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Tox > Old material > Flashcards

Old material Flashcards

1
Q

What are the properties of cholecalciferol rodenticide?

A

Cholecalciferol= Vitamin D3

Insoluble in water/soluble in most organic solvents/oil

No bait shyness (no offensive odor or flavor)

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2
Q

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

A

True

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3
Q

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

A

Extremely to highly toxic

[Don’t forget this handy dandy chart]

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4
Q

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].

A

Calcidiol–liver

Calcitriol–kidneys (and very potent).

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5
Q

What is responsible for increasing serum Ca2+ levels?

A

Calcitriol

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6
Q

Cholecalciferol is mainly excreted in:

A

Bile and feces

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7
Q

What is the MOA of cholecalciferol rodenticides?

A

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.*

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8
Q

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

A

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

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9
Q

Clinical signs of cholecalciferol rodenticide toxicity appear as early as:

A

24-36 hours post-exposure.

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10
Q

What are clinical signs of cholecalciferol toxicity?

A

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

PU/PD

Arrhythmias, hypertension.

Depression, weakness, muscle twitching, seizures, coma.

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11
Q

How would you treat cholecalciferol rodenticide toxicosis?

A

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.

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12
Q

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

A

False, it is a 1st generation anticoagulant rodenticide.

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13
Q

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.

A

True

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14
Q

First generation drugs like Warfarin are most toxic when:

A

They are ingested daily for a week.

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15
Q

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

A

Highly toxic

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16
Q

This species is the most susceptible to Warfarin toxicosis.

A

Dogs

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17
Q

This species is the most sensitive to Warfarin toxicosis.

A

Pigs>Dogs>Cats>Ruminants>Horses>Chickens

18
Q

Warfarin is metabolized in the liver via __________.

A

Hydroxylation

19
Q

The half life of Warfarin is:

A

19 hours

20
Q

The MOA of Warfarn is:

A

Inhibit Vitamin K epoxide reductase.

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

21
Q

Clinical signs of anticoagulant rodenticide toxicity are:

A

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

22
Q

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

A

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

23
Q

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

A

Fresh Frozen Plasma

Fresh whole blood

Cryoprecipitate

24
Q

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

A

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

25
Q

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

A

True

26
Q

What are some sources of ethylene glycol?

A

Antifreeze

Coolant

Industrial solvent

Rust remover

27
Q

Which species are the most sensitive to ethylene glycol toxicosis?

A

Humans and cats

28
Q

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

A

11 hours

29
Q

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.

A

Alcohol dehydrogenase

Aldehyde dehydrogenase

Aldehyde dehydrogenase

30
Q

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

A

Calcium oxlate

31
Q

What are the signs of ethylene glycol toxicity?

A

Direct GI irritation

Increased serum osmolality

CNS depression

Metabolic acidosis

Acute renal failure

Hyperglycemia

Low USG

Hypocalcemia

Azotemia

Hyperkalemia

32
Q

Why would you see a hyperphosphatemia with ethylene glycol toxicity?

A

If there is a rust inhibitor present

33
Q

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

A

True, there are no false positives with ethanol.

34
Q

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

A

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.

35
Q

Organophosphates irreverisbly inhibit ______________.

A

Acetylcholinesterase, hence causing spastic paralysis.

36
Q

T/F: Organophosphates undergo lethal synthesis.

A

True

37
Q

Phosphates are biologically ________,

while thiophosphates require ________.

A

Active

Bioactivation

38
Q

T/F: Organophosphates lead to muscarnic effects.

A

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

39
Q

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

A

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)

40
Q

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

A

True

41
Q

T/F: Carbamates do NOT undergo storage activation.

A

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

42
Q

What are the clinical signs of carbamate toxicity?

A

Similar to organophosphate toxicity.

Tox (3 decks)

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