene Glycol Treatment Rationale
"EtOH blocks the ALCOHOL DEHYDROGENASE" - Ethanol or fomepizole competitively inhibits alcohol dehydrogenase, preventing formation of toxic metabolites. Treatment must be given BEFORE metabolites form!
Excretion
Excretion is the removal of toxicants and their metabolites from the body. The primary routes are renal (urine) and hepatobiliary (bile/feces), with minor contributions from pulmonary (exhaled air), mammary (milk), and dermal routes.
Renal Excretion Mechanisms
Memory Aid - Ion Trapping for Enhanced Excretion
"ABBA" - Alkalinize urine for Basic drug toxicity is WRONG! Actually: Alkalinize for Acids (aspirin), Acidify for Bases. Weak ACIDS (like aspirin) are trapped in ALKALINE urine because the ionized form cannot be reabsorbed.
Enterohepatic Recirculation
Some toxicants excreted in bile are reabsorbed from the intestine and returned to the liver, prolonging their effects. This is called enterohepatic recirculation. Examples include: NSAIDs, digoxin, some rodenticides, and amatoxin (mushroom toxin). Multiple doses of activated charcoal can interrupt this cycle.
High-YieldHalf-life (t1/2) is the time required for plasma concentration to decrease by 50%. It takes approximately 5 half-lives to eliminate 97% of a toxicant from the body. Clinical signs may persist longer due to tissue binding.
| Conjugation Type |
Enzyme |
Clinical Notes |
| Glucuronidation |
UDP-glucuronosyltransferase (UGT) |
Most common Phase II reaction; CATS ARE DEFICIENT - causes prolonged effects of many drugs |
| Sulfation |
Sulfotransferase (SULT) |
Limited capacity; saturates at high doses |
| Glutathione conjugation |
Glutathione-S-transferase (GST) |
Critical detoxification pathway; GSH depletion leads to toxicity (acetaminophen) |
| Acetylation |
N-acetyltransferase (NAT) |
Genetic polymorphisms (fast/slow acetylators) affect drug toxicity |
| Methylation |
Methyltransferases |
Important for catecholamines and histamine |
| Parent Compound |
Toxic Metabolite(s) |
Clinical Significance |
| Ethylene glycol |
Glycolaldehyde, glycolic acid, glyoxylic acid, oxalic acid |
Metabolites cause metabolic acidosis and calcium oxalate crystal formation |
| Methanol |
Formaldehyde, formic acid |
Formic acid causes blindness and severe metabolic acidosis |
| Acetaminophen |
N-acetyl-p-benzoquinoneimine (NAPQI) |
NAPQI depletes glutathione causing hepatotoxicity |
| Bromethalin |
Desmethyl bromethalin |
Metabolite is more potent uncoupler of oxidative phosphorylation |
| Organophosphates (some) |
Oxon metabolites |
Desulfuration creates more potent acetylcholinesterase inhibitors |
| Mechanism |
Description |
Clinical Relevance |
| Glomerular filtration |
Passive filtration of unbound, small molecules |
Only free (unbound) drug is filtered; protein binding reduces excretion |
| Tubular secretion |
Active transport of organic acids and bases into tubular lumen |
Can be saturated; drug interactions at transporters |
| Tubular reabsorption |
Passive diffusion of lipophilic compounds back into blood |
pH manipulation (ion trapping) can enhance elimination |
Dose-Response Relationships
The dose-response relationship is a fundamental concept in toxicology, summarized by Paracelsus (1493-1541): "All things are poison, and nothing is without poison; the dose alone makes a thing not poison." This principle means that any substance can be toxic at a sufficiently high dose.
[Include Image: Figure 3. Sigmoid (S-shaped) dose-response curve showing threshold, linear portion, ED50/LD50, and plateau]
Key Dose-Response Terms
Memory Aid - LD50 Interpretation
"The LOWER the LD50, the LOUDER the alarm!" - A low LD50 means the substance is highly toxic (kills at low doses). Example: Botulinum toxin LD50 = 0.00001 mg/kg (extremely toxic) vs. Water LD50 = 90,000 mg/kg (practically nontoxic).
