Common Intoxications

Question 1

What is the mechanism of action of ibuprofen toxicity?

Where are there adverse affects? (2)

Answer 1

• competitive inhibition of COX enzymes results in
• Reduced production of prostaglandins
• Needed for general repair processes in the body
• adverse effects on
• homeostatic control of renal blood flow
• gastric mucosal integrity

Question 2

Name the 2 benefiical effects of prostaglandins in the GI tract

Answer 2

• Increased secretion of mucous & bicarb by gastric epithelium
• maintenance of mucosal blood flow

Question 3

What is the source of an iburprofen overdose? (2)

Answer 3

• Misguided attempts by owners to medicate pet
• Accidental access – just stealing a packet off the bench

Question 4

How does iburprofen dose affect the adverse effects?

Answer 4

Dose related effects are quite common (across a range of toxins too)
Low doe may just see gastric ulcer
Higher dose – signs of AKI (may or not be reversible)
Very high dose – seizures and imminent death

Question 5

Can veterinary NSAIDs have the same effect as iburprofen?

Answer 5

Carprofen and meloxicam – commonly use, wide therapeutic dose

• >5 times therapeutic dose à GI signs
• >10 times therapeutic dose à AKI

Question 6

What are the GI clinical signs of iburprofen toxicity?

Answer 6

GI signs (huge range):

• Nausea
• Vomiting, diarrhoea
• Anorexia
• Haematemesis
  
  • Especially if there is gastric ulcers
• Melaena
• Abdominal pain
  
  • Ulcer can cause significant pain

Worst case scenario:

• Major GI bleed
  
  • Pale mm
  • Hypovolaemia
• Ulceration progresses to perforation and septic peritonitis
  
  • Congested mm?
• Can be fatal

Question 7

What are the renal clinical signs of iburprofen toxicity?

Answer 7

Renal signs (v. relevant with iburprofen):

• Polydipsia
• Polyuria
• Weak/lethargic
• Signs of azotaemia
• Anorexia (due to GI injury or a build up of waste)
• Vomiting (due to GI injury or a build up of waste)

Worst case scenario:

• Oliguria (reduced urine output) à anuria (AKI has then become complete kidney failure at this point)
  
  • Catch them at oliguria and can potentially reverse kidney injury
• Death

Question 8

What are the increased risk factors with iburprofen toxicity? (4)

Answer 8

• Cats might be more at risk than dogs
  
  • Cats have a poor glucuronidation pathway which affects metabolism of many toxins
  • Dogs can deal with the toxins better than cats
• Pre- existing renal disease
  
  • Older dogs and cats
• Dehydration
• Hypotension – reduction in renal blood flow or GI integrity

Question 9

What in chocolate makes animals sick?

Answer 9

Theobromine

Question 10

What is the mechansm of action of theobromine toxicity?

Answer 10

• Theobromine is amethylxanthine = CNS stimulation
• ­Increased catecholamine release (adverse effect on contractility)
• inhibition of Ca re-uptake by cells = Increased ­ heart & skeletal muscle contractility
• high fat/sugar content of chocolate = vomiting/GI signs

Question 11

Which chocolate is most toxic?

Answer 11

Dark chocolate

Question 12

How would an animal have acces to theobromine? (2)

Answer 12

• Accidental
• Misguided owners

Question 13

What does theobromine toxicity depend on?

Answer 13

The type of chocolate, amount and the individual’s ability to deal with the dose which can vary.

Question 14

What are the variety of clinical signs for theobromine toxicity?
Mild signs, GI signs, Cardiotoxicois, CNS signs..

