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483 Cards in this Set
- Front
- Back
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what is the definitiv difference between toxicant and toxin
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toxicant=poison
toxin=poison from a biological source |
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Toxicity is the poisoning of a animal.
True or false? |
False
Toxicity is the relative potency of a toxicant Toxicosis is poisoning |
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The science of poisons, including chem properties and\
ID and bio effects |
Toxicology
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any subsance, harmful or not, that is foreign to the body
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Xenobiotic
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A pathalogical cndition that results from exposure to a toxicant
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toxicosis
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The relative potency of a toxicant
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Toxicity
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total amt of toxicant received by an animal
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dose
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amount of toxicant per unit animal weight
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dosage
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dose above which effects can be detected
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threshold dose
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the toxic effects become more severe as the dose increases
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Graded response
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LD50
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dose likely to cause death in 50% of a given spp/age/sex group
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What are the 10 most common causes of poisoning in dogs?
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Ibuprofen, Chocolate, Ant/Roach Baits, Rodenticides, Acetominophen, Pseudoephedrine, Thyroid hormones, Bleach, fertilizer
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What is THE most common cause of poisoning in cats?
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spot on permethrins
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Define toxicokinetics
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how xenobiotics are absorbed, distributed, metabolized, and excreted in a biological system
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Which part of biotransformation are cats lacking in?
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Glucoronidation
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What step of biotransformation are pig lacking in?
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Sulfation
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What step in biotransformation are dogs deficent in?
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Acetylation
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Explain enterohepatic recirculation?
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absorbed from SI--> goes to blood stream--> liver--> bile--> excreted into SI--> absorbed from SI and back around
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What is first order elimination?
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a constant rate of elimination is achieved per unit time
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What is zero order elimination?
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plasma concentration vs unit time is not proportional, saturation kinetics are involved
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Define antidote
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a remedy or other agent used to neutralize or counteract the effects of a poison
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what is a chemical chelator?
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a chemical/metal antidote to a poison in which bind to the toxicant to increase excretion
are usually nephrotoxic |
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How does a pharmacolgical antidote work?
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antagonizes or competes at the receptor site
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What is a functional antidote?
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Basically supportive care
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During what time period after poison ingestion are emetic agents most useful?
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usually 30-90 minutes post-ingestion
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When should you NOT use an emetic agent?
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animal has ingested a caustic agent/petroleum distillate, in species that can't vomit, asympotamtic animals, with Hx of seizures cardiac dz, recent abdominal Sx
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Which animals canNOT vomit?
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Rodents, Rabbits, Horses, Ruminants, Avians and Reptiles.
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Through what mechanism does Hydrogen Peroxide act as an emetic?
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local GI irritation
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Through what mechanism does Apomorphine act as an emetic?
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centrally acting
mediated through the dopamine receptorsin the CRTZ |
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What is a possible side effect of apmorphine?
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CNS depression
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What is a specific reversal agent of apomorphine'sCNS effects?
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Naloxone
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Will Naloxone reverse the vomiting effects of Apomorphine?
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NO
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What is a good choice of drug to induce emesis in cats?
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Alpha 2 agonists: Xylazine
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What type of substances can activated charcoal bind?
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large nonpolar substances
NOT useful for small polar or ionized particles. NOT for heavy metals. Re-administer after4-6 hrs if poison undergoes enterohepatic circulation |
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Will activated charcoal work against heavy metals?
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NO
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What is the best substance for dermal decontamination?
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liquid dishsoap
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What clinical signs can be mistaken for seizures?
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trembling, tremors, Sycope
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What are the top differenials for seizures?
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Toxicity, Encephalitis/meningitis, Trauma, Metabolic (hepatic encephalopathy, hypoglycemia), Neoplasia, Epilepsy
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What is the number one cause of seizures?
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Epilepsy
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Are episodic seizures common with toxicosis?
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NO
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What are the drug of choice for seizures?
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Benzodiazepines
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Strychnine is an ingredient in which household product
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pesticides
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What is the main species affected by strychnine poisoning?
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dog
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What is the toxic dosage for strychnine in dogs?
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0.75 mg/kg
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What is strychnines mechaism of action
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competitive reversible inhibition of NT glycine a Renshaw cell
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What is strychnine' general Mechanism of action?
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interferes wih POST-synpatic inhibition in the spinal cord and medulla leading to uncontrolled reflex activity of extensor muscles=rigidity
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Where is strychnine absorbed in the body?
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intestines
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How is strychnine metabolized?
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Liver
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How is strychnine excreted?
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Kidneys
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What are the clinical signs of strychnine toxicosis?
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anxiety, rigidity, violent tonic to titanic seizures, Sawhorse stance
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What is the actually cause of death due to strychnine toxicosis?