Therapeutic Index and Margin of Safety
The therapeutic index (TI) measures the relative safety of a drug. It is calculated as: TI = LD50/ED50 (or TD50/ED50). A larger therapeutic index indicates a wider margin between therapeutic and toxic doses.
High-YieldDrugs with NARROW therapeutic indices require careful dosing and monitoring. Examples include: digoxin, phenobarbital, aminoglycosides, theophylline, and chemotherapeutics. These are more likely to cause toxicity in clinical practice.
Dose-Response Curve Characteristics
Most dose-response curves are sigmoid (S-shaped) when plotted on a logarithmic scale. The curve shape provides important information about toxicity patterns:
- Steep slope: Small dose increase causes large response change (more dangerous)
- Shallow slope: Gradual response change with dose (more predictable)
- Potency: Position along the x-axis; more potent toxicants have curves shifted left
- Efficacy/Maximum effect: Height of the plateau (maximum response achievable)
| Term |
Definition |
Clinical Application |
| LD50 |
Lethal Dose for 50% of test population; expressed as mg/kg body weight |
Compares acute toxicity between substances; smaller LD50 = more toxic |
| TD50 |
Toxic Dose for 50%; dose causing a specific toxic effect in 50% of population |
Used when endpoint is toxicity rather than death |
| ED50 |
Effective Dose for 50%; dose producing desired effect in 50% of subjects |
Basis for therapeutic dosing |
| NOAEL |
No Observed Adverse Effect Level; highest dose with no adverse effects |
Used to establish safe exposure limits |
| LOAEL |
Lowest Observed Adverse Effect Level; lowest dose causing adverse effects |
Establishes lower boundary of toxicity |
| Threshold |
Dose below which no observable toxic effect occurs |
Assumed for most toxicants except carcinogens |
| Drug Example |
Therapeutic Index |
Clinical Implication |
| Digoxin |
Narrow (approximately 2-3) |
Requires careful dosing and monitoring; toxicity common |
| Phenobarbital |
Narrow (approximately 2-3) |
Anticonvulsant with risk of sedation/respiratory depression |
| Penicillin |
Wide (greater than 100) |
Very safe at therapeutic doses; dose flexibility |
| Metronidazole |
Moderate |
Generally safe but neurotoxicity at high doses |
| Route |
Onset |
Key Considerations |
Decontamination |
| Oral (Ingestion) |
Variable (minutes to hours) |
Most common in small animals; affected by gastric contents, pH, formulation |
Emesis, gastric lavage, activated charcoal |
| Dermal (Topical) |
Variable; may be delayed |
Lipophilic compounds absorb readily; damaged skin increases absorption |
Bathing with dish soap; clip hair if needed |
| Inhalation |
Rapid (seconds to minutes) |
Large surface area of lungs; gases and volatile compounds |
Remove from source; oxygen therapy |
| Parenteral (Injection) |
Very rapid (IV immediate) |
Bypasses absorption barriers; 100% bioavailability IV |
Limited options; supportive care |
| Ocular |
Rapid local; variable systemic |
Corneal damage from caustics; systemic absorption possible |
Copious irrigation (20-30 minutes) |
| Envenomation |
Minutes to hours |
Snake/spider bites; depth of injection affects spread |
Antivenin; supportive care |
Routes of Exposure
The route of exposure significantly affects the rate of absorption, onset of clinical signs, and appropriate decontamination methods. Understanding route-specific considerations is essential for case management.
High-YieldFor ORAL exposures, emesis is generally effective only within 1-2 hours of ingestion for rapidly absorbed substances. However, some toxicants (grapes/raisins, chocolate, extended-release medications) may remain in the stomach longer, extending the window for decontamination.
