Term
| Avicides: What is the most likely mechanism of exposure to non-target species? |
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Definition
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Term
Avicides
Are these agents selective for target bird species? If so, which and what is the mechanism by which they are selective? |
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Definition
• Yes. It is a pelleted poultry feed base that is palatable to starlings & blackbirds.
• Sensitive birds such as Starlings, Red-Winged Blackbirds and Crows contain LD50’s ranging from 1.8-3.8 mg/kg (sensitive = LD50’s <25mg/kg) |
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Term
Avicides
Are there specific treatments for 4-AP toxicosis outside of supportive and symptomatic treatments? |
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Definition
Minimize absorption (gastric lavage followed activated charcoal).
Pancuronium bromide (antag 4-AP)
Xylazine to control excitement
Propranololo (B-blockers) for tachyarrythmias |
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Term
Rodenticides
What is the most likely mechanism for exposure to non-target species? |
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Definition
| • The baits used can be attractive to pets. Some people mix baits with food to attract rodents. |
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Term
Rodenticides
For anticoagulant rodenticides, what is the major determining factor for the duration of toxicosis? |
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Definition
• Half life varies in species and depending on the actual compound. (duration of toxicosis is dependent on half-life)
• Warfarin –14 d
• Brodifacoum 30d |
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Term
Rodenticides
For anticoagulant rodenticide ingestion, if the animal is asymptomatic, what is the schema of treatment? |
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Definition
• Emetic, adsorbent and cathartic therapies for ingestion that has occurred w/in the last few hours
• Monitor PT (prothrombin time) or PIVKA (protein induced in vitamin K antagonism) levels at baseline, 48, and 72 hours to determine if decontamination was successful. If elevated PT initiate vitamin K1 therapy.
• Cattle and EQ, begin K1 therapy. If cannot, animal should be stalled and fed high quality alfalfa. |
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Term
Rodenticides
For anticoagulant rodenticide ingestion, if the animal is symptomatic, what is the schema of treatment? |
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Definition
| • Stabilize if shocky or dyspneic. If significant hemorrhage has occurred give whole B, plasma or a synthetic B product. Perform serial coagulation and CBC’s. High dose vitamin K1 (5mg/kg) may be indicated, and REST. |
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Term
Rodenticides
Which of the rodenticide agents may cause secondary poisonings via the eating of rodents that are killed? |
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Definition
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Term
Rodenticides
How is the mechanism of action of cholecalciferol related to its’ toxicity and treatment? |
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Definition
| • Cholecalceferol is Vit D3. Metabolized in the liver to calcifediol then in the kidneys to calcitriol. If there is a build up of Vit D3 there will be an increase in plasma calcium and phosphorous levels. Increased Ca will cause membrane permeability, altered Ca pump activity, decreased cellular energy production, and cellular necrosis. Mineralization of soft tissues may occur at levels 70X. |
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Term
Rodenticides
Are there specific toxicities or attributes associated with strychnine (gopher bait) poisoning? |
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Definition
| • Yes, highly toxic to animals. Symptoms range from slight ataxia and mm stiffness (low doses) to severe muscle spasms and convulsions (blocks glycine-inhibitory NT). |
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Term
Rodenticides
Why is there a difference in the potential toxicity of zinc phosphide in animals that can or cannot vomit? |
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Definition
• Induces vomiting in animals that can
• Non-target species frequently vomit recently ingested zinc phosphide thus preventing poisoning. Time is critical and early decontamination can improve prognosis. |
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Term
Respiratory Toxins:
What are three factors that can influence respiratory toxicosis across species? |
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Definition
• Tissue architecture: toxicants may selectively induce damage to specific tissues or cell population (ex. Water soluble gases such as formaldehyde and sulfur dioxide become trapped in the URT making them susceptible to oxidant injury).
• Metabolic capability
• Anatomic configuration (ex. Nasal cavities in dogs are far more complex than humans therefore less susceptible to deep lung effects of a toxic gas). |
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Term
Respiratory Toxins:
What factors are associated with Hydrogen Sulfide production and release that make it potentially dangerous? |
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Definition
| • The gas is formed by anaerobic bacterial decomposition of protein and other sulfur containing organic matter. It is heavier than air and accumulates in manure pits and holding tanks. The gas is rapidly released when waste slurry is agitated and can generate high concentrations in the range of 1000 ppm. Concentrations of 200 ppm has a paralyzing effect on the olfactory sensory apparatus blocking detection. |
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Term
Respiratory Toxins:
What is the mechanism of action of Carbon Monoxide and how is that related to observed toxicities and treatments? |
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Definition
• MOA: rapidly absorbed in the lungs, competing for binding sites with O2 on a variety of proteins including hemoglobin. Affinity for CO to hemoglobin is >>>> than O2. Complex forms carboxy-hemoglobin that has a severely reduced ability to carry O2.
