toxicology lecture 2 Flashcards
what are the 4 rodenticide toxicities
- warfarin
- bromethalin
- cholecalciferol (vitamine D3)
- 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 =
- intracavital bleeding (lungs and abd), melena, epistaxis etc.
- lethargy, excercise tolerance, inappetence, pallor, dyspnea
- sudden death - paricardium, cranium, thorax etc
- 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
thoracocentesis
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
- decomtamination
- supportive care (fluid and oxygen)
- atropine
- pralidoxime
- diazepram
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
what are the toxic doses for dogs and cats for acetaminophen toxicity
dogs 75 to 100 mg/kg
cats 10 mg/kg
what are the clinical signs of acetaminophen toxicity
methemoglobinemia (cannot carry oxygen) -more than 200 mg/kg in dogs and 10 mg/kg in cats -brown/ muddy mm -resp signs - distress hepatic dysfunction renal failure heinz body formation (cats)
what is the treatment of acetaminophen toxicity
decontamination
transfusion
oxygen and fluid therapy
what are the drugs used for acetaminophen toxicity
N-acetylcysteine
cimetidine
ascobric acid
what does N-acetylcysteine do
it increases synthesis and replenishes cellular gluathione stores by providing a glutathione precursor
what does cimetidine do
slowed metabolism of acetaminophen into toxic metabolites (not for cats)
what does ascorbic acid do
it reduces the methemoglobin to hemoglobins
what are permethrins and pyrethroids
insecticides frequently used in flea and tick meds
-extraction of chrysanthemom flowers
Pyrethroids are a deriative of pyrethrins - a more stable form which is more potent and toxic
what is the mechanism of toxicity for permethrins and pyrethroids
dermal and GI absorption (ingestion and grooming)
-disruption of action potential -> repetitive firing of signals -> neurotoxicity -> affects CNS and PNS
what is the clinical presentation of toxicity for permethrins and pyrethroids
within minutes/hours and up to 72 hours
- no specific findings in usual bloodwork
- few vet practices provide screening for presence of this toxicity
- most pets have history of recent dermal application of an insecticide
what are the clinical signs of toxicity for permethrins and pyrethroids
mild to moderately
hypersalivation, mild tremors, hypersensitivity/ depression, GI signs, V/D
what are severe clinical signs of toxicity for permethrins and pyrethroids
disorientation, hyperthermia, muscle fasciculations, generalized tremors, seizures
what is the treatment for pyrethrin toxicity
decontamination and supportive care (fluid/oxygen)
dermal exposure
oral exposure
medications - methocarbamol, diazepam/barbiturates
what is the prognosis of permethrins and pyrethroids
excellent in general
- fatal outcomes may occur (mostly in cats)
- secondary brain injury may come from prolonged seizure activity/hyperthemia
- severely overdosed (gave for dogs only to cats)
- patient in which treatment and supportive care are withheld
what is lily toxicitiy
can cause acute renal failure, we don’t know why but it has to deal with renal tubular necrosis
what are the clinical signs of lily toxicity
lily induced gastritis within 2 hours can cause vomiting, anorexia, depression
uremia in approx 12 hours
acute renal faily in 24 to 72 hours
-polyuria,oliguria, anuria, depression, dehydration, enlarged/painful kidneys
-severe azotemia, elevated creatinine
what is the treatment for lily toxicity
no known antidote fluid therapy, supportive care, intensive monitoring GI Decontamination and fluid diuresis peritoneal dialysis (only treatment in anuric cats)
what is the prognosis of lily toxicity
ARF within 18 hours if treatment is delayed
death occurs approx 3 to 7 days without proper treatment
