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182 Cards in this Set
- Front
- Back
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The majority of poison hotline calls are regarding what species |
a. Dogs-88% b. Cats-10% 2 |
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Which two breeds are overrepresented
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a. Goldens and labs 3 |
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What is the most common cause of death
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a. Pesticides or gardening products b. Human drugs 4 |
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Over 50% of FB ingestions are what
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a. Silica packets 5 |
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What is the definition of adverse drug event
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a. Voluntary reports from DVMs and consumers b. Lack a control group c. Difficult to prove cause and effect 6 |
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Reporting of ADE are required for who
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a. Animal pharmacy industry b. Voluntary for DVM and consumers 7 |
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What are the major categories for ADE
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a. Significant product defects-> w/in 3 days i. Label mistakes ii. Product malfunctioning from carrier b. Result in unexpected animal injury and or unexpected product effectiveness-submitted w/in 15 days i. Requires professional intervention ii. Causes permanent problems iii. Not on the label 8 |
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What are the 6 criteria for causality
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a. Info from scientific literature b. Previous documentation of clinical signs c. Alternative explanation for clinical sign d. Timing of events and dosage given e. Dechallenge (lessening of c/s when dose is low) f. Rechallenge (recurrence of sign when drug given again) 9 |
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One ADE is enoughto document or make changes to the label
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a. No 10 |
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What new cleaning item has the highest risk of FB
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a. Swiffer Wet Jet- non toxic 11 |
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What is the toxic dose for macademia nuts and what are the clinical signs
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a. 1 nut/kg b. Weakness, depression, vomiting c. Signs resolve after 24 hours 12 |
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What are the toxic doses for grapes
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a. 1-2 grapes/kg has been shown to cause ARF 13 |
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How does xylitol cause its clinical signs
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a. Promotes insulin release from the pancreas and causes hypoglycemia 14 |
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What part of the lilly is toxic
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a. All parts can cause ARF in cats (anuric RF in 2-4 days) 15 |
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Are lilies toxic to dogs
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a. Yes, cause GI upset 16 |
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Pennies from what time frame have zinc in them and cause intravascular hemolysis
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a. 1982-today 17 |
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Why is chocolate toxic
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a. Caffeine and theobromine cause cardiac arrhtyhmias, hyperexcitability, and GI upset, seizures 18 |
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How are centipedes poisonous
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a. Venomous stinging apparatus-> causes GI upset and irregular heart beat 19 |
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Is febreeze nontoxic
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a. Yes 20 |
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How do onions and garlic cause toxicity
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a. Hemolytic anemia b/c of Heinz body formation, methehemoglobinemia b. Treat w/ vitamin C for antioxidant effects 21 |
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Resolve spot is toxic
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a. No 22 |
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Are catepillars and butterflies toxic
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a. Yes, contain venomous glands and over 2,000 species are poisonous 23 |
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What type of toxicity do poinsettas cause
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a. GI upset 24 |
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How does vitamin A cause toxicity
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a. Bone lesions 25 |
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How does vitamin D cause toxicity
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a. Hypercalcemia 26 |
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Is lipstick poisonous
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a. Yes, can contain heavy metals sometimes b. Can be carcinogenic 27 |
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Is DEET mosquito repellant toxic
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a. Yes, very b. Causes muscle tremors c. Ataxia d. Seizures 28 |
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What is the MOA for DEET
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a. Acetylcholinesterase 29 |
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Which mosquito repellants are safe
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a. BT b. Bti produces toxins which are effective in killing various species of mosquitoes, fungus gnats, and blackflies, while having almost no effect on other organisms. Indeed this is one of the major advantages of B. thuringiensis products in general is that they are thought to affect few non-target species. 30 |
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With dermal exposures like to permethrin in cats, how should one treat
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a. Wash with mild detergent, rinse and towel dry b. If gets into eye, irrigate it for 10-120 minutes i. Check with fluroscein stain to make sure no ulcers 31 |