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respiration inhibition, tissue anoxia and exhaustion
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How do you diagnose Strychnine poisoning?
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Cyanosis, evidence of a struggle
Analysis of stomach contents, lavage fluid, liver or urine |
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How would you treat strychnine poisoning?
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control the seizures and supportive care: artificial respiration, dark quiet place, gastric lavage, multicombination seizure drug tx
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What kind of environment might you expect water hemlock to be found?
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moist, rich soil
ditches, streams, edges of pastures |
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Which species would you expect to be affected by waterhemlock poisoning?
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Livestock and people
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Which part of the water hemlock is the most poisonous?
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young leaves andf roots
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What is the toxic agent of water hemlock?
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Cicutoxin
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What are the clinical signs of waterhemlock poisoning
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salivation, muscle twitching and violent convulsions
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What is the general onset time of water hemlock poisoning
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rapid
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What is one of the most toxic plants in the US?
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waterhemlock
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How can you distinguish water hemlock from poison hemlock?
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in waterhemlock the veins go to the notches
in poison hemlock veins go to the tips |
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what are two plants that may be confused with water hemlock?
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wild parsnips and carrots
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What are the key points in diagnosing water hemlock poisoning?
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Hx: evidence of exposure or look for the plant in pasture
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What is the best treatment if you catch water hemlock poisoning early?
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rigorous GI decontamination, seizure control
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What is the prognosis for waterhemlock poisoning?
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poor
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What is the source of tetanus toxin?
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Clostridium tetani
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Where can you generally find the bacteria responsible for tetanus toxin production?
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feces, soil
it is common might be found in contaminated puncture wounds, castration, tail docking dehorning, fight injuries |
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Under what conditions do Clostridium tenani produce their toxin?
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anaerobic
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Which species are susceptible to tetanus?
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all species are susceptible
Horses are extra sensitive dogs and cats are a bit more resistant |
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What is the mechanism of action for tetanus toxin?
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prevents release of glycine
inhibits the inhibitory NTs leading to stimulation Retrograde movement along the axon to the wound |
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What are the clinical signs of tentanus?
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sustained contractions without twitching
stiffness and rigidity convulsions Sawhorse stance Lockjaw or Trismus Sardonic grin |
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What generally causes death due to tenanus poisoning?
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asphyxiation
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What are the treatment options for tentanus toxicity?
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Muscle relaxors (Methocarbamol)
diazepam and acepromazine Antibiotics and Antittoxin |
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Can tetanus antitoxin reverse the clinical signs?
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no
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How do you generally confirm a diagnosis of tetanus?
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based on clinical signs and history of exposure
No lab changes are expected |
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What common household product would you expect to find the toxin Metaldehyde?
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snail and slug baits
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What is the poisonous substance found in snail and slug baits?
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Metaldehyde
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Which species are susceptible to Metaldehyde poisoning?
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all species are susceptible
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What is the lethal dose of metaldehyde in a dog?
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100 mg/kg
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Which US region is most likely to experience higher numbers of metaldehyde poisoning?
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California and Oregon
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What is the proposed mechanism of action of metaldehyde?
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acetaldehyde production inteferes with GABA inhibitory NTs leading to reduced serotonin and NE
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What are the common clinical signs seen with metaldehyde poisoning?
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Fast onset within 3 hours
salivation, restlesness, anxiety Tremors followed by convulsions acidosis, hyperthermia deatth |
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What are the clinical signs of metaldehyde toxicosis in horses?
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sweating, tremors, diarrhea, colic
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What are the clinical signs of metaldehyde toxicosis in ruminants?
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ataxia and tremors
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There is a distinctive way to recognize metaldehyde poisoning?
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it has a distinctive odor of formaldehyde
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How do you diagnose metaldehyde poisoning?
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distinctive formaldehyde odor
submit stomach contents or lavage fluids |
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What is best for metaldehyde poisoning?
A hands off approach or aggressive treatment measures? |
Aggressive treatment measures
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How would you treat metaldehyde poisoning?
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activated charcoal and cathartics
enemas supportive care gastric lavage seizure control may show relay toxicity |
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which toxin is also used as a chemotherapuetic agent?
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5 FU
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which toxin is a pyrimidine antimetabolite?
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5 FU
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What is 5 FU's mechanism of action?
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interferes with RNA function in actively dividing cells
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Where are 5 FU's primary cell targets?
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GI cells, bone marrow cells
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What is the LD 50 of 5FU in dogs?
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30 mg/kg
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Most common clinical signs of 5 FU toxicosis?
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Seizures, Vomiting, Death/Euthanasia. Lethargy, respiratory distress
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Which companion animals species is more susceptible to the effects of 5FU
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cats
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If an animal initially survives the first 48 hours of 5 FU toxicosis, what system/clinical signs must be monitored for?
