Term
Which of the following is not considered a rodenticide?
a. Anticoagulants
b. Bromethalin
c. Cholecalciferol
d. Strychnine
e. Organophosphates
f. Zinc phosphide |
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Definition
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Term
The most commonly used group of rodenticides is:
a. Anticoagulants
b. Cholecalciferol
c. Strychnine
d. Bromethalin
e. Zinc Phosphide |
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Definition
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Term
Which of the following is NOT a first generation anticoagulant?
a. Warfarin
b. Diphacinone
c. Diphethialone
d. Chlorophacinone
e. All of the above are first generation anticoagulants |
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Definition
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Term
Which of the following is NOT a second generation anticoagulant?
a. Brodifacoum
b. Bromadiolone
c. Diphethialone
d. Chlorophacinone
e. All of the above are second generation anticoagulants. |
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Definition
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Term
| First generation anticoagulant products generally contain _____% of active ingredient, while second generation anticoagulant products generally contain _____% of active ingredient. |
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Definition
0.05%--first generation
0.005% second generation |
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Term
| T/F: second generation anticoagulants are designed for use in warfarin-resistant rats. |
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Definition
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Term
| T/F: oral absorption of anticoagulants is slow, usually taking hours to days. |
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Definition
| False--rapid--peak levels within minutes to hours |
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Term
Give the plasma half-life for the following compounds:
Warfarin:
Diphacinone:
Brodifacoum: |
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Definition
Warfarin--14 hours
Diphacinone--4.5 days
Brodifacoum--6 days |
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Term
| Anticoagulants are metabolized in the ____________ and excreted in the __________ and ___________. Some residues may transfer to both the ___________ and ________________. |
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Definition
Liver--metabolism
*Bile* and urine--excretion
Transfer to milk and placenta |
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Term
The main factor disrupted by anticoagulants in the Vitamin K cycle is:
a. Vitamin-K dependent carboxylase
b. Vitamin KH2
c. Vitamin K Reductase
d. Vitamin K Epoxide Reductase
e. Quinone |
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Definition
| d. Vitamin K Epoxide reductase |
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Term
When recycling of vitamin K is inhibited by anticoagulants, which clotting factor is affected early and which is affected late?
a. PTT (IX) early, PT (VII) late
b. ATT (VII) early, PTT (IX) late
c. PT (VII) early, PTT (IX) late
d. PTT (IX) early, ATT (VII) late
e. None of the above |
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Definition
| c. PT (VII) early, PTT (IX) late |
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Term
| The agent that causes anticoagulant-toxicity signs in animals that consume moldy sweet clover is ____________. |
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Definition
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Term
Which of the following regarding anticoagulant toxicity is true?
a. Toxicity is rapid, occuring within 12-24 hours
b. Factor IX is the first coagulation factor to demonstrate changes
c. A clinical coagulopathy manifests 3-6 days after ingestion of the rodenticide
d. PTT will increase before PT on the coagulation profile |
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Definition
c. A clinical coagulopathy manifests 3-6 days post ingestion; some can be as short as 36 hours though
PT drops first, PTT later
Anticoagulants display a delayed effect |
|
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Term
| T/F: anticoagulant toxicity therapy should be instituted if the estimated ingested dose is 1/4 of the LD10 value for the active ingredient. |
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Definition
True
Note that brodifacoum has a very low LD50 (0.22-4 mg/kg) when compared to the other anticoagulants. Its LD10 is 0.20 mg/kg. |
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Term
Which of the following scenarios is most likely to have an increased risk of anticoagulant toxicity?
a. A neonatal foal receiving sulfonamides for an umbilical infection
b. A 12 year old dog with hepatic cirrhosis
c. A herd of cattle eating a moldy hay bale
d. A Cushinoid horse due to iatrogenic corticosteroid administration receiving bute to help prevent laminitis
e. All of the above increase the risk of anticoagulant toxicity |
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Definition
e. All of the above
Geriatric/neonatal animals
Concurrent liver dz
Ruminants/horses--moldy sweet clover
Protein-displacing drugs (bute, sulfa, steroids, aspirin, platelet-inhibiting drugs) |
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Term
Which of the following scenarios is most likely to have an increased risk of anticoagulant toxicity?
a. A neonatal foal receiving sulfonamides for an umbilical infection
b. A 12 year old dog with hepatic cirrhosis
c. A herd of cattle eating a moldy hay bale
d. A Cushinoid horse due to iatrogenic corticosteroid administration receiving bute to help prevent laminitis
e. All of the above increase the risk of anticoagulant toxicity |
|
Definition
e. All of the above
Geriatric/neonatal animals
Concurrent liver dz
Ruminants/horses--moldy sweet clover
Protein-displacing drugs (bute, sulfa, steroids, aspirin, platelet-inhibiting drugs) |
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Term
For each of the following clinical signs of anticoagulant toxicity, explain why it happens.
