130. Rodenticide toxicity Flashcards

1
Q

What is the MOA of anti vitamin K rodenticides?

A

inhibit physiological recycling
of vitamin K by inhibiting vitamin K epoxide reductase
in the liver, which inhibits vitamin K synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the difference between first and second generation products?

A

second generation products more acutely toxics and longer half-lives

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

After the depletion of which clotting factors, clinical sign appears after ingestion of anti-vitamin K?

A

2 (prothrombin), 7, 9, 10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which anti thrombotic factors are affected by anticoagulants?

A

C, S, Z

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Which test can diagnose anti vitamin K toxicity the earliest?

A

Protein c levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

When should you recheck a coagulation profile after the 30 days course of vitamin K?

A

48h post cessation of vitamin K

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which are the routes of vitamin K administration and which one is preferred?
Which one is dangerous in the USA?

A

PO, SQ, IM
PO: preferred with food
Otherwise SQ
IM: can cause pain and bleeding.
IV: anaphylaxis in the USA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the prognosis?

A

Excellent to guarded depending on clinical signs at presentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the MOA of bromethalin?

A

uncouples oxidative phosphorylation, decreasing adenosine
triphosphate (ATP) production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the lethal dose 50% of bromethalin in cats and dogs?

A

0.3 mg/kg in cats and 2.4 mg/kg in dogs –> meaning that 50% that ingest this dose, will die

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

When do you see clinical signs?

A

if low dose up to 5 days, if high dose 2 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What lines of treatments can be considered if suspecting bromethalin intoxication?

A

Decontamination is the most important, rapidly absorbed 1.5 hour, activated charcoal q4-6 for 48-72h as undergo enterohepatic recirculation, intralipids to reduce blood levels, IVF, nutritional support, HTS or mannitol, anti epileptic drugs, MV.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Prognosis

A

guarded to poor if clinical signs develop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the MOA of cholecalciferol ingestion?

A

Cholecalciferol (vitamin D3) is rapidly absorbed and converted
to calcifediol in the liver. Calcifediol is then converted
to calcitriol (active vitamin D, 1-25-dihydroxycholeciferol)
in the proximal convoluted tubule of the kidney. Excess
levels of active vitamin D cause increased absorption of
calcium and phosphorus from the GI tract, bone, and
kidneys. Metastatic mineralization of tissues can occur at
calcium-phosphorus products over 60 (mg/dL), and can
affect many tissues throughout the body irreversibly.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

At what doses can we see clinical signs and can it be fatal?

A
  • 0.5mg/kg
  • 2mg/kg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are some clinical signs observed in cholecalciferol ingestion?

A

inappetence, vomiting, diarrhea, polyuria, polydipsia,
lethargy, depression, muscle tremors, and seizures

17
Q

What is the half-life of calcifediol?

18
Q

Is charcoal recommended in vitamin D3 intoxication and why?

A

yes, undergoes significant enterohepatic recirculation.

19
Q

What other medication is recommended to decrease GI absorption?

A

Cholestyramine
resin administration (0.3–1 g/kg PO q8h for 4 days,

20
Q

What is the MOA of Cholestyramine?

A

Cholestyramine binds to bile acids that are normally found in the intestine and forms an insoluble complex that is excreted in feces. With toxic exposures, toxins that are highly lipophilic and bound to bind acids will also be trapped in this insoluble complex and excreted in feces.

21
Q

What is the MOA for glucocorticoid use in case of hyperCa?

A

Inhibi the production of the active form of vitamin D (1,25-dihydroxyvitamin D), which significantly reduces calcium absorption in the intestines, ultimately decreasing circulating calcium levels in the blood

22
Q

What is the MOA Zinc and aluminum phosphide toxicity?

A

These salts produce phosphine, the active
agent, that may inhibit cytochrome C oxidase, disrupt
the mitochondrial membrane, and generate free radicals
that peroxidize lipids. Phosphine has rapid, directly toxic
effects on the heart, adrenal glands, and kidneys, and is
a corrosive agent.

23
Q

What caution must be taken when inducing emesis or when an animal who ate phosphide vomits?

A

It must be in a ventilated area as exposure to phosphine gas may result in fatigue,
headaches, vomiting, dizziness, and shortness of breath in
people if exposure doses are high enough

24
Q

T or F: Activated
charcoal is not indicated as the active compound is a gas,
mental status is likely to deteriorate rapidly, and addition
of liquid components to the GI tract increases rate of
production of the toxic gas.