Poisons produced by a biologic source (venoms, plant toxins, etc...)

Synonymous terms for the disease produced by a toxicant 

Amount of a toxicant necessary to produce a detrimental effect

All toxic effects are dose dependent

Effects during the first 24-hr period 

Effects produced by prolonged exposure (greater than or equal to 3 months)

Absorption: May occur through the alimentary tract, skin, lungs, via the eye, mammary gland, or uterus

Distribution: Via the bloodstream. Knowledge of the distribution characteristics of toxicants is necessary for proper selection of organs for analysis

Metabolism: Metabolism or biotransformation of toxicants bu the body is an "attempt to detoxify"

Excretion: Toxicants and metabolites is by the way of the kidneys, digestive tract, and some via milk

Dose: Primary concern

Route: Affects absorption, translocation, and perhaps metabolic pathways

Duration & Frequency

Age, size and health of animal: Capabilities of liver and kidneys vary with age, species, and health. Amont of toxicant required to cause pathology is generally correlated to body weight

Telephone triage

Assess the patient

Stabalize the patient

Prevent toxicant absorption: Oral exposure (emetics, gastric levage, activated charcoal). Dermal or ocular exposure (bathe and ocular flush)

Monitoring

Supportive therapy

Plants (Arrow, Johnson, and Sorghum grass)

Fertilizers & Pesticides

Apricots, peaches, chokecherries, and elderberry leaves and seeds/pits

Eucaluptus spp. (Implicated in small animals)

Toxin produced: Cyanogenic glycosides produced when cell structure is disrupted (freezing, chomping, or chewing)

Signs occur within 15-20 minutes - few hours after consume toxic forage

Bright, cherry red mucous membranes *

Excitement, tachypnea, dyspnea, tachycardia

Salivation, lacrimation, voiding feces and urine

Death (whole process doesn't last longer than 30-45 min)

* Dr. Christensen said this would be the most important one to know

Must be immediate

Break the cyanide-cytochrome oxidase bond and free cytochrome osidase to transport oxygen for respiration

Sodium nitrite IV

Sodium thiosulfate IV

DMAP IM

Hydroxylamine hydrochlorine IM

All animals susceptible (most common in cats & dogs)

Antifreeze, solvents, rust removers

Toxic dosages (dog = 4-6ml/kg, cat = 2.5ml/kg)

History (owner may have witnessed ingestion, pet may be walking drunk, vomiting lethargy, anorexia, and seizures)

Stage 1: 30 minutes-12 hours post ingestion. PU/PD, depression, incoordination, atazia, paresis, seizures, coma, hypothermia

Stage 2: 12-24 hours. Tachypnea, tachycardia, pulmonary edema, and congestion

Stage 3: 24-72 hours. Depression dehydration, vomiting, oliguric renal failure, seizures. May palpate enlarged and painful kidneys. 

Laboratory findings

Calcium oxalate crystalluria

In house detection kit

Ultrasound

Supportive therapy

Antidote: Fomepizole or ethanol within 8 hrs of ingestion

Grave prognosis if patient exhibiting clinical signs

Guarded prognosis if presents within 1-2 hours after ingestion

Toxic products: Methylxanthines (theobromine and caffeine)

Mode of action: Stimulates CNS, acts on the kidneys to stimulate diuresis, and increase contractility of cardiac and skeletal muscle

Unsweetened>Dark>Milk>White

6-12 hours post-ingestion

PU/PD, vomiting, diarrhea, restlesness

Hyperactivity, ataxia, tremors, seizures

Tachycardia, premature ventricular conractions, tachypnea, cyanosis, hypertension, hyperthermia, coma

Pancreatitis due to high fat content

Death due to cardiac arrythmias or respiratory failure

Symptomatic and supportive: Decontamination. Thermoregulation, fluids, monitor cardiac status, urinary catheterization, seizure/tremor control

Leaves, fruit, stems, and seeds: Leaves most toxic

Toxic componenet: Persin (fatty acid derivative)

Clinical signs: Vomiting/diarrhea, inflammatory mammory glands (rabbits, goats, cattle, horses), cardiac failure (goats, sheep, horses), and respiratory distress (birds - very toxic)

Treatment: Symptomatic and supportive

Happens only in some dogs

Mechanism: Unknown; primary injury proximal renal tubular cells

Clinical signs: Affected dogs develop anuric renal failure within 72 hrs of ingestion. Vomiting/diarrhea: 6-12hrs. Lethargy, anorexia, abdominal pain, weakness, dehydration, polydipsia, tremors

Treatment: Decontamination, fluid diuresis for 48 hrs, dopamine or furosemide to stimulate urine production

Farm animals: Ingest parasitic fungus that has replaces grain or seed of rye or forage plants

Mechanism of action: Vasoconstriction of arterioles*. Initially reduces blood flow which leads to complete necrosis of the extremities due to thrombosis.

