Toxicology

Front 1

What are the critical questions to ask when presented with a potentially poisoned patient? (5)

Back 1

1) Full background history

2) Ascertain the nature of the poison

3) When exposure to the toxin occurred

4) How much poison the animal was exposed to

5) The route of exposure

Front 2

What are the factors to consider with recommending home emesis?

Back 2

Depends on the length of time which has elapsed since exposure, the nature of the toxin, and the clinical status of the animal.

Front 3

What are the major steps for managing an acutely intoxicated patient? (6)

Back 3

1) Assessment of airway, breathing, & circulation (consider if intubation, assisted ventilation, &/or oxygen supplementation are needed)

2) Control of seizure activity & tremors (Diazepam IV; may need to combine w/barbiturate)

3) Assessment of hydration & metabolic derangements (full biochemical profile & blood gas analysis)

4) Gastrointestinal decontamination (emesis or flushing followed by AC)

5) Enhance elimination of toxin (IVFT, ion trapping, IFE, etc)

6) Supportive care (oxygen, hydration, temperature, electrolyte status, physical therapy, & nutrition)

Front 4

Paracetamol toxicity

1) What is the pathway of this toxin?

2) What are the dose toxicities for dogs? cats?

3) How does it affect the dog? cat?

4) What is proper treatment?

Back 4

1) Elimination is primarily via conjugation w/glucuronide & sulphates in the liver, followed by excretion of these non-toxic metabolites in bile & urine. Toxic metabolites can be produced (usually small amounts) via the cytochrome p450 pathway.

2) Dog: 200-600 mg/kg

Cat: 50-100 mg/kg

3) Dog: Liver is most susceptible to injury. Hepatocellular necrosis-->liver failure: depression, weakness, anorexia, vomiting, & jaundice. Methaemoglobin/haemoglobinuria.

Cat: RBC is most susceptible to oxidative injury. Hemoglobin-->methemoglobin. Cyanosis, chocolate-colored mucous membranes, heinz-body anemia (hemolytic). Also vomiting, ataxia, collapse, facial & pulmonary edema.

4) Reduce further absorption by induction of emesis or gastric lavage w/in 1-2 hours of ingestion then administer activated charcoal (AC) to reduce absorption of residual drug. Provide supportive care via supplemental oxygen, IVFT, & blood transfusion. Give specific therapy in this case of glutathione precursors to replenish cellular glutathione stores (e.g. SAMe).

Front 5

Ibuprofen (NSAID) toxicity

1) What is the pathway of this toxin?

2) What are the clinical signs?

3) What is proper treatment?

4) What are the factors that increase the risk of toxicity? (3)

Back 5

1) NSAIDs reduce the production of prostaglandins & thromboxane by direct inhibitionof cyclooxygenase (COX) enzymes. They are non-selective in nature & thus can affect COX-2 (desired target) & COX-1 (physiological response). Due to this they can cause a reduction of gastric prostaglandins & bicarbonate secretion leading to gastric ulceration +/- renal toxicity.

2) Vomiting, depression, anorexia, diarrhoea, melaena, & anuria/oliguria or PUPD.

3) Reduce further absorption by inducing emesis or gastric lavage if w/in 1-2 hours of ingestion. Administer AC-->continue every 6h for 72h due to enterohepatic circulation. Provide supportive therapy via IVFT to maintain renal perfusion. Provide specific therapy via Misoprostol, H2-antagonists, proton-pump inhibitors, & sucralfate.

4) age, hypoalbuminaemia, & concurrent use of glucocorticoids.

Front 6

Aspirin toxicity

1) What are the potential problems with this toxicity?

2) What are the clinical signs?

3) What is proper treatment?

Back 6

1) Ulcerogenic & nephrotoxic potential in addition to hyperventilation followed by a severe metabolic acidosis.

2) Pulmonary oedema, seizures, respiratory depression, & coma.

3) Reduce further absorption by inducing emesis or performing gastric lavage if w/in 1-2h of ingestion. Follow with administering AC-continue every 6h for 72h. Provide supportive therapy via IVFT to maintain renal perfusion. Provide specific therapy of Misoprostol, H2-antagonists, proton-pump inhibitors, & sucralfate. Additionally, elimination of salicylate can be enhanced by forced diuresis (combo of IVFT & diuretics) w/careful attention to fluid balance to avoid overload. Consider administration of bicarbonate if severe acidaemia is present.

Front 7

Ethylene Glycol toxicity

1) What is it & what is it found in?

2) What is the outcome highly dependent on?

3) How does it cause toxicity?

4) What are the clinical signs?

5) How to diagnose?

6) What is proper treatment?

Back 7

1) Organic solvent; Anti-freeze/de-icer. High palatability.

