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VM751 Exam I
| Term | Definition |
|---|---|
| dosage | amount of toxicant per unit animal mass or weight |
| toxin | a poison that originates from biological processes |
| toxicity | the quantity of poison that causes toxic effects |
| dosage | the amount of toxicant per unit animal mass |
| route of exposure | how the animal is exposed to the toxicant |
| threshold | the highest dose of toxicant where no toxic effects are observed |
| lethal | acute dose resulting in death |
| lethal concentration | lowest concentration of a chemical in a matrix, usually feed or water, that causes death |
| LD50 | the dose resulting in death of 50% of the animals |
| NOEL | the highest dose at which significant effect isn't detected |
| NOAEL | the highest dose at which no adverse effect was detected |
| LOEL | the lowest dose at which a significant effect is found |
| LOAEL | the lowest dose where significant adverse effect is found |
| effective | dose of a drug/tox that produces some desired effect in 50% of the population |
| therapeutic index | the ratio of LD50 to ED50 |
| SSM | ratio of LD1 to ED99 |
| acute | exposure to 1+ doses in <24 hours; most common in companion animals |
| subacute | exposure to 2+ doses in >24 hours and <30 days |
| subchronic | exposure lasting 1-3 months, usually in drinking water or plants for grazing animals |
| chronic | exposure for 3+ months |
| decontamination | treatment for toxicant exposure that inhibits and minimizes further absorption and promotes elimination |
| symptomatic, supportive care | treatment for toxicant exposure that treats the symptoms and stabilizes the patient for recovery |
| antidotal | treatment for toxicant exposure that counteracts the effect of the toxicant |
| caustic | ocular decontamination with physiologic saline and tepid water for 15- 20 min; recommend e collar |
| noncorrosive | ocular decontamination with physiologic saline and tepid water for 10- 15 min, also recommend e collar |
| dermal | decontamination for toxins that can be absorbed transdermally or that an animal can lick off while grooming |
| surfactant | substance needed to decontaminate oily dermal toxins |
| caustic | dermal decontamination using copious amounts of tepid water for 15- 20 min; want to dilute as much as possible |
| inhalant | decontamination focused around ventilating the area and possibly giving the patient humidified oxygen |
| injection | decontamination where you remove stinger or venom sac, also clean the area |
| 1- 2 hours | timeframe in which emesis is usually indicated for GI decontamination |
| increased | timeframe to induce emesis will be (increased/decreased) if the patient was fed |
| aspiration pneumonia, protracted emesis, hematemesis, damage from corrosive toxins | possible secondary complications to induced emesis |
| bezoar | toxins that form these can be recovered up to 4 hours after ingestion |
| 49 | % of toxin recovery from emesis induced 30 min after ingestion |
| 17- 62 | % of toxin recovery from emesis induced 60 min after ingestion |
| 1- 2 ml/kg | dose for using H2O2 to induce emesis at home |
| apomorphine | preferred emetic agent for dogs |
| dexmed | preferred emetic agent for cats |
| xylazine | emetic agent in cats that can produce profound respiratory and CNS depression |
| hydro | opiod that can be given if other emetic agents don't work in dogs and cats |
| gastric lavage | method of GI decontamination when emesis may be contraindicated |
| whole bowel irrigation | method of GI decontamination using polyethylene glycol electrolyte solution; usually for large quantities of slow release medications |
| activated charcoal | method of GI decontamination that binds non polar compounds |
| cholestyramine | method of GI decontamination that binds with bile acids to form a complex to be pooped out; good for toxins that undergo enterohepatic recycling |
| cathartics | increase the speed and transit time of GI to promote pooping things out; usually paired with charcoal |
| fluid therapy | decontamination that increases renal elimination by forcing diuresis |
| chemical | antidote that works directly on the toxin through binding to generate an inactivated product that can be excreted |
