Toxiocology cases Flashcards

1
Q

Define poison

A

A poison is a chemical which, when introduced to an organism, is capable of producing an unwanted effect.

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2
Q

Name hepatotxins, the use and the species affected

A
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3
Q

What are the top toxic agents in dogs?

A

Difenacoum or bromodiolone (anticoagulant rodenticide)

Chocolate

(including all types)

Ibuprofen

Paracetamol

Raisins, grapes, sultanas, currants

Xylitol

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4
Q

What are the top toxic agents in cats?

A

Lily species

Agent unknown

Benzalkonium chloride

Paracetamol

Meloxicam

Imidacloprid

Praziquantel

Moxidectin

Grapes, sultanas, raisins, currants

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5
Q

What are the top toxicc agents in rabbbits?

A

Anticoagulant rodenticides

(including bromadiolone and difenacoum)

Chocolate

Peace lily

Ivy

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6
Q

A 14 year old domestic short haired cat is presented with weakness and lethargy, progressing to collapse over 6 hours. On physical examination the cat demonstrates tachycardia dyspnoea, and hypersalivation. The mucous membranes are a dark red/muddy brown colour. The cat voids urine during examination which is also dark red. The cat has a history of chronic arthritis and has been on oral meloxicam. The owner ran out of the medication and gave the cat half an adult human paracetamol tablet the previous evening. Suspecting the signs to be an indication that the cat was painful, this morning the owner has given another half tablet in the past hour. You suspect paracetamol poisoning.

1) What emergency treatment may be indicated in this cat?

A

Antidote is acetylcysteine can be obtained from hospital and should be administered ASAP. Other emergency treatments include IVFT at shock rates. Indications for emesis <1-2 hrs so this cat may benefited is not drowsy, seizuring, already vomited and the substance doesn’t contain oily products, or additionally a strong acid or alkali- cats are made to vomit using an alpha two agonist. Apomorphine is ineffective in cats. A gastric lavage can be used in this case or additionally an absorbant with activated charcoal agents to prevent absorption in the GIT. If in doubt (which we might be in this case due to time) can use an absorbant.

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7
Q

A 14 year old domestic short haired cat is presented with weakness and lethargy, progressing to collapse over 6 hours. On physical examination the cat demonstrates tachycardia dyspnoea, and hypersalivation. The mucous membranes are a dark red/muddy brown colour. The cat voids urine during examination which is also dark red. The cat has a history of chronic arthritis and has been on oral meloxicam. The owner ran out of the medication and gave the cat half an adult human paracetamol tablet the previous evening. Suspecting the signs to be an indication that the cat was painful, this morning the owner has given another half tablet in the past hour. You suspect paracetamol poisoning.

The dark red/muddy brown mucous membrane colour is due to methaemoglobinemia – what is the mechanism of its formation in paracetamol poisoning and what are the clinical implications?

A

Methaemoglobin is an oxidised form of haemoglobin that cannot bind to oxygen which therefore results in a reduction in the oxygen carrying capacity in the blood therefore resulting in the clinical signs presented (tachycardia and dyspnoea). Paracetamol is metabolised in the liver by glucoronidation and oxidation, the glucuronide and sulphate conjugates are non toxic and therefore can be excreted in bile and urine. In most species the oxidation pathway is minor compared to glucoronidation (major pathway). Cats lack the enzyme (glucoronyl transferase) that conjugates the paracetamol products through glucoronidation. Therefore the oxidation pathway is exceeded/ saturatied therefore paracetamol is not metabolised and remains toxic. Any paracetamol that is not metabolised through the oxidation pathway is converted to an intermediate product that is called NAPQI which reacts with red cells through oxidation leading to methaemoglobins.

