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Principles of Toxicology > Poisons and Toxins > Flashcards

Poisons and Toxins Flashcards

1
Q

Define a poison

A

A substance that is capable of causing the illness or death of a living organism when introduced or absorbed

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2
Q

What are classified as natural poisons?

A

Plants
Animals
Fungi
Inorganic material

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3
Q

What are classified as chemical poisons?

A

Drugs and medicines (human or veterinary)
Pesticides (domestic or agricultural)
Household chemicals
Industrial chemicals

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4
Q

What is the mechanism of paracetamol toxicity?

A

Saturation of metabolic pathways - toxic metabolite conjugated by glutathione which is promptly depleted
Cats lack the metabolic capacity to detoxify paracetamol

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5
Q

What are the early clinical manifestations of paracetamol toxicity?

A

Progressive cyanosis
Brown/blue MM
Weakness and lethargy

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6
Q

What are the clinical manifestations of paracetamol toxicity between 4 and 24 hours?

A

Facial and paw oedema
Vomiting
Depression
Dark brown blood - mtheaemoglobinemia

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7
Q

What are the clinical manifestations of paracetamol toxicity that appear after a day has passed?

A

Severe methaemoglobinemia

Hepatic necrosis

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8
Q

What are the signs of methaemoglobinaemia?

A

Blue or brown mucous membranes
Arterial blood is chocolate brown in colour and remains dark on aeration
Cyanosis fails to respond to oxygen therapy

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9
Q

What level of paracetamol is toxic to dogs and cats?

A 
Dogs = 150mg/kg
Cats = 20mg/kg
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10
Q

What is the treatment for paracetamol toxicity?

A

Emesis with apomorphine in dogs and xylazine in cats
Activated charcoal
Antidote is acetylcysteine which is a precursor of glutathione
SAMe 90mg twice daily for 3 d the 90mg daily for 14 d
Ascorbic acid 30-40mg/kg every 6 hrs for at least 36 hrs

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11
Q

What is the dosing of acetylcysteine in cats?

A

For 20-60mg/kg paracetamol 140mg/kg by slow IV infusion over 6 hours
For >60 mg/kg paracetamol or if evidence of metHb 280mg/kg orally or by slow IV over 6 hours
After 6 hours 70mg/kg orally or IV over 20 minutes every 6 hours for 2-4 days

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12
Q

What is the dosing of acetylcysteine in dogs?

A

> 150mg/kg paracetamol or evidence of metHb 280mg/kg orally or by slow IV over 6 hours then 70mg/kg orally every 6 hours for 2-4 days

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13
Q

What should be monitored after paracetamol poisoning?

A

For 1 week liver function, clotting, renal function and full blood count

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14
Q

Why does NSAID toxicity occur?

A

Mainly due to COX-1 inhibition

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15
Q

What are the early manifestations of NSAID toxicity?

A

Gastrointestinal erosion, ulceration an possibly perforation
Vomiting and diarrhoea both may be bloody
Rarely CNS symptoms (ataxia, lethargy, drowsiness)

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16
Q

What are the late manifestations of NSAID toxicity?

A

Renal failure

Hepatic failure

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17
Q

What is the treatment for NSAID toxicity?

A

Decontamination using emesis or activated charcoal
Prevention of gastric ulceration using H2 receptor antagonists, proton pump inhibitors or ulcer healing or coating agent
Prostaglandin supplementation with Misoprostol
Maintenance of renal function with IVFT

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18
Q

What are the clinical effects of theobromine (chocolate) poisoning?

A

Vomiting, diarrhoea, polydipsia, salivation - dehydratioin
CNS/myocardial stimulation - tremor, convulsions, tachycardia, hypertension, arrhythmia
Renal failure
Fatal cases due to severe convulsions/circulatory failure

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19
Q

How is theobromine toxicity managed?

A

Emesis, repeat dose activated charcoal, adequate rehydration, surgery observation for up to 72 hours
Monitor vital signs, ECG, benzodiazepines for CNS stimulation, treatment of arrhythmia is lidocaine

20
Q

Where do tremorgenic mycotoxins come from?

A

Food waste and rubbish, mouldy bread, mouldy rice, dairy products, mouldy cream cheese, mouldy macaroni cheese, mouldy blue cheese and blue cheese, mouldy fallen fruit and nuts, silage, compost

21
Q

What is the mechanism of tremorgenic mycotoxin toxicity?

A

Penitrem A may interfere with release of neurotransmitters

May act synergisitically

22
Q

What are the clinical effects seen within 3 hours of tremorgenic mycotoxin ingestion?

A

Vomiting, ataxia, whole-body muscle tremors, rigidity with hyperextension of extremities, hyperactivity, hyperaesthesia, tachycardia, panting, tachypnoea, nystagmus and blepharospasm

23
Q

What are the clinical effects seen in severe cases of tremorgenic mycotoxin ingestion?

A

Severe tremors and opisthotonus, convulsions and coma with paddling
Rarely aspiration
Increased muscular activity - hyperpyrexia, exhaustion, rhabdomyolysis, dehydration and hypoglycaemia

24
Q

How is tremorgenic mycotoxin ingestion managed?

A

Decontamination by emesis, gastric lavage and activated charcoal
Anticonvulsants such as benzodiazepines, barbiturates, methocarbamol
Supportive care - rehydration, cooling measures, ventilation, antiemetics, observe for 24-48 hours

25
Q

What allium species are poisonous?