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Bone marrow suppression 5 days to 3 weeks later leading to severe neutropenia
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What are the protocols for treatment of 5 FU toxicosis?
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Decontamination via emesis (if less than 30 min), lavage and activated charcoal. GI protectants, antiemetics (cerenia), Abxs, seizure control, and monitor WBCs
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What is the mechanism of action of methylxanthines?
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antagonism of adenosine, inhibitory NT, increases Ca 2+ entering the cell, which inhibits sarcoplasmic reticulum, inhibition of cellular phosphodiesterase which increases cell signalling and stimulates the second messenger system, and stiumulates the sympathetic NS increasing levels of catecholamins
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What is the effect of methylxanthine on cellular signaling?
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it increases cell signaling and stimulatesd the second messenger system of the beta adrenergic receptors.
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What is the effect of methyxanthine on sarcoplasmic reticulums?
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It increases the calcium entering the cell which inhibits sequestration of calcium by the sarcoplasmic reticulums
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What is methylxanthines effect on the sympathetic NS?
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it stimulates the sympathetic NS leading to increased release of catecholamines.
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What common substances is the potential toxin, methylxanthine, found in?
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caffeine!
tea, coffee, cocoa beans, chocolate, OTC meds, herbal remedies |
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Where can methylxanthine be absorbed rapidly in the body?
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mouth
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Where is methylxanthine metabolized in the body?
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liver
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How is methylxanthine eliminated?
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in bile and urine
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What is significant about methylxanthines's elimination in bile?
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it has enterohepatic recirculation
* it also can be reapsorbed through the bladder wall |
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Which methylxanthine containing compound may actually take a long time to be absorbed?
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Chocolate is absorbed slowly, may take awhile to see effects.
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What is the general amount of methylxanthine needed to induce toxicity in dogs and cats?
small, med, or large amt |
large
100+mg/kg |
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What are the clinical signs of methylxanthine ingestion and toxicosis?
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vomiting and diarrhea
PD Restlessness, hyperactivity, ataxia, tremors, seizures tachycardia, PVCs, tachypnea, hypertension, arrhythmias, hyperthermia |
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How do you diagnose a potential methylxanthine toxicosis?
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often Hx and clinical signs
may look at serum, urine, liver kidney, fat stomach contents |
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What is the length of time methylxanthines can remain stable in serum?
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14 days
(plasma for 4 months) |
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What is the treatment protocol for methylxanthine toxicosis?
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decontamination (emesis)
control the signs and symptoms empty the bladder frequently supportive care |
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What should you do if you believe a dog has ingested chocolate?
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get them to vomit it up, it takes a long time to absorb and emesis is generally rewarding
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When an animal has ingested chocolate in the form of baked goods, which organ functions must be monitored?
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pancreas-pancreatitis
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Which household foodstuffs contain the largest amounts of methylxanthines and whose ingestion are most concerning?
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bakers chocolate
cocoa powder cocoa beans coffee beans |
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What must you be concerned about with ingestion of chocolate covered raisins in addition to methylxanthine toxicosis?
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raisins can cause kidney failure
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What must you be concerned about with a coingestion of chocolate macadamia nuts?
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tremors and weakness
in addition to methylxanthine poisoning |
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Caffeine poisoning should be treated more intensely than chocolate ingestion? T or F
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F
caffeine and chocolate ingestion have the same treatment protocols. |
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What is the toxic compound in Brazilian cocoa?
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Guarana
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What effects will Guarana show in the body?
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Positive ionotropic and chronotrophic effects on the heart
cerebral vasoconstriction renal and GI vasorelaxation |
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Does guarana have a small or large lethal dosage?
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small
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What are the clinical signs of guarana toxicosis?
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vomiting, hyperactivity, restlessness, PU/PD
tachycardia, arrythmias, muscle tremors, ataxia, seizures |
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What is the treatment approach for guarana toxicosis?
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early decontamination
control arrhythmias control tremors and seizures urinary catheter'IV fluids and supportive care |
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What are some common household items that might be responsible for sodium toxicosis?
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salt containing meds
brine, hypertonic sodium solutions feed mixing errors salt water as an emetic ocean water bullion cubes Play doh...homemade salt shakers |
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How can an animal develop indirect salt toxicosis?
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dehydration
alteration of body water balance: ingestion of osmotic agents |
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What are some osmotic agents that can be responsible for indirect salt toxicosis?
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glycol containing substances
paintballs activated charcoal high sugar solutions dry wall |
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Describe how sodium is absorbed and distributed in the body
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sodium is rapidly absorbed orally
distributes throughout the body and passively diffuses into the CNS where it becomes trapped because it must be actively transported out |
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What is the mechanism of sodium toxicosis?
