Toxicology

Phenoxyacetic acid herbicides

-2,4-D (scotts weed and feed), 2,4,5-T, Silvex -Low toxicity in most animals -cattle exposed to >20mg/kg for multiple days show clinical signs -Lethal dose is 100mg/kg for cattle but is over 500mg/kg for chickens and pigs -Normally causes weeds to overgrow so quickly they cannot maintain growth rate and die

Mechanism of action of Gossypol

-A chronic toxicosis. Plasma gossypol with time an is cumulative since it is lipophilic -Chelates iron and causes anemia, reduced protein availability -produces toxicity by inhibition of dehydrogenase leading to decreased energy and protein production; oxidative stress -Non ruminant are more sensitive

Ionophore toxicity

-Act my increasing intracellular Na+ and Ca++a, leading to mitochondrial swelling and cell death especially in muscle -LD50 is 1-2mg/kg -Usually result of feed-mixing errors -Poultry are the last sensitive to ionophore toxicity

Clinical signs of Aspirin toxicity

-Acute: nausea, vomiting, anorexia, fever and respiratory stimulation with high doses. Depression, lethargy, seizure, coma. Acidosis with anion gap. Reduced renal flow and renal failure -Chronic: gastric irritation and ulceration are the most common problems. Anemia, bone marrow depression, heinz bodies, thrombocytopenia in cats. -Toxic dose for dogs is 50mg/kg/day and 25 mg/kg/day for cats

How to treat CNS depression

-Analeptics -Doxapram to increase respiratory rate

Diagnosing ELEM

-Analysis of feed for fumonisin in conjunction with clinical signs -Severe liver injury and lesions: elevated serum cholesterol levels and increased ALP, ALT, sorbitol dehydrogenase, GGT and total bilirubin and bile acids -Post-mortem CNS necrosis and liquefaction

Treatment of clostridium tetani

-Antitoxin at early stages -Supportive therapy -prognosis is very poor

Things that can cause ventilatory muscle paralysis

-Botulism, tetanus, snake venom, OP insecticides, strychnine

Acute Renal Failure

-Characterized by decreased GFR and renal azotemia -Caused by transient damage to tubule, glomerulus, or vasculature -signs are vomiting, GI bleeding, polyuria/polydipsia, progressing to anuria, diarrhea, and tremors

Diagnosing NSAID toxicity

-Clinical signs -Anion gap due to acidosis -Increase in liver enzymes, jaundice -Decreased blood clotting time -Acute renal failure

Clinical signs of cardiac glycoside toxicity

-Clinical signs can occur from 1hr to weeks after ingestion -hyperkalemia is the hallmark sign -trembling, staggering, and dyspnea -Increase in Ca++ and intracellular Na+ -racing heart, and rhythm/arrythmia, weak pulse

Clinical signs of Slaframine toxicity

-Copious salivation "slobbers" sometimes the only sings -May see feed refusal -bloat, diarrhea, frequent urination

Why is the Proximal convoluted tubule prone to injury

-Cytochrome P450 and cysteine conjugated B-lyase are found here. Bioactivation results in damage -Loose epithelium allows compounds to move back and forth through the tissue causing more damage -It transports anions, cations, and heavy metals which can accumulate and cause injury to epithelial cells

Two disease caused by Fumonosin

-Equine leucoencephalomalacia -Porcine pulmonary edema

Prognosis of ethylene glycol toxicity

-For cats survival rate is highly dependent on treatment within the first 3-4 hours but mortality rate is at least 90% -In dogs survival is most likely if treatment is started within 6-8 hrs of ingestion. If azotemia is present at examination survival is slim. Those that survive will likely have renal failure -For luck survivors therapy can take up to 72 hours. Recovery can take 3-5 days if treated aggressively

Nitrate toxicosis

-Found in fertilizers, many plants, contaminated water -Nitrate gets converted to nitrite which causes vasodilation and oxidized ferrous iron in hemoglobin to the ferric state forming methemoglobin resulting in oxygen starvation of tissues -Susceptibility goes in order of pigs>cattle>sheep>horses

Mycotoxins

-Fungal metabolites which cause pathological, physiological and/or biochemical alterations usually on several organ systems -Can affect all species -There have been outbreaks of aflatoxins in dog foods and peanut butter

Tremorgenic mycotoxins

-Fungi of genera Penicillium, aspergillum, Claviceps -cause release of neurotransmitters from synaptosomes in the CNS -Clinical signs include diminished activity and immobility followed by hyper excitability, muscle tremor, ataxia, tetanic seizires, convulsions

Treatment of phenoxyacetic acid toxicity

-GI (emesis, lavage) or dermal (bath) decontamination -Activated charcoal/cathartic -ion trapping to enhance excretion: 1-2mEq/kg NaHCO3 if kidneys are normal. Avoid if kidneys are damages -Prognosis is good for treated animals

Treatment of cardiac glycoside toxicity

-GI decontamination -Treat arrhythmias with propranolol -treat hyperkalemia if needed -Use digoxin immune FAb fragments if propranolol is ineffective (antidote for digoxin and other glycosides)

Treatment of Cantharidin

-GI decontamination and protection (sucralfate) and antibiotics

Treating Ivermectin toxicity

-GI decontamination for recent exposures with activated charcoal -Supportive care including fluid and electrolyte therapy. Epinephrine and short-acting barbiturate (no benzodiazepam) -Prognosis for non susceptible breeds good if exposed to less than 5mg/kg but guarded for an breed of dog that has ingested more than 5mg/kg -test dogs if you are going to administer high dose of ivermectin

Treating anti-esterase toxicity

-GI decontamination, bathing for dermal exposure -Atropine sulfate for muscarinic signs, will not stop nicotinic signs -Oximes can reactivate AChE -Diazepam or barbiturates for seizures -Time

treating arsenic toxicity

-GI decontamination: emesis followed by activated charcoal and cathartic -Chelation therapy with antidote dimercaprol -Sodium thiosulfate before clinical signs -Supportive therapy -Prognosis is poor once symptoms appear

Treatment for methylxanthine toxicity

-GI decontamination: induce emesis -Monitor EKG: treat arrhythmias with lidocaine; if this fails use metoprolol -treat seizures with diazepam or barbiturates -Maintain respiration -Fluid diuresis may increase excretion

Clinical signs of phenoxyacetic acid toxicity

-GI effects: vomiting, diarrhea that may be bloody, oral and GI ulcerations -Muscle effects: hesitates to move and rigid skeletal muscles. Ataxia weakeness, posterior weakness -Seizures at high doses -Myotonia with serious toxicosis -Rumen atony -Renal tubular degeneration -hepatic necrosis

