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269 Cards in this Set
- Front
- Back
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Study of chemicals, drugs, or other substances that produce hermful effects in or on biological tissues.
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Toxicology
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What is the central aim of toxicology?
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To assess or predict the degree of harm associated with the use of various toxicants.
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List two major assumptions associated with the dose-response curve.
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Primary: There is a cause-and-effect relationship between dose and response
Secondary: Response is proportional to dose. |
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If we assume that the response of an individual to a dose is proportional, this causes us to assume the following 3 things:
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1. There is a receptor for the chemical on the target cell
2. The magnitude of the response is related to the concentration of the toxicant at the receptor 3. The concentration of the toxicant at the receptor is related to the dose of the chemical. |
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What type of dose response curve represents an "all-or-none" phenomenon. An example would be the number of animals responding to a given dose. This info is taken and created as a cumulative curve.
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Quantal curve
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This type of dose response curve measures parameters over a continuous scale.
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Graded
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Would measuring blood pressure be done on a graded scale or a quantal scale?
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Graded
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How is TI calculated?
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LD50 / ED50
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The first piece of infe sought when gauging drug safety; HOWEVER, not always accurate as it assumes that the ED and LD curves are always parallel.
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Therapeutic index
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A more conservative and accurate measure of relative drug safety.
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Standard safety margin (SSM)
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"Certain safety factor" is interchangeable with what term?
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Standard safety margin
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How is standard safety margin calculated?
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LD1 / ED99
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Is a drug more safe if its SSM is >1 or <1?
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Over 1
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Refers to comparing slopes of DR curves of one compound versus another.
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Comparative toxicity
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On a graded dose response curve, why is log dose often used on the X-axis instead of dose?
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Makes curve more linear and easier to read.
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List some advantages of using regression analysis for plotting dose-response data.
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All data can be used
Fewer restrictions on dosage schedules used Not limited to linear-linear analyses |
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Do endogenous dose response curves or exogenous dose response curves have an inverted, biphasic shape?
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Endogenous
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Homeostatic mechanisms regulate concentration of these substances and keep them in a narrow normal range. This causes the associated dose-response curve to be inverted and biphasic.
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Endogenous substances
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Any substance causing a deleterious effect in or on a biological system.
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Toxicant (poison)
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Toxicant originating from a biological source.
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Toxin
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Adjective that describes effect of toxicant on a living system.
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Toxic
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Disease caused by a toxicant
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Toxicosis
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Amount of toxicant required to produce detrimental results
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Toxicity
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Likelihood of poisoning occurring under specific conditions
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Hazard, or risk
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The obverse of risk (the likelihood of poisoning NOT happening)
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Safety
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What is selective toxicity?
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Injury to one kind of biological matter without injuring aother kind, even if they are in close proximity
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Effects of a single dose of toxicant, or multiple doses within 24 hours.
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Acute toxicity
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Animals suffering from acute toxicity are typically monitored for how long?
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7-14 days
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Effects of a toxicant administered over a period of 6 months to 2 years.
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Chronic toxicity
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How would the toxic potential of a chemical be classified if it is under 1 mg/kg?
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Extremely toxic
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List two examples of "extremely toxic" chemicals (toxic at <1 mg/kg)
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Botulinum toxin
Nicotine |
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How is a compound classified if its toxic potential is over 15 g/kg?
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Relatively harmless
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True or false: There is no such thing as a non-toxic chemical.
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True
The dose makes the poison. |
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1 ppm is equal to...
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1 mg/kg or 1 mcg/gm
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1 % is equal to 1 gram per
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1 gram / 100 mL
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1 mg% is equal to...
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1 mg/100mL, or mg/dL
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1 mcg% is equal to...
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1 mcg/100 mL or 1 mcg/dL
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What is a miliequivalent (meq)?
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MW (mg) / Valence
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Which will always be larger by an order of 1000: percent or ppm?
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PPM
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How can one easily convert percentage to ppm?
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Move the decimal four places to the right.
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How many ppm = 100 gm/ton?
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110 pom
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1 gm/ton = how many ppm?
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1.1 ppm
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1 lb chemical/ acre = how many mg/kg BW in the animal?
