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Toxicology

Terms in this set (191)

Toxicology
Science and study of poisons (toxicants) an dtheir effects on living organisms
Toxicant or toxic substance
Any solid, liquid, gas that interferes with life processes
Biotoxin
Toxicants from biological sources
- Endotoxin (bacterial)
- Zootoxin (animal)
- Phytotoxin (plant)
- Mycotoxin (fungal)
Variations in toxic responses
- concurrent D
- Age
- Species diffs
- Genetic Polymorphisms
Toxicokinetics
Movement of toxicant through the body --> ADME
Toxicokinetics ADME
Absorption
Distribution
Metabolism
Excretion
ADME: Absorption
Two most common routes of exposure/absorption are oral/GI and percutaneous/dermal
ADME: Metabolism
- Biotransformation (liver): making more water soluble for excretion via Phase I and Phase II reactions
- Bioactivation: Nontoxic or low toxic compound to a more reactive metabolite
ADME: Excretion
Excretion through feces, urine, exhaled through the breath, sweat it out, in your saliva, excrete thru breast milke, etc.
Toxicodynamics
What does the toxicant or metabolite do to the body
toxicant/metabolite effect on the body
Dependent on mechanism of action, usu. cellular damage, alter structure/function

- Bind and activate/block a receptor
- free-radical production
- lipid peroxidation
- alter cell pH
- s/t its unknown
Incidence of dog poisonings
>60%, avg of 4 yrs old
Incidence of cat poisonings
< 10%
Incidence of horse poisonings
<1%, little known
Small Animals: Most poisonings are _________
acute, involve single agent, show no sex predisposition, accidental (malicious is very rare), and ingested
SA poisonings: _______ % show no clinical signs
57 - 63%
SA poisonings: _______ % self limiting signs
25%
Most common CA toxicants
- human meds
- insecticides/rodenticides
- human food
- vet meds
- household toxicants
- plants
- herbicides
- outdoor products
Common substances toxic to DOGS
- antifreeze
- Rodenticides
- Insecticides
- Heavy Metals
- Oral meds/topical preparations
- Mycotoxins
- Plants
- Some human foods (chocolate)
Common substances toxic to CATS
- Rodenticides
- Insecticides
- Antifreeze
- Drugs (acetominophen, Ibuprofen)
- Plants
- Quaternary ammonium chloride
Common substances toxic to LIVESTOCK
- Insecticides
- Heavy metals
- Nitrate-nitrite
- Plants
- Mycotoxins
- Feed additives
- Miscellaneous farm chemicals
Approach to the poisoned patient
1. E to a known toxicant
2. E to an unknown substance that may be toxicant
3. Uncertain, but toxin is a rule out
Treat the ____ and not the ____
Patient, poison
Decontamination Goals
Remove the source of toxicant, prevent further E/bsorption (including people)
How to Decontaminate
- Remove source if known
- Induction of emesis for recently eaten
- Gastric lavage
- Gastrotomy or endoscopic removal
- Adsorbents
- Accelerate excretion (use of cathartics)
Detoxification Goal
Hasten elimination of absorbed toxicant
How to Detoxify
- Forced diuresis
- Ion trapping in the urine
- Antidotes
- IV lipid emulsion therapy
Toxicant: Antidote

Acetaminophen
N-acetylcystine
Toxicant: Antidote

Anticoagulants
Vitamin k1
Toxicant: Antidote

OP/OC
Atropine
Toxicant: Antidote

Ethylene glycol
Fomepizole; ethanol
Toxicant: Antidote

Iron
Deferoxamine
Toxicant: Antidote

Cyanide
Sodium thiosulfate
Toxicant: Antidote

Lead, arsenic
Succimer
Toxicant: Antidote

Amitraz
Yohimbine
Toxicant: Antidote

Opioids
Naloxone
Copper
D-penicillamine
Diagnostic Toxicology
- Requires a complete understanding of the case,
- evidence: clinical exam, CBC/chem, necropsy
-Hx and clinical pathology findings identify source of toxin, organ affected and rule outs
- Residues in food animal products must be considered
What is a toxicology MYTH
Toxicology "panel"
Dx Tox: Four Investigative Goals
1. Form a list of differentials based on the clinical signs and/or lesions
2. ID potential sources of the toxicant
3. Find evidence of E to the toxicant
4. Find evidence of absorption of the toxicant