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8
Q

A 14 year old domestic short haired cat is presented with weakness and lethargy, progressing to collapse over 6 hours. On physical examination the cat demonstrates tachycardia dyspnoea, and hypersalivation. The mucous membranes are a dark red/muddy brown colour. The cat voids urine during examination which is also dark red. The cat has a history of chronic arthritis and has been on oral meloxicam. The owner ran out of the medication and gave the cat half an adult human paracetamol tablet the previous evening. Suspecting the signs to be an indication that the cat was painful, this morning the owner has given another half tablet in the past hour. You suspect paracetamol poisoning.

1) What emergency treatment may be indicated in this cat? Antidote is acetylcysteine can be obtained from hospital and should be administered ASAP. Other emergency treatments include IVFT at shock rates. Indications for emesis <1-2 hrs so this cat may benefited is not drowsy, seizuring, already vomited and the substance doesn’t contain oily products, or additionally a strong acid or alkali- cats are made to vomit using an alpha two agonist. Apomorphine is ineffective in cats. A gastric lavage can be used in this case or additionally an absorbant with activated charcoal agents to prevent absorption in the GIT. If in doubt (which we might be in this case due to time) can use an absorbant.

By what method would you obtain a definitive diagnosis in this case?

A

Serum or urine paracetamol concentation. Clinical signs, history and relevant lab concentration- Heinz body anaemia. If methaemoglin is >15% serum chemisty profile: increased liver enzymes, urinalysis indication methaemoglobin are elevated.

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9
Q

A 14 year old domestic short haired cat is presented with weakness and lethargy, progressing to collapse over 6 hours. On physical examination the cat demonstrates tachycardia dyspnoea, and hypersalivation. The mucous membranes are a dark red/muddy brown colour. The cat voids urine during examination which is also dark red. The cat has a history of chronic arthritis and has been on oral meloxicam. The owner ran out of the medication and gave the cat half an adult human paracetamol tablet the previous evening. Suspecting the signs to be an indication that the cat was painful, this morning the owner has given another half tablet in the past hour. You suspect paracetamol poisoning.

1) What emergency treatment may be indicated in this cat? Antidote is acetylcysteine can be obtained from hospital and should be administered ASAP. Other emergency treatments include IVFT at shock rates. Indications for emesis <1-2 hrs so this cat may benefited is not drowsy, seizuring, already vomited and the substance doesn’t contain oily products, or additionally a strong acid or alkali- cats are made to vomit using an alpha two agonist. Apomorphine is ineffective in cats. A gastric lavage can be used in this case or additionally an absorbant with activated charcoal agents to prevent absorption in the GIT. If in doubt (which we might be in this case due to time) can use an absorbant.

Why are cats more susceptible than dogs to some toxins such as paracetamol?

A

Because they lack the enzyme glucoronyl transferase.

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10
Q

A 14 year old domestic short haired cat is presented with weakness and lethargy, progressing to collapse over 6 hours. On physical examination the cat demonstrates tachycardia dyspnoea, and hypersalivation. The mucous membranes are a dark red/muddy brown colour. The cat voids urine during examination which is also dark red. The cat has a history of chronic arthritis and has been on oral meloxicam. The owner ran out of the medication and gave the cat half an adult human paracetamol tablet the previous evening. Suspecting the signs to be an indication that the cat was painful, this morning the owner has given another half tablet in the past hour. You suspect paracetamol poisoning.

1) What emergency treatment may be indicated in this cat? Antidote is acetylcysteine can be obtained from hospital and should be administered ASAP. Other emergency treatments include IVFT at shock rates. Indications for emesis <1-2 hrs so this cat may benefited is not drowsy, seizuring, already vomited and the substance doesn’t contain oily products, or additionally a strong acid or alkali- cats are made to vomit using an alpha two agonist. Apomorphine is ineffective in cats. A gastric lavage can be used in this case or additionally an absorbant with activated charcoal agents to prevent absorption in the GIT. If in doubt (which we might be in this case due to time) can use an absorbant.

What is the primary target organ?

