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Toxicology > Unit 1 - Pesticides > Flashcards

Unit 1 - Pesticides Flashcards

1
Q

What is a pesticide?

A

A poison that is used to destroy pests of any kind

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2
Q

What is the most commonly used rodenticide?

A

anticoagulants

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3
Q

What species are more resistant to anticoagulants?

A

Cats

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4
Q

What compounds are 1st generation anticoagulants?

A

Warfarin, Diphacinone, and Chlorophacinone

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5
Q

What compounds are 2nd generation anticoagulants?

A

Brodifacoum, Bromadiolone, and Diphethialone

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6
Q

Are 1st or 2nd generation anticoagulants more potent?

A

2nd

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7
Q

Where are anticoagulants metabolized and excreted?

A

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

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8
Q

T/F - Anticoagulants can cross the placenta.

A

True

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9
Q

What is the MOA of anticoagulants?

A

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

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10
Q

What are the predisposing factors for anticoagulant toxicity?

A

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

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11
Q

What protein displacing drugs can predispose animals for anticoagulant toxicity?

A

Phenylbutazone, sulfonamides, aspirin, and corticosteroids

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12
Q

When is the onset of clinical signs for anticoagulant toxicity?

A

2-5 days - it is delayed

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13
Q

What clinical signs are associated with anticoagulant toxicity?

A

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

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14
Q

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

A

Whole blood

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15
Q

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

A

Purple, light blue

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16
Q

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

A

Liver for an anticoagulant screen

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17
Q

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

A

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

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18
Q

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

A

Shortly after ingestion

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19
Q

How is anticoagulant toxicosis diagnosed?

A

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

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20
Q

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

A

Elevated PT and PTT with normal platelets

21
Q

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

A

Stabilize the patients first

22
Q

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

A

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

23
Q

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

A

10 days, 2-4 weeks

24
Q

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

A

False - it is therapeutically ineffective and nephrotoxic to horses

25
Q

What differential diagnoses should you consider along with rodenticide toxicity?

A

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

26
Q

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

A

There is a high probability of relay toxicosis

27
Q

What happens when there is too little vitamin D3?

A

Decreased calcium, bone fragility, weakness, and death

28
Q

What happens when there is too much vitamin D3?

A

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

29
Q

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

A

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

30
Q

What is the MOA of cholecalciferol?

A
  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
31
Q

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

A

12-36 hours

32
Q

What clinical signs are associated with cholecalciferol toxicosis?

A

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

33
Q

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

A

Serum, urine, feedstuffs, and/or tissues

34
Q

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

A

GI, heart, lung, kidney

35
Q

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

A 
Ca >12
P >10
Azotemia
Increased 25 OH D3
Decreased PTH
36
Q

When do you have to worry about mineralization?

A

If Ca x P is >70

37
Q

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

A

Isosthenuric

38
Q

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

A

Increased Ca levels (2000-3000 ppm)

Increased Ca/P ratio

39
Q

What DDx should be considered with cholecalciferol toxicosis?

A

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

40
Q

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

A

Soft tissue mineralization

41
Q

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

A

Hemorrhage, erosion, and ulceration

42
Q

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

A

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

43
Q

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

A

Aortic plaques and vessel mineralization

44
Q

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

A

False - it is

45
Q

How is cholecalciferol toxicosis treated?

A

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

46
Q

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

A

Inhibit bone resorption

47
Q

What drugs can be used to inhibit bone resorption?

A

Calcitonin and pamidronate

48
Q

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

A

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

Toxicology (32 decks)

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