** Often all 4 CANNOT be met and a presumptive dx must be made
Dx tox: Historical Info
- Knowledge of a knwon E and circumsatcens
- Presence of poisons on premises or tehir availability should be determined (e.g. drugs, feed additives, rodenticides, insecticides)
- Food & water supply should be examined
- Know what Qs to ask
Dx Tox: Clinical signs
- Nature of signs and sequence of occurence important
- Details are often important
- Careful attention to changes in heart rate and rhythm --> Cardiotoxins
Parasympathetic signs
SLUDGE
- Salivation
- Lacrimation
- Urination
- Defecation
- GI upset
- Emesis
Parasympatholytic signs
- Bloat
- Dry mouth
- Mydriasis
Dx tox: Sample Collection from LIVE animals
- Whole blood
- Serum
- Urine
- Stomach content
- Feed (if suspect)
Dx tox: Sample Collection from DEAD animals
- Liver
- Kidney
- Brain
- Fat
- Urine
- GI content
Dx Tox: Sample collection enviro
- label containers w/location of sample
- each feed source
- dont pool feed from diff lots
- Water sources individually
- any sus materials
Dx tox: Diagnostic Failures
- Incorrect sample
- Inadequate sample size
- Improper sample storage
Chemical Burns; Acid burns
Acids cause coagulation necrosis --> barrier to further penetration


*alkali causes liquefactive
Chemical Burns; alkali burns
Alkalis cause liquefactive necrosis --> facilitates rapid, deep dissolution of tissue (much more severe)

*acid causes coagulation necrosis
Soaps
- Made by reacting alkali w/fat
- Primarily GI
- Alkali may cause caustic burns
- homemade soaps, dishwasher detergents often contain free alkali (lye = NaOH/kOH)
toxicity of soaps
Generally low, ingestion uncommon
Soaps & Detergents Treatment
- Emesis (only if alkali)
- Dilution (oral milk or water)
- Fluids/electrolytes if vomiting/diarrhea severe (or if cardiac signs)
Non-ionic Detergents
e.g. many handwashing detergents, shampoos, some laundry detergents
- usu. GI signs, mild corneal damage
- Ingestion is uncommon
Non-Ionic Detergents
low toxicity
Non-ionic Detergents Treatment
- Decontamination (flush skin/eyes)
- Dilution (oral milk or water)
- FLuids if vomiting/diarrhea severe
Anionic Detergents
e.g. sulfates, sulfonates in laundry detergent automatic dishwasher detergents, some shampoos
- esophageal damage a major concern
- ocular lesions more severe
- ingestion uncommon but very harmful, intravascular hemolysis possible
Anionic Detergent toxicity
mild to moderate (usually not fatal)
Anionic Detergent Treatments
- Decontamination (flush skin/eyes)
- Dilution (oral milk/water)
- Activated charcoal
- Fluids if vomiting/diarrhea severe
Cationic Detergents
e.g. Quaternary ammonuium compounds (detergents,, fabric softeners, sanitizers)

- Severe oral and esophageal caustic burns, severe ocular damage
- profuse salivation, hematemesis, weakness, seizures, coma, death
Cationic Detergents Toxicity
high to extreme
Cationic Detergents Treatment
- Decontamination (flush skin/eyes)
- dilution/deactivation (milk, egg whites)
- activated charcoal?
- fluids to correct electrolyte imbalances
- DO NOT INDUCE VOMITING
- DO NOT NEUTRALIZE ALKALI WITH ACID --> HEAT --> BURNS
What detergent do you NOT WANT to induce vomiting with?
Cationic Detergents
Other Alkali products
e.g. toilet bowl and drain cleaners
- ingestion is RARE but contact can occur
- Effects similiar to cationic detergents or worse
- may obliterate esophagus; gastic perforation
Other Alkali Products Treatment
Dilution and supportative care