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7 mg/kg BW
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1 lb chemical/ acre = how many ppm on the resultant forage?
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230 ppm on forage
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Evaluation of patient signs and symptoms to arrive at a cause.
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Diagnosis
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Initial determination of organ systems affected, needs correcting
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Clinical diagnosis
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Diagnosis decribing lesions in tissues
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Pathologic diagnosis
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Diagnosis that determines the cause or source of an illness. This is the most important diagnosis as it allows therapy to proceed.
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Etiologic diagnosis
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What types of information should be gathered when taking a good patient history?
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Owner data and patient data
Past and current health history Environment and diet CS and PM findings |
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Determining the chronology and progression of... are both important when investigating a toxicosis.
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Clinical signs
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Very important for CONFIRMING a diagnosis.
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Chemical analysis
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What kind of toxological samples are typically collected from live animals?
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Blood (EDTA or heparin)
Serum Urine Vomitus Bait Feces Hair |
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What are some important toxocological sampling sites when examining a dead animal?
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Liver
Kidney Rumen/stomach contents Body fat Brain (half frozen) if animal shows CNS signs |
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How much feed material should be sent to the lab if a toxicology test is to be done?
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1-2 lbs
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How much water should be sent if sampling for a toxicologic screening?
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Between 1 pint and 1 gallon
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What kind of container should be used to hold a water sample?
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Glass (NOT plastic!)
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This kind of sample should not be frozen, but instead refrigerated.
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Whole blood
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Why should tissues not be washed before being sent for toxicology testing?
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May wash away compound of interest or introduce contaminants.
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Should a toxicology sample be "clean," or sterile?
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Clean
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List some of the goals of supportive care when treating a toxicosis.
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Prevent or treat convulsions
Maintain respiration Treat for shock Correct/control cardiac dysfunction Correct fluid and elecytrolyte loss Maintain body temperature Alleviate pain Protect skin and mucous membranes |
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Describe decontamination following topical toxicant exposure.
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Wash or flush area liberally for an extended period of time
Use small amount of detergent for skin exposure, rinse! May clip or shave animal |
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Emesis may be induced for how long after oral exposure to a toxicant?
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1-2 hours after ingestion
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List some contraindications for causing emesis.
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Unconscious/semi-comatose or very depressed
Patient convulsing or ingested convulsant toxicant Caustic material Petroleum distillated or volatile hydrocarbons (risk lipid pneumonia) |
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What are three emetics that owners may try at home if a per ingests a toxicant?
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3% fresh hydrogen peroxide (1-2 mL/kg)
Syrup of Ipecac (1-2 mL/kg in dogs; 3.3 mL/kg in cats) LIQUID dishwashing detergent, 3 TBSP in 8 oz water (10 mL/kg) |
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List an emetic drug that is used in dogs. With what drug may it be reversed?
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Apomorphine, reverse with naloxone
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List an emetic drug that is used in cats. With what drug may it be reversed?
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Xylazine, reverse with yohimbine
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If a patient ingested a toxicant over 2 hours ago, what method of GI evacuation would be indicated?
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GI lavage, maybe with enema
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Describe the process for GI lavage.
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Best done with patient unconscious or anesthetized
Place endotracheal tube and INFLATE CUFF! Place fenestrated stomach tube Incline animal with head down, give saline/water at 10 mL/kg Aspirate fluids with syringe Repeat until lavage fluid is clear |
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List a common GI adsorbent and the dose at which it is administered across all species.
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Activated charcoal, 1-2 g/kg in water
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Activated charcoal is not useful for these molecules.
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CN or NH3
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Activated charcoal is often given with...
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Saline cathartic (MgSO4 or Na2SO4)
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Activated charcoal should not be given along with...
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Mineral oil
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Why shouldn't activated charcoal be given with mineral oil?
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Oil coats charcoal so it doesn't bind toxin
Oil may also stimulate toxicant absorption by chylomicrons in gut |
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List three cathartics that may be given to help move a toxicant out of the GI tract.
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Mineral oil
MgSO4 or Na2SO4 (saline cathartics) |
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When is surgical evacuation of the gut indicated?