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When should one avoid inducing emesis
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a. Species that does not vomit b. Patient has already vomited multiple times c. Substance is possibly corrosive i. Give milk at 1 ml/kg d. Patient has epilepsy e. Patient has seizure f. Patient has cardiovascular disease and could easily vagal and arrest 32 |
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What is the dose for activated charcoal
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a. 1-3 ml/kg and then give ½ that every 4-8 hours 33 |
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What is the treatment for acetaminophen toxicity
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a. N-acetylcysteine 34 |
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How does it work
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a. Provides glutathione which binds and inactivates acetaminophen metabolites 35 |
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What other drug can be given that will inhibit P450 enzymes
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a. Cimetidine 36 |
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What can be given to reduce methemoglobin in HB
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a. Vitamin C 37 |
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How long does it take supplemented vitamin K to help clotting times
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a. 6-12 hours 38 |
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How long should vitamin K be supplemented for in rodenticide toxicity
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a. 2-4 weeks 39 |
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Why is IM injection of vitamin K not recommended
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a. Can cause a coagulopathy 40 |
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What agents cause promote acetylcholinesterase activity
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a. Organophosphate b. DEET c. Carbamate insecticide 41 |
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What drug is recommended within 24 hours of ingestion of organophosphates
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a. 2-PAM-pralidoxime chloride i. Relieves nicotinic signs-> muscle fasciculations ii. Relieves muscarinic signs-> SLUD, bronchospasm 42 |
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What other two drugs can be given to relieve muscarinic signs
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a. Atropine b. Glycopyrrolate 43 |
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What are the two treatments recommended for ethylene glycol toxicity that must be given within 6-8 hours in a dog of ingestion and within 2-3 hours of ingestion for a cat
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a. Fomepizole (4-methylpyrazole) + ethanol (20% solution) 44 |
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What is the MOA
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a. Competitively inhibit alchohol and alcohol dehydrogenase thereby preventing formation of nephrotoxic metabolites (oxalates) 45 |
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What is the therapy for heavy metal toxicity
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a. Deferoxamine is the most effective chelator of iron. Deferoxamine therapy works best if administered within 12 hours of ingestion or exposure. Supportive care alone may not prevent mortality. b. Calcium ethylenediaminetetraacetic acid is a chelator useful in lead and zinc toxicity, although it is only available in injectable form. c. Meso-2,3 dimercaptosuccinic acid is another chelator useful in lead toxicosis. Lead should be removed from the gastrointestinal tract before initiating oral therapy to prevent chelation and enhancing lead absorption from the gastrointestinal tract. D-penicillamine can be effective for long-term oral therapy of lead toxicity. 46 |
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What treatment is recommended for metronidazole toxicity
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a. Diazepam 47 |
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What is serotonin syndrome
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a. Overdose or combination of MAOIs, SSRIs, and Tricyclic antidepressants so have increased amount of serotonin 48 |
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What are the clinical signs associated with this
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a. Myoclonus, agitation, hyperreflexia, tremors, diarrhea, hyperthermia, ataxia 49 |
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What can you treat with
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a. Cyprohepatidine b/c it is a serotonin antagonist 50 |
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What are four types of rodenticides that are toxic
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a. Anticoagulant b. Bromethalin c. Strichnine d. Zinc phosphide 51 |
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What are two types of anticoagulants
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a. 1st generation-warfarin b. 2nd generation-Brodifacoum, diphacenone, chloraphacione 52 |
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what test can be done when suspect anticoagulant rodenticide toxicity
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a. PIVKA b. However, the absence of vitamin K results in an increase in these precursors, which spill into the circulation and become known as Proteins Induced by Vitamin K Antagonism (PIVKA). Concurrently, the levels of active factors II, VII, IX and X are depleted. 53 |
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What is the MOA of Bromethalin rodenticides
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a. Uncoupling of oxidative phosphorylation which causes hyperexcitability in acute phase depression in chronic phase (depletes ATP stores and causes neurologic changes) 54 |
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What are the clinical signs associated w/t his toxin
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a. Muscle tremors b. Seizures c. HL hyperreflexia 55 |
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What is the toxic dose and how quickly does it work
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a. Toxic dose is 5 mg/kg and death w/in 12 hours 56 |
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What is the recommended treatment
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a. Activated charcoal b. No antidote 57 |
