Toxicology 2 Flashcards
Anticoagulant rodenticide toxicity
Anticoagulant rodenticide toxicity
Toxins inactivate the enzyme required to activate vitamin K
Active vitamin K is needed to produce coagulation factors II, VII, IX, and X
Depletion of coagulation factors leads to abnormal hemostasis
Depletion of coagulation factors leads to abnormal hemostasis
First-generation rodenticides (e.g. warfarin, pidone, diphacinone, chlorophacinone) decrease clotting factor levels for 7-10 days
Second-generation rodenticides(e.g. brodifacoum, bromdiolone) decrease clotting factor levels for 3-4 wks.
Clinical signs Anticoagulant rodenticide toxicity
lethargy, vomiting, anorexia, ataxia, diarrhea, hemorrhage, melena, dyspnea, epistaxis, external hemorrhage/bruising, pale mm’s, sudden death from excessive internal hemorrhage
Diagnosis Anticoagulant rodenticide toxicity
hx, clinical signs, prolonged bleeding time tests (PT, aPTT, ACT), response to vitamin K therapy
Treatment Anticoagulant rodenticide toxicity
Vitamkin K1 is the antidote for anticoagulant rodenticide toxicity
Administered at 5 mg/kg SC initially, than PO q24h or divided q12h for 3-4 weeks
Symptomatic and supportive therapy
Bromethalin
(Assault, Trounce, Vengeance)
Formulated as greet pellets in a packet
Potent neurotoxin causing hyperexcitability, muscle tremors, seizures, and death
Cholecalciferol
(Ortho Mouse-B-Gone, Rampage)
Rodenticide converted to vitamin D3 causes calcium reabsorption leading to hypercalcemia
Calcium deposition in soft tissues (e.g. blood vessels, kidney, stomach wall) can lead to hemorrhaging and renal failure. High calcium levels can lead to cardiac dysrhythmias and death
Zinc phosphide
(Acme Mole and Gopher Killer, Mr. Rat Guard, Phosvin)
Formulated as meal, pellet or strip
Reacts with HCl acid in stomach to form toxic phosphine gas-> smells like garlic/rotten fish, damages capillary endothelium and RBC’s within the kidneys, liver, and lungs
Supportive therapy including oxygen supplementation and IV fluid administration
If vomiting is induced, it should be done outside or in a well ventilated area
Clinical signs of Zinc phosphide
lethargy, salivation, vomiting, abdominal distension, pulmonary edema, cyanosis, hypotension, shock, seizures, death
Metaldehyde toxicity
snail/slug bait toxicity
Toxin causes serious CNS abnormalities in animals, its mechanism of action is unknown
Death may occur from respiratory failure as disease progresses
Clinical signs Metaldehyde toxicity
anxiety, hypersalivation, hyperesthesia, ataxia, muscle tremors, tachycardia, seizures, hyperthermia
Treatment Metaldehyde toxicity
No specific antidote
Treatment is supportive and symptomatic
Administration of sodium bicarbonate IV may be needed for severe metabolic acidosis
Ethylene glycol (antifreeze) toxicity
Toxin is metabolized by liver into metabolites that cause metabolic acidosis and renal failure
One of the metabolites, oxalic acid, may combine with calcium to form calcium oxalate crystals in the renal tubule
Ethylene glycol clinical signs appear in three progressive phases
Stage I– CNS abnormalities (depression, ataxia, knucking, seizures, coma, death), anorexia, vomiting hypothermia
Stage II– Cardiorespiratory abnormalities (tachypnea, tachycardia)
Stage III– Renal abnormalities (severe depression, vomiting, diarrhea, dehydration, azotemia, oliguric renal failure)
Ethylene glycol Diagnosis is based on…
hx, clinical signs, laboratory tests (metabolic acidosis, calcium oxalate monohydrate crystals in urine), and ethylene glycol poison test kit