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Foreign body-- metallic, ball, etc
Persistent materials such as sticky oils and tars, or heavy fibrous plant material |
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True or false: Many of the common toxicants seen in veterinary medicine have antidotes readily available.
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False. There are relatively few true antidotes available.
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List three major physiological mechanisms for elimination of absorbed toxicants.
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Exretion
Biotransformation Storage |
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The number one form of excretion of toxicants is...
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Renal excretion
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List some ways in thich a vet may assist in renal excretion of a drug.
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Diuresis to increase urine flow (mannitol or furosemide)
Ion trapping (ammonium chloride, ascorbic acid, sodium bicarb) Dialysis (for glycols, alcohols, etc) |
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How does the body carry out biotransformation of a toxicant?
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Stimulates hepatic microsomal enzymes
Increased metabolism to detoxify and increase excretion |
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How can fecal excretion of a toxicant be assisted?
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Catharsis
Binding agent, such as activated charcoal |
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List three major sites of toxicant storage in the body as metabolically inactive compounds.
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Fat, bone, hair
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List some important factors to consider when forming a differential diagnosis list for toxicoses.
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System affected
Onset time Morbidity Case mortality Seasonality Age predilection Species Course of disease Progression of clinical signs |
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List some of the top toxicoses in canines
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Anticoagulants
Ethylene glycol Tremorgens Garbage Theobromine |
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List some of the top toxicoses in cats
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Pyrethrins
Calcium oxalate plants Lillies Acetaminophen Ethylene glycol |
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List some of the top toxicoses seen in the equine.
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Fescue
ELEM (causes leukoencephalomalacia) Ionophores Black walnut Slaframine (mycotoxin) |
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List some of the top toxicoses of cattle.
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Vomitoxin (dairy cattle, a mycotoxin)
Plants (Yew/Buckeye/Oak/Fescue) Lead Nitrates Inorganic Arsenic |
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CS of imidacloprid toxicity
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Nicotinic stimulation then block
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Recovery period for imidacloprid toxicity
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12-24 hrs
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Is there an antidote for neonicotinoid toxicity?
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No
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Mechanism of action for fipronil.
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GABA antagonist, causes excitement
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Onset time for fipronil toxicosis
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Under 7 hrs
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Recovery period for fipronil toxicosis
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12-24 hrs
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How is fipronil toxicosis treated?
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TIME
GABA agonists (barbiturates and benzodiazepines) |
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Clinical signs of fipronil toxicosis.
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+/- excitement
Muscle fasiculations, tremors Lethargy and ataxia with fatigue |
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These are often combined with a microsomal enzyme inhibitor called piperonyl butoxide, for prolonged toxicity.
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Pyrethrins and pyrethroids
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Which pyrethroid group has a -CN group? How does this affect its distribution?
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Type II--> Crosses BBB
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How are pyrethrins and pyrethroids metabolized?
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Esterases
Mixed function oxidases Glucuronidation |
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Which species are sensitive to pyrethrin toxicity?
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Cats, fish, birds
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Mechanism of action for pyrethrins and pyrethroids
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Keep Na+ channels open, causing hyperexcitation
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Describe the two syndromes seen with pyrethroid toxicities.
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T syndrome from Type I compounds: tremors and hyperexcitation
CS syndrome from Type II compounds: Clonic-tonic seizures |
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How is pyrethrin toxicity treated?
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Wash animal
Treat symptomatically (prn anticonvulsants) |
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Recovery period and prognosis with treated pyrethrin toxicity
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Under 24 hrs, good px
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Mechanism of action for organochlorines
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Cyclodienes are GABA antagonists
Aliphatics prevent closure of Na+ channels |
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Are organochlorines hydrophilic or lipophilic?
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Very lipophilic
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Terminal half life for organochlorines
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1 week to 2 months
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This class of toxins has a two-stage excretion after being distributed to all tissues, with a rapid initial loss and a prolonged long-term excretion.
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Organochlorines
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Describe acute organochlorine toxicity. How common is it? How long does it last
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Rare
Nervous system stimulation Lasts over 14 days, but maximal signs within 36 hrs |
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How is acute organochlorine toxicosis treated? What is the prognosis?
