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152 Cards in this Set
- Front
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mechanism of action of nicotine?
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nicotinic receptor agonist: mimics ACh at sympathetic and parasympathetic ganglia, NMJ, some receptors in CNS
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clinical signs of nicotine toxicosis
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emesis early on (stimulates CRTZ), excitation, tachynpnea, salivation; later muscle weakness, depression, respiratory muscle paralysis, cyanosis, cardiac arrest, death
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How does ion trapping effect absorption and elimination of nicotine?
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acidifying the urine will trap it so it can be excreted
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treatment for nicotine toxicosis
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emesis, AC, bathe if dermal exposure, ATROPINE (parasympatholytic), acidify urine, DO NOT USE ORAL ANTACIDS (increases absorption)
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mechanism of action of imidicloprid
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bind post-synaptic ACh receptors-->accumulation of ACh-->overstimulation-->paralysis
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what accounts for the high margin of safety of imidicloprids?
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they are specific for insect ACh receptors due to higher concentration of ACh receptors in the insect than in the mammal
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what is the mechanism of action of poison hemlock?
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nicotinic nueromuscular blockers, initial stimulation followed by depression of autonomic ganglia and skeletal muscle
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clinical signs of poison hemlock toxicosis
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weakness, trembling, ataxia, slobbering, rapid pulse, dilated pupils, frequent urination/defecation, musty mousy odor on breath and urine, death due to respiratory paralysis
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what is the mechanism of action of lupine?
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bind ACh nicotinic receptors
initial stimulation followed by depolarizing blockade |
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clinical signs of lupine
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sheep: labored breathing, depression, coma, death
cattle: hypersalivation, bruxism, weakness, recumbancy, death |
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what is the mechanism of action of widow spiders?
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release and subsequent depletion of ACh
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clinical signs of widow bites
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pain at site of infection, muscle fasiculations, tonic-clonic tremors, muscle cramps, excessive salivation, flaccid paralysis
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treatment of widow bites
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pain management (opioids, benzodiazepines, corticosteroids), methocarbamol/Ca Gluconate for muscle tremors, Antivenin (test for HST first); most are self-limiting in 4-6 hours
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how can you identify widow spiders?
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shiny black abdomen, red hourglass or red spots, only in warmer parts of US
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What is the bacterial source of botulinum toxin?
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Clostridium botulinum
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How are animals exposed to botulinum toxin?
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anaerobic wounds, poorly ensiled food, eating carrion, maggots, decaying vegetation
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how can you diagnose botulinum toxicosis?
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history, clinical signs, mouse bioassay on feed/serum, ELISA
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mechanism of action of botulinum toxin
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inhibition of release of ACh
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clinical signs of botulinum toxicosis
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ascending progressive flaccid paralysis, inability to swallow, mayasthenia, death from respiratory paralysis
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treatment of botlulinum toxicosis
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antitoxin, antibiotics (penicillin), wound debridement, supportive care
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mechanism of action of larkspur
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NMJ blocker: prevents binding of ACh
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clinical signs of larkspur toxicosis
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stiffness, weakness, nausea, mild tremors, collapse, prostration, aspiration pneumonia, death from respiratory paralysis
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treatment of larkspur toxicosis
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remove source, phyostigmine/neostigmine to inhibit ACh-ase, relieve bloat
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tick paralysis clinical course
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ticks feeding >5 days, ascending paralysis, animal retains pain sensation and tail wagging, death from respiratory paralysis
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tick paralysis treatment
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remove all ticks, mechanical ventilation (if needed), tick preventative (Frontline)
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What clinical syndrome results in horses from ingestion of sorghum?
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Equine cystitis-ataxia syndrome
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What are the clinical signs of sorghum toxicosis in horses?
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ataxia, dog sitting, paralysis of bladder--constant urine dribbling, paralysis of perineum--vaginitis, loss of tone of rectum, flaccid paralysis of tail
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What is the toxic principle of sorghum?
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cyanide conversion to beta-cyanoalanine
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what is the mechanism of action of sorghum toxicosis?
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interferes with normal nerve development and function: swollen, demyelinated nerves, increased gitter cells in spinal cord
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how is hydrogen sulfide gas formed?