- AC will not bind

- Analgesics to control severe pain

- prognosis grave
Other Alkali Products toxicity
high to extreme
Ibuprofen Toxicosis
- dogs access bc improperly stored
- pets medicated by the client
- narrow therapeutic index in dogs and cats
- 30 mins to 3 hrs after ingestion
Physiological effects of Ibuprofen toxicosis
- GI adverse effects are seen at lower doses (e.g. gastric ulcers, higher dose = multiple organ toxicity)
- inhibits gastric mucus secretion, increases gastric acid production --> ulceration & hemorrhage
- corticosteroids exacerbate NSAID toxicity
Physiology effects of a higher dose of Ibuprofen Toxicosis
higher dose causes renal vasoconstriction, kidney damage, bleeding may be seen due to inhibition of platelet function
What is the #1 canine toxicosis (in some regions)
Ibuprofen toxicosis
_____ accounts for __% of canine and feline calls to some posion control centres
Ibuprofen toxicosis, 50%
Common signs of ibuprofen toxicosis
- GI (vomiting, anorexia, diarrhea, melena)
- Depression, ataxia
- Renal (gastric hemorrhage less common in cats, primary signs usu. renal)
Ibuprofen toxicosis Treatment
- If detected early, treatment aimed at reducing absorption (emesis, activated charcoal, cathartics)
- IV fluids may be required to ensure adequate renal perfusion
- GI perforations require sx
- Severe blood loss may necessitate transfusion
Drugs for treating Ibuprofen toxicosis
Omeprazole: Proton pump inhibitor, inhibits gastric acid secretion --> shortens recovery time

Misoprostol: PGE, analogue that protects GI mucosae, decreases gastric acid secretion, increases bicarbonate secretion
Acetaminophen toxicity with acute dosages in dogs
600mg/ks

*therapeutic dose is 15mg/kg
Acetaminophen toxicity with acute dosages in cats
10mg/kg
Acetaminophen Toxicosis
Metabolite directly damages plasma membranes --> damage most severe in liver, blood


- Glucuronidation and sulfation pathways are finites, so high doses result in increasing P450 metabolism

- Inhibts glutathione synthesis --> even more unconjugated toxic metabolite accumulates
Acetaminophen Toxicosis & cats
Deficient in enzymes required for hepatic glucuronidation, so even higher amounts of NAPQI toxic metabolite accumulate --> essentially no safe dos e
Acetaminophen toxicosis clinical signs DOGS
hepatic injury
- vomiting
- Anorexia
- Tachycardia
- Tachypnea
Acetaminophen toxicosis clinical signs CATS
feline RBCs far more prone to oxidative injury (diff hemoglobin structure) --> methemoglobinemia is the most prominent feature
Most prominent feature of feline acetaminophen toxicity
methemoglobinemia
Acetaminophen toxicosis treatment
1. Minimize absorption (emesis or gastric lavage, followed by activated charcoal)
2. Supportive Therapy (for electrolyte distrubances)
3. Source of glutathione (N-acetyl-cysteine) to speed conjugation of toxic metabolites --> administer immediately to affected cat; repeat every 4 hrs for 5 treatments

