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231 Cards in this Set
- Front
- Back
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What are the most common routes of toxin adsorption?
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Oral, Dermal, Inhalation
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What factors affect passive transfer of toxins?
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Concentration gradients, Lipophilicity, molecular size and ionization state.
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What is a phase one reaction with respect to metabolism?
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Converts apolar, lipophilic xenobiotics into metabolites that have greater polarity and hydrophilicity by exposing or adding polar groups.
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What is a phase two reaction with respect to metabolism?
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Metabolites are conjugated with a functional group that dramatically increases water solubility (ie, glucuronidation)
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Why are cats inefficient glucuronidators?
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Domestic cats are deficient in UDP-glucuronyltransferase.
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Why is renal excretion favored by the body?
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Because metabolites are hydrophilic.
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List the non-renal methods of excretion.
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biliary, salivary, sweat, milk, CSF, exhalational.
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How many half lives are necessary to virtually eliminate chemical residues from the body?
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20 half lives
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What are the three assumptions that must be satisfied for there to be a dose response relationship with respect to a toxicant?
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1. There is a site of action that the toxicant works upon.
2. Degree of response is correlated to the concentration of the chemical. 3. Concentration of the chemical is related to the dose. |
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What are the seven specific mechanisms of intoxication?
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1. Chemical injury.
2. Necrosis of epithelial cells. 3. Inhibition of or competition with enzymes. 4. Interference with body metabolism or synthesis. 5. Systemic hypoxia or anoxia. 6. Actions similar to normal metabolites or nutrients. 7. Functional effects on the nervous system. |
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What is the NOAEL?
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The no observable adverse affects level. Ie, the highest does at which no adverse affect is seen.
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What are the environmental factors that influence toxicity?
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1. Season (toxins available, plant stage).
2. Temperature (metaoblism, food and water intake). 3. Light factors (biological rhythms, photosensitization). 4. Housing (crowding, stress). 5. Air circulation (ammonia gas) |
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Define Dose.
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Total amount of toxicant received by an animal.
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Define Dosage.
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Amount of toxicant per unit of animal weight (mg/kg).
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Define Threshold dose.
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Dose above which effects can be detected.
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Define minimum toxic dose.
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Dose at which toxic effects are first seen.
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What are the downfalls of using LD50?
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Can see significant affects at less than this, doesn't tell you what the LD1 is, doesn't tell you the MTD.
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What is the difference between exposure and intoxication?
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Toxicant must reach the target organ at high concentrations for sufficient periods of time for there to be an effect.
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Why are canines more sensitive to methemoglobin formation?
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4 vs. 2 sulfhydryl groups on hemoglobin.
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Why do some dogs have a deficient P-glycoprotein BBB?
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Defective MDR-1 gene.
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What drugs are commonly affected by a deficient MDR-1 gene?
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Ivermectins, acepromazine, butorphanol, loperamide.
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List the top 5 canine toxin exposures.
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1. Human medications.
2. Chocolate. 3. Household cleaners. 4. Machinery fluids. 5. Illicit drugs. |
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List the top 3 cat toxin exposures.
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1. Canine permethrin spot-ons***
2. Accidental overdoses. 3. Suspected rodenticides. |
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What are some cat specifics that affect their toxicology.
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Fastidious groomers, eight reactive sulfhydrul groups (oxidative damage to RBC's), DEFECTIVE GLUCURONIDATION!
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What are the most common Large animal exposures?
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1. Insecticides
2. Wormers 3. Feed additives 4. Mycotoxins 5. Plants 6. Racetrack--> anything |
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What are 2 indications for at home induction of emesis?
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Cases where toxin ingestion is reliably witnessed and when time of arrival at the hospital will bring time elapsed since oral ingestion for > 1hr.
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When should at home emesis NOT be recommended?
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-The animal is mentally compromised (seizures, tremors)
-Showing respiratory distress -Pre-existing conditions that increase the risk of aspiration -Caustic or corrosive compounds |
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What is the dose and MOA of table salt as an emetic? Risks?
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1 Tbsp on the back of the tongue will irritate pharyngeal and gastric sensory neurons. Risk of hypernatremia so not highly recommended.
