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Common Rodenticide Toxicoses Flashcards

(56 cards)

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1
Q

T/F: Color of rodenticide indicates the type

A

False

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2
Q

How does one identify a rodenticide?

A

Packaging!

  • Active ingredient and strength
  • Weight of package
  • EPA registration number (unique to specific product)

Baits put out by services should be listed on owners’ invoices

Not all rodenticides are d-Con

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3
Q

What are the two anticoagulant rodenticide groups?

A 
Hydroxycoumarin class
Indandione class
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4
Q

General characteristics of Warfarin

A
  • Short-acting anticoagulant
  • Hydroxycoumarin
  • Repeated exposure important
  • Therapeutic doses:
  • .1-.2mg/kg q12h dog cat
  • .067-.167mg/kg q24h horse
  • Baits usually .025% (7mg per oz)
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5
Q

Decontamination dose of Warfarin

A

0.5mg/kg

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6
Q

What are some 1st generation longer acting indandiones?

A

Diphacinone, Chlorophacinone, Pindone

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7
Q

What are some characteristics of 1st generation indandiones?

A

Treat the same as second generation

EPA restrictions on consumer use: consumers can purchase, must have bait station

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8
Q

What are some 2nd generation long acting hydroxycoumarins?

A

Brodifacoum - most potent
Bromadiolone - shorter half life
Difethialone

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9
Q

What is the decontamination dose for 2nd generation hydroxycoumarins?

A

0.02mg/kg

Bait usually contains .005% (1.4mg per ounce of bait)

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10
Q

T/F: Only pest control operators can apply 2nd generation hydroxycoumarins

A

True

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11
Q

Kinetics of rodenticides

A 
Readily absorbed
Hepatic storage
Slow elimination
- Brodifacoum t1/2 6+-4d
- 8% Flocoumafen in liver 43 weeks post exposure
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12
Q

What is the MOA of rodenticides?

A
  • Inhibit vitamin K epoxide reductase to prevent vitamin K recycling
  • New coagulation factors not activated
  • Pre-existing active coagulation factors become depleted (II, VII, IX, X)
  • Hemorrhage
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13
Q

Clinical signs of anticoagulant toxicosis

A
  • Signs develop in 2-7d
  • Initially vague signs: lethargy, anorexia, weakness
  • As signs progress:
  • Dyspnea: hemothorax; pulmonary hmg
  • Abd distension: Hemoabdomen
  • Frank hemorrhage, bruising
  • Lameness; paralysis or seizures (rare)
  • Death
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14
Q

What animals are at increased risk for anticoagulant toxicosis?

A

Very young
- pups have 50% clotting factor levels of adults
- Case report of prenatal exposure to brodifacoum
Underlying health problems
Animals on highly protein bound medications (NSAIDs, sulfonamides, levothyroxine) could have increased amounts of circulating active anticoagulant- advise close monitoring

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15
Q

What are the trigger doses of anticoagulants?

A

Warfarin .5mg/kg

All others .02mg/kg

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16
Q

When should emesis be considered as a decontamination method for anticoagulant toxicosis?

A

Less than 4h after ingestion
Grain-based baits may stay in stomach longer
DO NOT attempt emesis in a hemorrhaging animal

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17
Q

T/F: the benefit of repeated doses of activated charcoal has not been proven

A

True

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18
Q

What are the vitamin K dependent coagulation factors?

A
  • II, VII, IX, X

- Involves extrinsic, intrinsic, and common coagulation pathways

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19
Q

Which coagulation test (PT or PTT) will detect impaired ability to coagulate first?

A

PT; Factor VII (extrinsic pathway) has shortest half life in dogs

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20
Q

How should asymptomatic animals be monitored after decontamination for anticoagulant toxicosis?

A

PT in 48-72h post-exposure

  • Baseline value is ideal, esp. if exposure time is questionable
  • Do not administer vitamin K1 before blood samples are drawn
  • Confidence in effectiveness of decontamination
  • Large breed dogs or multidog households: cost of tests vs. 1 month of vitamin K1
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21
Q

Equine Monitoring (asymptomatic animals only) for anticoagulant toxicosis

A

PTT may prolong before PT
- Factor IX may have shorter half-life than VII in horses?
- Lack of good info on equine coagulation factor half-lives
- Elevated clotting times may develop rapidly
Best to monitor both PT and PTT
- Baseline: same day is important
- Then q24h for 3d

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22
Q

What is the treatment for anticoagulant toxicosis?