Answer 14

Mild signs:

• Agitation
• Restless/hyperactive

GI signs:

• Vomiting
• Diarrhoea
• Polyuria/polydipsia

Cardiotoxicosis

• Tachycardia
• Arrhythmia
  
  • Supra ven t-cardia
  • VPCs
  • Listen to the heart and feel the pulse to identify this

CNS signs

• Ataxia
• Tremor/seizures
• Hyperthermia

Question 15

How can we manage theobromine toxicity? (6)

Answer 15

• Gastric decontamination
  
  • delayed gastric emptying ~6 hrs
  • Therefore may still be worth going through gastric decontamination up to 6 hour later
• Repeat doses of activated charcoal
  
  • enterohepatic circulation occurs
• Close monitoring
  
  • ECG – looking for arrhythmia
  • blood pressure – hypo or hypertensive and then means we can manage this
• IVFT to enhance excretion
• Drug options:
  
  • b blockers for tachycardia
  • diazepam for muscle tremors
  • anti convulsants
• Encourage urination = elimination of metabolites

Question 16

Where is rodenticide toxicity most common?

Answer 16

Dogs

Question 17

What are the sources of rodenticide poisoning? (5)

Answer 17

• 1st generation (need repeat exposure?)
  
  • warfarin
  • dicoumarol
• 2nd generation (more potent, single dose, longer acting) – more powerful the rat doesn’t need to keep coming back for the bait like the 1st gen
  
  • brodifacoum
  • bromadiolone
  • Difenacoum

Question 18

What is the mechanism of rodenticde toxicity?

Answer 18

• inhibits vitamin K epoxide reductase (responsible for activating vitamin K clotting factor system). Need vitamin K to activate.
• prevents conversion of vitamin K epoxide to its active form
• prevents activation of vitamin K dependent clotting factors
• II, VII, IX and X

Question 19

Other than anti-coagulants, what else is in rodenticide which can cause issues?

Answer 19

Cholecalciferol here but this is a vitamin D analogue

Question 20

What happens 1-3 day (or up to 7 days) after ingestion of rodenticide?

Answer 20

Spontaneous bleeding

Question 21

What are the clinical signs of rodenticide toxicity? (6)

Answer 21

• Thoracic haemorrhage – can be dyspneic:
  
  • haemothorax
  • pulmonary haemorrhage
  • submucosal tracheal bleeding
• GI bleeding
• Epistaxis
• Haemarthrosis
• CNS bleeds
• Venupuncture sites

Question 22

What are the clinical signs of rodenticide toxicity consistent with? (what is there is a defect in?)

Answer 22

Defect in secondary haemostasis

Question 23

How can we diagnose rodenticide toxicity?

Answer 23

• History
• access?
• Clinical signs
• delayed onset!
• Activated coagulation time – prolonged 2-20 times normal (not used as much)
• PT – prolonged 2-6 times normal
• APTT – prolonged 2-4 times normal (goes up second)
• Platelet count normal or slightly low (used up by bleeds)

Question 24

Which lab test is the first to beome abnormal with rodenticide poisoning?

Answer 24

PT – prolonged 2-6 times normal

Question 26

How can you manage rodenticide toxcity? (3)

Answer 26

* Decontamination if no clinical signs of bleeding * Too late to make them vomit.. * If already bleeding depends on how critical the patient is… * plasma transfusion to provide clotting factors * Fresh plasma or frozen plasma??? (fresh is better than frozen tho) * +/- whole blood/packed red cells * antidote: vitamin K (takes 6-12 hours to help) * long course for 2nd generation toxins * cage rest +/- oxygen? * Anaemic/hypovolaemic need to rest

Question 27

Where is ethylene glycol toxicity seen?

Answer 27

Cat

Question 28

What are the sources of ethylene glycol? (5)

Answer 28

* antifreeze * screen washes, brake fluid * inks, coolants * sweet aromatic smell & taste- attractive to dogs and cats? * ??malicious poisoning occ suspected – people are quick to blame people…

Question 29

What is the mechanism of ethylene glycol toxicity?

Answer 29

Converted by alcohol dehydrogenase in the body = toxic metabolites

Question 30

Ethylene glycol is metablised and the products formed can form issues, name what these are and the effects of these.

Answer 30

Question 31

What is the mechanism of action causing metabolic acidosis and hypocalcaemia with ethylene glycol?