Prognosis depends on dose and delay before treatment
Most common illicit drug consumed by dogs
Marijuana
Marijuana
- rarely fatal
- stimulates cannabinoid receptor 1 in brain
Marijuana ingestion signs
CNS signs
- bradycardia
depression
- ataxia
- mydriasis
- urinary incontinence
- vomiting
- hypothermia
Marijuana ingestion treatment
Supportative care
- control tempy
recovery may take up to 5 days
Amphetamines: tret narcolepsy, ADD
- CNS stims: seizues
- Arrhythmias
- Supportative treatment and AC
- DEcongestants containing pseudoephedrine can result in false positives on urine drug tests
Barbiturates: sedatives, anticonvulsants
- CNS depression, extreme hypotension
- supportive treatment, emesis (if not unconscious)/gastric lavage + AC
Benzodiazepines: anti-anxiety medications
- CNS depression
- Supportative treatment
- Antidote: Flumazenil
Cocaine
- CNS stimulation
- May be combines with lidocaine, amphetamines, caffeine, heroin, strychnine
- very rapidly absorbed:
Cocaine Treatment
Decontamination only useful if caught right away
- Supportive care: Diazepam for seizures, beta blocker for tachyarrhythmia, control temperature
LSD
- CNS stimulation or depression
- supportative care
- gastric lavage/AC may worsen signs?
Opioids
- Respiratory depression may be fatal
- Emesis, AC, gastric lavage
> Opioids cause pyloropasm, may remain in stomach for.a few hours
- naloxone is a competitive mu opioid-receptor antagonist that reverses all signs of opioid intoxication
PCP and Ketamine
- Inhibit NMDA receptors in brain - mimics schizophrenia
PCP and Ketamine Clinical Signs
- increased muscle tone, HR, BP
- Abnormal facial expression, jaw snapping, salivation, seizures, blank staring
PCP and Ketamine treatment
- supportative treatment, control seizures
Gasoline (petroleum product)
- may drink out of curiosity, dermal exposure --> licking
Clinical Signs of gasoline ingestion
- CNS depression

Main concern is aspiration: can dissolve tissues within minutes
> less than 1 mL of volatile hydrocarbon --> widespread destruction of alveolar membranes --> pulmonary edema, necrosis, agonal death
Gasoline Treatment
Supportative treatment (e.g. oxygen, decontamination of skin)

- Prognosis witha spiration or coma is poor/grave


- DONT INDUCE VOMITING/GASTRIC LAVAGE due to aspiration risk
Fatal dose of antifreeze for cats
1.5 mL/kg
Ethylene Glycol (antifreeze) physiological effect
- Hepatic alcohol dehydrogenase enzymes convert it to organic acids (e.g. formic, oxalic acid) --> metabolic acidosis

- oxalic acid crystalizes in renal tubules --> calcium oxalate crystals cause renal tubular necrosis --> renal failure
renal failure time for antifreeze in cats and dogs
1 day - cats

3 days - dogs
Clinical signs of antifreeze ingestion
renal failure, vomiting, CNS depression, dehydration
Ethylene Glycol (antifreeze) Treatment
1. 5.5ml/kg/hr IV of a 20% vodka solution (half vodka, half sterile saline)

2. early orevention with fomepizole antidote (ADH inhibitor) - prevents oxalic acid formation
Toxicity of antifreeze
Often Fatal
Propylene Glycol physiological effect
ADH converts it to lactic acid --> acidosis may be fatal, but no calcium oxalate crystals

reacts wth hemoglobin to form heinz bodies (esp. cats that can persist for several weeks
Propylene Glycol
less harmful to animals is found in de-icing fluids for cars and also in low amounts in some foods
Propylene Glycol Treatment
Supportive fluid therapy

Prognosis depends on delay prior to treatment

no specific antidote
Methanol
less harmful than it is to primates/humans

- windshield washer fluid, rubbing alcohol
Physiological effect of methanol
converted in liver to formaldehyde and formic acid (toxic in primates but domestic species convert it to CO2 and water
Clinical signs of Methanol
CNS depression, blindness not observed in most non-primate species
Methanol Treatment
No specific antidote

Monitor, fluid therapy to correct electrolyte imbalances, if necessary
Ionophores
Used as coccidiostats and growth promotants
Ionophores Examples
Monensin

Lasolacid

Salinomycin
Monensin: Mechanism of Toxicity
Not fully explains

likely sustained Na induced and Ca2+ effect in myocytes

Muscle contraction --> necrosis
Monensin Diagnosis
- Increased AST, CK, AP
- Cardiac troponin
- Reduced Ca and K
Monensin Differentials
- White muscle disease (selenium deficiiency)
- Cardiotoxins (yew, oleander)
Monensin Analysis
Ionophore screen in feed/tissue
- cattle > 33ppm, Poultry >110ppm