2) Early recognition of EG intoxication or quick, high chance of mortality.

3) Causes vomiting due to GI irritation & CNS depression; metabolized by alcohol dehydrogenase to glycoaldehyde, glycolic acid, & oxalate.

4) CNS depression, ataxia, stupor, +/- seizures. Severe metabolic acidosis. ARF.

5) Based on serum biochemical & urine abnormalities. High AG metabolic acidosis; low HCO3; high AG-before onset of ARF. Following onset of renal damage-->azotaemia, hyperphosphataemia, hyperkalaemia, hypocalcaemia, & hyperglycaemia. Isosthenuria is seen in dogs & reduced USG in cats due to osmotic diuresis. Calcium oxalate crystalluria is observed (3h-cat, 6h-dog). EG test kits are available. Sodium fluorescein in antifreeze solutions may be detected by Wood's lamp-check the paws, face, & vomitus. Renal ultrasonography may help.

6) Reduce further absorption (emesis or gastric lavage if 1-2h) then AC. Decontaminate the patient (wash paws, etc). Provide supportive therapy via aggressive IVFT to maintain renal perfusion. Consider peritoneal dialysis or haemodialysis (if available) early to aid excretion of EG. Bicarbonate therapy for metabolic acidosis. Mannitol to promote diuresis. Provide specific therapy via drugs that competitively inhibit alcohol dehydrogenase; ethanol or 4-methylpyrazole. Thiamine & pyridoxine enhance metabolism of glycoxylic acid to non-toxic metabolites.

Front 8

What are some causes of Acute Renal Failure (ARF) in dogs & cats?

Back 8

-Ethylene Glycol

-Easter Lily-->cats

-Raisin/grapes/sultana-->dogs

Front 9

1)What are the main classifications of neurotoxins?

2) What are the clinical signs & some examples of each?

Back 9

1) Excitatory neurotoxins & Inhibitory neurotoxins.

2) Excitatory neurotoxins: muscle twitching, tremors, tonic contractions, & seizures. Strychnine, metaldehyde, organophosphates/carbamates, certain recreational drugs (e.g. cocaine), & neurotoxic blue-green algae.

-Inhibitory neurotoxins: CNS depression & coma in conjunction w/respiratory depression & bradycardia. Alphachloralose & the avermectins.

-A combination of both signs may be observed in permethrin intoxication in cats, marijuana, or nicotine.

Front 10

Metaldehyde toxicity

1) What is it?

2) How does it cause toxicity?

3) What are the clinical signs?

4) How do you confirm intoxication?

5) What is proper treatment?

Back 10

1) A molluscicide

2) Inhibits GABA & decreases seizure threshold.

3) Abdominal discomfort, salivation, vomiting, diarrhea, tachycardia & tachypnea, hyperaesthesia, hyperthermia, & muscle tremors. +/-opisthotonus & convulsions. +/- CNS depression/narcosis. Liver failure may develop later.

4) By analysis of stomach contents, serum, & urine.

5) Gastric decontamination is preferable to emesis. Administer AC +/- sorbitol purgative. Provide IVFT, general nursing care (avoid external stimuli), cooling if hyperthermic. Muscle relaxants/anticonvulsant drugs therapy; diazepam +/- barbiturates. There is no specific therapy indicated but if there is severe metabolic acidosis then consider bicarbonate therapy. Can also consider Glutathione precursors to reduce the potential for liver damage/failure (e.g. SAMe).

Front 11

Permethrin Toxicity

1) Are dogs or cats more sensitive?

2) What does it affect?

3) What are the clinical signs?

4) What is proper treatment?

Back 11

1) Cats

2) Sodium channels-->repetitive nerve stimulation

3) Excitatory neurological signs (tremors, seizures) but you can see ataxia & depression.

4) Supportive tx in the UK. USA has methocarbamol-a central muscle relaxant.

Front 12

Chocolate Toxicity

1) What is the active ingredient?

2) What does it do?

3) What are the clinical signs?

4) How much is potentially lethal?
5) What is proper treatment?

Back 12

1) Theobromine

2) Antagonizes the effects of adenosine

3) Restlessness, panting, diuresis, vomiting, & diarrhea. +/-CNS excitation & cardiac arrhythmias.

4) 100-250 mg/kg.

5) Supportive w/IVFT; muscle relaxants/anticonvulsants or CNS signs. Antiarrhythmic drugs if cardiac arrhythmias are persistent. Beta-blockers for supraventricular tachycardia. Lignocaine for life-threatening ventricular tachycardia.

Front 13

Strychnine Toxicity

1) What is it?

2) How is it toxic?

3) What are the clinical signs?

4) How is intoxication confirmed?
5) What is proper treatment?

