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Toxin

Mechanism of action

Sign of toxicity

Diagnosis

Treatment

Atropine sulfate for muscarinic signs, dose to


Clinical signs
effect, will not stop nicotinic signs
Decreased AChE activity
Oximes can reactivate AChE before aging
(blood, brain)
Diazepam or barbiturates for seizures
Test dose of atropine
Chemical analysis for
specific compound

Anticholinesterase insecticides
Organophosphates
Carbamates
Variable toxicity
Toxicity usually occurs from misuse of
products or improper storage

Inhibition of acetyl cholinesterase Muscarinic (salivation, lacrimation,


urination, diarrhea, miosis, dyspnea,
bradycardia)
Nicotinic (muscle fasciculations beginning
with face, generalized tremors, weakness)
CNS ( respiratory depression, clonic- tonic
seizures)

Ethylene glycol (EG)


Major ingredient in normal antifreeze
Toxicity usually in small animals
Exposure most common in spring and fall
Animals often like EG

EG acts like ethanol producing


early signs of drunkness
Metabolism to glycolic acid
causes acidosis
Metabolism to oxalic acid which
combines with calcium to form
insoluble crystals

3 stages of intoxication
stage I (30 min 3 hrs) ,drunkness, ataxia
stage II (12- 24 hrs)
1. tachypnea, tachycardia (or bradycardia)
2. often not observed
stage III (12 72 hrs) oliguric renal failure

Acetaminophen
Present in many overcounter pain and odd
remedies

Metabolized extensively by the


liver by glucuronidation, sulfation
Activated by P450 to reactivate
compound detoxified by GSH
When GSH is depleted, toxicity
occurs

Methemoglobinemia, Heinz body


formation in cats
Cyanosis, dyspnea
Facial and paw edema
Anorexia, vomiting
Humans and dogs develop hepatic necrosis in
overdoses

GI decontamination
N- acetylcysteine (Mucomyst) to replenish and
substitute for GSH
Ascorbic acid used to treat methemoglobinemia
in cats, methylene blue in other animals

Monitor EKG
- treat tachyarrhthmias with lidocaine (not in
cats) or metoprolol
Treat seizures with diazepam or barbiturates

Methylxanthines
Antagonist of adenosine
Caffeine, theobromine, theophylline
receptors; causes CNS
stimulation, vasoconstriction and
Usually a problem with dogs due to eating
tachycardia
habits
Prevent Ca++ reuptake
Found in chocolate, coffee, medications
Unsweetened baking chocolate is especially Inhibits phosphodiesterase
toxic; as little as 0.2 oz/kg may kill a dog
Anticoagulant rodenticides
First generation compounds
o Warfarine (halflife=14-15 hrs)
o Short half life(hrs) low potency
Second genarampound
o Brodifacoum, bromodialone,
diaphacinone
o Long half life (15- 20 days); high
potency
Usually a problem in small animals
Large animals can develop similar
problems from sweetclover

Vomiting, diarrhea
Hyperactivity
Tachycardia, PVC, hypertension
Ataxia
tremors, seizures
coma

Inhibits Vit K epoxide reductase Delayed onset of clotting factors are


Increased prothrombin
(PT) time
consumed (3-5 days)
Results in depletion of Vit K
dependent clotting factors (II, VII, Initial signs are often depression, anorexia Increased activated
partial thromboplastin
and anemia
IX, X)
Pale mucosa, dyspnea, nose bleeds, bloody time (APTT or PTT)
feces and bloody gums
Chemical analysis
Abdominal pains
Hemorrhage and hematoma

Strychnine
Competitive inhibitor of glycine
Alkaloid used as pesticide to control
at post synaptic neurons
gophers, moles, rats and coyotes
Glycine is inhibitory so result is
Controlled in most states
disinhibition (simulatioin)
Still commonly used as a malicious poison
All species are sensitive but dogs are most
commonly poisoned

Toxicology

acidosis
anion and osmolal gap
crystalluria
crystals in kidney

Initial signs are anxiety and stiffness


grinning
violent tetenic seizures usually initiated by
sudden noise or light
saw horse stance
persistent rigid extension of all limbs
apnea due to rigidity

Traditional treatment is ethanol and bicarbonate


1. ethanol is competitive inhibitor of alcohol
dehydrogenase which is initial steps in EG
metabolism
2. bicarbonate used to correct acidosis
4- methylpyrazole and antizol are Alcohol
Dehydrogenaze inhibitors that can replace
ethanol