| functional | antidote that doesn't interact with the toxin, but will lessen the clinical signs |
| pharmacological | antidote that is usually an antagonist to the toxin or prevents formation of a toxic metabolite |
| anticholinergic | toxidrome with increased HR, BP, and temp, causes agitation, and mydiratic pupils |
| cholinergic | toxidrome with miotic pupils, increased bowel function, and increased sweat |
| opioid | toxidrome with decreased RR, HR, BP, temp, miosis, and lethargy |
| sympathomimetic | toxidrome with increased RR, HR, BP, temp, and sweat, mydriasis, agitation, and increased GI function |
| sedative-hypnotic | toxidrome with decreased RR, HR, BP, temp, and lethargy |
| Vd | refers to where in the body a drug is versus the concentration in the blood |
| blood | Vd <1 kg/L means the drug is concentrated where |
| tissue | Vd >1 kg/L means the drug is stored tissue, likely fat |
| concentration gradient, SA, permeability, macromolecule binding | factors that affect that passage of toxicants across biological membranes |
| solubility, metabolism, transporters, transit time | factors that affect intestinal permeability of oral drugs |
| lipophilic | compounds that get across skin |
| SA, permeability, solubility, perfusion | factors that affect dermal absorption |
| volatile | compounds that are easily inhaled |
| transporters | molecules that actively move compounds across membranes |
| metabolism | the amount of compound given is proportional to |
| liver | organ whose primary role is biotransformation and transfer of compounds to bile |
| liver | organ whose elimination is dependent on blood flow, enzymatic activity, and protein binding |
| poor | oral bioavailability of compounds with high liver extraction |
| kidney | organ whose elimination is dependent on filtration, active secretion, reabsorption, blood flow, and protein binding |
| diuresis | treatment that creates an unfavorable concentration gradient for reabsorption in the urine |
| alkinize | change to urine to enhance elimination of a weak acid |
| acifidy | change to urine to enhance elimination of a weak base |
| 100 mg/kg | xylitol toxic dose for hypoglycemia |
| 500 mg/kg | xylitol toxic dose for hepatic failure |
| xylitol | toxin that causes hypoglycemia, GI upset, and acute hepatic injury |
| methylxanthine | toxic compound in caffeine and theobromine from chocolate |
| xylitol | toxin where recommended treatment is early decontamination, supportive care for hypoglycemia, and monitoring for hepatic injury |
| 6 hours | caffeine half life in dogs |
| 18 hours | theobromine half life in dogs |
| 250- 500 mg/kg | theobromine toxic dose in dogs |
| 130- 250 mg/kg | caffeine toxic dose in dogs |
| 200 mg/kg | theobromine toxic dose in cats |
| 100- 150 mg/kg | caffeine toxic dose in cats |
| methylxanthine | toxin that blocks adenosine binding to purinergic receptors |
| methylxanthine | toxin that causes agitation, GI upset, increased RR and HR, hypertension, muscle tremors, PU/PD, and hypokalemia |
| methylxanthine | treat this toxin by inducing emesis, giving AC, U cath, fluids, treat seizures, and beta blockers |
| acids | household toxin that animals don't usually ingest a lot of bc it tastes bad |
| 2-4 | pH of acids that cause mild irritation |
| <2 | pH of acids that cause corrosive injury |
| acids | household toxin that causes protein coagulation and coagulative necrosis |
| alkalis | odorless, flavorless household toxin that animals will consume a lot of for this reason |
| 10-11 | pH of alkalis that cause mild irriation |
| >11 | pH of alkalis that cause corrosive injury |
| alkalis | household toxins that cause liquefactive necrosis that destroys lipid membranes causing edema and inflammation |
| stricture | tissue damage that can occur after ingestion of household alkalis and acids |
| emesis | GI decontamination that is contraindicated for household alkalis and acids |
| alkalis, acids | treatment for these toxins include decontamination with large volumes of water, GI protectants, IV drugs, fluids, analgesia, and monitoring for hemorrhage and sepsis |
| essential oils | common toxin to cats, partially due to their shitty livers |