- Rapidly etabolized residues
Monensin Treatment
- Feed change, supporative care, detox, and decontamination

- void cardiorespiratory exertion (putting cattle in a chute)
Monensin Toxicosis; Target Organs
Cardiac muscle: horses, donkeys, cattle

Skeletal Muscle: Sheep, pigs, and dogs
Monensin clinical signs
- Anorexia, decreased milk prod
- Mild Diarrhea and depression

- Dyspnea, ataxia, death from cardiac failure
% of High nitrate intake in plants
>1%
% of High nitrate intake in water
>1000 ppm
Acute Nitrate/nitrite toxicity in ruminants
Nitrates --> Convert to nitrite --> Nitrite binds to Fe3+ in heme oxidation to methemoglobin --> Hypoxia and vasodilation (nitric oxide/NO). Methemoglobinemia
Acute Nitrate/nitrite toxicity in ruminants Clinical and Necropsy signs
- weakness and collapse, ataxia, death

- Acute death, cyanoisis, dark brownish blood (variable)

- Nitrte (>20ppm) in ocular fluids

- Abortions 3 - 7 days after fetal hypoxia
Acute nitrate.nitrite toxicity in ruminants treamtment
IV methylene blue (1 or 2%: 1 - 10mg/kg IV)

reverses methemoglobinemia
Acute nitrate.nitrite toxicity in ruminants Prevention
Monitor feed nitrates, pasture levels, and intake in critical periods

safe levels <0.5%
Salt Poisoning
High sodium intake during water deprivation

precipitated by renewed access to water
Salt Poisoning: Dehydration Phase [water concentration]
1. Dehydration increases Na+ in plasma - 135 --> 160+ mEq/L

2. High Na+ by equillibration in astrocytes and CSF

"salty brains"
Salt Poisoning: Rehydration Phase
Water moves into salty brain!

1. Rapid rehydration reduces Na [] in plasma
2. Water influx into astrocytes and CSF bc excretion of Na is slower
3. Intracranial pressure increases
4. Perfusion decreases - ischemia and necrosis
5. Polioencephalomalacia
Salt Poisoning Diagnosis - Clinical
- Circumstantial: recent water restriction and increased salt intake
- CNS signs: dog sitting, wandering, bumping into things, circling, seizures, opisthotonus, paddling in a coma
Salt Poisoning Diagnosis - Laboratory
- High Na in serum and CSF

- Na analysis of feed (or water)
Salt Poisoning Diagnosis - Necropsy
- Polioencephalomalacia
- Eosinophillic meningoencehpalitis transiently in pigs
Salt Poisoning Treatment
No effective treatment
Salt Poisoning Prevention
reduce salt intake

gradually resupply water
Salt Poisoning differentials
Insecticide poisoning, pseudorabies, arsenic, Se intox, anything causing CNS signs
Non-protein Nitrogen (NPN) toxicosis: Clinical signs
- Urea, ammonium acetate, ammoniated feeds, etc

NPN --> ammonia --> amino acids in rumen

Hyperammonemia

- rapid onset salivation ataxia muscle spasms convulsions, death within hours of access to new feed mix
NPN toxicosis Diagnosis
- High rumen pH (8-10)

- Feed analysis
NPN Toxicosis Treatment
- Cold water to slow rumen metabolism
Cyanobacteria
Blue-green algae!