• Tx is to restore O2 to brain and heart. P’s tissues will appear pink w/cherry red blood. |
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Term
Respiratory Toxins:
Why does Nitrogen Dioxide cause considerable damage to the lungs but may not cause as much damage in the upper respiratory tract? |
|
Definition
| • NO2 combines with H2O in the air or exposed tissues to form corrosive nitric acid. NO2 is relatively insoluble in H2O so it passes through the URT w/little effect BUT produces damage to the lungs where the DURATION OF CONTACT IS LONGER and the MOISTURE CONTENTS IS GREATER. |
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Term
Respiratory Toxins:
What kind of animal is susceptible to toxicosis caused by overheating of cookware? |
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Definition
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Term
Respiratory Toxins:
How can cows eating forage high in tryptophan possibly lead to lung damage? |
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Definition
| • The reactive intermediates 3-MI cause lung damage, and after low level of exposure and recovery type II alveolar cells will proliferate. Cattle with intermediate signs can be pushed into acute syndrome if exercised, so they need to relax. |
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Term
Pharmaceuticals:
What is/are the major toxicities associated with the use of NSAIDs in companion animals? |
|
Definition
• Toxicities are related to inhibition of COX enzymes
o Renal damage at doses >175 mg/kg
o CNS effects (sz, ataxia, coma) at doses >400 mg/kg in dogs
o Cats: ulcer formation, renal damage, platelet aggregation inhibition, possible hepatic function
• Acute toxicity at doses 50-125 mg/kg in dogs may result in D, V, nausea, anorexia, gastric ulceration, and abdominal pain. |
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Term
Pharmaceuticals:
What phase II metabolizing system are felines deficient in? |
|
Definition
| • UGT’s: glucoronosyltransferase enzymes |
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Term
Pharmaceuticals:
What is/are the predominant toxic effects of acetaminophen in dogs? What about cats? |
|
Definition
• Dogs (600 mg/kg acutely): hepatocellular injury and necrosis, with V, anorexia, tachycardia, and tachypnea. At higher doses methemogloibinemia may become apparent with cyanosis, hemogloinemia, and hematuria.
• Cats (50-100mg/kg & as low as 10): methemoglobinemia with cyanosis, muddy mucous membranes, respiratory distress, edema of the face & paws, depression, hypothermia & vomiting. Heptotoxicosis is observed at high doses in males. |
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Term
Pharmaceuticals:
Is there a specific treatment for acetaminophen toxicosis? In a general way, how does it work? |
|
Definition
• NAC and or SAMe (dogs)
o N-acetylcysteine IV, S-adenosylmethionine
o NAC acts as a thiol donor and frees-up regular cysteine to be used in GSH (glutathione) anabolism which fxns in detox of reactive metabolites. |
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Term
Pharmaceuticals:
Why are dogs generally more likely to be poisoned by pharmaceuticals? And, how does this same general behavior factor in to venlafaxine poisoning in cats? |
|
Definition
• Dogs may chew on a bottle and accidently ingest the Rx.
• Cats readily eat venlafaxine tablets and capsules. |
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Term
Pharmaceuticals:
. How do you treat amphetamine toxicity? |
|
Definition
• Limit absorption: emetics, activated charcoals, and cathartics
• Supportive and symptomatic tx: acepromazine or chlorpromazine for agitation, barbiturates to control sz, cyproheptadine as a serotonin antagonist, propranolol to tx tachycardia
Increase elimination: IV fluids, ammonium Cl or ascorbic acid to acidify urine (leads to increased urinary elimination) |
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Term
Mycotoxins:
Why is aflatoxin toxicosis primarily hepatic whereas ochraotixn toxicosis is primarily renal? |
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Definition
• Chronic exposure to ochratoxin causes kidney dz related symptoms. High [renal] is d/t substrate for organic anion transporters in the kidney. MOA includes protein and mRNA pools reduced in kidney cells, and renal gluconeogenesis and phosphoenolphyruvate carboxykinase inhibition in rats and swine.
• Clinical signs of chronic exosure to aflatoxins are d/t liver dz (reduced wt gain, roughed hair coat, anemia, jaundice, anorexia, depression). |
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Term
Mycotoxins:
Why are ruminants relatively immune to ochratoxin-induced toxicosis? |
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Definition
| • The ruminal microorganisms detoxify ochratoxin |
|
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Term
Mycotoxins:
What toxicities are associated with ergot toxicosis and via what primary mechanism of action? |
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Definition
MOA: Agonist and antagonist activity at tryptaminergic, dopaminergic, and a-adrenergic R’s
Serotonin, Dopamine, Norepinephrine
Ex: alkaloids are antagonistic to dopamine D1 vasodilatory R’s, dompaminergic (agonist) activity at D2 R’s causes inhibition of prolactin secretion.
Vasoconstriction is produced by agonist activities and this effect varies depending on the vascular bed.
Toxicities →
Cutaneous and gangrenous lesions of the tail and extremities (assoc’d w/subacute or chronic ingestion, cold temps enhance the clinical effects)
Hyperthermia and production loss (reduces feed intake & milk production)
Reproductive failure (hyperthermia induced embryonic loss, agalactia, small weak foals, stillborns in PG EQ, prolactin secretion causes loss of corpora lutea and avortion in K9 and rodents)
Convulsive or nervous form (caused by acute ingestion of a large dose of sclerotia) |
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Term
Mycotoxins:
Why are trichothecenes also referred to as vomitoxin? |
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Definition
• deoxy-nivalenol (DON, vomitoxin) is a toxin of trichothecenes in domestic animals
o extra info: There is poor metabolism of deoxy-nivalenol (DON, vomitoxin) in swine which accounts for their sensitivity to the effects of these toxins. |
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Term
Mycotoxins:
Toxicities of zearalenone are primarily associated with its activity as a weak ______? |
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Definition
• Estrogen that binds to R’s for estradiol-17β
(clinical signs: hyperestrogenism & hyperemia and swelling of the vulva, mammary glnds and utereus as well as ovarian atrophy) |
|
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Term
Mycotoxins:
What are the primary toxicoses associated with fumonisin? |
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Definition
• PPE (porcine pulmonary edema)