| 0.4 g/kg | pennyroyal oil toxic dose |
| 1.9 g/kg | tea tree oil toxic dose |
| potpourri | cat toxin that can cause corrosive injury after just a few licks |
| pennyroyal, clove, wintergreen | essential oils that affect hepatobiliary system |
| citrus, peppermint, cinnamon, wintergreen | essential oils that affect the GI tract |
| citrus, pepperment | essential oils that affect the nervous system |
| wintergreen | essential oil that affects the respiratory and hemic system |
| citrus | essential oil that affects the musculoskeletal system |
| essential oils | decontaminate this toxin with water on skin, eyes, or GI tract; induce emesis if indicated |
| essential oils | treatment for this toxin includes antiemetics and hepatoprotectants |
| lithium disk | batteries that will develop a charge if stuck in the GI tract and then damage the tissue; typically won't rupture |
| dry cell | batteries that leak acid/base if ruptured that will then damage the tissue; heavy metals in casing can cause toxicosis, too |
| batteries | toxins that cause ulceration of skin and/or GI tract, can obstruct airways or cause stridor from esophageal obstruction, can fistulate the GI tract and cause hemorrhage, and can have affects secondary to heavy metal toxicosis |
| batteries | treatment for these toxins include endoscopy/surgery to remove them, GI protectants, analgesia, and abx if needed |
| milorganite | toxin in sewage-based fertilizer that can cause GI problems, muscle pain, and stiffness |
| cacao bean mulch | a non-food source of methylxanthine |
| fertilizer | toxicosis is unlikely since this toxin is poorly absorbed, but can cause GI signs |
| milorganite | fertilizer component where toxicosis includes musculoskeletal changes |
| EG | toxin in anti-freeze |
| oxalic acid | metabolite of EG that causes kidney damage |
| 4.4 mL/kg | lethal dose of undiluted EG in dogs |
| 0.9 mL/kg | lethal dose of undiluted EG in cats |
| alcohol dehydrogenase | enzyme that metabolizes EG/DEG into the toxic metabolites |
| EG, DEG | auto toxins that can cause GI upset, dullness and ataxia, metabolic acidosis, and renal failure |
| oxalate crystals | end produce of EG metabolism that causes the kidney damage |
| 0.5- 12 | hours after EG/DEG ingestion that cause GI upset, dullness, and ataxia |
| 12- 24, 36-72 | hours after EG/DEG ingestion that cause oliguric renal failure in cats and dogs, respectively |
| EG, DEG | diagnostics for this toxin include blood gas for acidosis, chemistry for renal function, and UA for crystals |
| fomepizaole, ethanol | pharmacological (?) antidotes for EG/DEG to compete for alcohol dehydrogenase to inhibit metabolism |
| propylene glycol | colorless, odorless "safer" antifreeze |
| propylene glycol | signs of this toxicity include ataxia, CNS depression, and lactic acidosis |
| 22 g/kg | toxic dose of propylene glycol for dogs |
| propylene glycol | treatment for this toxin include supportive care and monitoring of acid-base status |
| EG, DEG, PG | emesis is not contraindicated, but is often ineffective for these toxins due to rapid GI absorption |
| NSAIDs | class of pharmaceuticals that work through inhibiting COX enzymes |
| COX-1 | inhibition of this enzyme results in peptic ulcers and GI bleeding |
| COX-1, 2 | inhibition of these enzymes can cause hypertension and hemodynamic AKI |
| COX-2 | inhibition of this enzyme can cause myocardial infarct |
| 50-125 mg/kg | ibuprofen acute toxic dose in dogs |
| >175 mg/kg | ibuprofen renal toxicity dose in dogs |
| >400 mg/kg | ibuprofen toxicity causing CNS signs |
| ibuprofen | toxicity is primarily GI ulceration, but also renal damage, decreased hemostasis, usually no hepatic effects |
| ibuprofen | treatment for this toxin includes AC, fluids for renal failure, prostaglandin analog for GI protection; time to intervention is important |
| COX-2 | enzyme that is more readily inhibited by Rimdayl vs ibuprofen due to stereochemistry of Rimadyl |
| 5 mg/kg | toxic dose of naproxen |
| 23-86 mg/kg | aspirin toxic dose in dogs |
| 10-25 mg/kg BID | aspirin therapeutic dose in dogs |
| 10-20 mg/kg Q48 | aspirin therapeutic dose in cats |
| UGTs | a family of enzymes cats lack in their liver that often make them more susceptible to toxins |