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What is the dose and MOA of 3% Hydrogen Peroxide as an emetic? Risks?
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1 tablespoon via syringe will irritate pharyngeal and gastric sensory neurons via the glossopharyngeal and vagus nerves. Can cause mucosal erosions.
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How long does H2O2 emesis take?
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10-20 mins (better on a full stomach).
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What is the MOA of syrup of Ipecac as an emetic? Risks?
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Stimulates gastric mucosal receptors and the CRTZ. Effect may be delayed (30 mins) and if emesis is not achieved, gastric lavage is necessary as it is cardiotoxic. Max 15 mls.
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What is considered essential emergency care at home for a corrosive ingestions?
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Do NOT induce emesis! Have the pet ingest large quantities of water or milk and proceed to a vet hospital immediately.
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What is the basic approach to the poisoned animal?
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S-Stabilize
C-Clinically evaluate D-Decontaminate A-Apply antidote E-Enhance elimination S-Supportive care |
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How do you stabilize the poisoned patient?
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Airway (intubate), Breathing (assisted ventilation, supplemental O2), Circulation (compressions, FLUIDS),
address seizures and control body temperature. |
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What diagnostics should be preformed on a suspected intoxication?
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HISTORY! PE, Minimum database (CBC, Biochem, UA), Others as appropriate (ECG, Coags, radiographs, etc.)
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What is the purpose of decontamination?
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To prevent the absorption of toxin by removing as much as possible and binding what cannot be removed.
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What are some methods of GI decontamination?
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Emesis, Gastric lavage, gastrotomy, endoscopy, bowel irrigation, bind to prevent absorption (activated charcoal), apply cathartics to speed up removal, chelation.
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How do you decontaminate for a dermal exposure?
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Bathe the animal in a mild soap and water. If skin is burned by caustics, lavage copiously with saline.
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What is the purpose of an antidote?
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Antagonize or inactivate the toxin.
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Why do we enhance elimination of a toxicant?
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To push the toxin that has already been absorbed into the systemic circulation to be removed as quickly as possible.
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How do we enhance elimination of a toxicant?
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1. Diuresis
2. Decrease enterohepatic recirculation (mult. doses of activate charcoal) 3. Ion trapping 4. Chelation |
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When should forced diuresis not be used to enhance elimination?
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Patient is anuric or oliguric, has cardiac or cardiovascular issues.
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How do we use forced diuresis to enhance elimination of a toxin?
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High rates of fluids, add a diuretic (furosemide or mannitol). MONITOR RENAL FUNCTION!
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How do we use ion trapping to enhance elimination of a toxin?
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Acid diuresis with ammonium chloride. Basic diuresis with sodium chloride.
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How long do we have for In-clinic induction of emesis?
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Less than 30 mins is ideal, under 2 hours is reasonable, above 4 hours is questionable.
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How does the form of toxin effect the length of time that emesis is acceptable?
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Extremely toxic compounds mean that time of emesis can reasonable be increased. Liquid toxicants are rapidly eliminated (1-4 hours) whereas solids may take up toe 12 hours to be removed.
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What is the greatest toxicological concern relating to volatile hydrocarbons?
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Pulmonary lesions from aspiration. Provoke extreme inflammation.
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Which hydrocarbons are of greatest concern?
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Low viscosity hydrocarbons are the most dangerous (gasolene, kerosene, lighter fluid). High viscosity compounds (motor oil) are unlikely to cause pulmonary lesions.
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What is the greatest goal for treatment of hydrocarbon toxicity?
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Not allowing emesis to occur and therefore avoiding aspiration. Systemic toxicity is usually very low.
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How does apomorphine work for emesis?
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Dopamine agonist that acts on the CRTZ.
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How is apomorphine used for emesis?
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Tablets are reconstituted in saline and placed in the conjunctival sac. Should be flushed out after emesis (~6 mins). Can also use SQ, IV or IM.
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What are the side effects of apomorphine and how can they be treated?
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Prolonged vomitting, tachycardia, excitation, SEDATION,respiratory depression, bradycardia, and ocular irritation. Can be reversed with Naloxone.
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Why do we tend not to use apomorphine in cats?