Treatment of Nitrate toxicity

-IV methylene blue in a 1-2% aqueous solution at a rate of 1-2mg/kg body weight. Most effective in ruminants. Urine will become dark green -Use ascorbic acid in cats and horses -Educate farmers and ranchers regarding nitrate accumulation in weeds and forages intended for feeding/grazing -You can feed corn to cattle to increase rate of nitrite reduction by rumen flora

Symptomatic care

-Maintain body temperature -Alleviate pain -prevent irritation of skin and membranes with demulcents, milk, sucralfate

Mechanism of Action for Ethylene Glycol

-Major toxic agents are the metabolites produced by alcohol dehydrogenase -Glycolic acid causes metabolic acidosis -Glyoxylic acid causes CNS signs -Oxalate/oxalic acid causes renal damage and hypocalcemia by binding to calcium to form calcium oxalate

Fumonisin

-Metabolite of Fusarium spp. -Found on corn during years of drought followed by wet weather -Acts by inhibition of sphingosine-N-acetyltransferase causing increased levels of sphinganine which is cytotoxic -Also affects vascular endothelial cells leading to stroke, hepatic injury and pulmonary edema -Horses, ponies, swine and rabbits are susceptible.

Stage 3 clinical signs of ethylene glycol

-Most animals present in this stage -Polyuria progressing to oliguria an anuria -lethargy -anorexia, vomiting, seizures -oral ulcers, abdominal pain, dehydration and enlarged kidneys

Equine Leukoencephalomalacia

-Most common in late fall or winter -Main target organ is brain and liver -Acute onset of anorexia, ataxia, circling, drowsiness, blindness, and hysteria that get progressively worse over hours -Hyperexcitability, mania, and profuse sweating are terminal signs -Hepatotoxicity: characterized by jaundice and hepatic encephalopathy that may result in coma and convulsions -Nearly 100% mortality rate

Chronic Renal Failure

-Mostly related to secondary pathological changes triggered by initial injury -Secondary changes are compensatory mechanisms -Signs are primarily edema, hypocalcemia, parathyroid activity, and reduced red blood cell counts

Diagnosing salt toxicity

-Na levels >160 mEq/L especially if CSF>serum -Brain Na>2000ppm is diagnostic in swine and cattle -Differentiate from polio, lead, pesticides, encephalitis

Pharmaceuticals toxicity

-Neuroactive substance such as sleeping aids and antidepressants -Careless storage is the primary cause of toxicity -clinical signs can be similar to human toxicity

Treating hypertension

-Nitroprusside: constant iV infusion -Hydralazine: dogs require higher dose than cats

Ammoniated feed toxicosis

-Non protein nitrogen sources are often added to cattle feed -Found in high concentrations in some mineral licks -Affects bovine, caprine, and ovine species -Leads to excitability known as bovine bonkers

Diagnosing phenoxyacetic acid toxicity

-Oral and GI ulcers -Enteritis and rumen stasis -Congestion of kidney/liver -Hyperemia of lymph nodes -Clinical pathology to look for liver damage -Chemical analysis of serum, urine

Mechanism of action for arsenic

-Pentavalen form: gets reduced and metabolized in rumen and reduces availability of metabolic energy and then gets converted to trivalent form, producing toxicosis -Trivalent form: binds to -SH groups and disrupts cellular metabolism and inhibits oxidative phosphorylation enzymes reducing metabolism -Causes serious toxicity to GI epithelium and capillary endothelium leading to enteritis and shock -Pentavalent form can interact with mitochondria in the brain and affect metabolism. Trivalent is usually in the blood and affects oxidative metabolism

Disinfectant toxicity clinical signs

-Phenol: corrosive burns of oral-esophageal pathway, vomiting, hyper salivation, ataxia, panting; progresses to shock, cardiac arrhythmias, methemoglobinemia, hepatic and renal damage and coma -Pine oil: nausea, hypersalivation, bloody vomit, abdominal pain, ataxia,hypotension, respiratory depression, acute renal failure, pulmonary edema

Disinfectants toxicity

-Phenols(lysol) denatures and precipitates cellular proteins and destroys contacted cells -Pine oils (Pine-sol) directly irritating to GI tract . Detoxified by glucoronidation so cats are more susceptible to toxicity

Treatment of Ethylene Glycol Toxicity

-Prevent formation of toxic metabolites by giving 20% ethanol with bicarbonate or fomepizole. Don't use together -Ethanol contraindicated in animals with renal failure -Be cautious with alcohol. You do not want to exacerbate CNS depression

Clinical signs of salt toxicity

-Primarily CNS and include salivation, increased thirst, abdominal pain and diarrhea, progresses over several days into circling, wobbling, aimless wandering, head pressing, blindness, seizures and partial paralysis -Toxicity occurs when 2.2g/kg

Slaframine

-Produced by "black patch" fungus on red clover: rain high humidity and cool weather triggers growth -It is an ACh mimic that acts primarily as a muscarinic cholinergic agonist -Most common in horses and cattle

Ergot alkaloids

-Produced in small grains by claviceps purpurea. Similar alkaloids produced in fescue

Clinical signs of strychnine toxicity

-Rapid onset 10-120 mins with little to no vomiting -begins with anxiety, restlessness, stiff neck and gait, "grinning" as facial muscles stiffen, ears twitch -proceeds to violent tetanic seizures initiated by external stimuli, frequency increases with time, respiratory distress -Sawhorse stance, rigid extension of all 4 limbs -Death from respiratory failure and exhaustion

Metaldehyde

-Sources include fuel for small heaters and molluscicides -3-4 oz bait toxic to average size dog or sheep -Results in CNS excitation

Arsenic Sources and forms

-Sources: insecticides, medicine, food production, electronics, shellfish, water -Pentavalent and divalent forms

Nicotine (BlackLeaf 40)

-Stimulates than blocks nicotinic ACh receptor -Lethal dose is 1-2mg/kg

Toilet bowl cleaner

-They are acidic and contain sulfuric acid or hydrochloric acid -Signs include vomiting, salivation, dysphafia, abdominal pain, GI ulceration, dyspnea -Treat with dilution with milk or water and use steroids if strictures are a possibility -Emesis, lavage and activated charcoal are contraindicated

Clinical signs of Gossypol Toxicity

-Usually occurs with long term feeding but can be acute onset -At low levels produces weight loss, weakness, and dyspnea -Moderate anemia may be present, edema secondary to heart failure -Myocardial necrosis and congestive heart failure -Dairy cows and lambs may die suddenly with minimal lesions

Naproxen toxicity clinical signs

-Vomiting, black-tarry stool, diarrhea -anorexia,weakness, lethargy -painful abdomen -pale gums -facial twitching, seizures, depression, coma

Diagnosis of Cantharidin toxicity

-alfalfa hay consumption -beetles in hay or stomach -hypocalcemia, increased BUN -Ulceration of mucous membranes -Cardiac necrosis