A

Liver

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11
Q

A 14 year old domestic short haired cat is presented with weakness and lethargy, progressing to collapse over 6 hours. On physical examination the cat demonstrates tachycardia dyspnoea, and hypersalivation. The mucous membranes are a dark red/muddy brown colour. The cat voids urine during examination which is also dark red. The cat has a history of chronic arthritis and has been on oral meloxicam. The owner ran out of the medication and gave the cat half an adult human paracetamol tablet the previous evening. Suspecting the signs to be an indication that the cat was painful, this morning the owner has given another half tablet in the past hour. You suspect paracetamol poisoning.

1) What emergency treatment may be indicated in this cat? Antidote is acetylcysteine can be obtained from hospital and should be administered ASAP. Other emergency treatments include IVFT at shock rates. Indications for emesis <1-2 hrs so this cat may benefited is not drowsy, seizuring, already vomited and the substance doesn’t contain oily products, or additionally a strong acid or alkali- cats are made to vomit using an alpha two agonist. Apomorphine is ineffective in cats. A gastric lavage can be used in this case or additionally an absorbant with activated charcoal agents to prevent absorption in the GIT. If in doubt (which we might be in this case due to time) can use an absorbant.

What signs are likely to be seen in this cat as the toxicosis progresses

A
  • Early effects 1-4 hrs: progressive cyanosis, tachypnoea, dyspnoea, tachycardia, MM are brown in colour, weakness and lethargy may be absorbed
  • Late effects Methaemoglobinurea occurs at 4-24hrs. facial and paw oedema, depression, vomiting, anorexia, vocalisation, dark brown blood may be noticed in the presence of methaemoglobinaemia, anaemia, evidence of haemolysis. Less common effects include hyper/hypo thermia, ataxia and lethargy.
  • Later effects 2-7d: raised liver enzymes and bilirubin in cats, hepatic necrosis is not the casue of fatality in cats and die due to severe methaemoglobinaemia, other signs include intravascular haemolysis, jaundice and other evidence of liver damage, coma, convulsions and pulmonary oedema.
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12
Q

A 14 year old domestic short haired cat is presented with weakness and lethargy, progressing to collapse over 6 hours. On physical examination the cat demonstrates tachycardia dyspnoea, and hypersalivation. The mucous membranes are a dark red/muddy brown colour. The cat voids urine during examination which is also dark red. The cat has a history of chronic arthritis and has been on oral meloxicam. The owner ran out of the medication and gave the cat half an adult human paracetamol tablet the previous evening. Suspecting the signs to be an indication that the cat was painful, this morning the owner has given another half tablet in the past hour. You suspect paracetamol poisoning.

By what mechanism does paracetamol produce hepatocellular damage?

A

Any paracetamol that is not metabolised through the oxidation pathway is converted to an intermediate product that is called NAPQI which reacts with cell membrane molecules resulting in widespread hepatocyte damage and death leading to acute liver necrosis.

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13
Q

A 14 year old domestic short haired cat is presented with weakness and lethargy, progressing to collapse over 6 hours. On physical examination the cat demonstrates tachycardia dyspnoea, and hypersalivation. The mucous membranes are a dark red/muddy brown colour. The cat voids urine during examination which is also dark red. The cat has a history of chronic arthritis and has been on oral meloxicam. The owner ran out of the medication and gave the cat half an adult human paracetamol tablet the previous evening. Suspecting the signs to be an indication that the cat was painful, this morning the owner has given another half tablet in the past hour. You suspect paracetamol poisoning.

What is the specific antidote to paracetamol and explain its mechanism of action?

A

Acetylcysteine which is a precursor of gluthione which is used in the metabolism of highly reactive intermediate product NAPQI in red cells and liver. It also acts on NAPQI to form a conjugate that is excreted (although slow). Acetylcysteine can be oxidised in the liver to form sulphates that reacts with the paracetamol products that results in non-toxic products.