| glucoronidation | enzymatic process of putting a sugar on a substrate, adding a charge and making it harder to be reabsorbed in urine |
| 600 mg/kg | toxic dose of acetaminophen in dogs |
| BQI | toxic metabolite from acetaminophen metabolism |
| acetaminophen | pharmaceutical toxin that causes hepatic and renal injury; signs include vomiting, tachycardia, and tachypnea |
| methemoglobinemia | effect of severe acetaminophen toxicity |
| 10 mg/kg | toxic dose of acetaminophen in cats |
| hepatotoxicosis | toxic effect seen in cats at higher exposures than the ones causing methemoglobinemia |
| NAC | functional (?) antidote for acetaminophen toxicity by increasing GSH availability |
| acetaminophen | pharmaceutical toxin that is treated with GI decontamination, O2, fluids, blood products for anemia, and NAC or SAMe |
| psedudoephedrine | pharmaceutical toxin that acts as a sympathomimetic |
| pseudoephedrine | pharmaceutical toxin that causes peripheral vasoconstriction, cardiac stimulation, and enhanced CNS output |
| 5 mg/kg | toxic dose of pseudoephedrine |
| 11 mg/kg | lethal dose of pseudoephedrine |
| pseudoephedrine | pharmaceutical toxin that causes agitation, hallucinations sometimes, SyNS stimulation, muscle tremors, and hyperthermia |
| pseudoephedrine | treatment for pharmaceutical toxin includes GI decontamination, sedatives/anticonvulsants (except for diazepam), B blockers for cardiac effects, and urine acidification |
| chronic | overdose that is more likely to cause thyroid toxicosis |
| thyroid | toxicity that generally increases BMR; signs include agitation, GI upset, increased HR and RR, hypertension, abnormal PLRs |
| venlafaxine | SNRI anti-depressant that cats frequently eat for fun |
| venlafaxine | pharmaceutical toxin that causes mydriasis, V+, increased RR/HR, agitation, and ataxia; usually 1-8 hours after ingestion |
| cyprohetadine | serotonin antagonist that can be used for venlafaxine or amphetamine toxicity; functional antidote? |
| amphetamines | pharmaceutical toxin that acts as CNS stimulant; signs include agitation, hyperthermia, tremors, seizures, cardiac arrhythmias, and coma |
| respiratory | system that volatile compounds, gases, and small particles can all be toxic to |
| cell type, metabolism, anatomy | factors that affect respiratory toxicity |
| asphyxiation, irritation, edema, reactivity | acute responses to respiratory toxicity |
| fibrosis, emphysema, asthma, cancer | chronic responses to respiratory toxicity |
| ammonia | highly soluble respiratory toxin from decomposing excrement; highly caustic when inhaled |
| ammonia | resp toxicity where signs include tearing, shallow breathing, and nasal discharge |
| urea | a compound that can be ingested and converted to ammonia, causing lung damage |
| CO2 | end product of metabolism that can be a resp toxin at really high concentrations; impact is asphyxiation |
| CO2 | resp toxin where treatment is to provide fresh air; resolves quickly |
| CO | resp toxin that competes with O2 for Hgb binding causing asphyxiation; bright cherry red blood and mm |
| >60 | % carboxyhemoglobin in the blood that is fatal |
| CO | resp toxicity where best recovery is in hyperbaric or 100% O2; prognosis depends on degree of hypoxia |
| methane | relatively stable resp toxin that is a product of microbial degradation; main concern is flammability |
| 87- 90 | concentration of methane needed to see asphyxiation |
| H2S | lethal gas from anaerobic bacterial decomposition, usually in manure slurries; released when agitated |
| 200 | H2S ppm that causes olfactory paralysis |
| H2S | resp toxin that causes local inflammation and systemic intoxication; need artificial respiration to treat intoxication |
| NO2 | poisonous yellow-ish gas from fermentation of ensiled forage; problems occur when it is opened into poorly-ventilated areas |
| nitric acid | NO2 interacts with water and O2 in the tissue to form this toxic metabolite |
| more | brief exposure to high levels of NO2 is (more/less) toxic than long exposures to lower levels |
| >200 | ppm of NO2 that can cause immediate death |
| birds | animal species that is really susceptible to PTFE pyrolysis |
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