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Symptomatic treatment with anticonvulsants (GABA agonists)
Decrease absorption, wait PX okay but long withdrawal time |
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What is the effect of chronic organochlorine toxicity?
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Induction of microsomal enzymes that break down endogenous steroid hormones--> reduction of natural steroid hormones, like androgens
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This toxicant class is notorious for biomagnification in animal bodies.
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Organochlorines
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What are the clinical signs associated with chronic organochlorine exposure?
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Endocrine disruption
Reproductive or dermal effects Anorexia Adrenal involution Cancer? |
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How is chronic organochlorine toxicosis treated? What is the prognosis?
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Limit exposure (takes time for clearance)
Enhance metabolism if short half life Enhance excretion PX: guarded |
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Mechanism of action for amitraz.
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A2 agonist
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What are the clinical signs of amitraz toxicity?
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Depression, bradycardia, hypotension and/or intestinal stasis
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What is the onset for amitraz toxicity?
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30-120 minutes
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How long before amitraz toxicosis resolves?
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8-18 hours for CNS signs
36-48 hours for other signs |
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How is amitraz toxicosis treated?
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Alpha-2 antagonists
(Yohimbine, Tolazoline) |
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This drug acts as a fire ant "stomach poison"
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Hydramethylnon
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How is hydramethylnon toxicosis treated?
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Symptomatically for GI upset
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Clinical signs of hydramethylnon toxicosis
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Salivation, tremors, GI disturbances
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Effects of boric acid toxicosis.
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GI signs
Kidney damage |
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Treatment for boric acid toxicosis
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Symptomatic- demulcents
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Mechanism of action for DEET
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Decreases ability of insect to detect warmth and moisture
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Clinical signs of DEET toxicosis
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Encephalopathy in babies
CNS stimulation |
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Adverse effects of lufenuron toxicosis
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GI side effects
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List two insect growth regulators.
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Methoprene
Lufenuron |
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Most common sign of rotenone toxicosis. Also list a recent human toxic concern.
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Usually dermal irritation
Recent human concern as neurotoxicant |
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How much pure ethylene glycol would it take to kill a cat?
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1-2 tsp
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How much 50:50 ethylene glycol solution would it take to kill a 20 kg dog?
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8-9 fluid ounces
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Does ethylene glycol cross the blood brain barrier (BBB)?
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Yes
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What is the half-life of ethylene glycol in the body?
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4-8 hours
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Ethylene glycol is first converted into...
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Glycolaldehyde
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This step is the rate-limiting step in the body's metabolism of ethylene glycol.
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EG-->Glycolaldehyde
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What kind of symptoms are caused by the ethylene glycol metabolite, glycolaldehyde?
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CNS signs
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Primary toxicant in ethylene glycol toxicosis
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Glycolic acid
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Mist toxic of the ethylene glycol metabolites, but too short lived to be clinically important.
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Glyoxylic acid
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What are the early signs of ethylene glycol toxicosis? How long do they last?
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***CNS***
GI irritation CNS depression Muscle fasiculations Osmotic diuresis, PU/PD Duration up to 12h |
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What are the mid-range signs of ethylene glycol toxicosis? How long do they last?
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***Cardiopulmonary***
Anorexia, hypothermia, miosis Dehydration CNS depression increases Lasts from 12-24 hrs post exposure |
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What are the late clinical signs of ethylene glycol toxicosis? When do they dovelop?
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***Renal failure***
Severe lethargy or coma, may see seizures Anorexia, vomiting, oral ulcers (due to uremia) Occur beyond 24 hrs post exposure |
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How is ethylene glycol toxicosis diagnosed?
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Hx, CS
High renal calcium Increased renal echogenicity Serum and urine EG |
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Which metabolite of ethylene glycol is responsible for the severe systemic acidosis?
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Glyoxylic acid
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List some clin path data that would support ethylene glycol toxicosis.
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Elevated BUN, PO4, K, glucose
Decreased Ca |
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How is ethylene glycol toxicosis treated?
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4-MP within 8 hr in dog and 3 hr in cats (inhibits ADH enzyme)
Activated charcoal within 4-6h (+/-) If no 4-MP, give 20% EtOH within 4-6 hrs, as a CRI Diuresis Bicarbonate or LRS for acidosis Low protein diet |
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What is the prognosis for ethylene glycol toxicosis?