1. Anemia
2. Dyspnia
3. Epistaxis
4. Melena
5. Lameness
6. Ataxia/CNS signs
7. Sudden death
8. Abortion |
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Definition
1. Anemic--hemorrhage throughout the body d/t no clotting factors
2. Dyspnea--d/t anemia and hemothorax
3. Epistaxis--d/t lack of clotting factors
4. Melena--bleeding into GIT d/t lack of clotting factors
5. Lameness--hemarthrosis
6. Ataxia/CNS signs--subdural hematoma
7. Sudden death--hemothorax
8. Abortion--placental hemorrhage |
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Term
| T/F: platelet function is normal in animals with anticoagulant toxicity. |
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Definition
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Term
| _____________ is the diagnostic sample of choice in deceased animals, while _________________ is the sample of choice in live animals. |
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Definition
Liver
Blood (preferrably whole blood vs. serum) |
|
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Term
| T/F: increased clotting times 2x normal or more are common in acute anticoagulant toxicosis. |
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Definition
True
ACT: 2-10x normal
PT: 2-6x normal
APTT: 2-4x normal |
|
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Term
| List some differentials for anticoagulant toxicity: |
|
Definition
1. Dicoumarol--moldy hay
2. Idiopathic coagulopathy
3. Autoimmune thrombocytopenia
4. DIC
5. Hereditary (Von Willebrand's Disease)
6. Liver disease |
|
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Term
| T/F: Vitamin K3 is the treatment of choice for anticoagulant toxicity. |
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Definition
| False: K3 is ineffective as a therapy, though it might be beneficial as a preventative (except in horses--nephrotoxic) |
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Term
| What is the treatment of choice for anticoagulant toxicity? |
|
Definition
Vitamin K1--oral with a FATTY MEAL
treat for 10 days (warfarin)-4 weeks (brodifacoum, diphacinone)
Horses should not exceed 2 mg/kg/day |
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Term
| T/F: IV K1 is the therapy of choice for anticoagulant toxicity |
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Definition
| False: want oral route with fatty meal |
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Term
| Vitamin K1 therapy for anticoagulant toxicity has a lag time of ______ hours for effective coagulation. For immediate clotting factors, ___________ or ______________ should be performed. Clotting function should be monitored for ____ week(s) after therapy stops, and should be done by measuring ______ clotting factor. |
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Definition
3-6 hours
Blood or plasma transfusion
1 week
PT |
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Term
| Cholecalciferol rodenticides typically contain ______% active ingredient. |
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Definition
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Term
| T/F: cholecalciferol toxicosis in rodents is delayed 2-3 days after a single ingestion. |
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Definition
True
Same for other species as well |
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Term
1 IU of vitamin D3 = ___________ ug.
1 ppm D3 = ______ IU |
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Definition
1 IU = 0.025 ug
1 ppm D3 = 40 IU |
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Term
| ______________ is the plant derived form of vitamin D. |
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Definition
|
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Term
| T/F: Vitamin D2 is 10x more potent than D3 for calcium uptake. |
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Definition
| False: D3 is 10x more potent than D2 |
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Term
| Absorption of cholecalciferol is slow/rapid. |
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Definition
| Rapid--completely absorbed in the small intestine |
|
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Term
| Describe the toxicokinetics/metabolism of vitamin D3: |
|
Definition
Oral intake-->rapid absorption in SI-->circulates in plasma to liver and kidney:
1. liver metabolizes cholecalciferol to 25-hydroxy D3 via CYP 450 pathway
2. Kidney converts to 1,25 dihydroxy vitamin D (calcitriol)
Metabolites excreted mainly via bile to the feces |
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Term
| What is the rate-limiting step in the vitamin D3 pathway? |
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Definition
| Kidney--must convert 25 hydroxy D3 to 1,25 dihydroxy D3, which takes time |
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Term
| What is the daily Vitamin D3 requirement in dogs? |
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Definition
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Term
| ________ mg/kg cholecalciferol is considered toxic. |
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Definition
1-3 mg/kg
Dogs can die from dose as low as 5 mg/kg.