Vit K administration
Therapy should be continued for 10 14 days
with warfarine
21 30 days for second generation comounds

control seizures woth pentobarbital or


methocarbamol
prevent asphyziation
1.may require intubation and respiratory
support

Melaldehyde
Slug and snail baits
Generally 3.5% metaldehyde
Ingestion of 1-4 oz of bait will cause
toxicity in average dog
Toxicity is most common in dogs

Metaldehyde is hydrolyzed to
acetaldehyde by gastric acids
Further metabolism of
acetaldehyde to acidic products
thought to account to acidosis
Exact mechanism in unknown

Initial signs are anxiety, nystagmus


Progresses to salivation, vomiting, ataxia,
seizures, hyperthermia
Profound acidosis
formaldehyde- like smell

Control seizures with diazepam or barbiturates


GI decontamination
Treat acidosis with fluids and bicarbonate
Treat hyperthermia

Cholecalciferol
Vit D3
Used as a rodenticide and psoriasis
treatment
Usually sold as a bait preparation
Toxicity occurs at doses above 0.5 mg/kg

Metabolized to 1, 25dihydroxycholecalciferol
Increased serum Ca by increasing
GI absorption, decreasing renal
excretion, and simulating bone
resorption

Vomiting, diarrhea
PD/PU, radio-opaque kidneys
Elevated serum Cs (>11.5 mg.dl), BUN
and creatinine
Mineralized of soft tissues

IV saline and furosemide


Cortisone
Calcitonin
Low Ca diet and avoid sunlight
Continue treatment until Ca stabilizes in normal
range (up to 2 weeks)

Lead causes a mixture of meurologic, GI


Clinical signs
and hematopoietic signs
Whole blood lead levels
Neurologic signs include blindness,
of 0.6 ppm or greater
seizures, ataxia, head-pressing, raor- horses Decreased serum d Gi signs include anorexia, vomiting,
ALAD activity,
constipation the becomes diarrhea, colic
increased urine d-ALA
Hematopoietic signs include regenerative
anemia with nucleated RBCs, basophilic
strippling (dogs), increased zinc
protoporphyrin (dogs), elevated plasma
porphyrins (cattle)

GI decontamination using a cathartic or surgical


removal of large objects
Chelation therapy with Ca-EDTA, DMSA
(succimer), d-penicillamine
Thamine may improve symptoms in cattle
Control seizures with barbiturates

Lead
Multiple actions. May based on
Affects large and small animals; waterfowl the reaction of Pb with SH
groups of key enzymes and effects
Sources include old paints, oil, grease,
on calcium regulations
batteries, lead shot
Lead inhibits delta-aminolevulinic
Toxicity usually results from acute oral
acid dehydratase and heme
exposures
synthetase, both involved in heme
synthesis

Oxalate containing plants


Plants containing soluble oxalates
Many members of the Areaceae family of
produce hypocalcemia and renal
plants contain performed Ca-oxalate
injury due to precipitation of Cacrystals that cause mechanical injury to the oxalate crystals
mouth resulting in pain, salivation,
vomiting, dyspnea
Diffenbachia, caladium, philodendron,
calla liliy
Example are rhubarb, beets, lambs
quarters
Nitrates
Sources are plants and fertilizers
Ruminants are most susceptible due to
conversion of nitrate to nitrite in rumen

Nitrite oxidizes hemoglobin to


methemoglobin

Cyanide
Acts by inhibiting cytochrome
Released from cyanogenic glycosides
oxidase which inhibits oxidative
found in some plants (wild cherry and other phosphorylation
prunus spp), sudan and johnson grass

Toxicology

Detoxification with limewater and supportive


treatment of hypocalcemia and nephrosis

Methemoglobinema, chocolate brown


blood
Brownish cast to membranes
Cyanosis, dyspnea
tachycardia

Convert methemoglobin to oxyhemoglobim with


methylene blue(except cats, ascorbic acid)
Avoid overdosing methylene blue; can cause
methemoglobinemia
Avoid stressing animals

Initial signs are salivation and tachypnea


Progress to dyspnea, weakness, seizures,
tachycardia
Death in 20-120 min.
Cherry- red b;ood that clots slowly

Cyanide binds to Fe (III)


Convert hemo to methemo. With sodium nitrate
Promote detoxification of cyanide with sodium
thiosulfate