Answer 31

Calcium in blood and tissues combines with oxalic acid = calcium oxalate precipitates * proximal renal tubule and around small vessels = AKI * meninges = CNS signs * myocardium and lung = cardiorespiratory signs

Question 32

What are the clinical signs of ethylene glycol toxicity in stage 1?

Answer 32

Stage 1 (from 30 mins up to 12 hours) * CNS depression (ataxia, weakness) * vomiting

Question 33

What are the clinical signs of ethylene glycol toxicity in stage 2?

Answer 33

Stage 2 (12-24 hours) * cardiopulmonary phase * tachycardia, tachypnoea, arrhythmia * hypo/hypertension * pulmonary oedema * seizures

Question 34

What are the clinical signs of ethylene glycol toxicity in stage 3?

Answer 34

Stage 3 (24-72 hours but can be within 1-3 hrs in cats) * Renal phase * signs associated with azotaemia * oliguria = anuria

Question 35

How can we diagnose ethylene glycol toxcity?

Answer 35

* Clinical signs – weak, collapsed with some resp signs, tachycardia * Urinalysis: * calcium oxalate crystals within 3-6 hrs * isosthenuria * Increased­ protein, haematuria * Blood tests * Decreased iCa * azotaemia (­Increase urea and creatinine) * ­ Increase glucose – can be stress but when you see with the above it does tick the boxes * Increased osmolality, acidaemia, metabolic acidosis with an increased anion gap (often 40-50 mEq/l) Residues in urine * Ethylene glycol, oxalate detected in urine, blood and tissues * Colorimetric kits detect ethylene glycol in urine in the first 24 hours. * patient side tests suboptimal sensitivity

Question 36

What is the prognosis and treatment for ethylene glycol treatment?

Answer 36

* Prognosis very poor because often late stage presentation * Decontamination: if \<1 hr since exposure * emesis? * activated charcoal not helpful * Management as for AKI * IVFT * close monitoring of urine output * peritoneal dialysis? * Antidote: * ethanol (or vodka)-only if not azotaemic * inhibits alcohol dehydrogenase * Pure alchohol – vodka being the purest you can buy inhibits the first stage.

Question 37

What is the mechanism of toxicity for Household cleaners & bleach (Sodium hypochlorite)?

Answer 37

•Direct mucosal damage

Question 38

What are the clinical effects of consuming bleach/household cleaner?

Answer 38

* Hypersalivation * Vomiting * Lethargy * Reduced Appetite

Question 39

What is the treatment for consuming bleach and household items?

Answer 39

* Detoxification: dilution * Supportive care

Question 40

What is the strategic approach to poison cases?

Answer 40

* Identify the toxin * Prevent further exposure * When did access occur? * Identify the best treatment * Is treatment necessary? * Is treatment appropriate? * Consider the prognosis * If you know this then discuss with O. Esp things like ethylene glycol where we know there is a bad prognosis.

Question 41

What is the mechanim of bracken toxicity in LA?

Answer 41

* bone marrow suppression * retinal degeneration * thiamine deficiency

Question 42

What are the risk factors with bracken toxicity? (3)

Answer 42

* part of the plant consumed (rhizome, shoots) * palatability vs availability of other food * age (experience?) of animal?

Question 43

What are the clinical signs associated with sub acute disease with bracken toxicity? (6)

Answer 43

* depression and poor appetite * scouring (bloody) and tenesmus * pyrexia (reduced neuts =2ry infection common) * non regenerative anaemia * coagulopathy associated with reduced platelets * epistaxis * vaginal bleeds * bruising * weak =recumbent =death

Question 44

What is chronic disease of bracken toxicity? What are the clinical signs? (4)

Answer 44

Chronic disease (small amount consumed over a long period) àenzootic haematuria due to neoplastic disease in the bladder * persistent haematuria * severe cases = blood loss, dysuria with blood clots passed * +/- intestinal wall neoplasia * chronic weight loss