10-20 mg/kg single oral dose considered lethal. |
|
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Term
List the following species in order of highest to lowest cholecalciferol susceptibility:
Adult dogs
Cats
Puppies |
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Definition
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Term
| List 3 ways that cholecalciferol toxicity increases serum calcium levels: |
|
Definition
1. Increases Ca (and P) absorption from the gut
2. via PTH--increases osteoclast bone resorption
3. Renal retention of calcium via distal tubule resorption |
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Term
All of the following factors would be expected in a dog with cholecalciferol toxicity except:
a. Bradycardia
b. Low ADH
c. Hypersthenuria
d. Soft tissue mineralization
e. Azotemia |
|
Definition
c. Hypersthenuria
Should see hyposthenuria and diuresis, polyuria, azotemia, low ADH, and bradycardia |
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Term
Which of the following values is consistent for a dog with cholecalciferol toxicity?
a. Serum calcium levels of 13.2 mg/dL
b. Serum phosphorous levels of 9.4 mg/dL
c. BUN of 112
d. USG of 1.005
e. All of the above are consistent with cholecalciferol toxicity |
|
Definition
e. All of the above
Guidelines:
Calcium >12 mg/dL
Phosphorous >7 mg/dL
Hyposthenuria (1.002-1.006)
Typically diagnostics include serum calcium, serum iPTH, and serum vitamin D metabolites. Serum phosphorous not as common to measure. |
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Term
Clinical signs of cholecalciferol toxicity usually begin __________ after ingestion.
a. 2-4 hours
b. 12-36 hours
c. 3-5 days
d. 24-36 hours
e. 5-7 days |
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Definition
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Term
| T/F: thyroid hypertrophy or hyperplasia is a lesion sometimes seen with cholecalciferol toxicity. |
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Definition
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Term
For the following diagnostics, state whether they will be increased or decreased:
1. Serum calcium
2. Serum phosphorous
3. BUN
4. Creatinine
5., Vitamin D metabolites
6. Serum iPTH
7. Heart rate |
|
Definition
1. Serum calcium--increased
2. Serum phosphorous--increased
3. BUN--increased
4. Creatinine--increased
5. Vitamin D metabolites--increased
6. Serum iPTH--decreased
7. heart rate--decreased |
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Term
The following are differentials for cholecalciferol. Which will have increased serum PTH? Which will have decreased serum PTH?
1. Hypercalcemia of malignancy
2. Chronic renal failure
3. Primary hyperparathyroidism
4. Feline idiopathic hypercalcemia |
|
Definition
1. hypercalcemia of malignancy will have decreased serum PTH
2. CRF and primary hyperparathyroidism will have decreased serum PTH |
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Term
While all of the following are treatments that can be implemented for cholecalciferol toxicity, which is perhaps the most important?
a. Emetics, cathartics, activated charcoal
b. Saline diuresis
c. Furosemide
d. Prednisone
e. Calcitonin
f. Bisphosphonates
g. Calcium restriction, antiemetics, GI protectants |
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Definition
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Term
Which of the following works by blocking osteoclast activation and decreasing renal and GI uptake of calcium?
a. Prednisone
b. Calcitonin
c. Bisphosphonates
d. Furosemide
e. Activated charcoal |
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Definition
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Term
Which of the following acts to inhibit bone resorption?
a. Prednisone
b. Calcitonin
c. Bisphosphonates
d. Furosemide
e. Activated charcoal |
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Definition
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Term
A dog gets into a compound with a pungent acetyline/ garlic-like odor. What is the most likely culprit?
a. Anticoagulants
b. Cholecalciferol
c. Zinc Phosphide
d. Strychnine
e. Organophosphates |
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Definition
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Term
| T/F: zinc phosphide is also labeled as a fumigant. |
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Definition
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Term
| Zinc phosphide is ________% active ingredient in baits. |
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Definition
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Term
| T/F: Zinc phosphide is most toxic to animals on an empty stomach. |
|
Definition
False--more toxic to animals that have recently eaten
300 mg/kg toxic dose (empty stomach)
40 mg/kg toxic dose (with food)
gastric acid release leads to the hydrolysis of the bait |
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Term
| T/F: zinc phosphate causes a zinc toxicity that leads to the toxicosis of the animal. |
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Definition
| False: zinc toxicosis is different. Zinc phosphate is hydrolyzed in the stomach to form phosphine gas, which blocks cytochrome oxidase and membrane ion transport. The zinc moiety acts as a strong emetic. |
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Term
| The onset of clinical signs for zinc phosphide occurs in _________ to _________. |
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Definition
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Term
| List some clinical signs associated with zinc phosphide toxicosis: |
|
Definition
Vomiting (bloody)
Anorexia
Lethargy
Rapid deep respiration
Abdominal pain
Ataxia/weakness
Seizures, running, hyperesthesia |
|
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Term
Which of the following is a sign that points to zinc phosphide toxicosis?
a. Hepatic fatty changes
b. Myocardial and renal tubular damage
c. Lung edema
d. A and B
e. A, B, and C |
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Definition
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Term
| The tissue of choice for postmortem diagnosis of zinc phosphide toxicity is the ________________ and samples should be _____________ due to the volatile nature of the phosphine gas. |
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Definition
|
|
Term
| T/F: the prognosis for zinc phosphide toxicity is guarded. |
|
Definition
|
|
Term
| T/F: the prognosis for cholecalciferol toxicity is guarded. |
|
Definition
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