• ELEM (equine leukoencephalomalacia) |
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Term
Mycotoxins:
What is the name of the toxin associated with “slobber syndrome” and why does it cause slobbering? |
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Definition
• Slaframine
• The ketoimine metabolite acts as a parasympathomimetic agent to stimulate exocrine and endocrine glands. |
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Term
Mycotoxins:
Why are dogs more likely to have toxicoses associated with penitrem A and roquefortine exposure? |
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Definition
| Dogs exhibit scavenger behaviors and may get into the garbage and ingest moldy foods. |
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Term
Envenomations – Reptiles:
Most snake bites are from what group of snakes in animals? |
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Definition
| • Crotalidae (pit vipers) |
|
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Term
Envenomations – Reptiles:
Is coral snake toxin primarily neurotoxic or causing of local tissue pain and damage? |
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Definition
| CNS depression, mm paralysis, and vasomotor instability |
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Term
Envenomations – Reptiles:
Why should a dog potentially bitten by a coral snake be observed over an extended period of time? |
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Definition
| • Because venom can take up to 14 days to clear. Venom causes intravascular hemolysis, evere anemia, and respiratory paralysis. |
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Term
Envenomations – Reptiles:
How would you treat a cat presenting with a known coral snake bite and who is beginning to be symptomatic? |
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Definition
| • Supportive care and be prepared to ventilate & possibly broad-spectrum ab’s. |
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Term
Envenomations – Reptiles:
What are the 3 general types of rattlesnake venom? What do they cause in afflicted animals? |
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Definition
• Classic diamondback rattlesnake venom: marked tissue destrection, coagulopathy, and hypotension
• Mojave A Rattlesnake venom: severe nuerotoxicosis (non of the above)
• Intergrade found in multiple spp: all the above |
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Term
Envenomations – Reptiles:
Why will pit viper antivenins or vaccines potentially only be active against a sub-set of envenomations? |
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Definition
| • (rattle snake vaccine in general) The vaccine elicits an immune response to the major protein fractions of the Western diamondback rattlesnake. |
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Term
Envenomations – Reptiles:
How would you tell if a rattlesnake bite occurred and the potential seriousness in a dog who may have been bitten? What diagnostic tests can be done? |
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Definition
• (rattle snake vaccine in general) The vaccine elicits an immune response to the major protein fractions of the Western diamondback rattlesnake.
• Swelling, dyspnea, tachycardia, nausea, obtunded, mm. fasciculation, hypotension, V
• Dx: CBC & chemistry, PT and PTT, look for high levels of CPK for mm damage & blook smear to look for echinocytes, UA to check for hematuria and rhabdomyolysis
• Tx: anti-venin (pre-tx w/Benadryl, vax has not been correlated w/a better outcome), keep animal calm, IV crystalloid fluid therapy for hypovolemia, broad-spectrum AB’s |
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Term
Envenomations – Reptiles:
What does Gila Monster venom cause? How do you treat a known envenomation? |
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Definition
• PAIN!, sig bleeding, edema, hypotension, tachycardia, regional mm fasciculations, possible secondary infection esp if tooth fragment embedded in wounds. Felines exhibit tachypnea, tachycardia, and vomiting d/t pain.
Take lizard off (and remaining teeth), hospitalize, iv fluids, crystalloids, opioids (NSAIDS contraindicated), broad spectrum AB’s, clean wound |
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Term
Envenomations – Spiders and Bugs:
What species is especially sensitive to widow bites? How would you treat a known bite in this species? |
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Definition
• Cats.
• Tx is symptomatic. Opiods to control pain, diazepam & methocarbamol to control mm rigidity (Ca++ gluconate is no longer used)
• EQ origin antivenin is available & effective (cheap, long shelf life, DTH is rare) |
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Term
Envenomations – Spiders and Bugs:
What is the primary lesion seen after a recluse spider bite? How would you treat it? |
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Definition
bull’s eye” lesion
• Tx: necrotic lesions: chemical debridement w/Burrow’s soln (aluminum acetate) or H2O2 and bandaging. Control pruritis w/diphenhydramine. Administer Ab’s if infection is evident. For pain use NSAIDS (minor), or Opioids (severe). Dapsone is used to inhibit N0 migration and may limit the severity of the necrotic lesion. Experimental antivenins effective but not available. |
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Term
Envenomations – Spiders and Bugs:
Are tarantulas dangerous? |
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Definition
• Selenocosmia & Phlogiellus spp are dangerous
• Spp in the U.S. are not capable of delivering serious envenomation.
• Those w/toxic venom occur in SA, Africa, & Australia
• Venom contains a neurotoxin and potentially a necrotoxin and hemolytic toxin → mm spasms, edema, hemoglobinuria, jaundice, and circulatory shock may develop |
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Term
Envenomations – Spiders and Bugs:
What are the consequences of a scorpion sting? Is it a serious concern in dogs or cats? |
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Definition
• Blockage of VG-Na and K Ch’s from α & β scorpion toxin.
• Instant sharp pain; localized edema & pruritis are common; regional LNs may enlarge & potentially an allergic rxn characterized by swelling of the eyelids, tongue, and V; systemic signs vary but gen include numbness of the face, maylgia, tachycardia or bradycardia, resp depression, and sz’s.
• no evidence for envenomation in dogs & cats |
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Term
Envenomations – Spiders and Bugs:
What does tick toxin cause? How do you treat it? |
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Definition
• Toxin interferes w/synthesis and/or release of Ach at the NMJ resulting in LMN paresis and paralysis (effects similar to those of botulinum toxin).
• CS’s: ascending ataxia → paresis to paralysis. Paralysis of the resp mm leads to resp failure and death.