Clinical signs: Lameness, swelling and tenderness of fetlock and pastern joints. Sloughing distal limbs, ear tips, and tail

Control: Ergot free diet

Unknow toxin

Clinical signs: Vomiting - hours after exposure. Oliguric to anuric renal failure: 24-72 hrs (ataxia, seizures, hypothermia, dehydration). Death or euthanasia: 3-6 days after ingestion

Treatment: Supportive/Symptomatic (treat for kidney failure at least 48 hrs). Delaying treatment beyond 18 hrs frequently results in death/euthanasia due to severe kidney failure

Toxin: N-propyl disulfide

Clinical signs: Lethary, diarrhea. Delayed signs (hemolytic anemia, jaundice, ataxia, collapse, death)

Susceptibility: Cattle>Horses & Dogs>Sheep & Goats

Treatment: Supportive care, blood transfusions, anti-oxidants

Types: Anticoagulants - warfarin, brodifacoum, bromadiolone (inhibition of the recycling of vitamin K1 which inhibits activation of vitamin K coagulation factors. Hemorrhage most commonly into body cavities and lungs

Bromethalin - Inhibition of efficient production of ATP. Neurologic (seizures and paralysis)

Cholecalciferol  - Vit D3. Increased intestinal absorption of calcium resulting in hypercalcemia

Clinical signs: Anemia, weakness, depression, anorexia, petechiation, melena, hematuria, epistaxis, hyphema, hemothorax, hematemesis

Treatment/Antidote: Vitamin K1, transfusions

Types: Ibuprogen, aspiren, acetaminophen, naproxen, carprofen

Mode of action: Inhibitor of cyclo-oxygenase. Prostaglandins production is blocked (which can result in GI, liver, or renal toxicity.

ONE 325 mg Tylenol will kill a cat!: 50 mg/kg toxic dosage; 25 mg/kg for aspirin

NEVER mix NSAIDs or use in conjunction with steroids!

Gastrointestinal: Vomiting, diarrhea

Anorexia, depression, ataxia, seizures

Death, renal failure

Cats are more sensitive than dogs: 1-4 hrs post-ingestion develop signs. Methemoglobinemia (cyanosis, chocolate brown blood color, heinz body anemia, death can occur within 18-36 hrs with Tylenol)

Decontamination: Emesis, lavage, charcoal

Antidote: For Tylenol: N-acetylcysteine

Liver protectants

Ascorbic acid (Vitamin C)

Supportive therapy: Fluid therapy, correct acidosis, oxygen therapy, stomach protectants

Sugar substitute: Gum, candy, baking products

Mechanism of action: Rapid dose-dependent insulin release followed by potentially significant hypoglycemia

Clinical signs: Vomiting, weakness, disorientation, seizures, elevated hepatic enzymes, coagulation abnormalities. Symptoms develop in 30 minutes--can last 12 hrs. May cause hepatic necrosis in 8-12 hrs.

Treatment: Emesis, bolus IV dextrose then dextrose CRI, potassium suplimentation, liver protectans

Hypoglycemia = 0.1g/kg

Liver injury = 0.5 g/kg

Flea/tick shampoos, dips, foggers, topical, sprays: Often due to application of dog products, cats that overgroom or exposed to recently treated dogs

Clinical signs: Hypersalivation, depression, tremors, hyperthermia, vomiting, seizures, possibly death. Onset signs within a few hours but may be delayed up to 24 hrs.

Treatment: Decontamination, supportive care (bathe with Dawn dish soap, thermoregulation, IV fluids), control tremors and seizures (intravenous lipid solutions)

Most live if treated

Pesticides with a narrow margin of safety: 

Clinical signs: Cholinergic overstimulation, muscarinic (hypersalivation, miosis, frequent urination, increased secretions, etc...), Nicotinic - muscle fasiculation and weakness, CNS

Treatment: Decontamination, supportive therapy, Atropine 2-PAM

Cigarettes, chewing tobacco, patches

Mechanism of action: Rapidly absorbed across the respiratory tracts, skin and MM, and small intestine. Depolarizing action within the CNS

Clinical signs: Agitation, hypersalivation, vomiting, diarrhea, ataxia, tremors, weakness, seizures, tachycardia, hypertension (bradycardia and hypotension have been reported)

Treatment: Decontamintaion, IV fluids, symptomatic care. Nicotine has a short half-life, patients that survive the first 4-6 hrs have improved prognosis.

Enzootic hematuria: Most common poisoning; cattle most common. Weak, febrile, lose weight, labored breathing, pale MM

Bright blindness: Tapetal hyperreflectivity (most common in sheep)

Bracken staggers: Neurologic diseas in monogastrics; anorexia, weight loss, incoordination, crouching stance while arching back, trembling

Treatment: Discontinue exposure, thiamine-horses, blood or platelet transfusion-cattle. Essentially untreatable. 

Prevent exposure!