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what are the 4 rodenticide toxicities

1. warfarin
2. bromethalin
3.cholecalciferol (vitamine D3)
4. zinc phosphide


what are anticoagulant rodenticides

- they are Vit K antagonists (our body can recycle and reuse Vitamin K)
-interferes with the production of vitamin K dependent clotting factors in the liver


what is the lag period of the coagulation system when vitamin K is depleted

3-5 days between exposure and appearance of clinical signs


how long does is take to see clinical signs if vitamin K is depleted

about 3 days, because then all the stored of vitamin K will have been consumed


what is the 1st generation of anticoagulant rodenticide toxicity

warfarin base


what is warfarin base

-warfarin, diphacinone, pidone
-short acting anticoagulant
- depress clotting factors for about 7 to 10 days


what is the 2nd generation of anticoagulant rodenticide toxicity

coumarin base


what is a coumarin base

bromadiolone, brodifacoum, super-warfarin - greater potency and accumulation effects in the liver
-depressed clotting factos for approx a month


what are the LD50 values for bromadiolone (super-warfarin)

rats 1.125 mg/kg b.w.
mice 1.75 mg/kg b.w.
rabbits 1 mg/kg/ b.w.


what are the LD50 values for warfarin

rats 3mg/kg
mice 437 mg/kg
rabbits 800 mg/kg


what are the clinic signs of anticoagulant rodenticide toxicity

3- 5 days post ingestion =
1. intracavital bleeding (lungs and abd), melena, epistaxis etc.
2. lethargy, excercise tolerance, inappetence, pallor, dyspnea
3. sudden death - paricardium, cranium, thorax etc
4.mild thrombocytopenia (secondary to blood loss, do not interfere with platelet production or function
**check poo


what is the diagnosis of rodenticide toxicity

-prolongation of PT (prothrombin time) and greater than PTT (thromboplastin time) and development of CS


what is the treatment of rodenticide toxicity

antidote - vitamin K1


what is CNS rodenticide toxicity

bromethalin (fastra, tomcat)
decreases mitochronrial ATP production in brain and liver


in CNS rodenticide toxicity less than LD50 what are the paralytic signs and when do they start

1 -4 days
hind limb weakness, ataxia, tremors, loss of deep pain, decreased propriception


in CNS rodenticide toxicity more than LD50 what are the convulsant signs and when do they start

4 - 36 hrs
hyperthermia, seizures, hyperexcitability


what is calciferol rodenticide toxicity

cholecalciferol (vitamin D#)
-orhto-mouse-B-gone, quintox, rampage
-increase calcium absorption from food and bones -> soft tissues calcification, nephrosis, cardiac arrhythmia
-free calcium levels are high and lead to mieralization of blood vessels and tissues (organs) = system calcification


what are the clinical signs of calciferol rodenticide toxicity

12 - 36 hrs post ingestion
anorexia, vomiting, muscle weakness, PU/PD, arrhythmia, seizures, hypercalcemia


what treatment can be used for calciferol rodenticide toxicity

furosamide, prednisone, calcitonin (lowers the calcium level by excreting or slowing down)


what is zinc phosphide

- sweeneys toxic peanuts, ACME gopher killer pellets, mold guard
-forms phosphine gase -> interrupt mitochondria process -> cell death and cellular oxidative damage


what are the clinical signs of zinc phosphide

appears rapidly after ingestion
-vomiting, +/- hemorrhage, anorexia, deep/wheezy respirations, ataxia, and hypoxia
-hard to detect because it degrades rapidly


what are the treatment of zinc phosphide

sodium bicarbonate slows the hydrolysis into gas, induce vomit in a well ventilated area to prevent exposure


what is organophosphate and carbamate intoxication

-it inhibits acetylcholinesterase (AchE) and synatic cleft
AchE - is an enzyme that degrades the neurotrasmitter acetylcholine in the nervous system


what does having excessive Ach do in the synapse

it accumulates with overstimulates muscarinic and nicotinic receptors


what are the clinical signs of organophosphate and carbamate intoxication

V/D, urination, miosis, bronchospasm, bronchorrhea, lacrimation, salivation, bradycardia


what are the nicotinic signs of organophosphate and carbamate intoxication

muscle tremors, twitiching, weakness and paralysis


what the CNS signs of organophosphate and carbamate intoxication

seizures, and coma


what is the treatment of organophosphate and carbamate intoxication

-supportive care (fluid and oxygen)


what is acetaminophen toxicity

NSAID - 90% is metabolized by the sulfate and glucuronide pathways (liver and kidneys) -> nontoxic metabolites
5% is metabolized by NAPQI
-can be neutralized by bind with endogenous glutathione and then excretes it out


what should we know about cats and acetaminophen toxicity

they have reduced glucuronide metabolism and they are deficient in glutathione and less than 3% of acetaminophen in excreted