A

Vitamin K1
- If actively hemorrhaging
- If PT prolonged
- Instead of PT monitoring in smaller animals
Dose
- Dog, cat: 1.5-2.5mg/kg q12h
- Horse: 2.5mg/kg q12h
- May be given PO, SQ, IM
Give with fatty meal to increase absorption
Injectable product may be given orally
- Useful for treating neonates, rabbits, rodents

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23
Q

What is the duration of treatment for anticoagulant toxicosis?

Study These Flashcards
A 
Warfarin - up to 14d
Bromadiolone - 21d
Brodifacoum and all others - 30d
Dose dependent
Recheck PT 48-72h after last dose of K1
24
Q

Things to avoid when giving vitamin K1

Study These Flashcards
A 
IV: risk of anaphylaxis is too great (malpractice)
IM in a bleeding patient (may continue to bleed)
Exceeding recommended doses (risk of oxidative damage to RBCs)
Vitamin K3 (menadione) and vitamin k supplements (ineffective, k3 is nephrotoxic in horses, 100mcg = 15-25 capsules/kg
25
Treatment of hemorrhage
Replace deficient coagulation factors: fp, ffp, whole blood K1 to activate new coagulation factors as they are produced: occurs within 6-12h Supportive care: oxygen, thoracocentesis/abdominocentesis, restrict exercise
26
Prognosis of anticoagulant toxicosis
Excellent if tx started before CS are evident | If CS present, prognosis depends on the type of signs (hemothorax vs. hemoarthrosis) and severity
27
What are the minimum toxic dose and minimum lethal dose of Bromethalin?
MTD - .9mg/kg dog, .24mg/kg cat | MLD - 2.5mg/kg dog, .45mg/kg cat
28
What are the kinetics of bromethalin toxicosis?
``` Rapid absorption (Tmax-4h) Converted to desmethylbromethalin by liver (several times more toxic) Elimination t1/2 = 6d (rat) w/ enterohepatic recirculation (give repeated AC**) ```
29
Bromethalin MOA
- Uncouples ox phos - Dec ATP - Loss of ion pumps - Intramyelinic vacuolization - Axonal swelling - Inc ICP - Disrupted neuronal conduction - Inc cerebral lipid peroxidation
30
Acute CS of bromethalin toxicosis
Acute/convulsant syndrome - seen with supralethal ingestion - signs appear 2-24h post ingestion - Agitation - Hyperesthesia - Depression - Generalized tremors, seizures, running fits - Mortality 100%
31
Chronic CS of bromethalin toxicosis
Chronic/paralytic syndrome (lower doses) - 1-5d post exposure - dogs, cats - initially: ataxia, hind limb paresis, depresssion - Progression: tremors, tetraparesis, obtundaion - Terminally: decerebrate posture, seizures, coma
32
DDX of bromethalin toxicosis
Rabies, FIP, crypto, HE, GME, neoplasia, lead poisoning
33
What are the trigger doses for bromethalin toxicosis?
cat- .05mg/kg dog- .1mg/kg Emesis- if within 4h of ingestion AC- 1x vs. 3x over 24h vs 6x over 48h; depends on estimated bromethalin dose, success of emesis, time since exposure
34
What drugs decrease cerebral edema as treatment for bromethalin toxicosis?
Furosemide (1mg/kg q4-6h IV) Mannitol (250mg/kg q6h IV) Dexamethasone (2mg/kg q6h IV) - Good for vasogenic but not cytotoxic edema, so this one is iffy
35
How should bromethalin toxicosis be treated?
- Decrease cerebral edema - Manage tremors, seizures with diazepam or barbiturates - Minimize external stimulation (put in quiet, dark room) - Treatment often ineffective or signs resume when stopped
36
What is the prognosis for bromethalin toxicosis?
Varies with severity of signs - Mild depression, ataxia: good prognosis, recovery possible over 1-2mo - Severe neurologic signs (coma, paralysis) or acute/convulsant syndrome: grave prognosis
37
What is the minimum toxic dose of cholecalciferol?
0.5mg/kg
38
What is the decontamination dose of cholecalciferol?
0.1mg/kg
39
What is the major circulating form of cholecalciferol?