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anaerobic bacteria decomposing sulfur-containing organic matter--liquid manure pits
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mechanism of action of hydrogen sulfide gas
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direct mucosal irritant
high doses cause stimulation of carotid body chemoreceptors which leads to tachypnea-->acapnia-->asphyxia |
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clinical signs of hydrogen gas toxicosis
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tachypnea, cough, cyanosis, asphyxia, seizures, death
conjunctivitis death from cardiopulmonary arrest |
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treatment of hydrogen sulfide toxicosis
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fresh air, oxygen supplementation, mechanical ventilation if needed
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clinical signs of chlorphenoxy herbicides (2,4-D)
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low doses (walking through treated lawn) will cause mild GI upset
high doses cause muscle membrane rigidity and irritability, hesitancy to move, ataxia, weakness |
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Why are ionophores incorporated in beef cattle diets and how do they work?
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growth promotants
increase feed efficiency, shift VFAs to propionic acid, prevent bloat/lactic acidosis |
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what is the toxic mechanism of ionophores?
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net cellular imbalance of cations (Na, K, Ca)-->mitochondrial swelling-->positive cardiac inotropy initially, then negative inotropy of cardiac and skeletal muscle
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which species is the most sensitive to ionophores?
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horses most sensitive
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clinical signs of ionophore toxicosis
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cardiac muscle lesions in horses along with weakness, feed refusal, ataxia, tremors
cattle: diarrhea, anoreia, depression, tremors, rumenitis pigs: tremors, knuckling, dyspnea, myoglobinuria |
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clinical signs of macademia nut toxicosis
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weakness, vomiting, tremors, ataxia, depression, hyperthermia
rear legs more greatly affected than front |
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treatment for macademia nut toxicosis
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emesis if early
AC supportive care monitor for pancreatitis if chocolate covered |
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what are the steps in ethylene glycol metabolism?
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ethylene glycol broken down by alcohol dehydrogenase into glycoaldehyde-->glycolic acid-->glycoxylic acid-->oxaic acid
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clinical signs of ethylene glycol
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CNS depression
PU/PD vomiting diarrhea |
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clinical signs of glycolic acid
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acidosis
nephrosis |
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clinical signs of oxalic acid
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crystalluria--calcium oxlate crystals (mono- and dihydrate)
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describe stage 1 of ethylene glycol toxicosis
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neuro and GI signs (ataxia, vomiting, drukenness, depression, acidosis, PU/PD)
30 minutes to hours post-ingestion |
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describe stage 2 of ethylene glycol toxicosis
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severe metabolic acidosis, tachypnea, tachycardia, pulmonary edema and congestion
12-24 hours post-ingestion |
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describe stage 3 of ethylene glycol toxicosis
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onset of oliguric renal failure, abdominal pain
12-72 hours post-ingestion |
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treatment options for ethylene glycol toxicosis
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asymptomatic: emesis/gastric lavage, fluids, check chemistries
symptomatic: control seizures, fluids, correct acidosis with bicarb, 4-MP (inhibits alcohol dehydrogenase, only for dogs), ethanol CRI (7% concentration) USE 4-MP OR ETHANOL BUT NOT BOTH |
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how can you get the desired ethanol concentration for ethylene glycol treatment if you have 40 proof vodka and a 1L bag of fluids?
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40 proof = 20% solution
7% is desired concentration 7% / 20% = x / 1000ml x=350ml replace 350ml of fluid bag with vodka |
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clinical pathology seen with ethylene glycol toxicosis
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metabolic acidosis
hypocalcemia hyperglycemia hyperkalemia azotemia isosthenuria, casts, CaOx crystallyuria |
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diagnosis of ethylene glycol toxicosis
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commercial test kits: PRN EG not sensitive for cats (lower levels intoxicate cats), Kacey EG kit can test for cats but false positive if any alcohol has been given
quantitative test at human hospital wood's lamp on urine, stomach contents |
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what is the therapeutic mechanism of salicylates
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selective Cox-1 inhibitor at low doses-->reduced prostaglandins and thromboxanes
reduces inflammation |
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what is the toxic mechanism of action of salicylates?
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non-selective Cox inhibitor at high doses
deceased GI protection, inhibition of platelet aggregation, decreased renal perfusion, pyrexia, metabolic acidosis |
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clinical signs of salicylate toxicosis
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low dose: vominting, anorexia, melena, increased bleeding time
high dose: seizures, coma, tachypnea, pulmonary edema, vomiting, melena, fever, metabolic acidosis, hyperglycemia |
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treatment of salicylate toxicosis
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low dose/asymptomatic: emesis, AC, fluids, monitoring, anti-emetics
high dose: control seizures, thermoregulation, fluids with bicarb, GI protectants |
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clinical signs of spent hops ingestion in dogs
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malignant hyperthermia
agitation, abdminal discomfort, painful abdomen, pacing, vocalization, myoglobinuria |
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treatment of spent hops ingestion
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emesis
AC Saline cathartic gastric lavage fluids dantrolene for muscle relaxation |
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what is the toxic principle of blister beetles?