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14
Q

A 14 year old domestic short haired cat is presented with weakness and lethargy, progressing to collapse over 6 hours. On physical examination the cat demonstrates tachycardia dyspnoea, and hypersalivation. The mucous membranes are a dark red/muddy brown colour. The cat voids urine during examination which is also dark red. The cat has a history of chronic arthritis and has been on oral meloxicam. The owner ran out of the medication and gave the cat half an adult human paracetamol tablet the previous evening. Suspecting the signs to be an indication that the cat was painful, this morning the owner has given another half tablet in the past hour. You suspect paracetamol poisoning.

Is there any safe treatment which might reverse/treat the methaemoglobinaemia?

A

Methylene blue – increases methaemoglobin reduction through enzymes through NADPH. Ascorbic acid can also be used as it acts as an antioxidant and can reduce NAPQI binding to red cells.

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15
Q

A 14 year old domestic short haired cat is presented with weakness and lethargy, progressing to collapse over 6 hours. On physical examination the cat demonstrates tachycardia dyspnoea, and hypersalivation. The mucous membranes are a dark red/muddy brown colour. The cat voids urine during examination which is also dark red. The cat has a history of chronic arthritis and has been on oral meloxicam. The owner ran out of the medication and gave the cat half an adult human paracetamol tablet the previous evening. Suspecting the signs to be an indication that the cat was painful, this morning the owner has given another half tablet in the past hour. You suspect paracetamol poisoning.

List other supportive treatment that could be given to this cat

A

IVFT, SAMe antioxidants used to support the liver. Whole blood transfusions may be required in cats with a severe drop in PCV or evidence of severe haemolysis. Place the cat in an oxygen tank. Cimetidine is an antihistamine.

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16
Q

Mr Black, the elderly owner of “Percy” a 3 year old African grey parrot phones the veterinary practice at 5PM after coming home and finding the bird quieter than normal, unable to perch and sitting on the floor and unsteady on its feet.

Percy is on a commercial seed based parrot mix and does not like to eat much fresh fruit and vegetables.

The owners allow the bird free access to the house for 1-2 hours in the morning and evening when they are at home. During the day the bird remains in its large cage, in which it has been housed for 2 years. The owner reports no change in routine or diet. He noticed that Percy seems to have lost his appetite but was not too worried about it because he saw him still drinking frequently. He also has a couple of fish tanks. On initial examination the bird is clearly unsteady on its feet and on handling.

There is a small amount of black/dark green fluid faeces smeared on the underside of the tail feathers and around the cloaca.

Anaesthesia is performed to permit radiography and venous sampling for haematology and biochemistry: Blood sampling (maximum volume approx 2mls (0.5% of body weight))

Radiography: Lateral and ventrodorsal whole body views

Describe the mechanism by which toxicity is produced in this case. Lead is the toxin of choice

A
  1. Lead >10mg/dl can diffuse across the blood brain barrier and can have cellular and neurological effects. Cellular effects: activated G protein that opens calcium channels causing release of calcium from endoplasmic reticulum. Lead enters the cell through calcium channels and binds with calmodulin leading to inflammation, apoptosis, muscle contractions and immune responses inappropriately produced. neurological effects: lead disrupts communication through astrocytes and endothelial cells. Plasma moved into interstitial spaces lading to increase in ICP causing oedema, encephalopathies and irreversibly brain damage.
17
Q

Which organ systems may be affected by lead toxicity?

A
  1. CNS, repro, MSK, urinary, neuro, CRS.
18
Q

Devise a treatment program for a bird with lead toxicosis

A
  1. Treatment consists of an antidote: chelation therapy to bind the lead in the GIT. Three chelation agents can be used: DMSA, EDTA and D-penecillamine. Certain foods can also speed up the process including high fibre. Occasionally surgery may be indicated if a large piece of lead has been ingested.
19
Q

How would we treat an aggressive bird with lead poisoning?

A

he should be hospitalised and monitored closely for signs of improvement.

20
Q

How can we prevent lead toxicity in birds?

