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43 Cards in this Set
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What species is very sensitive to bromethalin?
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Cats
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What species is resistant to bromethalin?
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Guinea pigs (can't demethylate)
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What are the acute high dose clinical signs of bromethalin?
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mm tremors, seizures (sound and light induced), hyperthermia, death, rigor
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What are the low dose clinical signs of bromethalin?
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(12-72 hrs) CNS depression, coma, anisocoria, hindlimb ataxia, paralysis, extensor rigidity, decerebrate posture
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How do you diagnose bromethalin toxicity?
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History, white matter edema/vacuolization, bromethalin or metabolites in fat, brain, liver
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What are the treatments for bromethalin?
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1. Decon (emetics, repeated AC)
2. Cerebral edema=mannitol, dx, furosemide 3. Gingko biloba |
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Decribe the mechanism of action of bromethalin.
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GI abs--demethylated in liver by P450--biliary excretion--enterohepatic recirc
Uncouples ox phosphorylation in mitochondria (decr. ATP)--myelin splitting, cerebral edema, increase ICP |
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Define the mechanism of action of strychnine.
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Competitive glycine inhibitor: blocks inhibitory Renshaw cells in CNS=cholinergic excitation
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What are the clinical signs of strychnine?
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rapid onset of mm tremors, seizures, tonic extensor rigidity, "sawhorse stance", opisthotonus, resp. paralysis
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How do you diagnose strychnine toxicity?
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History, chemical analysis of stomach contents, liver, kidney, urine.
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What is the treatment for strychnine?
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1. gastric lavage and AC (NO emetic)
2. seizures: valium, pentobarbitol 3. mm relaxants: methocarbamol, 1/2 quickly, rest slow to effect |
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Describe the mechanism of action of Zinc phosphide.
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converted to phosphine gas in acid stomach--cytotoxic to lungs--pulmonary edema and neuro effects
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What are the clinical signs of zinc phosphide?
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Rapid=respiratory + CNS, vomiting, seizures, pulmonary edema
Delayed=liver/renal disease |
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How do you diagnose zinc phosphide toxicity?
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History, chemical analysis of stomach contents and phosphine odor
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What is the treatment for zinc phosphide?
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1. No AC (it is a small molecule)
2. No emetic (it is corrosive) 3. NaHCO3 lavage to decrease hydrolysis 4. Seizures: valium, pentobarbitol |
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What is the mechanism of action of anticoagulant rodenticides?
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Inhibits VitK epoxide reductase=depletion of VitK dependent coag factors
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What are the VitK dependent Coag Factors?
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II, VII, IX, X,
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How do you diagnose anticoag rodenticide toxicity?
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History, prolonged ACT, OSPT, APTT, (PT 1st)
anemia, hproteinemia, +/- schistocytes, hfibrinogenemia, thrombocytopenia, increased FDPs |
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What is the treatment for small dose anticoag rodenticide?
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Emetics + AC
Monitor for clinical signs +/- Vitamin K if needed |
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What is the treatment for >1/10 lethal dose of anticoag rodenticide?
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1. VitK1 (oral>inj, loading dose, then SID) will correct coagulopathy w/in 12-48 hrs
2. 1st gen: 7-10dd VitK tx. 3. 2nd gen: 21-30dd VitK tx. 4. IV fluids, O2 5. PCV<15%=transfuse |
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What is a 1st generation anticoag rodenticide?
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Warfarin, dicoumarol (clover based)
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How do you calculate the exposure dose of warfarin?
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find this out???
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What is a 2nd generation anticoag rodenticide?
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Brodifacoum, diphacinone
more potent and persisitent |
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What is the treatment for sticky traps?
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Clip and bathe
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What is the mechanism of cholecalciferol toxicity?
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VitD
absorbed--activated in liver, kidney--hydroxalated metabolites to GIT and bone--increase Ca absorption and Ca mobilization Hcalcemia, Hphosphatemia, dystrophic calcification |
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How much VitD is in cholecalciferol?
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Throw packs have 10X daily dog dose
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What are the clinical signs of cholecalciferol toxicity?
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24hr=asymptomatic
>24 hrs=GI, anorexia, constipation, colinc, vomiting (hematemesis), mm wkness 24-48 hrs=renal, Hcalcemia/hphosphatemia, azotemia, proteinuria, glucosuria, hyposthenuria |
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How do you diagnose cholecalciferol toxicty?
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Hypercalcemia
serum cholecalciferol (2wks) rads (mineralization) Path (hemorrhagic ge, myocardial degeneration, diffuse mineralization of lung, kidney, atria, stomach |
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What is the short term tx. for cholecalciferol?
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<4 hrs=emetics, AC + SC
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What is the treatment for cholecalciferol?
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caliuresis
.9% saline + furosemide Prednisone *if symptomatic=add calcitonin SQ and pamidronate disodium to decrease bone resorption, low Ca diet, decrease sunlight, +/- peritoneal dialysis |
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How long do you treat for cholecalciferol?
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Treat until Ca returns to normal for 72 hrs
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What are the ddx for cholecalciferol toxicity/Hcalcemia?
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Neoplasia, primary HPTH, secondary HPTH, feed error, juvenile Hcalcemia, rodenticides
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What is the risk of teflon?
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overheating, release noxious gases, mostly in birds
>550F |
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What are the clinical signs of teflon exposure?
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sudden death, dyspnea, seizures/neuro (hypoxia)
lungs dark red/hemorrhagic |
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What is the origin of organic dusts?
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bedding, feed, hay, silage, fecal material (indoors)
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What are the clinical signs of organic dust exposure toxicity?
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Waxing and waning
Heaves, COPD, RAO decreased performance, increased lower resp. dz. |
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What is the treatment for organic dusts?
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Feed pelleted feeds
reduce dust |
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What are the features of ozone?
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pungent "after rain" odor
highly reactive oxidant gas highly toxic |
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What are the clinical signs of ozone?
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airway irritation/inflammation, increased airway responsiveness, bronchiolitis, decreased mucociliary clearance, secondary infections
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How do you prevent ozone toxicity?
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decrease exercise and outside exposure on high ozone days
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What is the toxicity of ozone?
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O2 in presence of volatile organic compounds + sunlight=O3
penetrates small airways increased hospital admission, mortality in humans (worsens resp. dz.) |
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Characteristics of CO?
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odorless, colorless
from incomplete combustion (car/boat exhaust, kerosene/propane heater, charcoal grills, house fires) |
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What is the mechanism of CO toxicity?
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shifts O2-Hgb dissociation curve to left (prevents peripheral O2 dissociation)
bright red blood |