Back 13

1) Excitatory neurotoxin

2) Blocks the inhibitory effect of glycine at the level of the spinal cord, brain stem, & thalamus. Results in unchecked neuronal activity.

3) Highly exaggerated reflex arcs; mild to severe muscle spasm. +/- convulsion w/opisthotonus.

4) Gastric contents, serum, or urine.

5) Treatment is supportive.

Front 14

Organophosphates & Carbamates Toxicity

1) What are they?

2) How are they toxic?

3) What are the clinical signs?
4) How is intoxication confirmed?
5) What is proper treatment?

Back 14

1) Insecticides

2) Inhibition of acetylcholinesterase-->prolonged activity of acetylcholine at the NMJ.

3) Nicotinic signs: muscle tremors, generalized muscle tetany followed by weakness.

-CNS signs: anxiety, hyperactivity, tonic-clonic seizures to severe CNS depression.

-Muscarinic signs: salivation, lacrimation, urination, & defecation.

-Bradycardia, dyspnoea, & miosis may also occur.

4) *Route of intoxication determines the rapidity of onset of clinical signs. Cholinesterase activity of heparinised whole blood or atropine (low-dose).

Front 15

List 2 types of Inhibitory Neurotoxins

Back 15

1) Alphachloralose

2) Avermectins

Front 16

Alphachloralose Toxicity

1) What is it used in?

2) What effects tend to predominate?

3) What are the clinical signs?

Back 16

1) Rodenticide & bird poison

2) Depressant effects

3) Hypothermia, bradycardia, CNS & respiratory depression

Front 17

Avermectin Toxicity

1) What is it used in?
2) How does it work?
3) What are the clinical signs?

4) What is the prognosis?

Back 17

1) Ecto- & endo-parasiticides
2) Enhances GABA activity-->CNS depression
3) Bradycardia, respiratory depression, CNS depression & coma.
4) Dose-dependent & supportive care may be required for days-weeks.

Front 18

How are toxicoses associated with CNS depression treated?

Back 18

1) Induce emesis or gastric lavage if w/in 1-2h. Administer AC +/- sorbitol purgative.

2) Provide supportive therapy by IVFT, nutritionnal support, maintenance of body temperature, & respiratory support.

Front 19

Anticoagulant Rodenticide Toxicity

1) What is the common product ingested by dogs? cats?

2) How does this toxicity work?

3) What are the clinical signs?

4) What are the diagnostic tests & their results?

5) What is the proper treatment?

Back 19

1) Dogs: Rodenticide. Cats: Intoxicated rodent.

2) Inhibits vitamin K epoxide reductase.

3) Indicative of a secondary haemostatic disorder. Epistaxis, haemoptysis, dyspnoea due to haemorrhage into the lungs, haematoma formation.

4) PT & APTT. Prolongation of both-intrinsic & extrinsic coagulation factors are affected.

5) Reduce further absorption by inducing emesis or perform gastric lavage if w/in 1-2h of ingestion. Administer AC +/- sorbitol purgative. Provide specific therapy via Vitamin K1 therapy by SQ injection followed by oral administration (tx should be continued for a further 7d then coagulation re-assessed). Supportive therapy via blood transfusion, for both coagulation factors & O2-carrying capacity, if blood loss if life-threatening. Supplemental O2 may be required if intra-pulmonary haemorrhage is severe.

Front 20

What does Cholecalciferal rodenticide intoxication result in clinically?

Back 20

A combination of coagulopathy & hypercalcemia. Therapy is aimed at reduction of further exposure & treatment of hypercalcemia.

Front 21

Adder Bites

1) What areas does this typically affect?

2) What area is considered more severe?

3) What are the clinical signs?

4) What are the biochemical alterations?

5) What is the mortality rate?

6) What is the proper treatment?

Back 21

1) Head & face

2) The extremities

3) localized tissue necrosis, concurrent alteration in mentation, to death as a consequence of severe distributive shock, haemolysis, & DIC

4) Elevations in CK & liver enzymes

5) 3-4%

6) Supportive & symptomatic therapy via IVFT & analgesia. There is European adder anti-serum available-->may be of advantage in the management of severely affected cases.

Front 22

Investigation of suspected malicious poisoning

1) What should you take note of?

2) What steps should be taken in the investigation? (3)

Back 22

1) Careful notes & a detailed history

2) *Relate the clinical signs to potential intoxications.

*Collect appropriate samples which can be subsequently analyzed; serum & urine, vomitus/gastric contents. Consult a toxicologist for advice on sample collection & storage.

*PM exam & collection of appropriate tissues should be carried out in all fatalities. Collect tissue for histopathology (formalin fixation) & also for toxin assays (frozen).