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What is the MOA for strychnine poisoning
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a. Inhibits post synaptic buffering effects on glycine 58 |
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What are the clinical signs
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a. Stiff, apprehensive, hyperthermia, hyperactivity b. Toxic extensor rigidity 59 |
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How is it treated
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a. Muscle relaxers, sedatives, activatd charcoal 60 |
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What are the clinical signs of zinc phosphide
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a. Mins to hous-> Anorexia, lethargy, dyspnea, vomiting, agitation, muscle tremors, weakness, recumbency and death 61 |
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What are the treatments
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a. Emesis b. Milk of magnesia c. Gastric lavage to increase gastric pH 62 |
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Animals with organophosphate toxicity die from what
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a. Respiratory failure, aspiration from increased respiratory secretions, bronchoconstriction, suppression of the respiratory centers in the medulla 63 |
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Is there a blood test for OG toxicity
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a. Yes, called cholinesterase testing 64 |
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What are the various treatments used for OG toxicity
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a. 2-PAM b. Emesis c. Activated charcoal d. Cathartics (mineral oil) e. Detergent and bath f. Atropine g. Diazepam if there is seizuring or muscle tremors h. Methocarbomal i. IVF 65 |
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What are pyrethrins
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a. Organic esters derived from chrysanthemum 66 |
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What are pyrethroids
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a. Synthetic cohort that is typically more toxic and last longer 67 |
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What is the MOA for toxicity for pyrethrins/pyrethroids
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a. Prolongs Na conductance and increased depolarization resulting in repetitive nerve firing 68 |
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What are the clinical signs
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a. Salivation b. Depression c. Ataxia d. Anorexia e. Vomiting f. Topically i. Urticaria ii. Pruritis iii. Alopecia 69 |
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Is it fatal
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a. Rare but can occur from seizures 70 |
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What is the treatment
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a. Emesis b. Cathartics c. Activated charcoal d. Gastric lavage e. Bath f. Diazepam g. Methocarbaomol h. IVF 71 |
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What is the prognosis
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a. Excellent 72 |
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What type of pesticide is Amitraz
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a. Formamidine pesticide 73 |
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What types of products contain Amitraz
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a. Tick collars, mitoban dips 74 |
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What is the MOA for this pesticide
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a. Monoamine oxidase inhibitor b. Alpha-2 adrenergic agonist c. Inhibitor of prostaglandin synthesis 75 |
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What are the clinical signs associated with this drug
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a. Depression b. Sedation c. Ataxia d. Bradycardia e. Hypothermia f. Mydriasis g. Vomiting h. Diarrhea i. Polyuria j. GI stasis 76 |
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What is the toxic and what is the lethal dose
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a. Toxic dose is 10-20 mg/kg b. Lethal is 100 mg/kg 77 |
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What type of labwork abnormalities might one see
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a. Hyperglycemia, transient 78 |
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What are the treatments
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a. None specific b. Induce vomiting c. Retrieval of tick collar if FB d. Activated charcoal e. Cathartics f. Atipamazole, yohimbine g. Enema 79 |
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What type of botanical extracts are seen in flea and tick shampoo
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a. Linalool b. D-limonene 80 |
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What are some other botanical extracts that are toxic
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a. Pennyroyal oil b. Methapulgium c. Hedcoma pulegioides d. All from plants 81 |
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What kind of effects to botanical extracts have
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a. Hepatic necrosis b. Liver failure 82 |
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What are the treatments
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a. Gastric lavage b. Activated charcoal c. DO NOT INDUCE EMESIS d. N-acetylcysteine e. Cimetidine for p450 enzyme inhibition 83 |
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Where do avermectins come from
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a. Soil Streptomyces organisms and are known as macrocyclic lactones 84 |
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What are some examples of common avermectins
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a. Ivermectin, milbemycin, alemectin, moxidectin 85 |
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How are these toxic
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a. Genetic adverse reaction with MDR-1 genes 86 |
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Which breed of dogs have the MDR-1 genes
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a. Collies, Australian shepherd, Shelties, OES, GSD, long haired whippets, silken windhounds b. Homozygous individuals are most sensitive 87 |