• Tx: remove tick(s), supportive care esp resp support. Use topical insecticides where multiple ticks are embedded. In Aust a polyclonal dog antiserum is effective if tx’d in the early stages of paralysis. |
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Term
Envenomations – Spiders and Bugs:
What do you primarily need to worry about regarding bee and/or wasp stings? |
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Definition
| • Exposure to single stings from bees or vespids is rarely fatal. Attacks w/multiple stings must be tx’d w/more care w/regards to systemic effects. |
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Term
Biotoxins:
How does botulism occur and what does it cause? |
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Definition
• Ingestion of preformed toxin, ingestion of spores, or contamination of wounds with spores
• Blocks ACh release from presynaptic neuron resulting in flaccid paralysis. |
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Term
Biotoxins:
What are the best prevention strategies for botulism? |
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Definition
• Vaccination with C. botulinum toxins with toxoid to prevent clinical dz
• Also proper ensiling of poultry litter, examine feed for evidence of decaying carcasses, rodent control program, proper disposal of dead animals (deep burials) |
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Term
Biotoxins:
How is tetanus different from botulism? |
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Definition
• Prevents the release of NTs, esp glycine, from neurons in the CNS → uncontrolled mm contractions
• Botulism → flaccid paralysis |
|
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Term
Biotoxins:
What clinical signs are indicative of tetanus and in what group of affected animals do they occur? |
|
Definition
• Generalized musculoskeletal stiffness, elevated third eyelid, abnormal blinking.
• Carnivores → contraction of mm of the lip produces a sardonic grin
• Progression of CS’s: severe muscular rigidity leading to sawhorse stance (fixed stare, erect ears, reluctance to eat or drink d/t “locked jaw, ” an elevated tail and flared nostril. |
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Term
Biotoxins:
What are the best prevention strategies for tetanus? |
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Definition
| • Prevent intro of the org into any wounds or surgical sites, use clean needles & blades for vax, tagging & castration. Optimal = vax program |
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Term
Biotoxins:
What are the general toxicities that can be associated with blue-green algae ingestion? |
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Definition
• Anataoxin-a toxicity presents w/mm tremors & leads to resp paralysis death w/in 30 min
• Anatoxin-a (s) inhibits AChE (SLUDGE) death w/in 1 hr
• Microcystin or nodularin are hepatotoxic death w/in 24 hrs |
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Term
Biotoxins:
What are the treatments utilized for dogs that ingest blue green algae? |
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Definition
• No antidotes ∴ tx symptomatically and supportive care.
• Decontamination → emesis, activated charcoal, a cathartic as well as bathing if algae remain on the haircoat = In LA’s activated charcoal is limited, a chathartic and possibly washing.
• Hepatotoxicity → fluids, corticosteroids & other elements of shock therapy.
• Neurotoxicity → aggressive resp support and sz control as needed. (animals w/anatoxin –a(s) toxicosis may be tx’d w/Atropine. |
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Term
Biotoxins:
Why is blister beetle toxicosis most often observed in horses? |
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Definition
• b/c they consume alfalfa hay produced in the semiarid regios of TX & OK.
• More susceptible to toxic effects than other livestock |
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Term
Biotoxins:
What does cantharidin cause clinically? |
|
Definition
• is a vesicant & causes irritation characterized by acantholysis and vesicle formation leading to ulcers or erosions where the compound contacts a mucosal surface.
• Varies w/dose: depression & discomfort to severe colic.
• EQ: signs related to colic (restlessness, depression, sweating, congested mucous memebranes, increase HR & resp rate)
• Fever, pollakiuria, and D
• Less common signs include oral lesions, salivation stiff gait, and B-tinged urine |
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Term
Biotoxins:
What is the mechanism of action of toxins associated with toads? |
|
Definition
• Secretion from the parotid glands release bufodienolides, which are cardiac glycosides. They bind to and inhibit Na-K ATPase similar to other cardiac glycosides.
↑ extracellular [K], w↑intracellular Na → Ca influx from the cytosol via Na-Ca exchange results. This results in depressed electrical conducation |
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Term
Biotoxins:
What species is most likely to be affected by toad toxins? Why? What are the clinical signs and treatment options? |
|
Definition
• Dogs, they will mouth or bite toads.
• CS hypersalivation, V, & anxiety are initial signs. Animals will present w/neurolgic abnormalities, including convulsions, ataxia, nystagmus, stupor, or coma. Mucous membranes of the oral cavity may be hyperemic. Death occurs 15 min post CS onset.
Initial tx: decontamination of the oral cavity. Diazepam if sz’ing. Initial cardiac examination should include auscultation (bradycardia → IV atropine; sustained tachycardia → B-antagonists). If hyperkalemic, tx w/an infusion of insulin, glucose, and Na bicarbonate. Digoxin-specific Fab-fragment not evaluated in dogs yet. |
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Term
| Quaternary Ammonium Herbicides |
|
Definition
diquat, paraquat)
-restricted use only- “blue dye” added
-Ingestion, inhaled, skin absorbition
Signs: vomiting, colic, diarrhea, dehydration, pulm edema, liver failure, renal failure |
|
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Term
| Carbamate and Thiocarbamate Compounds |
|
Definition
terbucarb, asulam, carboxazole
-bind acetylcholinesterase |
|
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Term
| Phenoxyacetic, Methoxybenzoic acid Phenoxybutyric compunds |
|
Definition
2, 4-D: 2,4 dichlorophenoxyacetic acid
Dicamba: skin and eye irritant, vomiting, resp irritant, teratogen
“agent orange”= 2, 4-D + 2,4,5-T |
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Term
|
Definition
-nontoxic to animals when used correctly
-signs in dogs: myotonia, ataxia, posterior weakness, diarrhea, vomiting, metabolic acidosis
-scottish terrier: urinary bladder transitional cell carcinoma and increased risk for lymphoma
-cattle: large dose interferes with fxn
-increase plant palatability, NO3 and HCN |
|
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Term
| Dinitrophoenolic Compounds |
|
Definition
(dinoseb, binapacryl)
-highly toxic to all clases of animals
-LD 50 of 20-56 mg/kg body wt
signs: convulsions, vomiting, headache, sweating, laboured breathing, unconsciousness |
|
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Term
| Organophosphate Compounds |
|
Definition
(glyphosate, bensulide)
-broad-spectrum, non-selective systemic herbicides effective on all annual and perennial plants
-phosphanoglycine does not inhibit cholinesterase activity
-acute LD50 in rats is >5.6g/kg. |
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Term
|
Definition
-Nausea, vomiting, staggering, hindleg weakness in dogs and cats exposed to freshly sprayed plants
-not teratogenic or carcinogenic
-strongly attached to soils and organic water—no leaching into water |
|
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Term
|
Definition
-triazolopyrimidine compounds (bromacil, terbacil)
-phenyl urea compounds (diuron, fenuron)
-polycyclinc alkanoic acids (diclofop, fenoxaprop, fenthiaprop)
-sulfonylurea compound ‘escort’-metsulfuron methyl (chlorsulfuron, sulfometuron) |
|
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Term
| Triazine, Methylthiotrazine Compounds |
|
Definition
(atrazine, cyanazine)
-Deaths have been reported in sheep and horses grazing triazine-treated pastures 1-7 days after spraying.
