Unit 1 - Pesticides

Question 1

What is a pesticide?

Answer 1

A poison that is used to destroy pests of any kind

Question 2

What is the most commonly used rodenticide?

Answer 2

anticoagulants

Question 3

What species are more resistant to anticoagulants?

Answer 3

Cats

Question 4

What compounds are 1st generation anticoagulants?

Answer 4

Warfarin, Diphacinone, and Chlorophacinone

Question 5

What compounds are 2nd generation anticoagulants?

Answer 5

Brodifacoum, Bromadiolone, and Diphethialone

Question 6

Are 1st or 2nd generation anticoagulants more potent?

Answer 6

2nd

Question 7

Where are anticoagulants metabolized and excreted?

Answer 7

They are metabolized in the liver and excreted in the urine and bile

Question 8

T/F - Anticoagulants can cross the placenta.

Answer 8

True

Question 9

What is the MOA of anticoagulants?

Answer 9

It prevents the recycling of vitamin K. This results in the loss of clotting factors and thus hemorrhage

Question 10

What are the predisposing factors for anticoagulant toxicity?

Answer 10

Age, hepatic disease, protein displacing drugs, grazing animals, and physical exertion

Question 11

What protein displacing drugs can predispose animals for anticoagulant toxicity?

Answer 11

Phenylbutazone, sulfonamides, aspirin, and corticosteroids

Question 12

When is the onset of clinical signs for anticoagulant toxicity?

Answer 12

2-5 days - it is delayed

Question 13

What clinical signs are associated with anticoagulant toxicity?

Answer 13

Hemorrhage and blood loss, dyspnea, widespread ecchymosis (hematomas), lameness due to hemorrhage in joints, CNS signs, and abortion

Question 14

What sample should you take for ante-mortem anticoagulant toxicosis diagnosis?

Answer 14

Whole blood

Question 15

Whole blood for an anticoagulant screen and CBC should be collected in a ________ top tube and a __________ top tube for a PT/PTT test.

Answer 15

Purple, light blue

Question 16

What post-mortem sample is best for anticoagulant toxicosis diagnosis?

Answer 16

Liver for an anticoagulant screen

Question 17

What additional samples may be helpful for diagnosing an anticoagulant toxicosis?

Answer 17

Urine, stomach contents, suspect bait, and/or forage material

Question 18

When would it be appropriate to get stomach contents for a toxicosis sample?

Answer 18

Shortly after ingestion

Question 19

How is anticoagulant toxicosis diagnosed?

Answer 19

Hemorrhagic syndrome, increased clotting time, and/or detection of a compound

Question 20

What will the PT, PTT, and platelet counts be in a patient with anticoagulant toxicosis?

Answer 20

Elevated PT and PTT with normal platelets

Question 21

What treatment should be done first in cases of anticoagulant toxicosis?

Answer 21

Stabilize the patients first

Question 22

What treatments can be done for anticoagulant toxicosis after the patient is stabilized?

Answer 22

Administer vitamin K1, emesis and activated charcoal, transfusion, rest, and continued monitoring after therapy

Question 23

Treatment of vitamin K1 is entirely dependent on the compound. Treatment for Warfarin toxicity is done for ___ days and Brodifacoum toxicity is done for _______.

Answer 23

10 days, 2-4 weeks

Question 24

T/F - Vitamin K3 is an acceptable substitute for vitamin K1

Answer 24

False - it is therapeutically ineffective and nephrotoxic to horses

Question 25

What differential diagnoses should you consider along with rodenticide toxicity?

Answer 25

Hereditary coagulopathies, autoimmune thrombocytopenia, hepatic disease, DIC, and idiopathic coagulopathy

Question 26

What environmental and human health considerations should be considered in cases of anticoagulant toxicosis?

Answer 26

There is a high probability of relay toxicosis

Question 27

What happens when there is too little vitamin D3?

Answer 27

Decreased calcium, bone fragility, weakness, and death

Question 28

What happens when there is too much vitamin D3?

Answer 28

There is too much calcium resulting in mineralization which can lead to death

Question 29

What are the common sources of cholecalciferol that lead to toxicosis?

Answer 29

Rodenticide products, calcipotriene (Dovonex), vitamin supplements, and plants containing 1,25 dihydroxy D3

Question 30

What is the MOA of cholecalciferol?

Answer 30

1. Metabolism of vitamin D3 2. Increased 1,25 DiOH D3 3. Negative feedback 4. Excess 25 OH D3 causes metabolic effects 5. Increased Ca from the gut, bone, and kidney 6. Hypercalcemia and hyperphosphatemia 7. Mineralization and necrosis

Question 31

When does the onset of clinical signs occur with cholecalciferol toxicosis?

Answer 31

12-36 hours

Question 32

What clinical signs are associated with cholecalciferol toxicosis?

Answer 32

Anorexia, vomiting, generalized weakness, bradycardia, hypertension, PU/PD, and renal failure at 24 hours

Question 33

What samples may you want to take if you suspect cholecalciferol toxicity?

Answer 33

Serum, urine, feedstuffs, and/or tissues

Question 34

What tissue samples may you want to take for cholecalciferol toxicity?

Answer 34

GI, heart, lung, kidney

Question 35

What will your serum chemistry results say if you have cholecalciferol toxicity?

Answer 35

``` Ca >12 P >10 Azotemia Increased 25 OH D3 Decreased PTH ```

Question 36

When do you have to worry about mineralization?

Answer 36

If Ca x P is >70

Question 37

What will the specific gravity be in cases of cholecalciferol toxicosis?

Answer 37

Isosthenuric

Question 38

What will the calcium levels from a kidney sample be in cases of cholecalciferol toxicosis?

Answer 38

Increased Ca levels (2000-3000 ppm) | Increased Ca/P ratio

Question 39

What DDx should be considered with cholecalciferol toxicosis?

Answer 39

hypercalcemia of malignancy, chronic renal failure, primary hyperparathyroidism, and feline idiopathic hypercalcemia

Question 40

What is the primary lesion that you will see with cholecalciferol toxicosis?

Answer 40

Soft tissue mineralization

Question 41

What lesions will you see in the GI tract due to cholecalciferol toxicosis?

Answer 41

Hemorrhage, erosion, and ulceration

Question 42

What lesions will you see in the kidneys due to cholecalciferol toxicosis?

Answer 42

Pale, rough - gritty texture, tubular necrosis, and crystal mineral deposition

Question 43

What lesions will you see in the cardiovascular system due to cholecalciferol toxicosis?

Answer 43

Aortic plaques and vessel mineralization

Question 44

T/F - Cholecalciferol toxicosis is not a medical emergency.

Answer 44

False - it is

Question 45

How is cholecalciferol toxicosis treated?

Answer 45

Decontamination ASAP, IV fluids, furosemide, and prednisone to decrease osteoclast activity

Question 46

What is the goal of treatment in progressive cases of cholecalciferol toxicosis?

Answer 46

Inhibit bone resorption

Question 47

What drugs can be used to inhibit bone resorption?

Answer 47

Calcitonin and pamidronate

Question 48

What environmental and human health considerations need to be considered for cholecalciferol toxicosis?

Answer 48

All animals are susceptible, there is a potential for relay toxicosis, and it is excreted in milk