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Can result in extreme excitation and mania.
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How is xylazine used as an emetic?
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Used in cats, but not with heart disease.
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What are the side effects of xylazine?
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Sedation and respiratory depression.
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What can be used to reverse xylazine?
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Yohimbine or Atipamazole.
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When should gastric lavage be considered?
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When emesis is needed but it is not safe.
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When is gastric lavage contraindicated?
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Caustic or corrosive, volatile hydrocarbon, risk of GI perforation, sharp objects in the stomach, animal is seizuring.
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What are the risks of gastric lavage?
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Aspiration, anesthetic risk, injury to the GI tract.
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How do you perform Gastric lavage?
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Anesthetize the patient in right laterial recumbency and introduce a large stomach tube measured to the xiphoid. Place the animal with the head angled down 20 degrees and instill warm water (10 mls /kg). Manually agitate the stomach and let the end of the tube fall to drain. Save fluid and measure to ensure all of it is coming out. Repeat cycle 15-20 times until fluid is clear.
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What type of injury does alkaline ingestion cause?
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Liquefactive necrosis very rapidly
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What type of injury does acid ingestion cause?
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Coagulative necrosis
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How do you perform chemical neutralization of corrosives, and what is the risk?
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Alkali - use vinegar
Acids- use sodium bicarb Exothermic reactions may occur causing burns to the GI mucosa. |
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What is the appropriate in clinic treatment for corrosive ingestion?
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Do NOT induce emesis or perform gastric lavage. Dilute with fluids ASAP. Do NOT use activated charcoal. Consider chemical neutralization. Use endoscopy as soon as possible to evaluate for mucosal damage. Use surface protectants (sucralfate, kaopectate, peptobismol). Pain control of butorphanol or NSAIDS if not using corticosteroids.
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How does sucralfate work?
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Binds to mucosal erosions and protects underlying mucosa.
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How are corticosteroids used in chemical burn treatment?
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When started immediately after the burn at anti-inflammatory doses, they may reduce the development of stricture/scar formation.
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How does activated charcoal work?
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HUGE surface area allows toxins to be trapped in pores via Van Der Waals forces.
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What are the goals of activated charcoal?
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To bind as much toxin as possible and provide passage through the GI without absorption and to provide further absorption of toxins that are recycled through.
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What compounds are activated charcoal most effective on?
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non-polar, neutral and large
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What substances are activated charcoal not effective on?
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Metals, caustics, volatile hydrocarbons, detergents and alcohols
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When should activated charcoal be administered?
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Ideally as early as 30 mins post exposure (after emetic has worn off). Technically, it is never too late due to recirculation. Don't forget for dermal patients as well that may groom the toxin off.
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What dosage should be used for activated charcoal?
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The more the better. Strive for 10X the volume of toxin ingested. The actual dose is 2-5 mg/kg.
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What are the risks of activated charcoal?
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Emesis, aspiration, PU/PD, constipation, hypernatremia.
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When is activated charcoal contraindicated?
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GI obstruction, perforated GI, Caustic/corrosive, severe dehydration or electrolyte disturbances.
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Why are cathartics used?
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To speed up GI transit of toxins.
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Which cathartics are best to use and why?
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Osmotic cathartics are best as they are very effective and have little GI absorption.
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What are the risks of cathartic administration?
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vomiting, cramping, excessive diarrhea, dehydration, hypernatremia, hypermagnesemia
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When are cathartics contraindicated?
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GI obstruction, perforation, dehydration, osmotically active toxin. Dont use magnesium cathartics in CNS depressed patients. NEVER repeat cathartics.
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When should cathartics be instituted?
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Within 60 minutes of ingestion.
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What cathartics can be used in horses?
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Mineral oil (not with Activated charcoal), epsom salts (CAUTION!)
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What conditions must be met for Ion trapping to be effective?
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Toxin must be excreted primarily by the kidneys, must not be highly protein bound, must not be highly lipid soluble.
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How do we enhance biliary elimination?
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Repeated doses of activated charcoal (every 6 hours).
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When is chelation used?
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Metal intoxications
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What is the most common side effect of chelators?