-30 mg of atrazine/kg for 36-60 days were lethal to sheep |
|
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Term
|
Definition
Arsenicals
-EPA does not register because of livestock losses, environmental persistence, carcinogenesis
-single toxic oral dose for cattle and sheep is 22-25mg/kg body wt |
|
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Term
|
Definition
Livestock poisoned after ingestion of treated plants and from accidental consumption of Feed-mistakenly as salt!
-lethal dose is 1.1g/kg body wt for cattle
-hemolysis and methemoglobin
Tx: repeated doses of methylene blue |
|
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Term
| 5 most common toxins in dogs |
|
Definition
Anticoagulant rodenticide
Chocolate
envenomation
NSAIDS
Human prescription drugs |
|
|
Term
| 5 most common toxins in cats |
|
Definition
Topical insecticides
Toxic plants
Ethylene glycol (**treat w/in 3 hours!!)
Acetaminophren
envenomation |
|
|
Term
| Anticoagulant Rodenticides |
|
Definition
Warfarin-like (antag vit K, factors II, VII, IX, X)
-takes 1-7 days to see CS: dyspnea, coughing, hemoptysis, lethargy, anorexia, lameness, abdominal distension, bleeding, joint swell
TX: gastric decontamination, vit K supp, recheck Prothrombin Time in 48 hrs (tests factor VII). Relapse is common |
|
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Term
|
Definition
-not anticoagulant (inhibit CNS ATP prod)
-takes CNS signs 1day-2wks: acute (seizures, death), Chronic (ascending paralysis)
Tx: early GI decontamination
Supportive care: gingko, seizure prophylaxis, cerebal edema (mannitol) |
|
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Term
| Cholcalciferol Rodenticides |
|
Definition
-Vitamin D3 (hypercalcemia)
-CS in 36 days (lethargy, nausea, PU/PD)
TX: NaCl Diuresis, furosemide, corticosteroids, bisphosphonates
If you see it: clean out GI (vomit, charcoal) |
|
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Term
|
Definition
In cats, treat in 2-3 hrs
-it’s converted to a toxic metabolite
Sources: antifreeze, photography chemicals, solvent in paints
LD50 Cats: 2-4mlkg, t1/2=2-5 hrs
LD50 Dogs: 4-5mg/kg, t1/2=10hrs
3 phases: 1. CNS (ataxia, depress, nausea), 2. Cardio (tachypnea, tachycardia), 3. Renal (nausea, **azotemia, isosthenuria, oliguria)
**permanent kidney damage |
|
|
Term
| Ethylene glycol diagnosis |
|
Definition
Increased serum osmolality
-<3hrs to 48hrs
Serum ethylene glycol levels
-<3hrs-24-48hrs
Increased anion gap metabolic acidosis
-2-3hrs and beyond
Calcium oxalate crystaluria
-3-6hrs to 72 hrs
-hypocalcemia and hypothermia |
|
|
Term
| Ethylene glycol treatment and background |
|
Definition
Topical and gastric decontamination, IV fluid diuresis, inhibit metabolism***
Historical tx: competitive substrate for alcohol dehydrogenase, req intensive patient monitoring.
ENHANCES EG side effects: osmotic diuresis, serum hyperosmolality, CNS and resp depression |
|
|
Term
| Fomepizole 4-methylpyrazole (4-MP) |
|
Definition
Tx: for ethylene glycol
Potent inhbitor of alcohol dehydrogenase
Fewer side effects |
|
|
Term
|
Definition
Methyxanthines (theobromine, caffeine)
CS: restless, mm tremors, seizures, cardiac effects
LD50- .75-1.3oz/kg baking
-9x methyxanthines level of milk chocolate |
|
|
Term
|
Definition
Snail/slug killer
Liquid or meal(garden run off water common source)
CS: convulsions, hyperthermia (shake and bake)
TX: gastric decontamination (emesis, charcoal, enema), control convulsion, IV fluid |
|
|
Term
|
Definition
Pennies. Min tox dose: 2
CS: vomiting, diarrhea, anorexia, depression
Dx: hemolytic anemia, azotemia, inc liver enzyme, zinc level high
Tx: removal, chelation therapy-Ca EDTA |
|
|
Term
|
Definition
Moldy corn and peanuts
Fatal hepatitis in dogs
Tx: supportive care: SAMe, VitE |
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Term
|
Definition
Sugar subsititude
Rapid insulin release (hypoglycemia, hypokalemia)
CS: weakness, ataxia
Liver failure reported |
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Term
|
Definition
Nsaids: aspirin, ketoprfen, aleve
Acetaminophren: Tylenol
Tox b/c of failure to metabolize and size diff between humans and sm animals
Most common: carprofen |
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Term
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Definition
Decrease PGE, Gi ulceration/perforation, acute renal failure.
