Rodenticides Flashcards
What are the possible sources of anticoagulant rodenticides?
- used as prepared baits, or powders for mixing with bait material
- some used as medical anticoaguants
How can animals be exposed to anticoagulant rodenticides?
- ingestion of baits or eating contaminated food
- relay toxicosis (secondary)
- malicious poisoning
What are the properties of anticoagulant rodenticides?
- odorless and tasteless
- resistant in environment for weeks to months
- slow action
What factors can enhance the toxicity of anticoagulant rodenticides?
- vitamin K deficiency
- pre-existing liver disease
- enzyme inhibitors
- concurrent factors causing hemorrhage
- drugs displacing anticoagulant from binding sites
- steroids or thyroxine may increase receptor site affinity
Describe the mechanism of action of anticoagulant rodenticides
- inhibit vitamin K epoxide reductase
- leads to depletion of reduced vitamin K
- reduced carboxylation and activation of precursors of clotting factors
Which are the precursor clotting factors?
II, VII, IX, X
When is the onset and what are the clinical signs of anticoagulant rodenticide toxicosis?
- onset in 1-5 days
- hemorrhage signs: epistaxis, bloody discharge, hematuria, weakness, shock, hematomas, anorexia
- abortion in cattle
How do you diagnosis anticoagulant rodenticide toxicosis?
- detection in blood, serum, or plasma in live animal
- postmortem: liver, GI contents, vomitus, sample of bait
How would you treat anticoagulant rodenticide toxicosis if exposure is recent and the animal has a normal coagulation panel?
decontamination
- emesis, charcaol
How would you treat anticoagulant rodenticide toxicosis if there are no clinical signs, but prolonged coagulation?
- give vitamin K1 orally
- consider giving clotting factors
How would you treat anticoagulant rodenticide toxicosis if the animal is bleeding, but PCV is > 15-20% and stable?
- start with vitamin K therapy
- give clotting factors
- consider giving RBCs
How would you treat anticoagulant rodenticide toxicosis if the animal is bleeding, and PCV is < 15% and unstable?
- give clotting factors and RBCs
- start vitamin K therapy
What are possible sources of/ways of exposure to Cholecalciferol?
- ingestion of pesticides for rats/mice
- relay toxicosis
- vitamin D toxicosis: large doses, poisonous plants, ingestion of psoriasis medications
What are the properties of Cholecalciferol?
- Cholecalciferol = vitamin D3
- insoluble in water
- soluble in most organic solvents/oil
- no bait shyness
Describe the mechanism of action of cholecalciferol
- absorbed from GI tract
- binds to vitamin D binding protein in plasma and transported to liver
- metabolized in liver to calcidiol
- calcidiol transported to kidneys and metabolized to calcitriol
What are the effects of cholecalciferol toxicity?
- increased serum Ca
- causes hypercalcemia and hyperphosphatemia
- deposition of Ca in soft tissues
- tissue damage, hemorrhage, increased capillary permeability, and renal ischemia
- increased loss of Na and K
When is the onset and what are the clinical signs of Cholecalciferol toxicity?
- onset is 24-36 hours
- depends on tissues affected
- GI: anorexia, vomiting, ab pain, constipation
- Renal: PU/PD
- CV: arrhythmias, hypertension
- CNS: depression, weakness, seizures
What are the lesions of Cholecalciferol toxicosis?
- hemorrhagic gastroenteritis
- mineralization in affected tissues
How is Cholecalciferol toxicosis diagnosed?
- elevated serum Ca/P
- elevated calidiol and calcitriol
- radiographs: mineralization