A

Chelation agents efficacy has been proven in small animals but not in birds and has to be given IM so can cause muscle damage and pain- and if given IM you cannot give large amounts too.

21
Q
  1. What is the toxicant found in acorns?
A

Tannins – broken down to gallic acid and tannic acid (cause birth defects if eaten in sufficient quantities by pregnant cattle)

22
Q

A group of yearlings is moved to a new field bounded by mature trees. The trees include some mature Oak. The cattle have been grazing around the base of these trees for the last 5 days. A number of the animals are now demonstrating clinical signs including anorexia with dark faeces which have a mucoid covering film. It is noticeable that the animals are spending an increased time at the water trough. One of the cows rapidly becomes prostrate (lying stretched out on ground with face on the floor), is jaundiced and had a swollen abdomen. This animal subsequently dies and is submitted for necropsy.

These animals have acorn intoxication.

  1. What is the primary target organ and how might this relate to clinical signs in this case?
A

Kidneys – water trough time = Polydipsia, ulceration and damage causing diarrhoea

Tannic acid – ulceration of the mouth, oesophagus and rest of intestines, also damages the kidneys

It is the renal failure that causes most of the deaths `associated with acorn poising

Generally only affects small numbers of the herd as will only develop in those who eat large quantities

23
Q
  1. What is the mechanism by which the acorn toxicant produces its effects?
A

Acorns contain gallotanin, in the rumen this is broken town into tannic acid and gallic acid

Hydrolysed tannins can be absorbed and become bound to plasma proteins and endothelial proteins which leads to haemorrhage and fluid loss from blood vessels resulting in oedema

24
Q
  1. Which other plants may produce similar toxic effects on this target organ, the same organ as acorns?
A

Red root pig weed, bracken, ragwort, rhododendron

25
Q
  1. What are the likely post mortem findings of acorn toxicity?
A

Acorns in rumen occasionally

Dark brown colouration of kidney cortex

Dark red urine

Gastric ulceration

26
Q
  1. What can be done to support the surviving animals with acorn toxicity?
A

No specific antidote

Remove from acorn pasture in early stages – most recover in 2-3 days

Fluid therapy to keep kidneys functioning, broad spec Abs and single dose of laxative mineral oil may help in early stages

Cattle that survive normally economically worthless and PTS best option

Prevent by feeding calcium hydroxide (hydrated lime) can be a way of significantly reducing effect of toxin

27
Q

Which species are affected by acorn toxicity commonly?

A

Sheep and cattle

28
Q
  1. What is the normal prognosis in animals showing clinical signs of acorn toxicity?
A

BAD

29
Q

What is the plant? Toxicant? MOA? Clinical signs?

A

Top left = Azealia geisha red (toxic to goats)

  • Toxicant – grayanotoxins
  • MOA – prolonged Na channel activation and cell depolarisation leading to overstimulation of CNS
  • Clinical signs – within 6 hrs of exposure: depression, head pressing, severe salivation, abdominal cramps and bloat, vomiting, regurgitation, muscle tremors
30
Q

What is the plant? Toxicant? MOA? Clinical signs?

A

bracken (toxic to ruminants)

  • Toxin – thiaminase, ptaquiloside
  • MOA – effects cattle and sheep and causes bone marrow disease
  • CS – bone marrow suppression, retinal degeneration, thiamine deficiency and bladder cancer
31
Q

What is the plant? Toxicant? MOA? Clinical signs?

A

deadly nightshade (poisonous and causes goat polio)

  • Whole plant poisonous
  • MOA – contains atropine and related alkaloids which act on muscarinic receptors
  • CS – increase HR, nervous excitement, inability to stand, green diarrhoea, dilated pupils and gastric stasis
32
Q

What is the plant? Toxicant? MOA? Clinical signs?

A

Top right – rhododendron (toxic to all animals)

  • Toxin – andromedotoxin
  • MOA- same as Azealia
  • CS – GI signs predominate