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Nephrotoxicity
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What is deferoxamine used for?
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Iron and aluminum toxicosis as it complexes free iron.
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What is dimercaprol used for?
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Lead, arsenic, inorganic mercury, gold, copper
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When is dimercaprol contraindicated?
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Iron, selenium, cadmium, uranium
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What is D-Penicillamine used for?
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Iron and copper toxicity
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What are the three broad categories of antidotes?
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Pharmacologic categories
Chemical antidotes -Chelators -Antibodies |
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What are the 5 mechanisms of pharmacologic antidotes?
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1. Prevent toxic metabolite formation
2. Enhance toxic secretion 3. Compete for receptor site 4. Blockade of receptors causing toxic effect 5. Restoration of normal function |
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How do antibodies function as antidotes?
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They act directly on the toxicant to make it less toxic or enhance its excretion.
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What are antivenins?
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Antibodies against particular venoms.
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What is immunotoxicotherapy?
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The use of commercial antibodies that are in anti-toxin specific serum or monoclonal antibodies. Dosage is on toxic plasma concentration, not body weight.
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How is antivenin made?
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Low doses of vemon is injected into horses or sheep, and they hyperimmune plasma is collected and purified. This will form an immune complex with venom components.
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What is the antidote for viper intoxication and how should it be administered?
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Crotalidae polyvalent antivenin (equine) administered IV.
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What are the most common side effects of crotalidae antivenin?
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Allergic reactions and true anaphylaxis.
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When should antivenin be adminstered?
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Best if given within 4 hours, but as long as coagulation panels are still deteriorating, venom is still active and antivenin will be beneficial. (up to 72 hours)
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What is CROFAB and how does it work?
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Crotalidae polyvalent immune FAB (ovine) approved for use in NA crotalid snakes. The FAB fragment of a commercial antibody will bind the venom. It is very efficacious in dogs and has less side effects than hyperimmune plasma.
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What is digibind and how does it function?
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Digoxin immune FAB (Ovine) used for digoxin or digitoxin toxicity. The FAB binds the toxin and the immune complexes are cleared by the kidneys or reticulo-endothelial system.
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When do we use digibind?
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If cardiac glycosides have caused severe ventricular arrhythmias, progressive bradyarrhythmias, or second or third degree heart block not responsive to atropine.
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What is 2-PAM (Pralidoxime) and how does it work?
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Regenerates inactivated AChE in cases of organophosphate poisoning through hydrolysis of the enzyme
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What is Acetylcysteine and how is it used?
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Oral reducing agent used to treat acetaminophen toxicity.
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What is vitamin K1 and how is it used?
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Used for anticoagulant rodenticide toxicity. Should be given orally twice daily for 3-4 weeks.
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How are benzodiazepines reversed?
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Flumazenil
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How do we reverse alpha 2's?
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Yohimbine and Atipamazole
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How do we reverse opiods?
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Naloxone
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What are functional antidotes?
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Supportive therapies that are used to control clinical signs (ie. diazepam fro seizures)
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What are the general mechanisms of excitatory toxins?
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1.Increased synaptic transmission
2.Increased generation of action potentials 3.Physical neuronal damage |
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What are the clinical signs of excitatory toxins?
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Behavioural changes, agitation, tremors, seizures
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What is the prodromal sign of CNS intoxication?
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Agitation
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How is agitation treated clinically?
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Benzodiazepines-very effective but short acting.
Phenothiazines-lowers seizure threshold. Antihistamines-cyproheptadine or diphenhydramine. |
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What is a tremor, and how is it differentiated from a seizure?
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Tremors are uncontrolled motor activity without loss of consciousness. It can usually be interrupted by distracting the animal, whereas a seizure can not be interrupted.
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What is the drug of choice for treating tremors?
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Methocarbamol-skeletal muscle relaxant that is given slowly IV
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How are toxocogenic seizures differentiated from medical seizures?
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They are: persistent, gradually increasing in severity and duration, acute onset, combined with other signs.
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What diagnostics should be done before instituting therapy for toxocogenic seizures?
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Draw blood ASAP to check glucose and calcium.
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What is the 1st line treatment for toxocogenic seizures?
