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)
Which lab test is the first to beome abnormal with rodenticide poisoning?
PT – prolonged 2-6 times normal
How can you manage rodenticide toxcity? (3)
- 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
- plasma transfusion to provide clotting factors
Where is ethylene glycol toxicity seen?
Cat
What are the sources of ethylene glycol? (5)
- 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…
What is the mechanism of ethylene glycol toxicity?
Converted by alcohol dehydrogenase in the body = toxic metabolites
Ethylene glycol is metablised and the products formed can form issues, name what these are and the effects of these.
What is the mechanism of action causing metabolic acidosis and hypocalcaemia with ethylene glycol?
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
What are the clinical signs of ethylene glycol toxicity in stage 1?
Stage 1 (from 30 mins up to 12 hours)
- CNS depression (ataxia, weakness)
- vomiting
What are the clinical signs of ethylene glycol toxicity in stage 2?
Stage 2 (12-24 hours)
- cardiopulmonary phase
- tachycardia, tachypnoea, arrhythmia
- hypo/hypertension
- pulmonary oedema
- seizures
What are the clinical signs of ethylene glycol toxicity in stage 3?
Stage 3 (24-72 hours but can be within 1-3 hrs in cats)
- Renal phase
- signs associated with azotaemia
- oliguria = anuria
How can we diagnose ethylene glycol toxcity?
- 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
What is the prognosis and treatment for ethylene glycol treatment?
- 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.
- ethanol (or vodka)-only if not azotaemic
What is the mechanism of toxicity for Household cleaners & bleach (Sodium hypochlorite)?
•Direct mucosal damage
What are the clinical effects of consuming bleach/household cleaner?
- Hypersalivation
- Vomiting
- Lethargy
- Reduced Appetite
What is the treatment for consuming bleach and household items?
- Detoxification: dilution
- Supportive care
What is the strategic approach to poison cases?
- 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.
What is the mechanim of bracken toxicity in LA?
- bone marrow suppression
- retinal degeneration
- thiamine deficiency
What are the risk factors with bracken toxicity? (3)
- part of the plant consumed (rhizome, shoots)
- palatability vs availability of other food
- age (experience?) of animal?
What are the clinical signs associated with sub acute disease with bracken toxicity? (6)
- 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
What is chronic disease of bracken toxicity?
What are the clinical signs? (4)
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
What is it that causes toxicity with bracken poisoning in horses? What are the signs (3)
- Thiaminase causes
- chronic ataxia
- weakness
- paralysis
How can you prevent bracken toxicity in sheep? (3)
- 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
What are the mechanisms of copper toxicosis in LA? (2)
- direct irritant
- oxidative injury
- Heinz body
- methaemoglobinaemia
- haemolysis = nephrosis
What are the sources for copper toxicosis? (9)
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
What are the risk factors for copper toxicity in sheep?
- 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
What are the clinical signs for copper toxicosis? (9)
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
How can you diagnose copper toxicity in sheep?
- 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
How can you treat copper toxicity?
- Ammonium tetrathiomolybdate
- s/c every other day for 3 days….
Decreased Cu absorption and increased excretion from liver
•expense?
What are alfatoxins in poultry?
- 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
Which birds are at risk of alfatoxins?
- 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
What are the clinical signs of Aflatoxicosis? (7)
- 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
How can you treat aflatoxicosis?
- none
- aflatoxins don’t accumulate or persist
- recovery possible if moderate intoxication
- remove contaminated feed
How can you prevent aflatoxicosis? (5)
- 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?
Which other animals are affected by aflatoxins?
- 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
