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Toxicology > Unit 1 - Neurotoxic Rodenticides and Metaldehyde > Flashcards

Unit 1 - Neurotoxic Rodenticides and Metaldehyde Flashcards

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1
Q

What are the sources for Zn phosphide?

A

multiple baits and fumigant

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2
Q

What are the most commonly Zn phosphide poisoned species?

A

Dogs and wildlife

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3
Q

What is the MOA of Zn phosphide?

A

Zn phosphide is hydrolyzed in the stomach to phosphide gas (PH3), there is an increase in PH3 which inhibits cytochrome oxidase. This ultimately leads to cell death and necrosis

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4
Q

Why is Zn phosphide more toxic to animals that have recently eaten?

A

When there is a full stomach there is a decrease in stomach pH which results in increased acidity and hydrolysis

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5
Q

When is the onset of clinical signs for Zn phosphide toxicosis with a full stomach?

A

15 minutes - 7 hours

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6
Q

When is the onset of clinical signs for Zn phosphide toxicosis with an empty stomach?

A

12 -18 hours

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7
Q

If there is a large dose of Zn phosphide, how quickly does death occur?

A

Within 3 hours

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8
Q

What clinical signs are associated with Zn phosphide toxicosis?

A

Vomiting (+/- blood) and seizures are the most common
Anorexia, lethargy, dyspnea, and weakness
Colic in horses

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9
Q

What gross lesions are associated with Zn phosphide toxicosis?

A

Non-specific signs - congestion, hepatic fatty change, gastroenteritis, and rotten fish/garlic odor

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10
Q

What microscopic lesions does Zn phosphide cause?

A

Myocardial damage and renal tubular necrosis

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11
Q

What samples should be taken for suspect Zn phosphide toxicosis?

A

Stomach contents and vomitus

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12
Q

What necropsy/exam hazards are associated with Zn phosphide toxicosis?

A

Inhalation of PH3 gas from vomitus or stomach contents - causes migraines and respiratory distress

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13
Q

How is Zn phosphide toxicosis treated?

A

Decontamination ASAP and supportive care

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14
Q

What supportive care should be given for Zn phosphide toxicosis?

A

IV fluids - for acidosis
Dextrose, B vitamins, Low protein diet - for the tx of liver failure
Diazepam, barbiturates, methcarbamol, and anesthesia - to control seizures
GI protectants
O2 administration

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15
Q

What is the prognosis for Zn phosphide toxicosis?

A

Guarded - poor

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16
Q

What are the sources of strychnine?

A

Strychnine tree, gopher bait, and malicious poisonings

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17
Q

What is the MOA for strychnine?

A

It inhibits glycine from binding and the reflex arc is lost. This results in uncontrolled excitation of the reflex

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18
Q

When is the onset of clinical signs for strychnine toxicosis?

A

15 minutes - 2 hours

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19
Q

What clinical signs are associated with strychnine toxicosis?

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A 
Extremely hypersensitive to external stimuli
Tetanic seizures
Ataxia, restless, tremoring
Acute death
Vomiting (rare)
20
Q

What lesions are associated with strychnine toxicosis?

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A

There are no diagnostically significant lesions - hemorrhage and bruising and presence of bait in the stomach

21
Q

What is the most important sample to collect for a potential strychnine toxicosis case?

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A

stomach contents

Other sample options are urine, liver, kidney, and bait

22
Q

How is strychnine toxicosis treated?

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A

Supportive care, control seizures, decontamination, fluids, and decrease stimuli

23
Q

What are the sources of bromethalin toxicity?

24
Q

What species is more sensitive to bromethalin?

25
Bromethalin is metabolized in the ______, it is _______ so it concentrates in fatty tissue, it enters __________ circulation with bile salts, and is excreted in _______.
Liver, lipophilic, enterohepatic, bile
26
What is the MOA of bromethalin?
1. Bromethalin is metabolized to Des-methylbromethalin 2. Uncoupling of oxidative phosphorylation 3. Decreased ATP 4. Impaired Na pump 5. Na is unable to be pumped out 6. H20 flows to Na 7. Nervous tissue swelling
27
Clinical signs for bromethalin toxicosis is ______ dependent.
dose
28
When do clinical signs occur when there are low doses of bromethalin? High?
Low - 2-7 days | High - 4-18 hours
29
What clinical signs are associated with low dose bromethalin toxicosis?
``` Hindlimb paralysis and ataxia Depression Lateral recumbency Coma +/- tremors, vomiting, and anisicoria ```
30
What clinical signs are associated with high dose bromethalin toxicosis?
muscle tremors, seizures, hyperthermia, hyperexcitability to external stimuli
31
What fresh tissue would be ideal for bromethalin toxicosis diagnosis?
Brain, fat, stomach contents, and liver
32
What fixed tissue would be ideal for bromethalin toxicosis diagnosis via histopath?
Brain and spinal cord
33
What will you see on histopath in patients with bromethalin toxicosis?
Edema, +/- spongy degeneration of white matter
34
T/F - The antidote for bromethalin toxicosis is atropine.
False - there is no antidote
35
How is bromethalin toxicosis treated?
Decontamination - emesis and activated charcoal Dexamethasone or Mannitol to decrease the edema Control seizures - diazepam and pentobarbital IV lipid emulsion
36
What are the sources of metaldehyde?
Snail/slug bait
37
What seasons are you likely to see metaldehyde toxicosis?
Spring and summer
38
Where is metaldehyde absorbed?
in the GI tract
39
What is the MOA for metaldehyde toxicosis?
It is unknown - what we do know is that seizure threshold is decreased
40
When is the onset of clinical signs for metaldehyde toxicosis?
Minutes to hours
41
What clinical signs are associated with metaldehyde toxicosis?
Anxiety, +/- salivation, incoordination, hyperthermia (105 F), hyperesthesia, blindness, and respiratory failure (death soon follows)
42
What clinical signs do cats get with metaldehyde toxicosis?
Mydriasis and nystagmus
43
What gross lesions are associated with metaldehyde toxicosis?
GI inflammation, generalized organ congestion, and acetylene/alcohol breath odor of the stomach contents
44
What microscopic lesions are associated with metaldehyde toxicosis?
hepatocellular swelling and neuronal degeneration
45
What is the preferred sample for diagnosing metaldehyde toxicosis?
Stomach contents - MAKE SURE TO SEAL AND FREEZE Serum, urine, and bait are also acceptable
46
How is metaldehyde toxicosis treated?
Aggressive detoxification, control neurologic symptoms, IV fluids, and control hyperthermia

Toxicology (32 decks)

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