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Diazepam CRI (reduce dose by 25% every 4-6 hours) or midazolam IM.
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What are second and third line treatments for toxocogenic seizures?
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IV bolus of phenobarbitol (anesthesia will usually be reached with benzos on board).
Use IV propofol to effect as a last ditch attempt, or try inhalational anesthetics. |
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What 4 parameters should be repeatedly monitored if CNS excitatory signs are present?
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Body temperature, acid base (most will be acidotic), blood glucose, and myoglobinuria
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List 3 excitatory psychoactive drugs
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Marijuana, cocaine, and amphetamines
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Is home emesis indicated in marijuana toxicity?
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Yes
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What are the clinical signs of marijuana toxicity?
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Marked CNS signs-alternating excitation and depression, ataxia, mydriatic. Vomiting, tachypnea and tachycardia, hyperthermia.
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How is THC intoxication treated?
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Stabilize: Start a venous line and reduce agitation.
Emesis if CNS signs are not present. To reduce adsorption, give activated charcoal and sorbitol, then repeated AC for enterohepatic recycling. Provide supportive care for hyper or hypothermia. |
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What are the clinical signs for cocaine?
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Extreme excitation and hyperactivity, ataxia, mydriasis, vomiting, hypersalivation, tremors and/or seizures, tachycardia and tachypnea
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What metabolic derangement does cocaine toxicity result in?
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SEVERE metabolic acidosis
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How is cocaine toxicity treated?
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Induce emesis very quickly after ingestion. If heavy sedation has been achieved, perform gastric lavage. Provide supportive care for tremors and seizures. Monitor body temperature.
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Human drugs for ADHD often contain this toxin.
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Amphetamines
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What are the clinical signs for amphetamine toxicity?
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Hyperactivity, restlessness, tremors, seizure, mydriasis and hypersalivation. Tachycardia and hypertension.
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What is the MOT of amphetamines?
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Simulate catecholamine release peripherally and stimulate cerebral cortex, resp centre and RAS.
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What is the MOT of cocaine?
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Sympathomimetic effects by blocking the reuptake of serotonin and norepinephrine.
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How is amphetamine toxicity treated?
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Emesis if less than 30 mins or gastric lavage for larger quantities. Administer activated charcoal. Control CNS signs with benzodiazepines and the CV affects with B-Blockers or lidocaine. Provide fluid diuresis.
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What are the toxic components of chocolate?
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Methylxanthines - Caffeine and theobromine.
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What is the lethal dose of thebromine?
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100-250 mg/kg
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What is the lethal dose of caffeine?
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100-200 mg/kg
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What is the rule of thumb for treating chocolate toxicity (MTD)?
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Treat if ingestion is >20 mg of methylxanthines/kg, however if the owner is concerned, treat!
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What is the MOT for methylxanthines?
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Neuronal and muscular calcium disruption and cAMP receptor antagonization and accumulation
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What are the clinical signs of methylxanthine intoxication?
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Hyperactivity, tremors, seizures, vomiting and diarrhea, polydipsia, urinary incontinence, severe polypnea, tachycardia, cardiac arrhythmias, hypertension, hyperthermia.
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How do you treat chocolate toxicity?
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Stabilize with benzodiazepines, use B-blockers for tachycardia or lidocaine for arrhythmias. Control hyperthermia. emesis/gastric lavage, activated charcoal, diuresis.
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When should emesis be performed?
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Chocolate coats the stomach so emesis can be performed far later than normal (up to 4 hours).
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What is the prognosis for chocolate toxicity?
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Good, even with SEVERE toxicity.
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What important discharge instruction should go home with a chocolate patient?
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Remove all chocolate from the house, as they have developed a taste for it and will immediate return to it.
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What is the MOT of organophosphates and carbamates?
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AChE inhibition leading to hyperstimulation of ACh synapses.
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What are the clinical signs of organophosphate/carbamate toxicity?
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SLUD, vomiting and diarrhea, CNS excitation signs.
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What diagnostic samples should be taken for organophosphate/carbamate toxicity?
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Whole blood, brain, stomach contents, urine, skin
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Should emesis/gastric lavage be performed for organophostpates/carbamates?
