Rodenticides Flashcards

1
Q

Cholecalciferol

A

2 active forms of Vit D: plant derived (ergocalicerol/D2) and animal derived (cholecaciferol/ D3)
2 synthetic forms

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

Most common ways of cholecalciferol toxicity

A

Ingestion of rodenticides
Human medicine ingestion
Pet foods

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

Toxic dose of cholecalciferol

A

Vit D3 10x more potent than D2
Single oral lethal dose: 13 mg/kg

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

Mechanism of toxicity for cholecalciferol

A

Enhances Ca and P absorption from the gut
Enhances renal absorption
Mobilizes Ca from bone (hypercalcemia)

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

What are the differentials for hypercalcemia

A

Hyperparathyroidism
Addison’s dz
Renal dz
D- vitamin D
Idiopathic
Osteolytic
Neoplasia
Spurious

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

CS of cholecalciferol toxicity

A

Secondary to hypercalcemia (GI, renal, cardiovasc. and neuromuscular)
Depression, weakness and anorexia
36-48 hr after ingestion

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

Progressive signs of cholecalciferol toxicity

A

V, PU/PD, constipation and dehydration
Acute kidney injury, oliguria/ anuria
Calcification of renal tubules
Hematemesis/ melena

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

Minimum database for cholecalciferol toxicity

A

Monitor ionized Ca, P, BUN and creatinine
↑ total calcium (15-18 mg/dL)
Isothenuria

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

TX of cholecalciferol toxicity

A

GI decontamination
Reduce hypercalcemia
Supportive care (IV NaCl→ calciuresis and volume expansion)

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

Tx for acute ingestion for cholecalciferol toxicity

A

<6 hr
Induce emesis, AC

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

How do you tx the hypercalcemia associated with cholecalciferol toxicity?

A

Directed @ reducing blood Ca levels
Prevent acute kidney injury
Tx arrhythmias and supportive care (antiemetics and tx GI ulcers)

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

Medical tx for cholecalciferol toxicity

A

Glucos: after other causes of hypercalcemia rule out
Furosemide (lasix): after fluid deficits corrected
Salmon calcitonin: inhibits osteoclast activity, reduces resorption of Ca from bones
Bisphosphonate (pamidronate): Inhibits osteoclastic bone resorption, reduce Ca conc. within 48hr

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

Bromethalin

A

Used in warfarin- resistant in mice/ rats
Neurotoxic and accidental ingestion

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

Toxic dose of bromethalin

A

Cats sensitive (0.5 mg/kg) and dogs (5mg/kg)
CS seen @ lower doses

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

Toxicokinetics for Bromethalin

A

Rapidly absorbed from GI tract (peak plasma levels within 4 hrs)
Metabolized by liver to desmetheylbromethalin (more toxic)
High conc. in body fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

MOA of Bromethalin

A

Uncoupling of oxidative phosphorylation → ↓ ATP and reduced activity of Na and K ATP → brain electrolyte imbalances → fluid movement to the brain and SC

17
Q

Bromethalin primary target

A

CNS primary target
↑ intracranial pressure/ cerebral edema

18
Q

CS of Bromethalin

A

2-24 hr after ingestion: severe muscle tremors, hyperthermia, seizures and hyperesthsia (mortality 100%)
Delayed 1-2w: ataxia, patellar hyperreflexia, CNS depression, seizure then coma

19
Q

Electroencephalographic (EEG) for bromethalin toxicity

A

Seizure foci
Cerebral edema and hypoxia

20
Q

Postmortum confirmatory tests of Bromethalin

A

Diffuse vacuolization of white matter
In fat, liver, kidney and brain tissue

21
Q

Tx for Bromethalin

A

Emesis within 1 hr (no CNS signs)
Providing symptomatic and supportive care
AC (every 4-6 hrs, @ least 2-3x)

22
Q

How do you control cerebral edema and ↑ intracranial pressure associated with bromethalin?

A

Mannitol, hypertonic saline
Keep head elevated 30 degrees
No jug venipuncture

23
Q

Controlling seizures associated with bromethalin toxicity

A

Phenobarbitol, keppra, midazolam/ diazepam/ lorazepam

24
Q

Anticoagulant rodenticides generations

A

1st gen: warfarin based products (rats becoming resistant)
2nd gen: More toxic, longer duration (more common)
Brodifacoum, bromadiolone, etc

25
Q

Mechanism of toxicity of anticoagulant rodenticides

A

Depletion of K1 in liver → depletion of 2, 7, 9, 10 (PT elevated first then APTT)

26
Q

CS of anticoagulant rodenticides

A

Coagulopathy
Lethargy, anorexia, dyspnea, hemoptysis, lameness
Bleeding from any site

27
Q

Minimum database for anticoagulant rodenticides

A

CBC, Chem and coag panel
+/- blood typing (cross match), imaging
PT

28
Q

Acute ingestion tx of anticoagulant rodenticides

A

Induce emesis and AC
Check PT 48 hrs after ingestion (prolonged → oral Vit K every 2 hrs for 4w)

29
Q

Anticoagulant rodenticides tx for bleeding patients

A

Correct coag (fresh frozen plasma, fresh whole blood)
Vit K1 (with food)
Supprotive care (O2, blood products and fluids)

30
Q

Zinc phosphate

A

Gopher and mole control
Zinc phosphide + stomach acid = phophine gas release = V (hemorrhagic)

31
Q

CS of zinc phosphate toxicity

A

V, depression, dullness, weakness, seizure, convulsion and death (PPE required)

32
Q

Zinc phosphate tx

A

IV fluids, O2 supplement
N-acetyl cysteine, acid reducers, liver protectants