Tx: gastric decontamination (vomit, charcoal), monitor urine output, monitor signs of perforation/peritonitis |
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Term
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Definition
Prevention/client Ed
GI cdecontamination
Glutathione precursors (acetylcysteine)
Vit C (converts methehmoglobin to hemoglobin)
Supportive care |
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Term
|
Definition
Primarily cats
Renal damage
Tx: GI decon. 48 hrs diuresis
DON’T WAIT |
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Term
| Anuric/Oliguric Renal Failure Treatment |
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Definition
Fluid loading-central catheter
Careful monitoring (resp rate, ausculation, urine output)
Drugs: furosemide, mannitol, dopamine
Dialysis |
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Term
|
Definition
OTC flea and tick—overdose small and yng animals
Misuse of insecticides…dips and sprays, concentrated products |
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Term
| Organophosphates/carbamates |
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Definition
CS: CNS stim (seizures, ataxia, anxiety), Muscarinic signs (dyspnea, lacrimation, salivation, urination, defication), nicotinic activity (facial twitch, mm tremors, weakness, paralysis)
tx: Topical overdose…remove by bathing
Ingestion: GI decontamination
Symptomatic/supportive: atropin, diazepam, 2-PAM, iv fluids |
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Term
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Definition
Topical insecticide
Mech: alpha1&2 R: bradycardia, vasoconstric, hyperglycemia, GI stasis
CS: vomiting,s eizures, sedation, ataxia
Tx: iv fluids, GI and topical decontamination, Atipamizole: alpha R antag. |
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Term
| Antidepressant Drug Intoxication |
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Definition
| CS: CNS stim (seizures, ataxia, anxiety), Muscarinic signs (dyspnea, lacrimation, salivation, urination, defication), Nicotinic activity: facial twitching, mm tremors, weakness, paralysis |
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Term
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Definition
| Energy or elementary particles that can propagate through air and transfer energy to matter. Energy in Transit. |
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Term
|
Definition
| Radiation is of sufficient energy to eject electron |
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Term
| Types of ionizing radiation |
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Definition
| Electromagnetic, particulate radiation |
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Term
| Electromagnetic Radiation |
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Definition
|
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Term
|
Definition
| Electrons, protons, neutrons, z particles, heavy charged particles |
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Term
| Biologic effects of radiation |
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Definition
| DNA damage, mitotic death. Early effect in the skin bc it is rapidly dividing. Cancer. |
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Term
| Radiation units - Roentgen |
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Definition
| Roentgen - a unit for measuring the amount of gamma or xrays in air. |
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Term
| Radiation units - absorbed dose |
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Definition
| Energy deposited by radiation in mass of material at location of interest. Rad, Gray, joule/kg |
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Term
| Early lethal effects of radiation |
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Definition
| Cerebrovascular syndrome, GI syndrome, hematopoetic syndrome. All of these syndromes may be preceded by the prodromal radiation syndrome |
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Term
| Cerebrovascular syndrome (incapacitation syndrome) |
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Definition
| Death within hours. Symptoms vary with species and dose. Pathogenesis unclear. |
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Term
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Definition
| 3-8 Gy. Destruction of bone marrow stem cells leads to depletion of functional RBC, WBC and platelets. No signs until attrition of functioning cells. |
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Term
| Lymphocyte response to radiation |
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Definition
| Very sensitive to irradiation. Causes apoptotic death. Salivary and lacrimal cells behave similarly. |
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Term
| Hematopoetic Syndrome: Symptoms and pathogenesis |
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Definition
| Chills, fatigue, brusing, oral ulceration and epilation. Can get infections and hemorrhage. Death usually occurs before anemia. |
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Term
| hematopoetic syndrome treatment |
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Definition
| 4-5 Gy: Observation/symptomatic. > 5 Gy: isolation, antibiotics and supportive care. 8-10 Gy: bone marrow transplant? |
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Term
| Which animal is markedly sensitive to whole body irradiation? |
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Definition
| Burros. Extensive subarachnoid hemorrhage and edema. Vasculitis, meningitis, congestion, perivascular hemorrhage. |
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Term
| What does relative biological effectiveness (RBE) reflect? |
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Definition
| The fact that some types of radiation are more efficient than others in producting biological effects. The Q-factor aproximates RBE. |
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Term
| What is Radiation Protection Equivalent Dose? |
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Definition
| Combines physics (absorbed dose) with biology (RBE) in an attempt to estimate injury. Measured in rem (~rads) or Sieverts (~Gy) |
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Term
| Radiation vx radioactivity |
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Definition
| Radioactivity is spontaneously emmiting unstable atoms. Radiation is the energy or particles that are released during radioactive decay. |
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Term
| What gas gives us the most background radiation (esp in Colorado?) |
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Definition
|
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Term
| What national groups whatch over radiation safety? |
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Definition
| International commision of radiation protection, National council on radiation protection and measurements, DOE, NRC |
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Term
| What are the occupational radiation limits? |
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Definition
| Stochastic (cancer): 5 rem/yr (50 mSv). Lifetime dose should not exceed years in age times 1 rem. |
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Term
| Radiation limits of minors? |
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Definition
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Term
| Radiation limits of fetus (declared)? |
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Definition
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Term
| Effect on fetus for perimplatation (0-9 d), organogenesis (10d - 6wk), and fetal period(6wk - term). |
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Definition
| embryonic death, teratogenesis, growth/mental retardation. |
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Term
| Radiation effects on an embryo are NOT observed below ___ rem. |
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Definition
|
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Term