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Yes
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What are the antidotes for Organophosphate toxicity?
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Atropine or 2-PAM
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How is atropine given as an antidote for organophosphate toxicity?
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1/4 of the dose IV, confirm effects and give remainder SQ or IM.
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What is the classic exposure of cats to pyrethrins?
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Admin of OTC canine flea spot ons the cats. Cats may also groom off of dogs or eat treated insects.
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What are the clinical signs of pyrethroid intoxication?
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Hyperexcitability, tremors and seizures. Dyspnea, salivation and weakness
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How are pyrethroid toxicities treated?
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Control seizure with benzodiazepines, dermal decontamination and activated charcoal.
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What are the 4 main clinical signs of CNS depressive toxins?
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Behavioural changes, depression, coma, ataxia
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How is CNS depression commonly caused by toxins?
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Acidosis, muscular weakness, hypoxia and hepatic encephalopathy
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What are the components of nursing care of the unconscious patient?
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1. Maintain seizure control
2. Secure an airway and humidify air 3. Mouth care 4. Eye care (tears every 2 hrs) 5. Bladder care (catheter) 6. Colon care 7. Nutrition |
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When is parenteral nutrition indicated?
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If patient has not eaten for 2-3 days.
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How do horses become exposed to amitraz?
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Attempted treatment with cow/sheep product.
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How do dogs become exposed to Amitraz?
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Ingestion of flea/tick collars
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What is the MOT of Amitraz?
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Alpha-2 adrenergic activity
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What are the clinical signs of Amitraz toxicity?
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CNS-depression, ataxia and tranqulization. Hyperglycemia, decreased heart and resp rate, decreased GI motility.
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What is the treatment for Amitraz toxicity?
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Decontamination, administer Yohimbone or Atipamezole. Ileus may need to be treated with laxatives. HYDRATION!!! Do not treat bradycardia with atropine in horses.
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Why are the kidneys prone to toxic damage?
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Kidneys are the main site for excretion of most toxins. They are also concentrated in the kidney. 25% of the cardiac output goes to the kidneys.
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What are the main clinical signs of nephrotoxicosis?
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PU/PD, Oliguria, Anuria
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How can the kidneys be supported after a toxic insult?
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Replace fluid deficits in 6-12 hours and continue to provide maintenance fluids (2-3X normal maintenance). If urine prod'n drops below 0.25ml/kg/hr, add a pharmacological diuretic (dopamine is controversial).
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How are metabolic abnormalities resulting from kidney failure corrected?
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Administer bicarbonate and carry out fluid diuresis.
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What electrolyte abnormality must be corrected in the case of renal failure? How do you correct this?
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Hyperkalemia corrected by using insulin and dextrose concurrently. Can also use calcium gluconate.
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Over what time period should the fluid deficit be replaced in a patient with nephrotoxicosis?
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6-12 hours
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Why is chronic treatment necessary after an acute bout of nephrotoxicosis?
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Kidneys will go through a period of renal tubular regeneration, and will not be able to concentrate urine. Hydration is critical.
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How long should a patient be monitored after an acute nephrotoxicosis?
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10-30 days
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When do the 3 phases of Ethylene glycol toxicity occur?
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Phase 1: 1-4 hours
Phase 2: 4-6 hours Phase 3: 12-72 hours |
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What are the clinical signs associated with Phase 1 Ethylene glycol toxicity?
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CNS signs: Behavioral changes, ataxia, depression, poss. seizures. Renal: initial diuresis resulting in dehydration. CV: Tachycardia. Resp: polypnea
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What are the clinical signs associated with Phase 2 Ethylene glycol toxicity?
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Acidemic phase: GRadual worsening of the CNS signs, progressing to coma and death. Increased polypnea (compensatory) and vomiting.
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What are the clinical signs associated with Phase 3 Ethylene glycol toxicity?
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Renal failure due to accumulation of oxalate crystals in the kidney. Oliguria/Anuria. Renomegaly.
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When is the EG test kit most effective at detecting EG?
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Phase 1.
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Why should treatment be began if suspicion is strong but test results do not support EG toxicity?
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EG concentrations below the minimum detectable amount may be fatal in cats.