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Good in dogs treated with 4MP within 5-8 hrs, cats treated with 4MP within 3 hrs
Poor if acidosis at 6 hrs If renal involvement, grave |
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Sources of methanol
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Windshield washer antifreeze, paint, varnish removers
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Sources of ethanol
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Alcoholic beverages, bread dough
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This group of animals is especially sensitive to methanol toxicosis due to an inability to metabolize formate (a byproduct).
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Primates
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Metabolites formed as methanol is broken down.
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Formaldehyde and formic acid
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What are some clinical signs associated with short-chain alcohol toxicosis?
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CNS problems (1 hr onset, 12 hr duration)
Vapor irritation of eyes, oral mucous membranes, trachea PRIMATES have blindness 8-24 hours after exposure |
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How is alcohol toxicosis treated in nonprimates?
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Activated charcoal
Monitor vitals Fluids Intubate if needed |
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How is alcohol toxicosis treated in primates?
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Give EtOH or 4MP to prevent formate accumulation
Give folinic acid as source of folates to help formic acid metabolism |
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Does baking chocolate or unsweetened cocoa have more theobromine?
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Unsweetened cocoa
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List some methylxanthines.
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Caffeine
Theophylline Theobromine |
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How much milk chocolate per kg is toxic to a dog?
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2 oz/kg
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Systems affected by methylxanthine toxicosis.
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CNS, cardiac, urinary, GI
("Energizer Bunny" syndrome) |
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How is methylxanthine toxicosis diagnosed?
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History and CS
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How is methylxanthine toxicosis treated?
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Emesis within 1-3 hrs
Gastric lavage with activated charcoal instead if CNS signs present Diazepam/methocarbamol/pentobarbital Fluids B-blockers |
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Is the cat or dog more susceptible to NSAID toxicosis?
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Cat
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This NSAID causes idiosyncratic hepatic necrosis in some Labrador retrievers.
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Carprofen
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Systems affected by NSAID toxicosis.
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GI, renal
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How is ibuprofen toxicosis diagnosed
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History of access
Elevated BUN and creatinine Leukocytosis with left shift if GI ulcer perforation Serum analysis U/S of ulcers Renal papillary necrosis |
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How is NSAID toxicosis treated?
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Fluids at 2X maintenance with bicarb for ion trapping and tx acidosis
Sucralfate Omeprazole MISOPROSTOL (prostaglandin E) Use GI protectants for 3-5 days or until signs have resolved |
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These dog breeds are highly susceptible to ivermectin toxicosis. Why?
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Herding breeds, collies, etc.
Due to a mutation in P-glycoprotein, which affects the blood-brain barrier |
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How does ivermectin work?
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Increases activity of GABA receptors
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System affected by ivermectin and the key clinical signs that distinguish this toxicosis
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CNS
mydriasis, blindness |
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What is the disease course for ivermectin toxicosis?
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2 days to 7 weeks
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In this toxicosis, the resultant blindness may be reversible.
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Ivermectin
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How is ivermectin toxicosis diagnosed?
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History of administration
Test for genetic susceptibility |
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How is ivermectin toxicosis treated?
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Short acting barbiturate or propofol for convulsions (not benzodiazepines)
IV physostigmine Epinephrine for anaphylactic reactions |
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What is the mechanism of action for piperazine?
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GABA agonists in the brain
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Which body system is affected in piperazine toxicosis, and what key clinical signs are observed?
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CNS
See myoclonus, hyperesthesia, vomiting, convulsions |
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How is piperazine toxicosis diagnosed?
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History of administration
Necropsy to rule out pre-existing renal or brain disease |
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How is piperazine toxicosis treated?
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Short acting barbiturates and IV fluids
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Systems affected by pseudoephedrine.
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CNS and cardiac
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What are two consequences of muscle tremors associated with pseudoephedrine toxicosis?
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Rhabdomyolysis and renal failure
Hyperthermia and DIC |
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How is pseudoephedrine toxicosis diagnosed?
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History and CS
Hyperglycemia and hyperinsulinemia Hypokalemia |
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How is pseudoephedrine toxicosis treated?