Ammonia, oven cleaners, and drain cleaner toxicity

-alkaline products that cause caustic ulceration -Esophageal ulceration occurs at pH of around 12 most of these products have a pH of 14 -Symptoms include vomiting, salivation, dysphagia, abdominal pain, GI ulceration, dyspnea -Treatment is dilution with milk or water, steroids if stricture is possible, symptomatic

Mechanism of toxicity of ergot alkaloids

-alkaloids are dopamine serotonin agonists which produce hallucinations -Activity at dopamine receptors in pituitary lead to decreased prolactin secretion -Smooth muscle contractions can occur and may cause abortion and ischemia

Diagnosing Porcine Pulmonary edema

-analysis of feed for fumonisin in conjunction with clinical signs -Increase in serum and tissue sphenoid bases -Increased liver enzymes, total bilirubin, bile acids, and cholesterol -Post-mortem pulmonary pathology indicating pulmonary edema, hepatic lesions, necrosis

When to use emesis

-animals with suspected oral exposure. Should be induced within 60 minutes of known toxic ingestion -Don't use for corrosive agents -only induce emesis if no vomiting has occurred yet and if activated charcoal is not an option

Diagnosing Anticholinesterase toxicity

-appropriate history and clinical signs -Atropine challenge: give preanesthetic dose. Wait 15 mins to observe normal signs of atropine if observed toxicity is not due to cholinesterase inhibitor -Decreased RBC AChE >50% inhibited -Non-specific pathology

NSAID toxicity

-at high doses they uncouple oxidative phosphorylation and increase lactic acid leading to metabolic acidosis

Lesions associated with arsenic toxicity

-at very high exposures you might not see any -Brick red gut -Fluid GI contents sometimes foul smelling -Soft yellow live, red congested lungs -Damage to glomerulus and tubules in kindney

Clinical signs of Zolpidem toxicity

-ataxia -vomiting -lethargy -disorientation -hyper-salivation -hyperactivity and panting also possible

Fluid therapy in toxicosis

-balanced electrolyte solution for shock and dehydration -Monitor urine output -Inotropic drugs like dobutamine

Things that cause respiratory center depression

-barbiturates, opiates/opiodes -ethylene glycol -hypnotics, sedatives -Tricyclic antidepressants -Crude oil

Diagnosing cholecalciferol toxicity

-based on ingestion, clinical signs, and hypercalcemia -most common finding is rapid increase in plasma phosphorous (within 12 hrs) followed by an increase in plasma calcium (24-48 hours) -Low parathyroid hormone -Increased BUN and creatinine -Low urine spec grav with calciuria -High hydroxycholecalciferol levels in bile and kidney

Diagnosis of alprazolam toxicity

-based on suspected ingestion and clinical signs

Bee envenomation

-bees envenomate by stinging; stinger remains on skin for some species, can only sting once and can be lethal -63 identified components: 50% mellitin, 12% phospholipase A2 3% hyaluronidase

Alprazolam (xanax) toxicity

-benzodiazepine -Acts at limbic, thalamic, and hypothalamic level of CNS -clinical signs of toxicosis include ataxia, depression, vomiting, tremors, tachycardia, diarrhea, and ptyalism -clinical signs usually appear within 30 mins of ingestion

Enterotoxins

-bind to intestinal epithelium increasing permeability and causing fluid loss and decreased absorption of nutrients -Salmonella, E. Coli, bacillus, strep and C. perfringens -Causes vomiting, diarrhea, abdominal pain, stasis with gas accumulation and bowel distention

Toad poisoning

-bufo secrete toxins for defense -B. marinus and B. alvarious are commonly lethal -eggs and tadpoles are also toxic

Wasp envenomation

-can sting repeatedly and often attack in groups -kinins are the primary pain-inducing substances. Some contain neurotoxins or alarm pheromones that alert the swarm to intruders

Mechanism of Action NSAID toxicity

-causes gastric ulceration -Causes renal toxicity mainly by the inhibition of prostaglandin synthesis and renal blood flow -Vasoconstrictive acute renal failure -Acute interstitial nephritis -Fluid and electrolyte imbalances -Renal papillary necrosis -Chronic renal failure

Ways in which toxicants cause toxicity

-cellular damage: can result from free radical damage, inhibition of energy productIon, disruption of enzyme function -organ system dysfunction: not associated with specific cellular injury but lethal to intact organism

Diagnosing methylxanthine toxicity

-chemical analysis of stomach contents, plasma, serum, urine, or liver -theobromine can be detected in serum for 3-4 days after ingestion b/c of long half life

Factors related to the toxicant

-chemical structure -affinity -vehicle

Diagnosing strychnine toxicity

-clinical signs -hyperthermia is often present in dogs -chemical analysis of bait, stomach contents, or liver -Elevated CPK and LDH in serum -Lactic acidosis, hyperkalemia and leukocytosis common lab findings -Rule out other compounds that can cause seizures

Signs of tick toxins

-clinical signs appear 6-14 days after attachment of tick -loss of appetite and voice -incoordination -ascending flaccid paralysis -excessive salivating and committing -respiratory distress -death due to respiratory paralysis

diagnosing toad poisonings

-clinical signs begin immediately with hyper salivation, foaming, head shaking, vomiting -other signs include hyperemic gums, arrhythmias, near signs, hyperkalemia -Death can occur in as little as 15 mins

Clinical signs of ivermectin toxicity

-clinical signs begin within hours to a day of ingestion -ataxia, disorientation, lethargy, mydriasis, coma, blindness, some bradycardia -recumbency and seizures more common in collies -respiratory distress typically precedes death

Porcine pulmonary edema

-clinical signs include inactivity, increased respiratory rate and decreased HR -Signs occur about 12 before the development of pulmonary edema -Lethal edema occurs within 4-7 days of consuming contaminated feed -Respiratory distress manifested as increased respiratory rate and effort with abdominal and open mouth breathing occurs within hours of death -Cyanosis of mucus membranes

Soap and shampoo ingestion

-clinical signs include vomiting and diarrhea -treat by dilution with milk or water -rarely ever fatal

Clinical signs of cyanide toxicity

-clinical signs occur within 15-20 mins to a few hours after animals consume toxic forage -classic symptom is cherry red blood that is slow to clot -May smell almonds in stomach contents -Sudden death, dyspnea, weakness, tremors

Clinical signs of Cantharidin

-colic, frequent urination, diaphragm contraction with heart beat, shock -Causes severe irritation and ulceration of oral, GI, and bladder epithelia -Causes cardiac toxicity

Acetaminophen toxicity

-common poisoning -metabolized in liver by glucoronidation, sulphonation and oxidation pathways -cats are extremely sensitive due to lack of glucoronidation

