Unit 1 - Pesticides Flashcards
What is a pesticide?
A poison that is used to destroy pests of any kind
What is the most commonly used rodenticide?
anticoagulants
What species are more resistant to anticoagulants?
Cats
What compounds are 1st generation anticoagulants?
Warfarin, Diphacinone, and Chlorophacinone
What compounds are 2nd generation anticoagulants?
Brodifacoum, Bromadiolone, and Diphethialone
Are 1st or 2nd generation anticoagulants more potent?
2nd
Where are anticoagulants metabolized and excreted?
They are metabolized in the liver and excreted in the urine and bile
T/F - Anticoagulants can cross the placenta.
True
What is the MOA of anticoagulants?
It prevents the recycling of vitamin K. This results in the loss of clotting factors and thus hemorrhage
What are the predisposing factors for anticoagulant toxicity?
Age, hepatic disease, protein displacing drugs, grazing animals, and physical exertion
What protein displacing drugs can predispose animals for anticoagulant toxicity?
Phenylbutazone, sulfonamides, aspirin, and corticosteroids
When is the onset of clinical signs for anticoagulant toxicity?
2-5 days - it is delayed
What clinical signs are associated with anticoagulant toxicity?
Hemorrhage and blood loss, dyspnea, widespread ecchymosis (hematomas), lameness due to hemorrhage in joints, CNS signs, and abortion
What sample should you take for ante-mortem anticoagulant toxicosis diagnosis?
Whole blood
Whole blood for an anticoagulant screen and CBC should be collected in a ________ top tube and a __________ top tube for a PT/PTT test.
Purple, light blue
What post-mortem sample is best for anticoagulant toxicosis diagnosis?
Liver for an anticoagulant screen
What additional samples may be helpful for diagnosing an anticoagulant toxicosis?
Urine, stomach contents, suspect bait, and/or forage material
When would it be appropriate to get stomach contents for a toxicosis sample?
Shortly after ingestion
How is anticoagulant toxicosis diagnosed?
Hemorrhagic syndrome, increased clotting time, and/or detection of a compound
What will the PT, PTT, and platelet counts be in a patient with anticoagulant toxicosis?
Elevated PT and PTT with normal platelets
What treatment should be done first in cases of anticoagulant toxicosis?
Stabilize the patients first
What treatments can be done for anticoagulant toxicosis after the patient is stabilized?
Administer vitamin K1, emesis and activated charcoal, transfusion, rest, and continued monitoring after therapy
Treatment of vitamin K1 is entirely dependent on the compound. Treatment for Warfarin toxicity is done for ___ days and Brodifacoum toxicity is done for _______.
10 days, 2-4 weeks
T/F - Vitamin K3 is an acceptable substitute for vitamin K1
False - it is therapeutically ineffective and nephrotoxic to horses
What differential diagnoses should you consider along with rodenticide toxicity?
Hereditary coagulopathies, autoimmune thrombocytopenia, hepatic disease, DIC, and idiopathic coagulopathy
What environmental and human health considerations should be considered in cases of anticoagulant toxicosis?
There is a high probability of relay toxicosis
What happens when there is too little vitamin D3?
Decreased calcium, bone fragility, weakness, and death
What happens when there is too much vitamin D3?
There is too much calcium resulting in mineralization which can lead to death
What are the common sources of cholecalciferol that lead to toxicosis?
Rodenticide products, calcipotriene (Dovonex), vitamin supplements, and plants containing 1,25 dihydroxy D3
What is the MOA of cholecalciferol?
- Metabolism of vitamin D3
- Increased 1,25 DiOH D3
- Negative feedback
- Excess 25 OH D3 causes metabolic effects
- Increased Ca from the gut, bone, and kidney
- Hypercalcemia and hyperphosphatemia
- Mineralization and necrosis
When does the onset of clinical signs occur with cholecalciferol toxicosis?
12-36 hours
What clinical signs are associated with cholecalciferol toxicosis?
Anorexia, vomiting, generalized weakness, bradycardia, hypertension, PU/PD, and renal failure at 24 hours
What samples may you want to take if you suspect cholecalciferol toxicity?
Serum, urine, feedstuffs, and/or tissues
What tissue samples may you want to take for cholecalciferol toxicity?
GI, heart, lung, kidney
What will your serum chemistry results say if you have cholecalciferol toxicity?
Ca >12 P >10 Azotemia Increased 25 OH D3 Decreased PTH
When do you have to worry about mineralization?
If Ca x P is >70
What will the specific gravity be in cases of cholecalciferol toxicosis?
Isosthenuric
What will the calcium levels from a kidney sample be in cases of cholecalciferol toxicosis?
Increased Ca levels (2000-3000 ppm)
Increased Ca/P ratio
What DDx should be considered with cholecalciferol toxicosis?
hypercalcemia of malignancy, chronic renal failure, primary hyperparathyroidism, and feline idiopathic hypercalcemia
What is the primary lesion that you will see with cholecalciferol toxicosis?
Soft tissue mineralization
What lesions will you see in the GI tract due to cholecalciferol toxicosis?
Hemorrhage, erosion, and ulceration
What lesions will you see in the kidneys due to cholecalciferol toxicosis?
Pale, rough - gritty texture, tubular necrosis, and crystal mineral deposition
What lesions will you see in the cardiovascular system due to cholecalciferol toxicosis?
Aortic plaques and vessel mineralization
T/F - Cholecalciferol toxicosis is not a medical emergency.
False - it is
How is cholecalciferol toxicosis treated?
Decontamination ASAP, IV fluids, furosemide, and prednisone to decrease osteoclast activity
What is the goal of treatment in progressive cases of cholecalciferol toxicosis?
Inhibit bone resorption
What drugs can be used to inhibit bone resorption?
Calcitonin and pamidronate
What environmental and human health considerations need to be considered for cholecalciferol toxicosis?
All animals are susceptible, there is a potential for relay toxicosis, and it is excreted in milk