| What are the doses that the radiology personnel at the VTH get per year? |
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Definition
| Large animal: 1.8 rem. Fluoroscopy: 0.25 rem. Other diagnostic machines: 0.05 rem. Other clinicians, students 50 mrem. |
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Term
| Radiation badges: type used most often? |
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Definition
| Aluminum oxide sandwiched in plastic and sealed in light tight covering. |
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Term
|
Definition
| As low as reasonably achievable. |
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Term
| What are the employer responsibilities for radiation safety? |
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Definition
| Registration with state, certified inspection, warning signs, provide personnel dosimeteres, provide employee training, access to individual records |
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Term
| Employee responsibilities? |
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Definition
| Become familiar with rules, follow them, notify of concerns. |
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Term
| In vet med most toxicities are _____, but in humans they are usually chronic. |
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Definition
|
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Term
| What samples would you take from an animal you suspect has a toxicity? |
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Definition
| Live: Blood, serum, urine, vomit. Postmortem: feed, stomcah contents, eye, liver, kidney, brain, hair, fat (wrap in aluminum foil not plastic) |
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Term
| Mercury: What form is absorbed? |
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Definition
| Ionized form of Hg+ or Hg++ (8-10%) or bacteria can tranform to methyl mercury which is lipid soluble and abosorbed 80-90%. |
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Term
|
Definition
| treated grain, wood pulp, felt industry, gold mining, Hg in thermometes, electrical devices, fluorescent lamps, physical chem labs. In wildlife near military bases. |
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Term
| Target tissue of mercury? |
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Definition
| nervous, kidney, cardiovascular, GI, hematopoietic |
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Term
| Clinical sings of mercury intoxication? |
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Definition
| Motor disturbance, blindness, cerebral development, GI problems |
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Term
| Diagnoses of mercury intoxication? |
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Definition
| If chronic test the hair. If acute test blood, urine, liver, kidney. PM will see gastric ulcers, tubular necrosis, and MeHgs will cause crebellar hypoplasia. |
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Term
| Tx for mercury intoxication? |
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Definition
| Give egg white (lots of SH) and charcoal, followed by succimer. Not much you can do from chronic cases. |
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Term
|
Definition
| Mainly found as an oxide in insecticides, herbicides, treated wood and in well water in Nevada. |
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Term
| Target tissue and mech of action of arsenic? |
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Definition
| Will bind with lipoic acid (in the TCA cycle) and effect energy metabolism. Tissues with high oxidative energy (actively dividing cells) are targeted. Intestinal epi, epidermis, kidney, liver. |
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Term
| Clinical signs of arsenic intoxication? |
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Definition
| Abdominal pain, ataxia, watery diarrhea, dehydration. |
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Term
| Diagnoses of arsenic intoxication? |
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Definition
| History, urine and liver As levels, hair if chronic. |
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Term
| Treatment for arsenic intoxication? |
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Definition
| GI detox, dimercaprol (british anti-lewisite, lots of SH groups), or the newer succimer. |
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Term
|
Definition
| Batteries, fishing weights, lead based paints, lead shot, pastures near lead smelters, grease, leaded gas. |
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Term
|
Definition
| The metallic lead isn't toxic unless it is ingested. It reacts with acid to form Pb++ wich will take the place of Ca++. Absorbed from the GI tract by active transport. |
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Term
| Target tissues and mech of action of lead? |
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Definition
| CNS mostly, hemolyphatic system, GI. Will bind to RBC membranes and accumulate in soft tissues. Binds to the sulfhydryl groups, effects RBC formation. When chronic it will accumulate in bone. |
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Term
| Clinical signs of lead toxicity? |
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Definition
| Mostly CNS: blindness, aggression, head pressing, circling, roaring, anorexia, anemia. |
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Term
| Diagnoses of lead toxicity? |
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Definition
| History with clinical signs, immature RBCs with basophilic stippling, blood and kidney lead levels, radiography for lead objects in GI tract. Need to differentiate bw PEM and water deprivation. |
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Term
| Treatment for lead toxicity? |
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Definition
| Remove any lead from GI tract. Give Ca-EDTA or succimer. |
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Term
| What post mortem changes will you see in an animal with lead toxicity? |
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Definition
| Rumen: laminar cortical necrosis. Degeneration and necrosis of renal tubular epitheliu. Intranuclear inclusion bodies. In waterfowl, mm wasting and Pb shot in gizzard. |
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Term
|
Definition
| Something deliberately added. |
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Term
| What is a feed constituent? |
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Definition
|
|
Term
| What is a feed contaminant? |
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Definition
| Unintended substance in the feed. |
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Term
| What mineral will inhibit Cu absorption? |
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Definition
| Molybdenum. Sulfur will increase the problem. In monogastrics Fe and Zn can also inhibit Cu absorption. |
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Term
| Mechanism of Mo toxicity/Cu deficiency? |
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Definition
| Di, tri and tetra thiomolybdate will bind to Cu and make in unavailable. With dec in Cu there will be a deficiency in Cu based enzymes. |
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Term
| Clinical signs of Mo tox/Cu def? |
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Definition
| Chronic diarrhea, bleached/dull hair, spontaneous fractures, dec immune response, dec weight gain and milk production, ADR, CNS signs (swayback in lambs). |
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Term
| Diagnosis of Mo tox/Cu def? |
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Definition
| Low serum, liver Cu levels. Feed Cu:Mo <4 and S:Mo < 100:1 (want a ratio of 8:1 Cu:Mo and Mo should be more than 1/100th of S). Determine blood Mo. |
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Term
| Treatment of Mo tox/Cu def? |
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Definition