Mechanism of action of methylxanthines

-competitive antagonist of adenosine receptors causing CNS stimulation, vasoconstriction and tachycardia -prevents Ca++ reuptake leading to increased skeletal and cardiac muscle contractility -Inhibits phosphodiesterase and increases cyclic AMP and GMP concentrations

Ionophores

-compounds that form lipid soluble complexes with cations facilitating ionic transport across membranes -Used as antibiotic -Approved for use in dairy cattle to improve efficiency of milk production. -Also have several other off label uses

Diagnosing arsenic toxicity

-consider when there is a sudden onset of gastroenteritis or sudden death especially in animals near water -Liver or kidney arsenic >5ppm -examine stomach contents or vomitus -Gets readily absorbed in GI tract to take samples as soon as possible

Diagnosis of Slaframine toxicity

-consumption of clover, identification of black patch in clover -Differentiate from OPs, botulism

Treatment for black widow envenomation

-control muscle spams and pain -calcium gluconate for cramps -anti-venom -supportive care, especially respiratory

Treating tachycardia and arrhythmias

-correct acid-base, electrolyte or fluid disorders -lidocaine -Propranolol

Treatment of brown recluse envenomation

-dapsone to treat dermal lesions -treat with fluids and bicarb if hemoglinuria -administer abx to prevent secondary infections -analgesics for pain -clean necrotic lesions with burrows solution or hydrogen peroxide -debridement of necrotic tissue -bandage

Cathartics

-decrease GI transit time, increase movement of toxins, or charcoal-toxin complex, and decrease possible absorption of the toxin -Use as adjunct to activated charcoal therapy -Mineral oil (don't use with charcoal), Saline cathartic

Clinical signs of Anticoagulant rodenticide toxicity

-delayed onset of clinical signs as clotting factors are consumed -Initial signs are often depression, anorexia, and anemia -Dyspnea, nosebleeds, bleeding gums, and bloody feces -Hemorrhage and hematoma -Prolonged bleeding from injection sites is usually noted

Treating phenol toxicity

-demulcents (milk or eggs) -gastric lavage or emesis if no caustic burns -activated charcoal if no caustic burns -supportive therapy including IV fluids and respiratory support -1% methylene blue for methemoglobinemia

Diagnosing cyanide toxicity

-diagnose by history of ingestion and unclothed red blood -analysis of frozen stomach contents

Diagnosis and treatment of Zolpidem toxicity

-diagnosis based on suspected ingestion and clinical signs -Treatment is supportive and symptomatic

How to treat seizures

-diazepam is a treatment of choice. 0.5mg/kg every 10 mins -Phenobarbital or pentobarbital -Methocarbamol

Treating pine oil toxicity

-dilute with milk, egg white or water -b/c of aspiration pneumonia, emesis and lavage are contraindicated -follow dilution w/activated charcoal and cathartic -Supportive therapy including renal perfusion, acid-base and electrolyte balance

Pit viper envenomation signs

-distinct fang marks -immediate swelling, pain and bruising at site of bite -hypotension, shock, tachycardia, tachypnea -anticoagulation -tissue necrosis -cats more resistant than dogs

Brown recluse envenomation

-dogs are most susceptible from lying on them -venom contains several necrotizing enzymes -sphingomyelinase D binds to cell membranes and cleaves head off lipids -tissue necrosis -victim's immune response determines severity

Clinical signs of arsenic poisioning

-dose dependent -intense abdominal pain, gastroenteritis -Weakness, staggering gair -Salivation, trembling -Vomiting -PU/PD progressing to oliguria and anuria -Dehydration, thirtst -Posterior paresis -Cold extremities due to poor perfusion -Subnormal temperature -May live for 1-3 days

Dishwasher detergent toxicities

-due to high alkalinity -signs include vomiting, diarrhea, salivation, GI pain, and oral, esophageal, and gastric erosions -Treat with dilution with milk or water , analgesics, and possibly steroids for inflammation

General supportive care includes

-ensuring adequate urine output -Monitoring respiratory, cardiac and neurological status -Manage clinical signs as they develop -Manage secondary hepatic or renal injury -Administer GI protectants/anti-emetic

Mechanism of zearalenone action

-estrogen receptor agonist -causes hyperestrogen syndrome -vulvovaginitis and estrogenic responses in swine -rapid detection kits available

Toxins associated with an increased anion gap

-ethylene glycol -ethanol -iron -methanol -Salicylates -Strychnine -Anion gap of >30mEq/L is clinically significant and suggest metabolic acidosis

Diagnosing ergotism

-evidence of sclerotia in feed, or fescue in forage matter -chemical analysis of feed and forage for ergot metabolites

1st generation anticoagulant rodenticides

-ex. Warfarin -short half-life (15 hours) -Low potency, requires multiple feedings -LD50=10-50mg/kg

Zinc toxicity

-found in galvanized metals and post 1982 pennies -With the stomach's acidic environment zinc is freed and forms zinc salts which are corrosive to mucosa -Oxidative damage that leads to hemolysis -Seen in dogs and aquatic zoo animals

Strychnine

-from seeds of stychnos-nux vomica (indian tree) -alkaloid used to control pocket gophers -restricted-use pesticide -Often used as a malicious poison -LD50 values range from 0.5-3mg/kg. Higher for birds -Rapidly absorbed needs to be treated aggressively

Things to collect during a history

-heath history -current clinical history: how long was problem present, when was animal observed sick, if animal found dead when were they last seen healthy, size of the herd -Clinical signs based on systems -Environment: indoor only? indoor/outdoor? fenced yard vs. free roaming? -Diet and water source

4 parts to accurately diagnosing any toxicity

-history -Clinical signs -Pathology/Necropsy -Chemical analysis

Diagnosing Ivermectin toxicity

-history of administration -Brain ivermectin concentration >100ppb -Can also measure in GI content, liver, fat, and feces -No diagnostic bloodwork

Diagnosing Gossypol toxicity

-history of cottonseed ingestion -cardiac necrosis, edema, vacuolozation -chemical analysis of gossypol

Diagnosis of Ammonia Toxicosis

-history of exposure -clinical signs very important -Differentials include OP pesticides, cyanide, grain overload, meningitis, and encephalitis. -Analysis of feed of blood/rumen fluid for ammonia levels -Increased ammonia, glucose, BUN, and decreased blood pH may help diagnosis NPN overdose

Diagnosing Anticoagulant rodenticide toxicity

-history of exposure -evidence of a coagulopathy -response to vitamin K1 therapy -Run hematological tests for PT and PTT. Increased time with normal platelet counts are indicative of toxicity

Diagnosing tick toxicosis

-history of tick infestation -presence of dermacentor, ixodes ticks -ascending paralysis and loss of voice

Diagnosing grape/raisin toxicity

-hypercalcemia -hyperphosphatemia -Increased Ca xPO4 -Elevated BUN and serum creatinine