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cantharidin
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clinical signs of blister beetle intoxicosis
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low dose: depression, anorexia, discomfort
high dose: restlessness, depression, mucosal ulcers, pollakiuria, fever, synchronous diaphragmatic flutter, muscle fasiculations |
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diagnosis of blister beetle intoxicosis
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cantharidin assay on urine, gut contents (collect early samples)
finding parts of beetles in hay |
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how are horses intoxicated by blister beetles?
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beetles swarm in alfalfa hay during blooming and then are trapped in hay when it is chopped releasing cantharidin
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treatment of blister beetle intoxication
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change diet
AC mineral oil fluids: dilutes toxin, increases renal excretion pain relief |
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COX enzyme roles
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Cox1: GI protectant, platelet function, renal perfusion
Cox2; inflammatory mediator |
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organs affected by NSAID toxicosis
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GI epithelium
kidneys liver (idiosyncratic in some dogs) CNS at very high doses |
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clinical signs of NSAID toxicosis
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GI: melena, hematemesis
kidneys: RENAL PAPILLARY NECROSIS, PU/PD, oliguria/anuria |
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treatment of NSAID toxicosis
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emesis, AC, SC, fluids (diuresis for 48-72 hours), GI protectants
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mechanism of action of cholecalciferol
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changed to calcitriol in kidneys/liver-->calcium resorption from gut and bones-->demineralization of bone, calcification of soft tissues
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how should you monitor cholecaciferol exposures?
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chemistry panals to check calcium levels
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treatment of cholecalciferol toxicosis
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decontaminate early: emesis, AC
treat hypercalcemia: IV saline (competes with calcium at tubules), furosemide, prednisone, phosphate binders, lowCa/Phos diet, avoid sunlight, bisphosphonates (stops bone resorption) |
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plants that produce cholecalciferol-like actions
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Cestrum: day blooming jessamine
Solanum (nightshade) Trisetum |
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mechanism of injury of soluble oxalate containing plants
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crystallization of calcium oxalate in renal tubules-->renal tubular necrosis
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what metabolic effects can be seen with soluble oxalate containing plants?
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hypocalcemia
azotemia |
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which soluble oxalates are water soluble and easily absorbed from the gut?
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sodium and potassium oxalates
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clinical signs of borate and boric acid
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CNS, renal effects
but, most clinical cases are only self-limiting GI distress |
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What is not known about grape and raisin toxicity?
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mechanism of action is unknown
toxic principle is unknown |
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clinical signs of grape/raisin toxicosis
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acute renal failure (azotemia), increased serum calcium
vomiting-->depression-->ataxia |
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treatment of grape/raisin toxicosis
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fluids, monitor urine output
early and aggressive decontamination |
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lesions seen in grape/raisin toxicosis
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renal proximal tubular necrosis
mineralized tubular debris, proteinaceous casts epithelial regeneration BASEMENT MEMBRANE REMAINS INTACT |
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clinical signs of red-rooted pigweed ingestion
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ventral edema, depression, weakness, trembling, incoordination, azotemia, fluid distended abdomen, hypocalcemia, hyperphos
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necropsy findings of red-rooted pigweed
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ascites
perirenal edema swollen and pale kidneys proximal and distal tubular necrosis |
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what is the toxic principle for oak poisoning?
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gallotannins
tannic acid |
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what part of the plant is toxic
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buds, twigs, leaves, acorns
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clinical signs of oak poisoning?
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constipation, brown colored urine in cattle, anorexia, depression, rumen atony, diarrhea, colic in horses
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prevention of oak poisoning
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feed animals well so they won't want to eat acorns
calcium hydroxide reduces binding tannic acid (expensive$$$) |
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which lilies are toxic to cats?
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Easter
Tiger Japanese Rubrum day lilies |
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which lilies are not actually lilies and therefore not toxic to days?