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What sdoes the MDR-1 gene code for
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a. Regulates the amount of drug that can cross the BBB 88 |
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What are the clinical signs
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a. Depression b. Ataxia c. Blindness d. Coma e. Muscle tremors f. Seizures 89 |
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How long can clinical signs last
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a. Days to weeks 90 |
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How is it treated
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a. Wash b. Emesis c. Activated charcoal d. Lipid IV therapy 91 |
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Which of these drugs has the longest half life
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a. Ivermectin-2d, Selamectin-11 days, moxidectin -19 days 92 |
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Where is a common source for lead toxicity
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a. Paints in homes build before 1977 93 |
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Once ingested, how does the metal become activated
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a. Acidic stomach environment favors ionization of the lead that is then rapidly absorbed by the duodenum 94 |
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Can a bullet be a source of lead toxicity
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a. No 95 |
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Where besides the red blood cell is iron stored in the body
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a. Bones, lead will displace calcium in bone matrix b. Stored in grey matter after it crosses the BBB 96 |
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How is lead excreted
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a. Excreted in feces unabsorbed 97 |
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If not excreted or stored where else can lead be found
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a. In renal tubular interstitium 98 |
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How does lead cause its clinical signs
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a. Interfere with calcium b. Binds to cellular and enzymatic sulfhydryl groups c. Alters vitamin D metabolism d. Inhibits membrane associated enzymes e. Impairs heme synthesis f. Alters smooth muscle contraction g. Decreases cerebral blood flow h. Alters neurotransmission 99 |
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What are the clinical signs
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a. GI upset b. Behavioral changes c. Ataxia d. Tremors e. Seizures f. Agitation g. Pu/Pd h. Blindness i. Dementia j. Pica k. Vestibular signs l. Coma m. Megaesophagus 100 |
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What will one see on labwork
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a. Anemia b. Basophilic stipling c. nRBC 101 |
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Why is it important to completely decontaminate a patient before starting chelation
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a. Chelation can cause increased absorption of lead 102 |
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What is used to chelate lead
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a. Calcium EDTA (not normal EDTA) b. British anti-lewisite i. Increases urinary and biliary excretion ii. Contraindicated with patients with hepatic disease iii. Nephrotoxic iv. Pain at injection site c. Penicillamine-oral drug that binds other essential minerals including iron, zinc, copper that could be nephrotoxic, blood dyscrasias d. Succimer- PO or rectal administration, less nephrotoxic, does not bind essential minterals does not enhace absorption 103 |
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What is something one must watch out for once chelation is started
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a. May see rebound effect as there is redistribution 104 |
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What is the prognosis
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a. Favborable for moderate signs but guarded for CNS signs 105 |
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What is the toxic substance in ethylene glycol
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a. 1,2-dihydroxyethone 106 |
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What substance is now added to ethylene glycol to help it become less palatable
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a. Denatonium benzoate 107 |
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What are the minimum lethal dosages
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a. Dogs: 4.4 ml/kg b. Cats: 1.4 ml/kg 108 |
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How is ethylene glycol absorbed
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a. Rapidly through the gastrointestinal tract and metabolized primarily by liver 109 |
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How is ethylene glycol metabolized
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a. Alcohol dehydrogenase and broken down into glycoaldehyde 110 |
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Once glycoaldehyde is formed, what is the next product
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a. Glycolic acid 111 |
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How is glycolic acid broken down into oxalic acid
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a. Via lactate dehydrogenase 112 |
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How are calcium oxalate crystals created
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a. Calcium binds to the oxalic acid in the renal tubules 113 |
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What are the three stages with ethylene glycol
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a. Stage 1= w/in 30 minutes b. Stage 2=w/in 8-24 hours c. Stage 3=w/in 1-3 days 114 |
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What clinical signs are associated with each stage
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a. Stage 1=drunk phase i. Vomiting ii. Pu/pd iii. Ataxia iv. Hyporeflexia b. Stage 2 i. Acidosis ii. Depression iii. Hypothermia iv. Muscle fasciculations v. Coma c. Stage 3 i. ARF ii. Anuric iii. Oral ulcers iv. Salivation v. Vomiting vi. Anorexia vii. Seizures 115 |
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How is EG toxicity diagnosed