Clinical signs of ammonia toxicity/imidazoles

-hyperexcitability: nervousness, rapid blinking, dilated pupils, trembling, ataxia, rapid respiration, SLUD, tonic convulsions induced by stimuli -If tox is caused by imidazoles animals will alternate between hyper excitability and normal behavior -The onset of clinical signs is rapid. 15 mins-several hours. Death occurs within 24 hours -If ammonia toxicity; death occurs when blood ammonia >2mg/dL

Ventilation may be needed if there is

-hypoventilation and hypercapnia (PCO2>45mmHG) -Metabolic acidosis (venous pH 7.35) -Hypoxia (PaO2<65mmHg). Treat with 40% oxygen

Treatment of Anticoagulant Rodenticide toxicity

-if ingestion has occurred within the last few hours use emetic, absorbent and cathartic therapy -Vitamin K administration: 0.25-2.5mg/kg for short acting or 2.5-5.0 mg/kg for long-acting -Continue therapy for 10-14 days for warfarin or up to 30 days for second generation compounds -May need transfusion in severe cases

Treating coral snake envenomation

-if neuro signs develop administer antivenom immediately (anaphylaxis may occur) -monitor respiratory fxn. May need ventilator -broad spectrum abx and symptomatic wound care -pts should be monitored for a min of 24 hours -prognosis is good when prompt care is received

Treatment of imidazole/ammonia toxicosis

-imidazoleL no treatment, just feed removal -Ammonia: no specific treatment can give 5-10 gallons of cold water and 1 gallon vinegar by stomach tube to acidify rumen and convert ammonia to less absorbable form -Prognosis is poor for recumbent animals

treating toad poisonings

-immediate oral decontamination with water -activated charcoal if no seizures -diazepam/barbiturates for seizures -atropine for bradycardia but don't give for salivation -propanolol/lidocaine for arrhythmias -fluid replacement -digoxin immune fab for severe near signs and hyperkalemia

Clinical signs of zearalenone toxicity

-in ferrets and pigs, symptoms depend on sex and maturity -In cattle and sheep males regress testis and have feminization, females have abortions and pseudopregnancy

NSAIDs

-include aspirin, ibuprofen, naproxen -absorbed well from stomach and intestinal mucosa -dogs are sensitive to ibuprofen -Cats are sensitive to aspirin due to lack of glucoronidation -Block prostaglandins

Methylxanthine toxicity

-includes caffeine, theobromine, theophylline -found in chocolate, coffee, medications -Toxicity commonly occurs around holidays -Unsweetened baking chocolate is especially toxic -Caffein tablets and cocoa bean mulch for horses are also causes

Diagnosing ionophore toxicity

-increased muscle enzymes and myoglobinuria -Elevated AST, CK, LDH, alkaline phosphatase, BUN, bilirubin -Decreased K and Ca due to high intracellular concentrations -Chemical analysis of feeds, liver -Differentiate from other causes of colic

Treating NSAID toxicity

-induce emesis and activated charcoal several times -Address GI ulceration(H2 inhibitors/sulcralfate) and acute renal failure -Supportive care -Consider transfusion for animals with significant hemorrhage/severe anemia

Treatment of alprazolam toxicity

-induce emesis with apomorphine if the ingestion is recent and no signs are present -use gastric lavage with activated charcoal if toxic dose -specific benzodiazepine antagonist, flumazenil may be used for severe CNS depression associated with toxicosis -Close monitoring is needed -fluids and additional medications may be needed

Treatment of cyanide toxicity

-induce methemoglobin formation with sodium nitrite to bind cyanide to sodium -Give sodium thiosulfate to increase formation of thiocyanate by rhodanese. Thiocyanate is non-toxic and eliminated -if necessary treat metHb with methylene blue

Cardiac glycosides

-inhibit the sodium potassium ATP-ase pump through competition with potassium for binding sites

Mechanism of Action of Anticoagulant Rodenticides

-inhibits Vitamin K1 epoxide reductase -Prevents formation of Vitamin K dependent clotting factors II, VII, IX, X

Zolpidem (ambien) toxicity

-inhibits neuronal excitation by binding to the benzodiazepine omega-1 receptors -rapid absorption from GI tract and highly bioavailable

Mechanism of action of Cantharidin

-inhibits protein phosphatases -mucosal irritant

Clinical signs of brown recluse envenomation

-initial bite causes little to no pain -3-8 hrs after it becomes red, swollen, and tender and forms a typical bulls eye and non-healing ulcer -can become necrotic -hemolytic anemia, fecer, weakness, and leukocytosis may occur -diagnosis is difficult if but isn't seen

Clinical signs of grape/raisin toxicity

-initial sign is vomiting followed by symptoms of acute renal failure

Clinical signs of fire ant stings/bites

-intense pain at the site of the sting -dogs develop erythematous puristic papillose that generally resolve in 24 hrs -no reports of anaphylaxis in animals -multiple stings similar to signs in bee/was sting

Mechanism of toxicity for Cholecalciferol/Vitamin D3

-it becomes metabolized to 1,25-dihydroxycholecalciferol -This causes massive increases in serum calcium by increasing GI absorption, decreasing renal excretion, increasing synthesis of calcium binding protein, mobilizing bone calcium -Calcium can go into tissue and cause crystallization

Why is the kidney a common site of toxicity

-it receives a lot of blood flow (22-25% of CO) -it concentrates compounds -helps excrete compounds especially xenobiotics

Clinical signs of Endotoxin

-lethargy -fever followed by hypothermia -diarrhea -abdominal pain -shock -extremely bad smelling feces

Treating enterotoxins and endotoxins

-limit absorption of material -support cardiovascular fxn -correct fluid and electrolyte imbalances -prevent bacterial proliferation and septicemia

Endotoxin

-lipopolysaccharide from gram negative cell walls -activates inflammatory processes and causes release of TNF, prostaglandins, histamine -Result is circulatory collapse, activation of pancreatic enzymes and autodigestion leading to pancreatitis, activation of clotting cascade, uncoupling of oxidative phosphorylation in heart

Liver toxicosis

-liver has ability to regenerate and repair itself -Intrinsic injury may lead to steatosis, necrosis, and cholestatis -Occurs as dose-dependent reaction to toxicant -Often caused by reactive products of xenobiotic metabolism

2nd generation anticoagulant rodenticides

-long half-life (20 days) -high potency, kills in single feedings -LD50=0.25mg/kg

Diagnosing acetaminophen toxicity

-look for common clinical signs as well as hemolysis, heinz bodies and elevated liver enzymes

Ethylene Glycol

-major ingredient in antifreeze -2nd most common cause of fatal poisonings in animals -Most frequently used as a malicious poisoning -Exposure common in spring and fall -Very high rate of mortality due to delays in presentation -tastes sweet to animals tend to like it -Lethal dose in cats is 1.5ml/kg of undiluted antifreeze or 1tbsp of 50:50 antifreeze:water -In dogs lethal dose is around 7ml/kg or 4.5 oz of 50:50 mixture -The ethylene glycol metabolites are what actually causes the poisoning