Memory Aid - When NOT to Induce Emesis
"CANS Cannot vomit safely" - Caustics (acids/bases), Altered consciousness, Neurologic signs (seizures), Sharp objects/petroleum products. These are contraindications to emesis induction!
| Hepatotoxin |
Mechanism |
Clinical Findings |
| Acetaminophen |
NAPQI metabolite depletes glutathione; centrilobular necrosis |
Elevated ALT/AST; methemoglobinemia in cats; treat with N-acetylcysteine |
| Xylitol |
Unknown mechanism; massive hepatic necrosis in dogs |
Hypoglycemia (rapid onset) followed by hepatic failure (24-72 hours) |
| Amatoxin (mushrooms) |
Inhibits RNA polymerase II; prevents protein synthesis |
Delayed onset (6-24 hr); severe hepatic failure; high mortality |
| Blue-green algae (microcystins) |
Inhibits protein phosphatases; massive hepatocyte necrosis |
Acute hepatic failure; often fatal within hours |
| Aflatoxins (mycotoxins) |
Hepatocellular damage and carcinogenesis |
Acute liver failure or chronic disease/cancer with long-term exposure |
| Nephrotoxin |
Mechanism |
Clinical Findings |
| Ethylene glycol |
Oxalic acid metabolite precipitates as calcium oxalate crystals in tubules |
Acute kidney injury; oliguria/anuria; calcium oxalate crystalluria |
| Lilies (cats) |
Unknown nephrotoxin; acute tubular necrosis |
ALL parts toxic to cats; AKI within 24-72 hours; often fatal |
| Grapes/raisins |
Unknown; idiosyncratic acute tubular necrosis in dogs |
Variable sensitivity; some dogs severely affected, others not |
| NSAIDs |
Inhibit prostaglandins needed for renal blood flow |
Papillary necrosis; decreased GFR; especially risky with dehydration |
| Aminoglycosides |
Accumulate in proximal tubular cells; cause necrosis |
Non-oliguric AKI; granular casts; usually reversible if caught early |
| Neurotoxin |
Mechanism |
Clinical Signs |
| Organophosphates/Carbamates |
Inhibit acetylcholinesterase; accumulation of acetylcholine |
SLUDGE/DUMBELS signs; treat with atropine and pralidoxime (OPs) |
| Permethrin (cats) |
Sodium channel prolongation; repetitive nerve firing |
Tremors, seizures, hyperthermia; cats lack glucuronidation |
| Metaldehyde |
GABA inhibition; decreased serotonin |
Severe tremors, seizures, hyperthermia (snail bait toxicity) |
| Bromethalin |
Uncouples oxidative phosphorylation; cerebral edema |
Tremors progressing to paralysis, seizures; no antidote |
| Ivermectin (MDR1 dogs) |
GABA agonist; crosses BBB in susceptible breeds |
Ataxia, blindness, coma; herding breeds at risk (Collies, Shelties) |
| Lead |
Multiple mechanisms; interferes with heme synthesis and nerve function |
GI signs and neurologic signs; nucleated RBCs, basophilic stippling |
Target Organ Toxicity
Target organ toxicity refers to the preferential accumulation of toxic effects in specific organs. Certain organs are particularly vulnerable due to their high blood flow, metabolic activity, or concentration mechanisms.
[Include Image: Figure 4. Diagram showing major target organs for toxicity (liver, kidney, nervous system, heart) with common toxicant examples]
Hepatotoxicity (Liver)
The liver is the most common target organ for toxicity because: (1) it receives blood directly from the GI tract via the portal vein, (2) it is the primary site of biotransformation, and (3) hepatocytes can bioactivate compounds to toxic metabolites.
Memory Aid - Hepatotoxicity Markers
"All Labs Tell Stories" - ALT (most liver-specific), AST, ALP (biliary), Bilirubin, Bile Acids (function test). Elevated liver enzymes indicate hepatocellular damage; decreased albumin and prolonged PT indicate hepatic dysfunction.
Nephrotoxicity (Kidney)
The kidneys are vulnerable because they receive 25% of cardiac output, concentrate toxicants in tubular fluid, and have active transport mechanisms that can accumulate certain compounds in tubular cells.
High-YieldLILIES ARE EXTREMELY TOXIC TO CATS! All parts of true lilies (Lilium and Hemerocallis species) can cause acute kidney injury. Even small exposures (pollen on fur that is groomed off) can be fatal. Early aggressive fluid therapy is critical.
Neurotoxicity (Nervous System)
Memory Aid - Cholinergic Toxidrome (SLUDGE/DUMBELS)
"SLUDGE" - Salivation, Lacrimation, Urination, Defecation, GI upset, Emesis. Also "DUMBELS" - Diarrhea, Urination, Miosis, Bradycardia (or bronchospasm), Emesis, Lacrimation, Salivation. Think of organophosphates and carbamates!