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Acepromazine/chlorpromazine IV or IM for tremors and CNS activity
Monitor cardiac function Urinary acidification to enhance excretion of weak base Cool baths for hyperthermia |
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Clinical signs of phenoxyacetic acid (2,4-D)toxicosis.
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GI
Muscle Dogs: Myotonia, paresis in hindlimbs |
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Toxic ruleouts for hind-limb paresis in the dog.
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Phenoxyacetic acid
Promethalin Botulism Mycotoxins Macadamia nuts |
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How is phenoxyacetic acid toxicosis diagnosed?
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2,4-D levels above 700 ppm in dog serum, over 40 ppm in dog urine.
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How is phenoxyacetic acid toxicosis treated?
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Symptomatic: fluids with bicarbonate for acidosis and ion trapping in urine
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How can phenoxyacetic acid toxicosis be prevented?
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Keep dogs off treated lawn until dry
Keep livestock off of treated pasture for 1-2 weeks |
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List two dipyridil herbicides.
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Paraquat
Diquat |
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These herbicides have two toxic syndromes based on the dose level.
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Paraquat
Diquat |
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Describe the high dose toxicosis associated with paraquat. (System, onset)
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Affects CNS
Onset under 2 hr |
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Describe the moderate dose toxicosis associated with paraquat.(System, onset)
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GI, respiratory, renal
Onset 1-3 days |
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How long after inital paraquat exposure does "hit and run" lung damage occur, as evidenced by dyspnea?
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2-7 days
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Describe the high dose toxicosis associated with diquat. (System, onset)
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Affects CNS
Onset under 2 hr |
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Describe the moderate dose toxicosis associated with diquat.
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GI and renal signs
No lung toxicosis |
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How is dipyridil toxicosis diagnosed?
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Sodium dithionite test for paraquat in urine or plasma
Increased BUN/creatinine in moderate dose cases with isosthenuria/hematuria/glycosurua |
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How is dipyridil toxicosis treated?
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Fuller's earth or bentonite clays
Activated charcoal Fluids and diuretics Antioxidants |
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What is the mechanism of action for dipyridils?
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Free radical formation
(Paraquat metabolized in lung-- damages lung) |
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What clinical signs are associated with triazine herbicide toxicosis?
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CNS signs
hyperesthesia |
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How is triazine toxicosis diagnosed?
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Stomach contents or liver for analysis
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How is triazine toxicosis treated?
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Symptomatic
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Why should atropine not be used to treat thiocarbamate toxicosis?
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Not a cholinesterase inhibitor
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This herbicide class has a orange-yellow dye that stains the animal's hair green and causes dermal effects.
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Dinitroanaline (Pendimethalin)
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|
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How is dinitroanaline toxicosis treated?
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Symptomatic
Remove stain with waterless hand cleaner Blot off and shampoo |
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WhaT about glyphosate causes advere effects?
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Anionic surfactant
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What system is affected by glyphosate toxicosis, and what is the onset time?
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GI irritation
Onset under 24h |
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What body system is affected by fluziafop-p-butyl herbicide?
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GI
|
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Fungicide found on seed corn
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Captan
|
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What body system is affected by captan toxicosis?
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Respiratory
|
|
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How can captan toxicosis be prevented in cattle fed seed corn?
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Dilute treated corn with 3:1 with clean seed corn,
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|
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True or false: Carbamate herbicides are acetylcholinesterse inhibitors.
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False
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Delayed onset rodenticide that increases abdorption of calcium from bone, renal tubules, and GI tract.
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Cholecalciferol
|
|
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Psoriasis cream that is an analog of 1,25-OH cholecalciferol.
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Calcipotriene
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|
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Organ systems affected by cholecalciferol, and onset time for CS
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GI, renal, cardiac
Onset time 18-36 hours (8-24 with calcipotriene) |
|
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How is cholecalciferol toxicosis diagnosed?