Organophosphate induced delayed neurotoxicity

-may cause delayed neuropathy characterized by axonal degeneratio of long motor neurons, hindlib weakness, paralysis. No treatment

Diagnosing ethylene glycol toxicity

-measure EG concentration in blood. Serum peaks at 1-6 hours but will be gone from urine and serum by 24 hours. -Serum biochem will show hyperglycemia and hypocalcemia -Anion and osmolal gap - There are kits for testing -Azotemia, elevated BUN and creatinine will be present in stage 3 -Calcium oxalate crystals can be found via ultrasound -Cats can have toxicosis with levels below detectable measures on diagnostic kits

Clinical signs of acetaminophen toxicity

-methemoglobinemia and hepatotoxicity -usually accompanied by tachycardia, hyperpnea, weakness, and lethargy -cats usually develop methemoglobinemia within a few hours followed by heinz body formation -Liver necrosis is clinical sing in dogs

Clinical signs of chronic zinc toxicity

-most often seen in cattle and onset is several weeks -PU/PD -Diarrhea, Anorexia -Hemolytic anemia -Lameness -Lesions

Clostridium tetani

-mostly affects cattle -caused by spores in puncture wounds, can be ingested -toxin acts by blocking release of GABA and glycine -Results in overstimulation of muscles leading to stiffness and tetany

Clinical signs of anti-esterase toxicity (AChE)

-muscarinic: SLUDGE-M -Nicotinic: muscle fasciculations beginning with face, eyelid and tongue, generalized tremors, weakness, paralysis -CNS: respiratory depression, ataxia, nervousness, clinic-tonic seizures -Signs may last 1-5 days

Clinical signs of black widow envenomation

-muscle cramping and spasm -rapid weight loss -abdominal rigidity -restlessness, writhing -vocalization -hypertension -tachycardia -cats are most sensitive to venom and they often eat spiders which causes severe pain, vomiting, diarrhea, and respiratory collapse

Zearalenon

-mycotoxin, metabolite of fusarium -most grains can be affected, toxin production occurs primarily during storage -heat stable and resistant to most mold retardants -affects most animals but chickens are resistant

Treatment of Ionophore toxicity

-no specific treatment or antidote -Feed change to non-ionophore must be made immediately until all diagnostic procedures are completed -offer supportive therapy -recovered animals may die later on due to exercise intolerance

Treating fumonisn toxicity

-no treatment available -change feed -isolate affected animals -pigs usually recover within 48 hours of removing contaminated feed

Stage 2 clinical signs of ethylene glycol

-occurs 12-24 hours after ingestion -tachypnea, tachycardia or bradycardia -often not severe and not recognized by owner -Cats typically remain depressed

Stage 1 clinical signs of Ethylene glycol

-occurs 30 mins to 3 hours following ingestion -drunkenness, ataxia, CNS depression -nausea, vomiting -PU/PD in dogs -usually missed with unobserved signs

Clinical signs of acute zinc toxicity

-occurs within a few days -vomiting -depression, anorexia -hemolytic anemia -jaundic -pancreatitis -Lesions:enteritis, renal, hepatic, and pancreatic necrosis

Black widow envenomation

-only females are toxic -venom contains alpha latrotoxin that creates pores in the membranes allowing Ca+++ entry and releasing massive amounts of neurotransmitters causing sustained muscle spasm

Tick toxins

-only in certain species (dermacentor, Ixodes) -Holocyclotoxin is produced in the salivary glands -Decreases ACh release at neuromuscular junction resulting in weakness and paralysis. May act of Na+ channels

Treating pit viper envenomations

-only proven therapy is antivenin -symptomatic and supportive care -copperhead bites can be managed with antihistamines for inflammation -Rattlesnake and moccasin bites often managed with fluids and corticosteroids for shock and for inflammation

Clinical signs of coral snake envenomation

-onset can be delayed up to 12 hours -salivation due to inability to swallow, dyspnea, weakness, hyporeflexia, CNS depression, paralysis

Cholecalciferol/Vitamin D3 toxicity

-overdosage of vitamin supplements or exposure to rodenticide -toxic at >0.5mg/kg -Lethal around 10-15mg/kg -Dogs and cats are more commonly affected

Clinical signs of neurotoxicity can be grouped as

-peripheral vs. central -excitatory vs. depressive

Diagnosing zearalenone toxicity

-presence of more that 1-2ppm in swine feed -reversal of symptoms occurs 7-10 days after change of feed -Activated charcoal or high fiber may reduce elimination times due to extensive enterohepatic recycling

Treating Strychnine toxicity

-primary goal is to control seizures and prevent asphyxiation -administer pentobarbital or methocarbamol -Emesis before signs, gastric lavage once anesthetized; follow with activated charcoal and forced diuresis. Must be aggressive -Ion trapping with ammonium chloride can be used to trap strychnine if animal is not acidotic -If acidosis develops treat with bicarbonate

Gossypol

-problem for large animals especially if feed is enhanced with cottonseed -found in pigment glands of cottonseed, provides insect resistance -levels vary with preparation and type of cotton. Inactivated by heating -Cottonseeds contain high level of energy, protein and fiber which is why they are used in feed

Ivermectin

-produced by soil fungus streptomyces avermitilis -GABA-A receptor agonist. Increases GABA release and enhances GABA binding -dose of 200g/kg can cause ataxia and disorientation -Collies, shepherds and shelties can experience toxicity with doses as low as 80-100ug/kg

Treating grape/raisin toxicity

-recommended following ingestion of any quantity -emesis, lavage, or activated charcoal for recent ingestion -fluid therapy for a minimum of 72 hours -Supportive therapy:furosemide, dopamine mannitol, hemodialysis, or peritoneal dialysis -No method is preferred over the other since we don't know why its toxic -Dopamine facilitates kidney function and blood flow

Clinical signs of ergotism in cattle

-reduce feed intake and weight gain, heat intolerance, retain winter coat -Necrotizing ergotism: lameness, gangrene of extremities that may result in sloughing of feet, ears, and tail during cold weather -Fat necrosis -Poor reproductive performance

Treating cholecalciferol toxicity

-reduced dietary calcium and phosphorus -GI decontamination within 6-8hrs -Monitor serum calcium from admission and every 24-48hours -Normal saline and furosemide: promotes Ca excretion -Prednisolone to reduce bone resorption, intestinal calcium absorption, and kidney calcium resorption -Calcitonin -Pamidronate to replace calcitonin -Sulcralfate or milk of magnesia for ulceration -Phosphate binders are good ideas