Question 45

What is it that causes toxicity with bracken poisoning in horses? What are the signs (3)

Answer 45

* Thiaminase causes * chronic ataxia * weakness * paralysis

Question 46

How can you prevent bracken toxicity in sheep? (3)

Answer 46

* limit access to pastures with bracken if grazing is poor * avoid access to recently ploughed land where there might be exposed rhizomes and new shoots * control bracken by burning, ploughing, reseeding and herbicide

Question 47

What are the mechanisms of copper toxicosis in LA? (2)

Answer 47

* direct irritant * oxidative injury * Heinz body * methaemoglobinaemia * haemolysis = nephrosis

Question 48

What are the sources for copper toxicosis? (9)

Answer 48

Feed: * concentrate feed with * high Cu * low Mb * pasture, silage, root crops from ground with added pig/poultry manure * distillery by-product feeds * concentrate with palm oil or molassed sugar beet pulp Others: * cattle supplements/licks containing copper * sulphate foot baths * fungicide treated timber * pasture treated with Cu sprays for snails (liver fluke) * water, soil

Question 49

What are the risk factors for copper toxicity in sheep?

Answer 49

* highly susceptible * ­ in Texels, Blue Faced Leicesters? * growing lambs \> ewes * liver cells have high affinity for Cu * mitochondrial and lysosomal storage * slow excretion of Cu in bile * stress related release of liver copper stores = disease * shearing * movement * weather

Question 50

What are the clinical signs for copper toxicosis? (9)

Answer 50

Acute haemolytic crisis: * red/brown urine * icterus/jaundice rather than pale mm * weak/collapsed * tachypnoea/tachycardia Liver necrosis: * anorexia * severe GI signs (diarrhoea) à dehydration, shock * abdominal pain/colic * icterus/jaundice * weak/collapsed

Question 51

How can you diagnose copper toxicity in sheep?

Answer 51

* Lesions * icterus, large pulpy spleen * ‘Gunmetal’ bluish black kidneys * tan/bronze liver * swollen necrotic hepatocytes * vacuolation * periportal fibrosis * Diagnosis * Increased­ serum bilirubin * Increased­ AST, SDH and LDH * copper levels? * serum * liver * kidney

Question 52

How can you treat copper toxicity?

Answer 52

* Ammonium tetrathiomolybdate * s/c every other day for 3 days…. Decreased Cu absorption and ­increased excretion from liver •expense?

Question 53

What are alfatoxins in poultry?

Answer 53

* most common and economically important mycotoxin * produced by Aspergillus flavus +/- Aspergillus parasiticus * Source: * grains, maize, soyabeans, peanuts, millet * warm and humid conditions in storage * Aflatoxin B1 is the most toxic

Question 54

Which birds are at risk of alfatoxins?

Answer 54

* Ducklings \> turkeys \> goslings \>chickens * adult hens are the least susceptible * Consequences of contaminated feed vary with * species * age and sex (M\>F) * nutritional status * level of intake/concentration in feed

Question 55

What are the clinical signs of Aflatoxicosis? (7)

Answer 55

* reduced appetite * weakness * Reduced efficiency of food conversion * Reduced growth rate * Reduced egg production and hatchability * immune suppression * coccidiosis, Marek’s disease, salmonella * abnormal pigmentation +/- bruising

Question 56

How can you treat aflatoxicosis?

Answer 56

* none * aflatoxins don’t accumulate or persist * recovery possible if moderate intoxication * remove contaminated feed

Question 57

How can you prevent aflatoxicosis? (5)

Answer 57

* hygiene * ensure litter is not mouldy and/or move mobile systems onto fresh ground * store food appropriately (dry place) * buy smaller quantities of food in winter * protective role of some food additives?

Question 58

Which other animals are affected by aflatoxins?

Answer 58

* young, newly weaned, pregnant or lactating animals are more susceptible * young pigs * pregnant sows * calves * adult cattle, sheep and goats usually only susceptible to chronic exposure