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Question 1

What are the properties of cholecalciferol rodenticide?

Answer 1

Cholecalciferol= Vitamin D3

Insoluble in water/soluble in most organic solvents/oil

No bait shyness (no offensive odor or flavor)

Question 2

T/F: Young animals are more sensitive to cholecalciferol rodenticides than adults.

Answer 2

True

Question 3

Toxic dose of cholecalciferol is 0.5-20 mg/kg in the canine which means it is how toxic?

Answer 3

Extremely to highly toxic

[Don’t forget this handy dandy chart]

Question 4

Cholecalciferol is absorbed from the GIT where it goes to the liver and is metabolized to ___________, [this is the main form in circulation] which eventually makes its way to the kidneys where it is metabolized to ____________ [which is very potent].

Answer 4

Calcidiol–liver

Calcitriol–kidneys (and very potent).

Question 5

What is responsible for increasing serum Ca2+ levels?

Answer 5

Calcitriol

Question 6

Cholecalciferol is mainly excreted in:

Answer 6

Bile and feces

Question 7

What is the MOA of cholecalciferol rodenticides?

Answer 7

Causes hypercalcemia and hyperphosphatemia.

*Note that PTH levels will be low in an attempt to lower serum Ca2+ but b/c there is an overdose it will be unable to compensate and lower Ca2+ levels.*

Question 8

Hypercalcemia as a result of cholecalciferol toxicity can lead to what?

Answer 8

Deposition of Ca2+ in soft tissues such as kidney tubules, cardiac and lung tissues, vascular walls and stomach.

Question 9

Clinical signs of cholecalciferol rodenticide toxicity appear as early as:

Answer 9

24-36 hours post-exposure.

Question 10

What are clinical signs of cholecalciferol toxicity?

Answer 10

Hematemesis, melena, vomiting, constipation, dehydration, shock.

PU/PD

Arrhythmias, hypertension.

Depression, weakness, muscle twitching, seizures, coma.

Question 11

How would you treat cholecalciferol rodenticide toxicosis?

Answer 11

Emesis, activated charcoal (repeated doses)

Possible IV Lipid therapy

Restricted Ca2+/Ph diet.

Supportive care

Treat the hypercalcemia: saline diuresis, furosemide, soduim bicarb, glucocorticoids, salmon calcitonin, [remember calcitonin TONES down the Ca2+], biphosphonates.

Question 12

T/F: Warfarin is a 2nd generation anticoagulant rodenticide.

Answer 12

False, it is a 1st generation anticoagulant rodenticide.

Question 13

T/F: Warfarin has a relatively slow onset of about 24-36 hours and can be as long as 1 week for 1st generation drugs.

Answer 13

True

Question 14

First generation drugs like Warfarin are most toxic when:

Answer 14

They are ingested daily for a week.

Question 15

The acute oral LD50 of Warfarin is 20-50 mg/kg which means it is how toxic?

Answer 15

Highly toxic

Question 16

This species is the most susceptible to Warfarin toxicosis.

Answer 16

Dogs

Question 17

This species is the most sensitive to Warfarin toxicosis.

Answer 17

Pigs>Dogs>Cats>Ruminants>Horses>Chickens

Question 18

Warfarin is metabolized in the liver via __________.

Answer 18

Hydroxylation

Question 19

The half life of Warfarin is:

Answer 19

19 hours

Question 20

The MOA of Warfarn is:

Answer 20

Inhibit Vitamin K epoxide reductase.

Reduce carboxylation and activation of precursors of clotting factors II, VII, IX and X.

Question 21

Clinical signs of anticoagulant rodenticide toxicity are:

Answer 21

Hemorrhage, although there may be no external evidence of bleeding.

Question 22

T/F: Vitamin K1 (Phytonadione) is used to treat Warfarn toxicity.

Answer 22

True, and do NOT give this IV!!! Needs to be given IM or SQ or orally!!

Question 23

What 3 blood products would you use for a hemorrhaging patient with anticoagulant rodenticide toxicity?

Answer 23

Fresh Frozen Plasma

Fresh whole blood

Cryoprecipitate

Question 24

How long would you treat a Warfarn toxicosis patient with Vitamin K for?

Answer 24

1 week, if you didn’t specifically know it was Warfarin you would treat for 3-4 weeks.

Question 25

T/F: Ethylene glycol lowers the freezing point of water.

Answer 25

True

Question 26

What are some sources of ethylene glycol?

Answer 26

Antifreeze Coolant Industrial solvent Rust remover

Question 27

Which species are the most sensitive to ethylene glycol toxicosis?

Answer 27

Humans and cats

Question 28

The half-life of ethylene glycol toxicity in dogs is:

Answer 28

11 hours

Question 29

Ethylene glycol is oxidized by _____ \_\_\_\_\_\_\_ to glycoaldehyde. Glycoaldehyde is oxidized by _________ \_\_\_\_\_\_\_ to glycolic acid. Glycolic acid is oxidized by ______ \_\_\_\_\_\_ to glyoxylic acid which is metabolied to oxalic acid, glycine, formic acid, hippuric acid, and benzoic acid.

Answer 29

Alcohol dehydrogenase Aldehyde dehydrogenase Aldehyde dehydrogenase

Question 30

Hypocalcemia as well as these types of crystals are common with ethylene glycol toxicity:

Answer 30

Calcium oxlate

Question 31

What are the signs of ethylene glycol toxicity?

Answer 31

Direct GI irritation Increased serum osmolality CNS depression Metabolic acidosis Acute renal failure Hyperglycemia Low USG Hypocalcemia Azotemia Hyperkalemia

Question 32

Why would you see a hyperphosphatemia with ethylene glycol toxicity?

Answer 32

If there is a rust inhibitor present

Question 33

T/F: The Catachem test is the most common bedside test you'd use to determine if a patient had ethylene glycol toxicosis.

Answer 33

True, there are no false positives with ethanol.

Question 34

T/F: Ethanol 20% is the best choice of treatment for Ethylene gycol toxicity.

Answer 34

False, although it is a treatment option, the side effects make it not as desirable as using Fomepizole (4-MP) which is the BEST treatment option.

Question 35

Organophosphates irreverisbly inhibit \_\_\_\_\_\_\_\_\_\_\_\_\_\_.

Answer 35

Acetylcholinesterase, hence causing spastic paralysis.

Question 36

T/F: Organophosphates undergo lethal synthesis.

Answer 36

True

Question 37

Phosphates are biologically \_\_\_\_\_\_\_\_, while thiophosphates require \_\_\_\_\_\_\_\_.

Answer 37

Active Bioactivation

Question 38

T/F: Organophosphates lead to muscarnic effects.

Answer 38

True, think of \*DUMBELS\*--Diarrhea, Urination, Miosis, Bronchospasm, Emesis, Lacrimation, Salvation.

Question 39

With Organophosphate poisoning you can conduct an Atropine response test and if it's positive you will see this:

Answer 39

Dry skin and mucous membranes, increased heart rate, moderately dilated pupils and decreased bowel signs which indicates a LOW liklihood of organophosphate poisoning. (Vs if no signs were seen then you'd be highly suspicious of organophosphate poisoning)

Question 40

T/F: 2-PAM is a viable option for treatment of severe organophosphate poisoning.

Answer 40

True

Question 41

T/F: Carbamates do NOT undergo storage activation.

Answer 41

True, (vs Organophopshates which DO undergo storage activation.)

Question 42

What are the clinical signs of carbamate toxicity?

Answer 42

Similar to organophosphate toxicity.