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peace lily
calla lily these plants contain oxalates though |
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clinical signs of lily toxicosis
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vomiting, salivation, lethargy, anorexia
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clinical pathology of lily toxicosis
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azotemia, hyperK, hyperphos
epithelial casts |
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histology of lily toxicosis
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kidneys: diffuse acute renal tubular necrosis, granular and hyaline casts
BASEMENT MEMBRANE INTACT |
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treatment of lily toxicosis
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emesis, AC
fluids peritoneal or hemodialysis goal is to keep them alive until the tubules regenerate |
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lesions resulting from chronic ochratoxin in swine
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pale enlarged kidneys
rough irregular surface of kidneys renal cortical streaking Loss of brush border, glomerulosclerosis, thickened basement membrane |
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what was the cause of the massive pet food recall of 2007? What were the histologic findings?
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melamine PLUS cyanuric acid
they must be in combination for renal effects to manifest crystals in distal nephrons, renal intersitial edema, corticomedullary hemorrhage |
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what does the development of teratogensis depend on?
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dependent on the stage of gestation at the time of ingestion
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mechanism of action of veratrum (False hellebore)
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jervanine acts directly prechondrogenic stem cells during mesenchymal differentiation into cartilage
cyclops |
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mechanism of action of nicotiana (tobacco)
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piperadine alkaloids are NMJ blockers that prevent normal fetal movement-->scoliosis, kyphosis, lordosis, cleft palate, torticollis
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mechanism of action of conium (poison hemlock)
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NMJ blocker that prevents normal fetal movement-->scoliosis, torticollis, kyphosis, cleft palate
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mechanism of action of lupine (Lupinous)
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ammodendrine is an NMJ blocker that prevents normal fetal movement-->crooked calf syndrome
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what are the 4 main syndromes associated with endophyte infected fescue?
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fescue foot
summer slump: most common, impaired thermoregulation fat necrosis equine fescue toxicosis: agalactia, abortion, foals are overmature with overgrown hooves |
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how can agalactia from fescue poisoning in mares be treated?
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domperidone 10-15 days prior to parturition
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why are ruminants susceptible to nitrates?
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rumen converts nitrates (safe) to nitrites (toxic)
monogastrics excrete nitrates unchanged |
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how do plants accumulate nitrates?
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stress/damage by drought, frost, herbicides, hail-->decreased photosynthesis-->nitrates don't get incorporated normally and thus accumulate in lower stalks
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what environmental conditions favor nitrate accumulation in plants?
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low water
high temerpatures unusually cool weather herbicides |
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what is the underlying cause of clinical signs with nitrate toxicosis?
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methemoglobinemia (Fe3+)
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what is the treatment for nitrate toxicosis?
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methylene blue IV slowly
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In which trimester of cattle gestation does ingestion of juniper or pine needles cause abortion?
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third trimester
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what is the toxic principle with juniper or pine needle ingestion that causes abortion?
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isocupressic acid
reduces uterine blood flow to fetus |
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which species is sensitive to zearalenone?
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swine are sensitive
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clinical signs of zearalenone toxicosis
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prepubertal gilts: most critical period is 7-10 days post-mating, implantation period
fetal resporption, mummies, reduced litter size, stillborn atrophy of testes in young males mammary gland enlargement in castrated males |
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mechanism of action of zearalenone
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acts as a weak estrogen
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effect of gossypol on reproduction
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pigs: reduced conception rate, abortions, reduced litter size
cattle: decrease sperm motility histologic changes in testes |
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what are the major components of snake venom?
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hyaluronidase: allows penetration of other toxins by destroying collagen
phospholipase A: rupture of myofibrils myotoxins: destroy muscle cells hemorrhagic toxins: coagulopathies |
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clinical effects of snake bites
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immediate intense pain at bite site
tissue destruction, coagulopathy, hypotension marked regional swelling echymosis, petichia cardiac arrhythmias, tachypnea neurotoxicosis without tissue destruction |
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what is the major cause of death from snake bites?
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death from hypovolemic shock
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treatment of pit viper bites
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do not use: cold packs, toruniquets, sucking out venom,
keep calm, maintain bite site below heart fluids antibiotics no steroids IV antivenin if available |
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difference between pit vipers and coral snakes
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pit vipers: retractable fangs
coral snakes: fixed fangs, have to chew to envenomate |
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how can you identify recluse spiders?
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violin shaped body
long, thin legs |
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clinical effects of recluse spider bites
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dermal necrosis
initial blister-->vesicle-->erosion systemic signs: vomiting, hemolysis, fever |
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treatment for recluse spider bites
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most require no treatment
clean wound well sugar bandage broad spectrum antibiotic |
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what are sclerotia?
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ergot bodies
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what are the toxic principles of ergot toxicosis?