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a. Commercial kits available i. Cross react w/ diazepam and glycerol (in pet food) ii. Cannot detect concentration less than 50 mg/dL 116 |
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How is it treated
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a. 4-methylprazole (4-MP) i. Competitively inhibits alcohol dehydrogenase b. Ethanol-also competitively inhibits alcohol dehydrogenase but can cause CNS and respiratory depression 117 |
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When is the best time to give 4-MP
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a. Cats- w/in 3 hours b. Dogs-w/in 8-12 hours c. Best if given w/in 32 hours 118 |
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How is propylene glycol toxic
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a. 1,2 propandiol b. Used instead of ethylene glycol 119 |
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What is the lethal dose in dogs
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a. 9 ml/kg 120 |
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What is the effect of propylene glycol in pet food
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a. Causes Heinz body anemia 121 |
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What are the clinical signs
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a. Ataxia and depression 122 |
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How is this material metabolized in the body
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a. Metabolized in the liver forms 2 isomers: i. L-isomer goes into citric acid cycle ii. D-isomer contributes to lactic acid 123 |
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What is the name of the substance used for brake fluid, hydraulic fluid, lubricants and cooking fuels that is less toxic than EG but more than PG
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a. Diethylene glycol 124 |
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What is the toxic dose
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a. 3.6-11.6 ml/kg 125 |
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What are the clinical signs
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a. Depression b. Vomiting c. Renal failure 126 |
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What is the result to a dog or cat that ingests petroleum compounds (gas, kerosene, diesel fuel)
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a. Aspiration of hydrocarbons causes respiratory epithelial necrosis 127 |
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What are the clinical signs associated with these products
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a. Salivation b. Pawing at the mouth c. Gagging d. Dyspnea e. Cyanosis f. Tremoring g. Convulsions h. Cardiac arrthmias 128 |
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What is the prognosis
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a. Good for motor oil and mineral oil 129 |
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What is methanol
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a. Methanol ingested in large quantities is metabolized to formic acid or formate salts, which is poisonous to the central nervous system, and may cause blindness, coma, and death in people but dogs and cats metabolize formic acid so not likely to be toxic 130 |
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How does nicotine toxicosis manifest
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a. Nicotine mimics Acetylcholine at PNS and sympathetic ganglia and causes hyperactivity 131 |
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What are the clinical signs
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a. Vomiting b. Salivation c. Tremors d. Dyspnea e. Tachypnea f. Muscle weakness g. Paralsysi h. Death is from respiratory muscle fatigue 132 |
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What are the toxic dosages
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a. Dog 12 mg/kg (40# dog=1 cigarrette) b. Dog lethal-9.2 mg/kg 133 |
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What is the treatment
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a. Supportive 134 |
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What is the MOA behind minoxidil (hair growth enhancer)
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a. Alters K channels in smooth muscle of vessels 135 |
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What are the clinical signs
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a. Hypotension b. Vasodilation c. Severe CV compromise leading to pulmonary edema and or pleural effusion 136 |
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Why is metabolism slowed in cats
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a. b/c metabolism occurs via conjugation with glucuronic acid 137 |
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What is xylitol and what is the MOA for its toxicity
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a. 5 carbon sugar b. Dose dependent rise in insulin 138 |
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What are additional issues with xylitol not related to hypoglycemia
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a. Hepatic necrosis b. Toxicity in cats is not known 139 |
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What is the toxic dose
|
a. 100 mg/kg b. Hepatic necrosis= 1000 mg/kg 140 |
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Do all dogs showing signs of hepatic necrosis have hypoglycemia
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a. No 141 |
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How is it treated
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a. Emesis b. Do not give activated charcoal c. Feed small frequent meals d. IV dextrose e. Hepatoprotectants f. K supplementation 142 |
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What toxin causes signs consistent with GI foreign body that looks like kibble filling the entire stomach on radiographs
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a. Expandable polyurethane glue 143 |
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What is the time frame
|
a. Clinical signs develop in 12 hours b. Can see radiographic changes in 4-5 hours 144 |
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How is it treated
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a. Treat like FB removal-friable material though b. Do not induce vomiting 145 |
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What are the osmotically active ingredients in paint balls