| Increase dietary Cu:Mo ~8, give CuO boluses PO (be careful with sheep so they do not get a toxic dose). |
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Term
|
Definition
| Feeding horse, pig, or poultry mineral to sheep or cattle. Putting sheep/cattle on pasture fertilized with pig or poultry manure. |
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Term
| Mech of action and target tissues of Cu toxicity? |
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Definition
| Cu will accumulate in the liver and cause damage to liver and RBCs. |
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Term
| Clinical signs of Cu toxicity in sheep? |
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Definition
| Hemoglobinuria, icterus, anoxia, death. |
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Term
| Diagnoses of Cu toxicity? |
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Definition
| Measure kidney and liver Cu values. Post mortem will see kidney gunmetal blue, liver swollen, friable with fibrosis in portal areas. |
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Term
| Treatment of Cu toxicity? |
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Definition
| Feed a Cu deficient diet and add thiomolybdate to bind the Cu. |
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Term
|
Definition
| Pennies minted after 1982, galvanized surfaces, industrial/fumes. |
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Term
| Target tissues and mech of action of Zn toxicity? |
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Definition
| GI and RBCs. Mech is not well established, but will dec RBC enzymes causing direct damage to the RBC membrane. |
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Term
| Clinical signs of Zn toxicity? |
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Definition
| In dogs/cats: vomiting, diarrhea, depression, icteric, hemoglobinemia, hemoglobinuria. Birds: depression, anorexia, weight loss, fluffed feathers, seizures. |
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Term
| Diagnoses/PM findings of Zn toxicity? |
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Definition
| Serum Zn measured with royal blue tubes, check for regen hemolytic anemia, basophilic stippling, heinz bodies, nucleated RBCs. PM will see hepatic heosiderin, hepatocellular necrosis. |
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Term
| Treatment of Zn toxicosis? |
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Definition
| Remove foreign object from GI, give Ca-EDTA to birds, supportive therapy, blood transfusion. |
|
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Term
|
Definition
| water, plants from high sulfur soils, molasses based diets, corn gluten. |
|
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Term
| Target tissue and clinical signs of sulfur toxicity? |
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Definition
| CNS: blindness, anorexia, head pressing, recumbency. |
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Term
| Mech of action of Sulfur? |
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Definition
| Will be reduced by rumen bacteria to sulfide (H2S, HS-) and get absorbed into blood or lungs. It inhibits cytochrome system and will dec energy production. |
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Term
| Diagnoses of Sulfur toxicity? |
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Definition
| Determine water SO4 and feed S levels, measure rumen gas cap S. Differentiate between Pb toxicity and H2O deprivation. |
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Term
| Treatment for sulfur toxicity? |
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Definition
| Supportive, dec S intake, feed roughage and thiamine. |
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Term
| Postmortem findings in sulfur toxicity? |
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Definition
| May smell H2S from rummen (rotten egg), rumen contents may be black, PEM lesions of the brain. |
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Term
| What are sources of salt toxicity? |
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Definition
| Brine water, high dietary salt with poor or inadequate H2O, restricted water intake (most common) from frozen water, failure of water system or neglect. |
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Term
| Mech of action of salt toxicity? |
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Definition
| Increased serum Na+ leads to inc in brain and CSF Na+. Dec in brain glycolysis, energy. Na will be trapped in the brain and CSF. |
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Term
| Target tissue and clinical signs of salt toxicity? |
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Definition
| CNS: blindness, aimless wandering, head pressing, circline, depression, weakness. |
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Term
| Diagnosis of salt toxicity? |
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Definition
| History with excessive Na intake or limited water intake, dehydration, high serum/CSF Na. Need to differentiate bw PEM and Pb toxicity. PM: cerebral edema, high brain and eye Na. |
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Term
| Treatment for salt toxicity? |
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Definition
| Rehydrate slowly over 48-72 hrs. Give IV hypertonic saline solution to reduce cerebral edema. |
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Term
|
Definition
| Feed additive in TMR in increase rate of growth/fattening. Also in liquid supplements/lick tanks. |
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Term
| Target tissues and mech of action of NPN/Urea? |
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Definition
| Rumen and CNS. Urea will overwhelm the liver, so ammonia is increased in blood and brain (neurotoxic). Will decrease a ketoglutaric acid, TCA cycle, so less ATP, so more anaerobic metablism producing lactate. |
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Term
| Clinical signs of NPN/Urea? |
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Definition
| Uneasiness, mm/skin tremors, mm weakness, abdominal pain (colic). |
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Term
|
Definition
| History, rumen pH>8, dieary urea analysis, rumen fluid, vitrous fluid, serum NH3. |
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Term
|
Definition
| Infuse the rumen with vinegar/acetic acid or cold water. Mainly prevent! Feed <33% of total N as NPN and slowly acclimate to NPN. Don't feed it with a full roughage diet. |
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Term
| Mech of ionophore toxicity? |
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Definition
| Hydrophobic molecules that bind cations (Ca,Mg,Na,K). They form lipid-sol complexes that are transported across membranes resulting in cellular imblance of cations. |
|
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Term
|
Definition
| growth promotants or coccidiostats. Ie monensis |
|
|
Term
| Source of toxic dose of ionophores? |
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Definition
| Result of mixing error, consumption by non target species, careless storage of premixes. |
|
|
Term
| Toxicokinetics of ionophores? |
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Definition
| High bioavailability, widely distributed, extensively metabolized, excretion via biliary elimination, short half life. |
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Term
| Clinical signs of ionophore toxicosis? |
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Definition
| Most ass with dec ATP production. Anorexia, sweating, colic, hypotension, recumbency, death. |
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Term
| Treatment for ionophore toxicity? |
|
Definition
| Activated charcoal, fluids, Se and Vit E. Poor prognosis. |
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|
Term
| Diagnosis of ionophore toxicity? |
|
Definition
| Clinical signs, clin path results, pathologic lesions, ionophore conc in feed and tissues. |
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