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Serum P elevated 12 hrs post exposure
Serum Ca elevated 24 hours post exposure Depressed serum intact PTH |
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How is cholecaliferol toxicosis treated?
|
Monitor Ca levels
Normal saline IV at 2-3 times maintenance Furosemide and prednisolone for several weeks |
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How does prednisolone help treat cholecalciferol toxicosis?
|
Antagonises vitamin D at the gut, bone, and kidney
|
|
|
Are dogs or cats more sensitive to bromethalin toxicosis?
|
Cats (but dog cases= cat cases)
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|
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What is the mechanism of action for bromethalin?
|
Uncoupler of oxidative phosphorylation, causing ion imbalance and fluid accumulation in myelin sheaths--> paralysis and respiratory arrest
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Describe the syndrome seen with high doses of bromethalin.
|
Onset within 24h
Convulsant syndrome -loss of bark -anisocoria -paralysis with possible forelimb extensor rigidity |
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Describe the syndrome seen with lower doses of bromethalin.
|
Onset between 1-5 days
Paralytic syndrome with hind limb paresis/paralysis and decerebrate posture |
|
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Describe the syndrome seen in cats with bromethalin toxicosis.
|
Vocalization
Ileus with abdominal distension Decerebrate posture Bladder paralysis |
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What is a decerebrate posture?
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Forelimb rigidity and hindlimb flaccidity
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What gross lesions are seen in association with bromethalin toxicosis?
|
Brain edema and spongiosis
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|
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How is bromethalin toxicosis treated?
|
Dexamethosoone and furosemide for edema
Phenobarb or diazepam for seizures Activated charcoal and sorbitol |
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|
This rodenticide comes in a bait that has a characteristic garlic or fishy odor.
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Zinc phosphide.
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|
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Relatively how toxic is Zn phosphate?
|
Very toxic
|
|
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What is the mechanism of action for zinc phosphide toxicosis?
|
Phosphine gas produced in the stomach--> free radical production and blockage of cytochrome oxidase
Zinc phosphide may cause later hepatic and renal damage |
|
|
What systems are affected by Zn phosphide and what is the onset time for CS to appear?
|
CNS, GI, respiratory
(vomiting is consistent CS) Onset 15 mins to 4 hr |
|
|
What is the duration of disease caused by Zn phosphide?
|
4-48 hr
|
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A patient presented with CNS, respiratory, and GI signs. He died in the midst of a tonic convulsion. On necropsy, the stomach contents had a garlicky odor. What could possibly be the cause of death?
|
Zinc phosphide
|
|
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How is Zn phosphide toxicosis diagnosed?
|
Phosphine gas in vomitus, stomach, liver or kidney
Elevated Zn concentrations in stomach, serum or liver Hypomagnesemia |
|
|
A dog just ate a Zn-phosphide pellet. What can the owner give at home before rushing the dog to the clinic?
|
Maalox (Al + Mg(OH)2)
|
|
|
How is Zn phosphide toxicosis treated?
|
Maalox
Emetic/gastric lavage with activated charcoal Fluids with bicarbonate Glucose Pain medication |
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|
Avicide coated on whole corn bait.
|
Avitrol
|
|
|
What is the mechanism of action for avitrol?
|
Enhances cholinergic transmission (+)
Blocks K+ current of repolarization following AP |
|
|
What is the system affected by avitrol, and what are the onset and duration of clinical signs?
|
CNS
Onset 10-15 mins Duration under 4 h in dogs, <15 mins in birds |
|
|
How is avitrol toxicosis diagnosed?
|
Presence of corn in stomach
Rapid rigor mortis |
|
|
How is avitrol toxicosis treated?
|
Diazepam for seizures in dogs
Xylazine for seizures in horses Propranolol for arrhythmias |
|
|
What is the mechanism of action for coumarin rodenticides?
|
Vitamin K antagonist--. Creates immature clotting factors (PIVKAs) that can't bind Ca++
|
|
|
When is the onset of bleeding problems associated with coumarins?
|
2-5 days
|
|
|
What systems are affected by coumarin toxicosis?
|
Hematopoetic
Respiratory |
|
|
How is coumarin toxicosis diagnosed?
|
Coagulogram- prolonged clotting times (especially PT)
Low PCV with normocytes Normal fibrinogen and FDP |
|
|
How is coumarin toxicosis treated?
|
Replace clotting factors and correct hypovolemia
Vitamin K1 IM or IV for 3-4 weeks |
|
|
A bitter, chemically stable alkaloid used as a rat poison
|
Strychnine
|
|
|
Where is strychnine metabolized?