Treatment of bees, wasps, and hornet stings

-removal of retained stinger -cold compress to relieve swelling and pain -monitor patients for anaphylactic reactions

Treating zinc toxicity

-remove foreign bodies -Emesis -symptomatic treatment. Fluids and blood products -Proton pump inhibitors or H2 blockers to decrease absorption of zinc salts and gastroprotection

Treatment of ergotism

-remove source and prevent secondary infections -Metoclopromide and domperidone increase prolactin secretion and can normalize the gestation in affected mares

Treating Slaframine toxicity

-remove source, maintain hydration and electrolytes -Can be treated with atropine -Clinical signs cease within 48 hrs of animal being removed from contaminated pasture. Rarely fatal

Treating acetaminophen toxicity

-replace glutathione stores, increase productivity of the two other pathways and manage the hematological sings -early decontamination only if recently ingestion -give the glutathione precursor N-acetylcysteine -reduce methemoglobin with ascorbic acid -can consider administering cimetidine in cats -Supportive care: fluids, blood transfusions, oxygen therapy

Steps in dealing with toxicosis

-respiratory maintenance -Control CNS activity -Control cardiovascular function -Stabilize patient -Obtain complete history

Mechanism of action of toad poisonings

-secretions contain many compounds -biogenic amines: cause vasoconstriction, hypotension, hallucination, GI effects -bufogenins: inhibit sodium potassium ATPase activity similar to cardiac glycosides. Produce potentially toxic cardiac arrhythmias

Grape and raisin toxicity

-seems to only affect some dogs -mechanism of action is unknown -there is a lack of dose response seen -lowest dose shown to cause renal failure is 4-5 grapes and for raisin 3g/kg

Diagnosing zinc toxicity

-serum zinc levels>10ppm -liver zinc>200ppm -Decreased PCV, regenerative anemia, thrombocytopenia -Heinz bodies -Elevated liver, kidney, and pancreatic enzymes -Hemoglobinuria -Xrays

bromethalin

-single dose rodenticide -kills in 3-5 days so you may see delayed toxicosis -Parent and metabolite uncouple oxidative phsophorylation in CNS

Treatment of salt toxicity

-slow rehydration over a 2-3 day period -Serum sodium levels should be lowered at a rate of 0.5-1.0 mEq/L/hr -IV hyperosmotic fluids low in Na -Loop diuretic to prevent pulmonary edema during fluid therapy

Clinical signs of bee, wasp, or hornet stings/bites

-small local swollen or edematous and erythematous plaque at site of sting -large local regional allergic reaction -anaphylaxis can cause death (reported in dogs) -systemic toxicity is uncommon but is caused by delayed hypersensitivity

Fire ant envenomation

-some bite, others sting, some can do both. Some can spray formic acid -Complex mixture of compounds largely consisting of alkaloids -Piperidine causes dermal necrosis when injected in the skin -Animals with limited mobility most severely affected

Clinical signs of clostridium tetani

-stiffness and reluctance to move -twitching and tremors of the muscles -Lockjaw -Unsteady gait with stiff held out tail -Bloat in ruminants -Later signs include collapse, spasm and death

LMW substances

-substance in venom that contains prostaglandins, histamine, and epinephrine -causes pain, inflammation and hypotension

Treatment of tick toxicosis

-supportive therapy -atropine sulfate -anti-emetics -fluid replacement therapy -oxygen -prognosis is good if treated

Factors related to the environment

-temperature -pH

Using Activated charcoal

-the earlier the more effective -Give repeated doses every 4-6 hours -Can give alone or after emesis/gastric lavage -Contraindicated for corrosive agents and non-polar materials. (acids, alkalis, alcohol/glycols, metals, oils, petroleum distillates, detergents) Make sure if animal is sedated it has airway protection -Do not give oral meds for at least 2 hours

Mechanism of action of acetaminophen toxicity

-toxic effects due to formation of the metabolite NAPQI -When glutathione stores depleted NAPQI binds to macromolecules and proteins and causes liver tissue necrosis and increased methemoglobin -Erythrocyte injury is predominant problem in cats: methemoglobin and heinz body production -Hepatic effect dominate in dogs, mice, rats

Bleach ingestion

-toxicity due to alkalinity and corrosive effect -causes liquefactive necrosis -clinical signs are vomiting and abdominal pan -Dilute with milk or water -emesis or lavage except with very caustic exposures -Activated charcoal and cathartics

Cantharidin

-toxin found with grasshopper populations as beetle lays eggs on grasshopper larvae -Usually affects horses -6-250 beetle can be lethal

Treatment for Gossypol toxicity

-treat by feeding high protein diet; add vit A, iron and lysine and remove gossypol sources -symptomatic treatment

Clinical signs of Cholecalciferol/Vitamin D3 toxicity

-typically appears 36-48 hours after ingestion -Anorexia, weakness, depression -thirst and polyuria -Calciuria -Diarrhea, dark feces due to intestinal bleeding and vomiting -Hypertension, bradycardia, and ventricular arrhythmia -Crystallization of tissues when Ca*P >70mg/L

Organophosphate pesticides

-used in flea collars, dips, fly, and and roach bait. -Include Parathion, malathion, chlorpyrifos -Highly water soluble and capable of acute toxicity -irreversibly inhibit AChE activity which leads to cholinergic overstimulation within minutes to hours

Cyanide toxicity

-usually a problem with consumption of wilted leaves and seeds of wild cherry, white clover or fresh sorghum -Also found in fertilizers, pesticides, rodenticides, fumigants, combustion -non toxic when dry, as hydrogen cyanide is volatile -Mechanism of toxicity: inhibits cytochrome oxidase

Garbage/carion toxicity

-usually protein rich foods during warm months -have enterotoxins and endotoxins -can be due to bacteria or performed toxins

Coral snake envenomation; mechanism of action

-venom is composed of small polypeptides and enzymes -neurotoxic due to bungarotoxin -acts by binding ACh causing paralysis -binding neurotoxin to postsynaptic receptor appears to be irreversible -enzymes can cause local tissue necrosis, myoglobinemia in cats and hemolysis in dogs

Clinical signs of methylxanthine toxicity

-vomiting, diarrhea, diuresis -Hyperactivity, "bounce" -panting -tachycardia, hypertension -Ataxia -Tremors, seizures -Coma -Death from arrhythmias or respiratory failure

Salt toxicity

-water deprivation of consumption of large amounts of salt are the most common causes -Most often seen in pigs but can be seen in other animals -high Na levels in plasma causes diffusion into CSF. When plasma NA drops sodium leaves CSF slowly attracting water leading to an increase in CSF volume and pressure

Differential diagnosis for cholecalciferol toxicity

-with ethylene glycol with will have much higher kidney calcium than with cholecalciferol. You will also have a greater Ca:P ratio in EG -Differentiate from paraneoplastic syndrome, juvenile hypercalcemia, and hyperparathyroidism