|
a. Polyethylene glycol b. Sorbitol c. Glycerol 146 |
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What is the effect of these ingredients
|
a. Results in hypernatremia b. Ataxia seizure c. Hyperchloridemia d. Hypokalemia 147 |
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How is this treated
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a. Decontamination b. Correction of electrolyte abnormalities c. Seizure control d. Supportie care e. Induce emesis if consumption w/in 2 hours f. NO ACTIVATED CHARCOAL g. Warm water enema 148 |
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What is the maximal rate to lower sodium
|
a. 0.5-1 mEq/L/hr 149 |
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What is the MOA behind grape/raisin toxicity
|
a. Unknown b. Idiosyncratic c. Get acute tubular necrosis , especially proximal tubules 150 |
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How quickly to kidney values go up
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a. w/in 48 hours b. Anuria is common 151 |
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What is the toxic dose
|
a. 0.7 ounces/kg of grapes b. 0.11 ounces/kg raisin oil 152 |
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What are some other labwork abnormalities
|
a. Acidosis, hyperkalemia 153 |
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What is the treatment
|
a. Emesis b. Activated charcoal c. Diuresis d. Phosphate binders e. Diuretics if anuric f. Control vomiting Prognosis- a. variable 155 |
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Which lilies are toxic
|
a. Easter lilies b. Star gazer lilies c. Tiger lilies d. Japanese snow lilies e. Day lilies 156 |
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Which lilies are not toxic
|
a. Peace lilies b. Callalilies 157 |
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How quickly does one see clinical signs
|
a. GI upset in 12 hours b. Lab abnormalities within 24-72 hours 158 |
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What is the MOA
|
a. Unknown 159 |
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How is this toxicosis treated
|
a. Emesis if within 2 hours b. Activated charcoal c. Cathartics d. Diuresis for at least 48 hours 160 |
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What is the prognosis
|
a. Variable 161 |
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Estradiol is the most active what
|
a. Endogenous estrogen 162 |
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What is DES
|
a. DES is a synthetic nonsteroidal compound with estrogenic activity. It is usually administered orally, metabolized by the liver, and finally eliminated in urine and bile. The half-life of oral DES in humans is 3 to 4 days. 163 |
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What is the short term side effects from estrogen like compounds
|
a. Pancytopenia 164 |
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What is the MOA for this
|
a. Binds to estradiol-1-B which may be present in high numbers in the bone marrow b. Secretion of myelopoiesis inhibiting factor 165 |
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What are the long term side effects
|
a. Risk of pyometra b. Teratogenic c. Embryotoxic 166 |
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What drugs are contraindicated in estrogen toxicity
|
a. GC b/c of immunosuppression 167 |
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What are progestins used for
|
a. Suppression of estrus b. Treatment of false pregnancies c. Paraphimosis in dogs 168 |
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What is the only approved form of megesterol acetate
|
a. Medroxyprogesterone acetate 169 |
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What are the short term effects
|
a. Not servious and reversible b. Lethargy c. Polyphagia d. Weight gain e. Behavioral changes 170 |
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What are the long term effects
|
a. Iatrogenic addison’s disease b. Insulin resistance c. Cystic endometrial hyperplasia d. Mammary neoplasia 171 |
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What are aflatoxins
|
a. Compounds produced as secondary metabolites from fungi (aspergillosis and penicillium) 172 |
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Which is one is most toxic and common
|
a. B1 173 |
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Which types of products do you find them in
|
a. Corn, peanuts, cottonseed 174 |
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What are the toxic dosages
|
a. Median lethal dose i. Dogs: 0.5-1.8 mg/kg b. Oral lethal dose i. Cats: 0.55 mg/kg 175 |
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How are aflatoxins metabolized and where are they concentrated
|
a. Metabolized quickly b/c highly lipophilic and protein-bound b. Absorbed completely in the duodenum c. Metabolites concentrated in the liver 176 |
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What are the two phases of aflatoxin toxicosis
|
a. Phase I-B1 metabolized by P450 enzyme to B,8,9 epoxide b. Phase II-B 8,9, epoxide is conjugated to glutathione via glutathione s-transferase c. The B,8,9 epoxide binds to cells affecting DNA protein synthesis d. Results in hepatic necrosis 177 |
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How is it diagnosed
|
a. Ante-mortem i. Test food ii. M1 urine test b. Post mortem i. Liver bx shows fatty degeneration of hepatocytes w/ centrilobular necrosis and cholestasis 178 |
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How is it treated
|
a. Remove toxin b. Emesis and activated charcoal c. IVF d. Vitamin K e. Vit B f. Hepatoprotectants g. N-acetylcysteine 179 |
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What are the most common types of nephrotoxins in cats
|
a. Lillies, cholecalciferol, ethylene glycol 180 |
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What are the most common types of nehrotoxins in dogs
|
a. EG b. NSAID c. Cholecalciferol d. Aminoglycosides 181 |
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NSAIDS are divided into what two groups
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a. Carboxylic acids: aspirin, naproxen, ibuprofen, flunixin b. Enolic acids: Phenylbutazone, Piroxicam 182 |
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Which nephrotoxin should always be considered for all cases of ARF
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a. Cholecalciferol 183 |
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What is the common result in dogs on high dosages of NSAIDS
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