Calcifediol
40
What is the most active form of cholecalciferol and the form responsible for toxicosis?
Calcitriol
41
General facts about Calcitriol
.5mcg tablets Dose in dogs is 1-30ng/kg Binds vit D receptor 2000x better than cholecalciferol Hypercalcemia can be seen at higher doses
42
General facts about Calcipotriene
Calcitriol analogue .005% cream, ointment, or solution (for psoriasis) Minimum lethal dose 36ug/kg (dogs)
43
How do the plasma and terminal half lives vitamin d analogues differ?
Calcitriol - shortest (p: 5-8h, t:3-5d) Calcifediol - middle (p:19-29h, t:19d) Cholecalciferol - longest (p:19-25h, t:weeks to months)
44
What is the MOA of calcitriol?
- Inc intestinal absorption of Ca and P - Inc bone resorption (Ca and P) - Inc renal tubular reabsorption of Ca (lesser role) - Net result: Inc serum Ca and P - As CaxP inc above 60, soft tissue mneralization is more likely to occur (metastatic calcification)
45
What is the result of metastatic calcification?
Acute renal failure
46
How does acute renal failure occur in cholecalciferol toxicosis?
Mineralization of kidneys, cardiac muscle, blood vessels, GIT, lungs, ligaments, soft palate Additional direct renal effects of hyper Ca - Impaired [] of filtrate - Renal vasoconstriction causing dec. GFR
47
What is the chronology of cholecalciferol toxicosis?
CS within 12-18h Elevations in serum P within 12h Increased serum Ca within 24h Renal failure may be detectable by 24-48h
48
T/F: in cholecalciferol toxicosis, serum P is elevated before serum Ca
True
49
What are the CS of ARF?
Vomiting, depression, PU/PD, anorexia, hematemesis, diarrhea, occassionally other signs: dyspnea, arrhythmias
50
What are the trigger doses of cholecalciferol?
dog- .1mg/kg | cat- any
51
How should one handle decontamination of cholecalciferol?
``` Emesis if ingestion less than 4h ago Cholestyramine = anionic exchange resin - 300mg/kg PO q8h for 4d - For any ingestion Activated charcoal 1-3x for large ingestion and alternative for smaller ingestion Intralipids? ```
52
Initial monitoring and treatment for hypercalcemia
Baseline: Ca, P, BUN, creatinine, and calculate CaxP Monitor blood values daily for at least 72h - No change in 4d, stop If CaxP rising, diurese at twice maint rate w/ .9% NaCl - Na competes for reabsorption w/ Ca in renal tubules - Treat until Ca normalizes
53
What are some treatment options for hypercalcemia?
.9% NaCl fluid diuresis Furosemide (2.5-4.5mg/kg PO q6-8h) - Increases Ca excretion - Thiazide diuretics are contraindicated b/c they decrease Ca excretion Corticosteroids - Dexamethasone (.25mg/kg IV SQ q6h) or Prednisolone (2-3mg/kg PO q8-12h) - Dec bone resorption, dec intestinal absorption, and inc renal Ca excretion Pamidronate Phosphate binder (eg AlOH3) Low Ca diet
54
Why is Pamidronate effective in treating hypercalcemia?
``` Bisphosphonate drug Inhibits osteoclastic bone resorption Early admin regimen: - Single initial dose - May need to repeat in 5-7d 1.3-2mg/kg diluted in .9% saline slow IV infusion over 2h ```
55
Continued treatment for hypercalcemia
Once serum levels improve, wean off saline diuresis Send home on oral furosemide, prednisolone, and phosphate binder for 2-4wk Monitor serum Ca daily for 5-7d post-diuresis -> 2x weekly for 2wk -> weekly Continue all therapies until CaxP is <60 (d-wk)
56
Prognosis of hypercalcemia
Good if initiate treatment early Worsens with prolonged inc Ca and P - Long term prognosis depends upon the degree of soft tissue mineralization - Lesions from soft tissue mineralization are poorly reversible and may result in long term sequelae or sudden death

Toxicology (3 decks)

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