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What blood gas results may indicate EG toxicity?
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PH less than 7.3, Anion Gap >25 mEq/L
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Should emesis and activated charcoal be given to a patient with EG toxicity?
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Yes, if CNS signs are not too severe.
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What is a complication of using activated charcoal as part of a treatment for EG toxicity?
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Very effective at binding ethanol which is a common antidote used for EG toxicity.
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What are the windows of opportunity for treating EG toxicity with an antidote in dogs? Cats?
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Dogs: 8-12 hours
Cats: 2-4 hours |
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What are the common antidotes used for EG toxicity?
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Ethanol and Fomepizole (4-MP)
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How can ethanol be properly titrated in order to avoid over suppression of the CNS when combined with EG?
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Titrate the dose until a stuporous, barely unconscious state has been reached. (usually a bolus followed by CRI).
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How is fomepizole given?
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4 IV boluses in both dogs and cats (higher doses for cats)
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How much lily must be ingested to be lethal to a cat?
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2-3 leaves of part of a flower
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What is the MOT for lillies in cats?
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Poorly understood but causes severe renal tubular necrosis and the debris will block collecting ducts. Basement membrane is not affected so they can regenerate.
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What are the clinical signs of lily toxicity in cats?
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VOMITING! Salivation, tremors, anorexia, depression. Progressive signs of renal failure: dehydration, lethargy, oliguria.
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What is the prognosis for lily intoxication?
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Good to excellent if the plant material is still in the vomitus, or if renal failure is not advanced.
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What is the MOT for grapes?
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Not known. Renal tubular necrosis.
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What are the clinical signs of grape toxicity?
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VOMITING (Uremia?), dehydration, anorexia, abdominal pain, oliguria/anuria.
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How large should feed samples be for submission for toxicology?
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500 g
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How large should water samples be for submission for toxicology?
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1L
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How large should forages be for submission for toxicology?
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3 inches
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Why are large urine samples required for toxicological analysis?
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Chemicals are often diluted in the urine
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What type of toxin are hair samples reliable for?
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Heavy metals
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What kinds of cardiac monitoring are required in small animal toxicosis?
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Regular auscultation, ECG, pulse oximetry, and blood pressure
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What kinds of toxins can cause bradycardia?
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Antiarrhythmics, adrenergic agonists, calcium channel blockers, organophosphates and carbamates
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What toxins can cause hypotension?
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Anything that causes bradycardia, plus nitrates/trites, cyclic antidepressants, ethanol, opiods, and nitroprussides.
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What are the treatment options for hypotension?
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Fluid therapy: crystalloids for mild and colloids or blood producs for severe. Dobutamine if there is a contractility problem. For SEVERE hypotension, consider dopamine or epinephrine.
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What are the treatment options for bradycardia?
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Atropine or glycopyrollate.
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What are the treatment options for tachycardia and hypertension?
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Keep the environment quiet, administer benzos and anxiolytics. Use B-Blockers for primary tachycardia.
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What drugs/toxins are usually associated with hypertension and tachycardia?
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Neuroexcitatory drugs
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What cardiac arrhythmia is commonly associated with digoxin intoxication?
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Ventricular tachycardia leading to fibrillation
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How can Ventricular tachycardia be treated?
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Correct any electrolyte abnormalities, give lidocaine or procainamide. Digibind.
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What is the antidote to digitalis intoxication?
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Digibind
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What are some hemoglobin (or methemoglobin inducing) toxins?
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NSAIDS, nitrites, chlorates
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What is the triad of oxidative damage to RBC's?
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Methemoglobinemia (hemoglobin destruction), heinz body formation, hemolyis
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Why are certain lab animals resistant to methemoglobinemia?
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High activity of an enzyme called methemoglobin reductase.
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What is methemolgobinemia?
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Oxidation of ferrous hemoglobin to ferric hemoglobin, such that it can no longer accept oxygen
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What are the clinical signs of hemoglobin damage?
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Blood is dark brown, eventually MM will be too, cyanosis and dyspnea, weakness & recumbency.
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What are heinz bodies?
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Denatured hemoglobin covalently binds to red cell cell membranes.