Primitive photosynthetic bacteria

- blooms under conditions favoring competition w/plant algae
- warm sunny weather, Eutrophication (animal wastes, phosphates)
- Water pH 6 - 9

- Hepatotoxic and/or neurotoxic
Microcystis and Noduaria: Hepatotoxic
Inhibit protein phophatases (disrupts cytoskeleton leading to endothelial separayion in hepatic sinusoids and zonal hemorrhage/necrosis

Vomiting in some species, colic, diarrhea (often bloody), sudden death from hepatic encephalopathy
Microcystin Hepatotoxicity
Inhiits protein phosphatase 2A

- Cellular hyperphosphorylation

- Cellular injury and necrosis

- Loss of structural associations
Anatoxin Neurotoxicity
Anatoxin-a produced by cyanobacteria

acute anterioir paralysis and sudden death
Factors affecting mycotoxin production
- Plant substrate
- Growth conditions
- Geo locations
- Type consumed
- Exposure
- Animal susceptibility
- Feeding systems
Growth conditions affecting mycotoxin production
- Humidity
- Temp
- pH
- Oxygen
Plant substrates affecting mycotoxin production
- Plants favor selected pathogens and saprophytes
- Composition (starch)
- Damage (stress, insects, other fungi)
Ergot
Sclerotia (dark resting body, mass of hyphal threads) of claviceps spp

Grows in various grains

produce toxic ergot alkaloids

Constrict arterial smooth muscle ischemia of extremities

Exacerbated by cold
Mycotoxin Overview 1
- Toxic secondary metabolites produced by fungi

- Ranking depends on agricultural practice and climate
- Residues w/human risk important to feed producers

toxin production depends on various conditions
Mycotoxin Overview 2
- Fungi flourish in high moisture conditions
> field contamination by plant pathognes
> Storage contamination by saprophytes

Grains (esp corn), nits, or vegetation (pasture, hay)
> levels usually below those responsible for overt toxicity
____ % worlds crop harvest are contaminated with fungi
25%
Diagnostic and Management Qs for Mycotoxins
- Is there visible mould?
- Do field or storage conditions favour toxin production?
- What assayed levels are meaningful?
- How to deal with moldy feed?
*No successful treatment, focus on prevention
4 Types of Mycotoxins
- Zearalenone
- Trichothecenes
- Aflatoxins
- Fumonisin
Zearalenone Mycotoxicosis Dx
- Estrogenic lesions or infertility
- Pink Fusarium mould contamination of grain, corn
- Conditions for production (cool, high moisture)
Zearalenone Mycotoxicosis Species Resistant
Pigs > 1ppm (gilts) > 3ppm (sows) > 9 ppm (boars)

Cattle > 12 ppm (heifers)
Poultry --> very resistant
Zearalenone Mycotoxicosis Treatment/Prevention
- Withdraw or dilute feed
- Divert feed to cattle (not dairy) or poultry
- Prevent moisture and fungal contamination
Trichothecenes
- Over 170 structurally
- Few impt to animal toxicosis
- Fungi grow in cool and damp conditions
Trichothecenes Progress
- Proliferate on plants in the field
- Further fungal growth in feed storage
- Toxins produced under cool and moist conditions
> Over wintered grain and forage
> Moisture >15%
> T-2 toxin + vomintoxin @ 6-12C (Zearalenone is 19 - 20C)
What temp does Trichothecenes and Zearalenone cause T-2 toxin and vomitoxin?
6-12C, 19 - 20C respectively
Trichothecenes Clinical Signs
1. Poor growth/production
2. Feed refusal (or vomition)
3. Irritation of skin and mucosal membranes
4. Cytotoxic to replicating cells @higher doses
Which 2 species are particularly susceptible to Fumonsins?
Pigs and horses
Fumonisins
- Hepatotoxic, vasotoxic, and neurotoxic
- Horses fed mouldy corn
Which species is resistant to Fumonisins
Poultry
Fumonisins clinical effects
- Acute porcine pulmonary edema (PPE)
- Cardiotoxic in pigs
- Hepatotoxicity in various species
- Esophageal cancer in humans
Tremorgens
Neuro-excitatory toxins

Tremors and convulsions if severe
3 species that are the most susceptible to Tremorgens
Sheep
Cattle
Dogs
2 species most susceptible and 1 resistant to Ochra toxins
Sus: Pigs and Dogs

