Rodenticides

Question 1

source of exposure of anticoagulant rodenticides

Answer 1

ingestion of baits or eating contaminated feed;

malicious poisoning;

secondary toxicosis

Question 2

MoA: Anticoagulant rodenticides

Answer 2

inhibit vitamin K epoxide reductase → reduction of coag factors II, VII, IX, XII (1972)

Question 3

Clinical signs associated with anticoagulant rodenticides

Answer 3

onset in 1-5 days

signs of hemorrhage (vary on site of bleeding)- hematuria, bleeding from venipuncture sites, hematomas,

weakness, shock, tachypnea/dyspnea, anorexia, lethargy, abortion in cattle

Question 4

Dx of anticoagulant rodenticides

Answer 4

Chemical analysis: blood (preferred), serum or plasma;

prolonged coag factors, anemia, thrombocytopenia, hypoproteinemia, radiographs (signs of hemorrhage)

Question 5

treatment of anticoagulant rodenticides

Answer 5

vitamin K1 (K3 not effective - side effects) PO - don’t give IV→ anaphylaxis!!

Coag factors (FFP, cryoprecipitate)

Question 6

DDx of anticoagulant rodenticides

Answer 6

spoiled sweet clover (cattle, horses)

vitamin K deficiency (swine, poultry)

DIC, liver disease, thrombocytopenia

Question 7

T/F 1st generation anticoagulant rodenticides like Warfrin are effective after one dose and hava a long half life

Answer 7

False

2nd generations - more acutely toxic

1st generations - most toxic when ingested daily over 1 week

Question 8

exposure: cholecalciferol

Answer 8

ingestion of rodenticides, relay (secondary) toxicosis, large doses of vit. D (feed additives, multivitamins, lotions), plants with vit. D analogs, psoriasis medication

Question 9

MoA: cholecaliferol

Answer 9

causes hypercalcemia and hyperphosphatemia, can lead to mineralization of soft tissues

Question 10

Clinical Signs: cholecaliferol

Answer 10

nonspecific (depends on tissues affected), anorexia, V+ (+/- blood), abdominal pain, constipation (+/- melena) dehydration, shock, PU/PD (hyposthenuria), arrhythmias, hypertension, depression, weakness, muscle twitching, seizures, coma, death

Question 11

Dx cholecalciferol

Answer 11

history and clinical signs, lab findings, rads - mineralization of soft tissues

Question 12

treatment of cholecalciferol

Answer 12

decontamination- emesis, activated charcoal (repeated doses), restrict therapy, supportive care

Treat the hypercalcemia - saline diuresis, furosemide, glucocorticoids, bisphosphonates

Question 13

lab results: cholecaliferol

Answer 13

hypercalcemia, hyperphosphatemia, elevated calcidiol and calcitriol, decreased PTH, azotemia, proteinuria, glucosuria

Question 14

DDx for cholecaliferal

Answer 14

DRAGONSHIT

Question 15

exposure: bromethalin

Answer 15

ingestion of bait, secondary (relay) toxicosis - not reported but possible

Question 16

MoA: bromethalin

Answer 16

uncoupling of oxidative phosphorylation, lack adequate ATP, insufficient energy for Na/K pumps

Brain and spinal cord: main targets (rely heavily on ox phos), ion pump dysfunction→ fluid imbalance, edema, increased pressure

Question 17

clinical signs: bromethalin

Answer 17

may be acute or delayed

Acute-less common; CNS excitatory signs - muscle tremors, hyperthermia, hyperexcitability, running fits, generalized seizures

Subacute- more common; progressive, hind-limb ataxia, proprioceptive defects and paresis; can progress to paralysis, loss of deep pain, patellar hyperreflexia, UMN bladder, CNS depression, V+, anorexia, dementia, positional nystagmus, Schiff-sherrington, seizures, death due to resp. Failure

Question 18

DDx: bromethalin

Answer 18

neurotoxins - strychnine, metaldehyde

trauma, neoplasia, encephalitis

Question 19

treatment: bromethalin

Answer 19

no specific antidote,

decontamination - emesis, activated charcoal with sorbitol (cathartics) - avoid Mg cathartics (CNS depressive) repeated dosing q 4-8hrs x 2-4 days;

supportive/symptomatic care - Mannitol (cerebral edema), diazepam/phenobarb (seizures and tremors), nutritional support

Question 20

bromethalin is considered a

Answer 20

General Use Pesticide (GUP)

Question 21

MoA strychnine

Answer 21

block postsynaptic effect of glycine in the spinal cord

Question 22

clinical signs: strychnine

Answer 22

rapid onset and rapid death

Early signs: apprehension, panting, nausea/V+, mydriasis, stiffness, muscle twitching, hyperthermia

Progresses to: tonic seizures (excitable by external stimuli) and opisthotonos, “sardonic grin” death from resp. failure

Question 23

treatment of strychnine

Answer 23

decontamination - emesis, gastric lavage (bicarb and antacids in it), activated charcoal (repeated doses);

supportive care - fluids, O2, keep in quiet place and avoid stimuli, diazepam/methocarbamol (tremors) treat seizures;

may need to be sedated 24-72 hours

Question 24

T/F strychnine and bromethalin and GUPs

Answer 24

False

strychnine is a “Restricted Use Pesticide” (RUP)

Question 25

what should be avoided with strychnine

Answer 25

opioids, phenothiazines, neuromuscular blockers, and dissociative anesthetics