Cardiotoxicity (Heart)
High-YieldSPECIES SENSITIVITY varies greatly. Horses are extremely sensitive to ionophores (monensin toxicity is often fatal). Cats cannot tolerate permethrin. Dogs lack the ability to vomit when they have eaten certain toxins. Always consider species differences!
| Cardiotoxin |
Mechanism |
Clinical Findings |
| Cardiac glycosides (digitalis, oleander) |
Inhibit Na+/K+-ATPase; increase intracellular calcium |
Bradycardia, AV block, ventricular arrhythmias; treat with digoxin-specific Fab |
| Chocolate (theobromine) |
Methylxanthine; adenosine receptor antagonist, PDE inhibitor |
Tachycardia, arrhythmias, hyperactivity, seizures; dogs more sensitive |
| Ionophores (monensin) |
Disrupt ion gradients; myocardial necrosis |
Cardiomyopathy; horses extremely sensitive; no specific treatment |
| Beta-blockers |
Block cardiac beta-1 receptors |
Bradycardia, hypotension, hypoglycemia; glucagon for treatment |
| Emetic Agent |
Species |
Dose |
Notes |
| Apomorphine |
Dogs |
0.03-0.04 mg/kg IV; 0.25 mg/kg conjunctival |
Emetic of choice in dogs; reversed by naloxone |
| Hydrogen peroxide 3% |
Dogs only |
1-2 mL/kg PO (max 45 mL) |
OTC option; may cause gastric irritation; do not use in cats |
| Xylazine |
Cats |
0.44 mg/kg IM |
Only 50% effective; causes sedation; reverse with atipamezole |
| Dexmedetomidine |
Cats |
5-10 mcg/kg IM or SC |
Alternative to xylazine; reverse with atipamezole |
| Parameter |
Details |
| Standard Dose |
1-2 g/kg PO; may give with cathartic (sorbitol) for first dose |
| Multiple Dose Protocol |
1 g/kg every 4-6 hours for 24-48 hours for enterohepatic recirculation toxins |
| Effective Against |
Most organic compounds, alkaloids, barbiturates, salicylates, theophylline, NSAIDs, chocolate |
| NOT Effective Against |
Heavy metals, alcohols, petroleum products, strong acids/bases, xylitol, salt, fertilizers |
| Contraindications |
Altered mentation (aspiration risk), GI perforation, ileus, dehydration, will interfere with oral antidotes |
General Decontamination and Supportive Care
The management of poisoned patients follows the same principles as any emergency: stabilize the patient first, then prevent further toxicant absorption, enhance elimination, provide specific antidotes when available, and deliver supportive care.
[Include Image: Figure 5. Flowchart showing approach to the poisoned patient - stabilization, decontamination decision tree, supportive care]
Initial Stabilization
Always address life-threatening problems first, regardless of the suspected toxicant:
- Airway: Ensure patent airway; intubate if necessary
- Breathing: Provide oxygen; assist ventilation if hypoventilating
- Circulation: IV access; fluid therapy for hypotension; treat arrhythmias
- Disability (neurologic): Control seizures; protect from injury
- Exposure/Environment: Thermoregulation; prevent continued exposure
Gastrointestinal Decontamination
Emesis Induction
Emesis is most effective when performed within 1-2 hours of ingestion. Effectiveness decreases over time but may still be beneficial for substances that remain in the stomach longer.
Memory Aid - Emesis Contraindications
"CHIPS Cannot Vomit" - Caustics (acids/alkalis), Hydrocarbons/petroleum products, Impaired consciousness, Prior vomiting (extensive), Sharp objects, Seizure risk. These patients need alternative decontamination methods!
Activated Charcoal
Activated charcoal adsorbs toxicants in the GI tract, preventing systemic absorption. It is most effective when given within 1 hour of ingestion but may be beneficial for several hours depending on the toxicant.
High-YieldActivated charcoal does NOT bind: heavy metals (iron, lead, lithium, zinc), alcohols (ethanol, methanol, ethylene glycol), petroleum products, cyanide, strong acids/bases, or xylitol. Know these exceptions!