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What is the clinical impact of heinz body formation?
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Deformed RBC's are phagocytosed and destroyed in the RES. IE hemolysis.
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What are the possible treatments for oxidative toxins?
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Oxygen therapy, fluids to dilute hemoglobinuria, blood transfusion after applying antidote, oxyglobin for dogs. Treat with reducing agents like ascorbinc acid, sodium sulfate or N-acetylcysteine.
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Why is N-acetylcysteine an antidote for oxidative toxins?
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Source of sulfhydryl groups as well as glutathione replenishment
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What is the MOT of acetaminophen?
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Toxic metabolite NAPQI causes oxidation of RBC's and hemolysis. Accumulation in the liver causes hepatic necrosis.
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Why are cats more susceptible to NSAID toxicity than dogs?
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Most NSAIDS are metabolized by glucuronidation, and cats are deficient in glucuronyl transferase.
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What are the clinical signs of acetaminophen toxicity in cats?
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Cyanosis from methemolgobinemia and anemia.
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What are the clinical signs of acetaminophen toxicity in dogs?
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Hepatic necrosis so liver signs.
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How long after intoxication with the antidote N-acetylcysteine be effective?
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Never too late!
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What is the treatment protocol for acetaminophen toxicity?
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Decontamination, administer N-acetylcysteine. consider supportive treatments: SAMe, sodium sulfate, Ascorbic acid, cimetidine (inhibits P-450 enzyme which creates toxic NAPQI).
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What are the clinical signs of hemolytic toxins?
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depression, anemia, icterus, hemoglobinemia, hemoglobinuria, mudddy mucous membranes.
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How is Acer rubrum intoxication treated in horses?
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Decontaminate with gastric lavage and cathartics. Support with diuresis, transfusion and oxygen therapy. Consider used of ascorbic acid.
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What are the mechanisms of toxicity for NSAIDs?
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1. Drop in protective prostaglandin activity.
2. Oxidative damage to RBC's 3. Decreased circulation for vital areas (GI mucosa, kidneys) 4. Increased tubular resorption of sodium and water |
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How is NSAID toxicity treated?
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Decontaminate, provide antiemetic for protracted vomiting, transfuse if severe bleeding ulcer, begin gastroprotectants (sucralfate, omeprazole and famotidine, misoprotol). Ensure good hydration for renal function.
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What predisposing factors will make NSAID toxicity worse?
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Decreased renal perfusion, GI disease, age, stress, hypotension, cardiac disease, and dehydration
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What are the clinical conditions that can result from a hepatic intoxication?
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Hepatic encephalopathy and coagulopathy
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How is hepatic encephalopathy treated?
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High carb and low protein diet. Use lactulose to trap NH4 in the gut and decrease ammonia production.
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How are coagulopathies resulting from hepatic intoxication treated?
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Give vitamin K, transfuse plasma and give oxyglobin.
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What biochem abnormality can result from severe hepatic intoxication that may require treatment?
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Hypoglycemia
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How are acute hepatic toxicities managed?
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Give fluids (use dextrose to maintain glucose levels) and give hepatoprotectants (N-acetylcysteine and SAMe, vitamine E)
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What is the source of xylitol?
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Sugarless gums and candies.
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What is the MOT of xylitol?
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Induces secretion of insulin from the pancreas and is hepatotoxic. Results in a profound hypoglycemia.
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What are the clinical signs of xylitol toxicity?
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Lethargy and seizures
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How is xylitol toxicity treated?
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Decontaminate, treat hypoglycemia STAT with IV dextrose, oral corn syrup. Give hepatoprotectants.
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How are anticoagulant toxicities treated?
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Decontaminate (unless clinical signs are present, then it is too late). Transfuse with whole blood or plasma (fresh) and give oxyglobin. Institute oral vitamin K1 therapy with a fatty meal and continue for 3-4 weeks. Can give IM or SC but watch for bleeding. Do NOT give IV as may cause anaphylaxis.
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How is bromethalin toxicity treated?
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Induce emesis (4 hour window), give activated charcoal for 3-4 days. Give mannitol for cerebral edema and dexamethasone. Careful with IV fluids.
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