SA toxicology Flashcards
Within what time limit should emesis be performed whilst treating toxicosis?
Within 3 hours
- 6hrs for aspirin
- 12hrs for chocolate
In cases of occular contamination how long should the animals eye be irrigated?
With what?
Saline
20-30 minutes
What is the MOA of apomorphine?
What are the potential routes of administration?
Dopamine agonist
Can be administered parenterally or inserting a tablet into the conjunctiva until effect
Activated charcoal is an example of what type of substance?
What is its MOA?
Adsorbents
Binds the poison and prevents absorption from the GI tract.
If using activated charcoal to treat drug intoxication how often should the half dose be readministered?
Why?
Every 4-8 hrs
The substance interferes with enterohepatic circulation
eg NSAIDs, methylxanthines, ivermectin
What are the contraindications to emesis?
- Vomiting already
- No gag reflex
- Central depression - unconscious, depressed
- Seizuring
- Corrosives, irritants or volatile products have been ingested
Why is apomorphine NOT used in cats?
The have few CNS dopamine receptors & so the drug is not effective as an emetic
What is a cathartic?
Give an example.
Speeds up defacation
eg Liquid paraffin
Which clotting factors are effected by vitamin K antagonism?
2, 7, 9, 10
Vitamin K antagonists such as warfarin competitively inhibit K1 epoxide reductase and prevent factor activation.
Describe the effect that vitamin K antagonists have on coagulation screening assays.
Initially a prolonged PT (since factor 7 has the shortest half life)
Secondly prolonged PT and APTT
Konakion
Vitamin K1
Cholecalciferol
Inactive form of vitamin D
What clinical signs are seen with Cholecalciferol intoxication?
Hypercalcaemia
Outline the differentials for hypercalcaemia.
- H - hyperparathyroidism
- A - addisons
- R - renal
- D - vitamin D toxicosis
- I - idiopathic
- O - osteolysis
- N - neoplasia
- S - spurius - dehyd/lipaemia
- G - granulomatous
What clinical signs are seen with intoxication with Cholinesterase inhibitors?
- D - diarrhoea
- U - urination
- M - miosis
- B - bronchoconstriction
- B - bradycardia
- E - emesis
- L - lacrimation
- S - salivation
Muscarinic, nicotinic and CNS effects
Examples of cholinesterase inhibitors.
Organophosphates
Carbamates
Insecticides/ fungicides
What three drugs are used in treatment of cholinesterase inhibitors?
- Diazepam - reduce seizures
- Atropine - muscarini antagonist
- 2-PAM - reduce nicotinic associated muscle tremors
Why do most pyrethroid intoxications occur?
What clinical signs are associated with intoxication?
Giving a dog prep to a cat - cat licks off prep whilst grooming + cutaneous absorption
- XS salivation
- tremors
- ataxia
- depression
- hyper/hypothermia
Paraquat
C/S
Toxic herbicide
- GIT
- Acute tubular necrosis
- Pulomnary oedema and haemorrhage - lung accumulation
- Usually fatal
The ingredient that is toxic in slug pellets is …..
MOA
C/S
Metaldehyde - reduced GABA inhibition
- Hyperaesthesia
- Neurotox/hepatotox
- Anxiety/restlessness
- Salivation
- Tremors
- Tachycardia
- Seizures
- Death
Why can paracetamol NOT be used in cats?
They are unable to glucoronidate paracetamol and so toxic intermediates of metabolism accumulate
How does paracetamol cause toxicity?
C/S
Causes oxidative damage to RBCs and formation of methaemoglobin.
- V+
- Abdo pain
- Tachycardia
- MetHb mm - chocolate coloured
- Depression
- Hepatic failure
Cimetidine
cytochrome P450 inhibitor - may reduce formation of toxic intermediates of paracetamol toxicosis
N-acetyl cysteine
Acts as glutathione - aids glucoronidation