Gastric Lavage
Gastric lavage is reserved for cases where emesis is contraindicated but removal of gastric contents is critical. The patient must be anesthetized and intubated with a cuffed endotracheal tube to protect the airway. It is less effective than emesis and should be performed within 1-2 hours of ingestion for maximum benefit.
Dermal and Ocular Decontamination
Enhanced Elimination Techniques
High-YieldIntravenous Lipid Emulsion (ILE) therapy has revolutionized treatment of lipophilic toxicoses. Standard protocol: 20% lipid emulsion, 1.5 mL/kg IV bolus over 1 minute, followed by 0.25 mL/kg/min CRI for 30-60 minutes. Monitor for pancreatitis and lipemia.
Common Antidotes
Memory Aid - Anticoagulant Rodenticide Treatment
"Vitamin K1 for 4 weeks minimum!" - Treatment duration depends on the generation: first-generation (warfarin) = 2-3 weeks; second-generation (brodifacoum, bromadiolone) = 4-6 weeks due to longer half-life. Check PT at 48-72 hours after stopping treatment.
Supportive Care Essentials
Most poisoned patients require supportive care as the foundation of treatment, regardless of whether a specific antidote exists:
- IV fluid therapy: Correct dehydration, support blood pressure, enhance renal excretion
- Thermoregulation: Cooling for hyperthermia (metaldehyde, serotonin syndrome); warming for hypothermia
- Antiemetics: Maropitant or metoclopramide for intractable vomiting
- Gastroprotectants: Omeprazole, sucralfate for GI irritation/ulceration
- Seizure control: Diazepam or midazolam first-line; phenobarbital or propofol for refractory seizures
- Analgesia: Opioids preferred; avoid NSAIDs in patients with potential renal compromise
- Monitoring: Serial assessments of vital signs, blood glucose, electrolytes, acid-base status
| Exposure Type |
Decontamination Protocol |
| Dermal (skin) |
Bathe with liquid dish soap and warm water; rinse thoroughly. Clip hair if necessary (long-haired animals). Use PPE to protect staff. Multiple baths may be needed for oily substances. |
| Ocular (eye) |
Irrigate with saline or water for minimum 20-30 minutes. Assess for corneal damage with fluorescein. Alkaline substances (caustic) cause more severe damage than acids. |
| Technique |
Mechanism/Use |
Examples |
| IV fluid diuresis |
Increases urine output to enhance renal excretion |
Most toxicants with renal elimination |
| Urinary alkalinization |
Sodium bicarbonate increases urine pH to trap weak acids in ionized form |
Aspirin, phenobarbital |
| Multiple-dose activated charcoal |
Interrupts enterohepatic recirculation; GI dialysis |
Phenobarbital, theophylline, digoxin |
| Hemodialysis |
Removes small, water-soluble, minimally protein-bound toxicants |
Ethylene glycol, methanol, salicylates |
| Intravenous lipid emulsion |
Creates lipid sink for lipophilic toxicants |
Ivermectin, permethrin, local anesthetics, baclofen |
| Antidote |
Toxicant |
Mechanism |
| N-acetylcysteine (NAC) |
Acetaminophen |
Replenishes glutathione; provides sulfhydryl groups for conjugation |
| Fomepizole or Ethanol |
Ethylene glycol, Methanol |
Competitive inhibition of alcohol dehydrogenase; prevents toxic metabolite formation |
| Atropine |
Organophosphates, Carbamates |
Competitive muscarinic receptor antagonist; controls SLUDGE signs |
| Pralidoxime (2-PAM) |
Organophosphates only |
Reactivates acetylcholinesterase before aging; give within 24-48 hours |
| Vitamin K1 |
Anticoagulant rodenticides |
Cofactor for synthesis of clotting factors II, VII, IX, X |
| Naloxone |
Opioids |
Competitive opioid receptor antagonist; short duration of action |
| Flumazenil |
Benzodiazepines |
Competitive benzodiazepine receptor antagonist |
| Atipamezole |
Alpha-2 agonists |
Alpha-2 receptor antagonist; reverses dexmedetomidine, xylazine |
| Digoxin-specific Fab |
Cardiac glycosides |
Binds and inactivates digoxin and related compounds |
| Methylene blue |
Methemoglobinemia |
Reduces methemoglobin to hemoglobin; use cautiously in cats |