A

Leeks, onions, shallots, spring onions, garlic and chive

26
Q

What animals are susceptible to allium toxicity?

A

Dogs, cats, sheep, cattle and goats

27
Q

What is the mechanism of action of allium toxicity?

A

Organosulphoxides in plants convert to organic sulphur compounds (n-propyl disulphide G6PD) when traumatised which enters erythrocytes and reduces the protective effect of glutathione
Mixed sulphide bond forms between Hb and glutathione resulting in Heinz bodies
Damaged erythrocytes removed from the circulation inducing anaemia

28
Q

What are the clinical effects of allium toxicity?

A

Signs of haemolysis can be delayed for 1-5 days
GI effects (vomiting, inappetance, onion smelling breath)
Heinz body anaemia (lethargy, pale MM, tachycardic, tachypnoeic)
Haematuria and haemoglobinurea
Urine may smell of onions
Mild methaemoglobinaemia
In severe cases icterus due to haemosiderin in the liver

29
Q

What is the toxic does of allium?

A

Not known as seems to vary

30
Q

How is allium toxicity managed?

A

Emesis, activated charcoal
Monitor haematology, IV fluids
High protein diet may promote restoration of glutathione stores
Supplement oxygen and oxyglobin may be given in severe cases or a blood transplant

31
Q

What is the mechanism of toxicity of anticoagulant rodenticides?

A

Vitamin K is essential for production of factors II, VII and X which are essential for the production of fibrin
Anticoagulants inhibit Vitamin K epoxide reductase so there is a depletion of Vitamin K and therefore a reduction in factors II, VII and X

32
Q

What are the clinical effects of rodenticide toxicity?

A

Rare as clotting factors have long half life so there is a delay between exposure and clinical effects
Elevation of clotting or PTT
Main effect is haemorrhage but may present with dyspnoea, lethargy, weakness or anorexia
Bruising, bleeding from gums, nose, GI tract and wounds

33
Q

How is rodenticide toxicity managed?

A

Decontamination if <2 hours previously
Blood tests
Vitamin K therapy if symptomatic or elevations in PTT

34
Q

What is the dose of Vitamin K used to treat rodenticide toxicity?

A

2-5mg/kg IM or SC daily at multiple injection sites until PT normalises
Once PT normalised Vitamin K orally for 2-3 weeks 2-5mg/kg in divided doses gradually reducing

35
Q

What important information needs to be collected to assess the severity/likely severity of rodenticide toxicity?

A 
Full trade name/active ingredient
Household or commercial product
Lifestyle
Concentration %
Acute/chronic exposure
Amount eaten
36
Q

What are the different types of molluscicides?

A

Metaldehyde
Methiocarb
Aluminium sulphamate
Ferric phosphate

37
Q

What is the mechanism of toxicity of molluscicides?

A

Not fully understood
Increase in muscular activity leading to hyperthermia
Rapid cellular necrosis and metabolic acidosis

38
Q

What are the clinical effects of molluscicide toxicity?

A

Hypersalivation, vomiting, diarrhoea, ataxia, panting, tremors, convulsions, hyperthermia
Respiratory and cardiac effects less common

39
Q

How is molluscicide toxicity managed?

A

Emetics? Gastric lavage? Activated charcoal

Managements of convulsions using benzodiazepines or propofol CRI

40
Q

What are the mechanisms of toxicity of European adder poisoning?

A

Significant morbidity but low mortality
Hypovolaemia and oedema due to increased vasular permeability due to release of mediated histamine, serotonin, bradykinin and prostaglandin
Local haemorrhage due to cytolytic and haemolytic factors
Cardiac effects due to impaired cirulation and poor perfusion of the myocardium
Renal impairment due to hypovolaemic shock

41
Q

What are the local clinical effects of European Adder poisoning?

A

Localised painful swelling
Swelling oedema may last days
Necrosis is rare

42
Q

What are the systemic clinical effects of European Adder poisoning?

A 
Shock, collapse and hypotension
Pain, panting, hypersalivation, mental status change, hyperthermia, bruising, pale MM, tachypnoea, lameness
Coagulopathy
Renal effects
Hepatic effects
Cardiac effects
43
Q

How is European Adder toxicity managed?

A 
Keep animal still and quiet
IVFT
Antivenom
BP, pulse, respiration, temperature
ECG
Check for coagulopathy, renal and hepatic parameters
44
Q

What are the indications for using antivenom to treat European Adder poisoning?

A

Any animal with bite to face or with severe swelling
Swelling beyond the next major joint proximal to bite
Hypotension unresponsive to IVFT
Evidence of coagulopathy
Any ECG abnormality

45
Q

What is the dose of European Adder antivenom used?

A

10ml ampoule diluted in 2-3 volumes of isotonic saline by slow IV injection or by IV infusion over 30 minutes

46
Q

What are the two types of adverse reaction to antivenom?

A

Anaphylactic reactions - urticaria, vomiting, fever and tachycardia. In severe cases hypotension and bronchospasm
Serum sickness occurs days later characteristed by fever, urticaria, joint pain and lymphadenopathy

47
Q

What are other treatment options that could be used instead/as well as antivenom?

A

Analgesia
Antibiotics
Antihistamines
Steroids

Principles of Toxicology (3 decks)

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