Resistant: Cattle
Aflatoxins
- Can be seen w/ blue or green fluorescence UV
- Mainly on corn, sorghum, peanuts, small grains
- Grow in storage in humid warm conditions
- Highly potent human toxins
- Wide variation in susceptibility
Alfatoxins Clinical Manifestations
- Hepatotoxic
- Immunosuppressive
- Hepatocarcingogenic
Rotenone Source/Exposure
Topical treatment of cattle lice and mites, flea control products
- Excessive use of powders and dips (i.e. cat grooming and oral exposure)
- Intentionally in water to kill fish, easily absorbed through gills
Rotenone toxicity
Birds fish and cats are most susceptible

Acute toxicity most common
Rotenone Clinical Signs
Vomiting (low dose) but may progress to lethargy, tremors, seizures (high dose) --> respiratpry failure, dyspnea, and death
Rotenone Dx
History, pulomonary congestions, GI irritation
Rotenone Treatment
- Minimize absorption; bathe with detergen; non specific detox
- correct acidosis if present
- diazepam for seizures
Rotenozone
Good
Pyrethrins and Pyrethroids Clinical signs
- Paresthesia, abnormal behaviour
- Irritation: salivation vomiting diarrhea
- Hyperexcitability, tremors, and seizures , dyspnea, weakness and death
- Highly toxic to cats and fish
Pyrethrins and Pyrethroids Treatment
minimize absorption! bathe with detergent, general detoxification, and and control seizures/spasms
Pyrethrins and Pyrethroids Dx
No specific clinical or pathologic lesions; tissue anaysis not useful

- CBC; stress leukogram, biochem, hyperglycemia

- R/O organophoshates, metaldehyde
Pyrethrins and Pyrethroids progonsis
Excellent except in cats with spot-on its gaurded
Organophosphates & Organocarbamates Source/Exposure
Still widely used
- Insecticides, fly, ant, and roach baits, shampoos collar, dips and sprays

- contaminated feed stuffs
- Improper use of plant insecticides
Organophosphates & Organocarbamates Toxicity
- Errors in use, mixing, or storage of unused materials

- High acute toxicity, rarely chronic

- Cats more susceptible than dogs

- poultry have lower tolerance than mammals

- Metabolized and excreted rapidly, AChE regeneration concerns!!
AChE regeneration takes ______ weeks
2 weeks
Organophosphates & Organocarbamates clinical signs
SLUDGE

acute posioning within 30 mins usually 6 hours
Organophosphates & Organocarbamates Prognosis
Very poor, high mortality

- early treatment and minimal exposure improves it
-carbamates have better prognosis (bind less tightly)
Metaldehyde Sources and Exposure
- slug and snail bait (pets like it)
- Coastal/lowland wet lands
- Common in dogs also in cats and sheep
Metaldehyde Clinical Signs
"Shake and Bake"
- Acute toxicity: anxiety, restlessness, ataxia
- Hypersalivation, mydriasis, tremors, ataxia, incoordination
- Severe muscle tremours, opistheotonos, convulsions, hyperthermia
Metaldehyde Dx
- No specific lesions
- Acetaldehyde in stomach (odour). Submit contents frozen
- Test blood cholinesterase to R/O OP toxicosis
- Acidosis due to acetaldehyde production
Metaldehyde Treatment
- Emesis
- AC
Seizure control
- IV fluids
- Sodium bicard to reverse acidosis
- Monitor temp and cool with wet towels and fans
- no specific antidote
Metaldehyde Prognosis
- Depends on dosage, time elapsed, speed of trtmnt
- Good with aggressive treatment and supportive care
Forms of Metal
- Metallic
- Inorganic salts
- Organic
Dose-Responses to Metals
Response shifts under influence of other factors
- other metals
- free radicals
- Genetics
- Disease
Toxicology of Metals: Mechanisms
1. Association with polar groups

2. Ionic interactions with charged residues

3. Generation of free radicals

4. Haptens and Immunostimulants
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