Common Intoxications Flashcards
What is the mechanism of action of ibuprofen toxicity?
Where are there adverse affects? (2)
- 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
Name the 2 benefiical effects of prostaglandins in the GI tract
- Increased secretion of mucous & bicarb by gastric epithelium
- maintenance of mucosal blood flow
What is the source of an iburprofen overdose? (2)
- Misguided attempts by owners to medicate pet
- Accidental access – just stealing a packet off the bench
How does iburprofen dose affect the adverse effects?
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
Can veterinary NSAIDs have the same effect as iburprofen?
Carprofen and meloxicam – commonly use, wide therapeutic dose
- >5 times therapeutic dose à GI signs
- >10 times therapeutic dose à AKI
What are the GI clinical signs of iburprofen toxicity?
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
What are the renal clinical signs of iburprofen toxicity?
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
What are the increased risk factors with iburprofen toxicity? (4)
- 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
What in chocolate makes animals sick?
Theobromine
What is the mechansm of action of theobromine toxicity?
- 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
Which chocolate is most toxic?
Dark chocolate
How would an animal have acces to theobromine? (2)
- Accidental
- Misguided owners
What does theobromine toxicity depend on?
The type of chocolate, amount and the individual’s ability to deal with the dose which can vary.
What are the variety of clinical signs for theobromine toxicity?
Mild signs, GI signs, Cardiotoxicois, CNS signs..
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
How can we manage theobromine toxicity? (6)
- 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
Where is rodenticide toxicity most common?
Dogs
What are the sources of rodenticide poisoning? (5)
- 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
What is the mechanism of rodenticde toxicity?
- 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
Other than anti-coagulants, what else is in rodenticide which can cause issues?
Cholecalciferol here but this is a vitamin D analogue
What happens 1-3 day (or up to 7 days) after ingestion of rodenticide?
Spontaneous bleeding
What are the clinical signs of rodenticide toxicity? (6)
- Thoracic haemorrhage – can be dyspneic:
- haemothorax
- pulmonary haemorrhage
- submucosal tracheal bleeding
- GI bleeding
- Epistaxis
- Haemarthrosis
- CNS bleeds
- Venupuncture sites
What are the clinical signs of rodenticide toxicity consistent with? (what is there is a defect in?)
Defect in secondary haemostasis
How can we diagnose rodenticide toxicity?
- 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)
Ethylene glycol is metablised and the products formed can form issues, name what these are and the effects of these.