|
Liver, half life of 10-12 hrs
|
|
|
What is the mechanism of action for strychnine?
|
Binds glycine receptor, removes neuroinhibitory influence--> hyperexcitation
|
|
|
What are some of the key clinical signs of strychnine toxicosis?
|
Tetanic seizures (bilateral and symmetrical)
Saw horse stance Risus sardonicus Hyperesthesia Respiratory distress--> asphyxiation |
|
|
How is a diagnosis of strychnine toxicosis made?
|
History and CS (no clonic-tonic sz)
Laboratory data Rapid rigor mortis |
|
|
How is strychnine toxicosis treated?
|
Active convulsions: Na pentobarbital (GABA mimetic)
Prior to convusions: Diazepam and a quiet, dark room Respiratory assistance PRN Gastric lavage if less than 1 hr Activated charcoal NO ACEPROMAZINE |
|
|
How does metaldehyde act on the body?
|
Severe CNS toxicant that acts on GABA system
|
|
|
What are the affected systems with metaldehyde toxicosis?
|
GI and CNS, "Shake and Bake" syndrome
|
|
|
Describe the "Shake and Bake" syndrome seen with metaldehyde toxicosis.
|
Early on: Tremors (Shake)
--clonic tonic convusions Later on: Hyperthermia (Bake) Relapse in a few days with severe liver problems |
|
|
How is metaldehyde toxicosis diagnosed?
|
History, CS, clonic-tonic convulsions and fever
|
|
|
How is metaldehyde toxicosis treated?
|
Control convulsions with diazepam or pentobarbital
Keep animal cool Emetics and/or gastric lavage EARLY! BE AGGRESSIVE! Activated charcoal Lactated Ringer's. |
|
|
List some relatively nontoxic household cleaners.
|
Liquid/bar soaps
Fabric softener Liquid dishwasing detergent Shampoo |
|
|
List some highly toxic/caustic household cleaners.
|
Ammonia (alkaline)
Toilet bowl cleaner (acid) Oven cleaner (alkaline) Drain cleaner (alkaline) |
|
|
How should one address ingestion of a non-caustic household cleaner causing GI upset?
|
Dilute with milk or water
|
|
|
List the 4 types of detergents, from least toxic to most toxic
|
Nonionic
Anionic Amphoteric Cationic |
|
|
What are the systems affected by a cationic detergent?
|
GI, CNS
|
|
|
What are the systems affected by an anionic detergent
|
GI, RBC (hemolysis)
|
|
|
Why can ingestion of automatic dishwasher detergent lead to hypocalcemia?
|
Anionic detergents mixed with alkaline builders to bind calcium
|
|
|
Phenols and pine oil disinfectants cffect which organ systems?
|
GI, hepatic, renal
|
|
|
Alkaline cleaners cause this kind of pathology when ingested.
|
Liquefactive necrosis: Keeps penetrating soft tissue until neutralized
|
|
|
Acid cleaners cause this kind of pathology when ingested.
|
Coagulative necrosis
|
|
|
In the event that an animal has gotten into an unknown household cleaner, what would the first treatment be?
|
Dilute with milk or water
|
|
|
How well are volatile hydrocarbons absorbed into the body?
|
Very well
|
|
|
This species is very sensitive to the effects of hydrocarbons.
|
Cats
|
|
|
List the organ systems affected by volatile hydrocarbon toxicosis.
|
CNS depression
Respiratory |
|
|
List a secondary issue seen in conjunction with volatile hydrocarbon ingestion.
|
Aspiration pneumonia
|
|
|
If an animal gets into gasoline and suffers no ill effects, after how long may it be assumed that the chance of disease is minimal?
|
6-12 hrs with no CS
|
|
|
How is ingestion of volatile hydrocarbons treated?
|
Emesis if over 1 mL/kg BW unless depressed
|
|
|
Rose fertilizers may cause this pathology due to high iron content.
|
Liver necrosis
|
|
|
Fertilizer ingestion (excluding rose fertilizer) affects this system in small animals. What is the disease onset?
|
GI system
Under 2 hr |