A slightly toxic substance requires a dose of _______ to cause toxicity

0.5-500mg/kg

A highly toxic substance requires a dose of _________ to cause toxicity

1-50mg/kg

With ___% metHb the patient will by asymptomatic with maybe some changes in membrane color

10%

With ___% metHb the patient will exhibit cyanosis, and blood and membranes will appear brown

15%

A practically nontoxic substance requires a dose of __________ to cause toxicity

5-15 g/kg

with ___% met hemoglobin the patient will have serious signs such as ataxia, seizures, and coma

50%

A moderately toxic substance requires a dose of __________ to cause toxicity

50-500mg/kg

with greater than ____% metHb the patient will die

70%

An extremely toxic substance requires a dose of ______ to cause toxicity

<1mg/kg

A relatively harmless substance requires a dose of __________ to cause toxicity

>15g/kg

The ABCs

Airway, breathing, circulation

________ and ______ are widely used by homeowners and professionals for rodent control

Anticoagulant and anticoagulant rodenticides

Dogs and cats with anti-esterase toxicity tend to display

CNS stimulation and convulsions

Dose-response relationship

Central concept of toxicology; assumes a cause and effect relationship and that response is proportional to dose

Who is the father of toxicology

Paracelsus

Toxicants you can identify in serum

Some metals, nitrate, nitrite, ammonia

Additive

Sum of the effects are equal to 1+1=2. Adds on to the toxic effect

Natural toxins

Toxic plants, microbes, vitamins, venoms

Toxicants you can identify in vomitus

Various poisons, heavy metals, anticoagulants, antifreeze

Toxicant

a compound that causes toxicity . May be natural or man-made

Dogs are deficient in ________ when it comes to drug metabolism

acetylation

Why is emesis, lavage and activated charcoal not mentioned as part of ethylene glycol treatment in some formularies

activated charcoal does not bind well if at all. Also ingestion probably occurred long before symptoms so these methods are probably useless in most cases unless the ingestion was observed

Toxicants you can identify in urine

alkaloids, some metals, abx, drugs, oxalates, cantharidin

If toxic agent has been identified use specific ______. Unless there isn't one for that toxin at which point treatment is symptomatic and supportive

antagonist

Antidote

any substance that prevents/relieves the effects of a toxicant. No antidote works on all toxicants

Diagnosing cardiac glycoside toxicity

based on history, access to plants, and clinical signs as well as analysis of vomit

Peptides in venom

cause many direct toxic effects and allergy

Enzymes in venom

cause toxicity and allergy -hyaluronidase- spreading and potentiating factor, catalyzes the cleavage or glycoside bonds -Collagenase breaks down capillary walls -protease degrades proteins and causes necrosis

Toxicants you can identify in fat

chlorinated pesticides and dioxins

Toxicants you can identify in brain

chlorinated pesticides, pyrethrins, cholinesterase, metals

Horses with anti-esterase toxicity tend to display

colic and dehydration

Antagonist

compound A prevents full impact of compound B

Synergism

compounds come together and increase effect significantly

Toxicology

concerned with identification, treatment, and assessing risks of poisons

For corrosive agents or strong acids and bases you should use ____ instead of emesis. This can be done with milk, water, or eggs

dilution

Factors related to exposure

dose, route of entry

Pregnancy has the potential to alter

drug metabolism

The two most common methods of decontamination are _______ and ______

emesis and activated charcoal

Sub-acute toxicosis

exposure over 7 to 90 days Ex. pesticides on lawn

In suspected nitrate deaths you should save the ______ for analysis of nitrate

eye

Xenobiotic

foreign substance

Only decontaminate animal after it has been

fully stabilized

Cats are deficient in ________ when it comes to drug metabolism

glucoronidation

Toxicants you can identify in blood

heavy metals, anticoagulants, antifreeze, cholinesterase, cyanide, chlorinated pesticides

Hymenoptera

includes bees, wasps, hornets, and fire ants

Antidotes can be harmful so they should not be used ____________

indiscriminately

Unconscious, paralyzed and severe respiratory distress patients are candidates for ________

intubation

Neurotoxicants are the _____ class of chemicals inducing toxicosis

largest

Toxicants you can identify in kidney

metals like As and Pb, phenolic compounds, oxalates

Toxicants you can identify in liver

metals, aflatoxin M1, alkaloids

Chlorpurifos causes more severe nicotinic signs in cats due to _______ tolerance

muscarinic

Both _____ and ______ substances are capable of causing neurotoxicity

natural, synthetic

Is presence of Fusarium on corn indicative of Fumonosin

no

Manmade toxins

not naturally occurring. Includes pesticides, cleaning products, pharmaceuticals, and industrial chemicals

The most important veterinary toxicants are absorbed by ______ or _______ routes

oral or dermal

The heart of an animal that has died from gossypol toxicity will look

pale and modeled

Chronic toxicosis

protracted exposure 6 months -lifetime Ex. lead in paint or arsenic from well water

What is the most common site of toxin induced renal injury

proximal convoluted tubule

Mechanism of action of Strychnine

rapidly absorbed and distributed to blood, liver, and kidney -Rapid elimination; complete in 48-72 hors -Competitive antagonist at postsynaptic spinal cord and medulla glycine receptors -Glycine is an inhibitory transmitter so antagonism results in disinhibition of all muscles

Lipid infusion

relatively new therapy. IV lips promising adjunct to conventional treatments

Cattle with anti-esterase toxicity tend to display

rumen stasis and severe depression

Sheep with anti-esterase toxicity tend to display

severe depression

Acute toxicosis

single dose exposure or several doses within a 24 hour period. Ex. snake venom, ingesting medications or rodenticides

Factors related to the subject

species, age, health status of the animal, sex

Pigs are deficient in ________ when it comes to drug metabolism

sulfation

If a patient is hyperthermic or hypothermic stabilizing them becomes

the priority

Why is bicarbonate given with ethanol in treatment of ethylene glycol intoxication

to balance out the ethanol thats not bound and correct metabolic acidosis

Purpose of acetaminophen toxicity treatment is

to keep glutathione up so NAPQI has something to bind to

Drug Metabolism

usually detoxifies a compound and increases its elimination

Clinical signs of Ionophore toxicity

usually occur 12-72 hours after ingestion -Anorexia, colic, profuse sweating on flanks can be seen in horses -Cattle exhibit similar signs to horses but with diarrhea and respiratory difficulty -Poultry are down with legs and wings stretched out -Dogs may exhibit posterior paresis and paralysis with lasalocid -Cats develop polyneuropath from salinomycin

Bioactivation

when metabolism increases the toxicity of a compound. Happens in acetaminophen, aflatoxins, and benzo[a]pyrene and some prodrugs