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ergopeptine
ergoline alkaloids |
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which ergot and fescue diseases are similar in presentation?
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gangrenous ergot
fescue foot |
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what is the proposed mechanism of action of black walnut?
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ischemia of laminae-->laminitis
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treatment for black walnut exposure
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remove from source
remove shoes, provide soft bedding phenylbutazone |
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mechanism of iron toxicosis
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direct GI irritant
high dose: iron binding capacity exceeded and free iron enters cells increased lipid peroxidation-->membrane damage |
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clinical effects of iron toxicosis
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phase 1: GI upset, melena, hematemesis
phase 2: apparent clinical recovery phase 3: 12-96 hours, recurrence of GI signs, metabolic acidosis, shock phase 4: 2-6 weeks, stricture formation |
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how can acute iron toxicosis be diagnosed?
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deferoxamine challenge: vin rose color urine
measure serum iron and total iron binding capacity |
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treatment of iron toxicosis
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emesis, AC if early
MgOH to ppt iron in gut so it isn't absorbed deferoxamine: chelates iron, use until red color of urine is gone |
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mechanism of action of acetomenophine
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sulfonation pathway normally used for excretion
sulfonation exhausted-->glucoronidation no glucoronidation-->P450 metabolism to NAPQI NAPQI binds cellular macromolecules-->cell death |
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treatment of acetomenophine toxicosis
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emesis, AC, SC
N-acetylcystine ascorbic acid antioxidant cimetidine to inhibit P450 fluids, whole blood |
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cats versus dogs with acetomenophine toxicosis
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cats: methemoglobinemia, facial/paw swelling
dogs: liver necrosis |
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clinical effects of cycad ingestion in dogs?
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vomiting, depression, anorexia, diarrhea
seizures due to hepatic damage |
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treatment for cycad ingestion
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emesis
AC/SC GI protectants fluids, electrolytes |
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mechanism of action of aflatoxin
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disrupt normal cellular catabolic and anabolic functions
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clinical effects of aflatoxins
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chronic disease
reduced weight gain, icterus, rough hair coat, anemia, GI upset |
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management of aflatoxin contaminated feed
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prevent damage during growth/harvest
dry corn to 15% moisture or less NovaSil additive to bind toxin |
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what part of the cockelbur is toxic?
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seeds
2 leaf cotyledons |
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clinical effects of cockelbur toxicosis
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depression, abdominal pain, anorexia, salivation
muscle fasiculations, extensor rigidity, opisthotonos, paddling coma and death |
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mechanism of action of pyrrolizidine alkaloid plants
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bioactivation by P450 to toxic pyrroles-->cytotoxic and antimitotic effects
progressive hepatic damage |
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clinical effects of pyrrolidizine plants
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acute: liver failure, anorexia, depression, ascites
chronic: icterus, photosensitvity, unthrifty |
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lesions with pyrrolidizine plants
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hepatocytomegaly
fibrosis bile duct proliferation |
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mechanism of action of blue-green algae
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dysfunction of intracellular regulatory proteins
microcystins disturb cytoskeleton |
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clinical effects of blue-green algae
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acute death from hemorrhagic shock
hepatic damage secondary photosensitization if survive |
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diagnosis of blue-green algae
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identification of bacteria in water, gut contents
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mechanism of action of latana
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triterpene acids-->intrahepatic cholestasis
damage to bile canilicular membranes |
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clinical effects of latana toxicosis
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ruminants
acute: bloat, photosensitization, anorexia, icterus chronic: photosns, cracking/desquamating skin, cloudy cornea, light sensitive |
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mechanism of action of sesquiterpene lactones
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bind -SH groups-->inactivate essential enzymes-->metabolic acidosis, hypoglycemia
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clinical effects of sesquiterpene lactones
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acute: spewing sickness
chronic: poor BCS, weight loss |
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clinical effects of alsike clover
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horses only
photosensitization: dew poisoning possible concurrent liver disease |
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lesions associated with alsike clover toxicosis
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bile duct proliferation, lobular fibrosis
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xylitol mechanism of action in dogs
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potent stimulation of insulin release-->rapid drop in glucose
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clinical effects of xylitol in dogs
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vomiting, depression
seizures hypoglycemia liver failure possible but not understood |
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treatment of xylitol poisoning
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emesis
AC NOT USEFUL feed meals with extra sugar if asymptomatic dextrose bolus, frequent small meals, potassium in fluids liver protectants |