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Na inhibits glycolysis--> reduces ATP available for Na/K pump--> excess sodium builds up
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What is dangerous about rehydrating a salt toxocosis patient?
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Rapid rehydration of hypernatremia leads to cerebral edema
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List in order the species susceptible to salt poisoning from most to least susceptible
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cats<dogs<cattle<swine
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What is the unique pathology of salt toxicosis in swine?
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eosiniphilic vascular cuffing
eosinophilic meningeoencephalitis |
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What are the clinical signs of salt toxicosis in swine?
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restlessness, thirst, pruritis, aimless wandering, headpressing, seizures, death
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What are the clinical signs of salt toxicosis in cattle?
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ataxia, head pressing, blindness, tremors, seizures
NO eosinophilic cuffs Polioencephalomalacia |
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Is activated charcoal a good treatment option for sodium ion toxicosis? Why?
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No, not good for heavy metal, may lead to free water loss
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If it is chronic hypernatremia, can you rapidly bring the sodium levels down?
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NO
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If it is acute hypernatremia, can you rapidly bring the sodium levels down?
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yes
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What are the major issues associated with paintball ingestions?
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acid bas imbalances
electrolytes disturbancces neuro signs Hypernatremia* |
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How do paintballs cause their toxic effect?
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They are osmotically active and pull free water into the gut, so lead to loss of free water and rapid shifts of sodium levels
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Polyethelene glycol is a common ingredient of _____.
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paint balls
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Dipropylene glycol is a common ingredient of paint balls and causes ____.
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CNS depression and acidosis
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Propylene glycol, when ingested, causes ___.
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Low MW-> systemic signs,. CNS depression, liuver injury
High MW--> not absorbed and draw water into the gut leading to hypernatremic signs. |
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Glycerol and Sorbitol are both cathartics commonly found in ____.
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paintballs.
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What clinical signs do we expect with paint ball ingestion?
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vomiting, ataxia, disorientation, muscle fasiculations, tremors, occassionally diarrhea and seizures
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How would you treat paintball ingestions?
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emesis if >5 balls/20 lbs
lavage if larger amt monitor electrolytes and acid base status control seizures |
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Can you use activated charcoal for suspected paintball ingestions?
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NO, contraindicated
exacerbates osmotic effect |
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When testing for a suspected toxicosis where the substance is known...what other substance can trigger a positive result on an ethylene glycol test kit?
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paint balls...because they contain polyethelene glycol, glycerol, and dipropylene glycol
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What is the proposed mechanism of amphetamines and methamphetamines?
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enhances release and decreases upake of catecholamines and serotonin
Directly stimulates alpha and beta adrenergic receptors, dopamine receptors |
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Can amphetamines penetrate the BBB?
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yes, easily penetrate
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At what speed are amphetamines absorbed?
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very rapidly
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How are amphetamines metabolized and excreted?
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hepatic metabolism
renal excretion |
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Why is the acid base status of the patient important when considering an amphetamine poisoning?
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because the excretion of the drug is faster in acidic urine and much slower in alkaline urine
Ion trapping |
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What are the common signs of amphetamine toxicosis?
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Hyperexcitability
Mydriasis Tachycardia Hypertension Agitation Seizures |
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What is a common cardiac presentation of an amphetamine toxicosis?
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High BP but lower HR
because the body compensates to bring the HR down |
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What are the treatment options for amphetamine toxicosis?
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gastric lavage
activated charcoal cyproheptadine: serotonin antagonist beta blockers: for tachycardias urinary acidification |
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What drug class must be avoided with amphetamine poisoning?
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Benzodiazepines
use phenothiazines instead |
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What common household products can the toxin Psuedoephedrine be found in?
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decongestants and cold meds
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What is the ingestion size (small, med, large) needed to produce clinical signs with pseudoephedrine ingestion?
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very small dose
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Some systemic diseases put a patient more at risk for pseudoephedrine ingestion related death. Which are these?
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cardiac and seizure disorders
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all natural can be assumed to also mean non toxic.
T or F |
F
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What is the active ingredient of Ma Haung?
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Ephedra
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Where can the ephedra plant be found?
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desert regions of China and Mongolia
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What are the active portions of the Ephedra plant?
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young canes, dried rhizomes and roots
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What are the general times of onset of action and duration of activity for Ephedra?
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rapid onset (within 30 minutes)
long duration (36-48 hrs) |
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What are the clinical signs of Ephedra ingestion?
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stimulation signs
peripheral vasoconstriction cardiac stimulation increased BP, tachycardia Agitation and CNS stimulation: mydriasis, restlessness, tremors, seizures |
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What drug does Sida cordifolia resemble?
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Ma Huang
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What are the true medical uses of cocaine?
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Topical aneshetic
Tx Horner's syndrome |
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The active ingredient of the Coca leaf is _____.
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cocaine
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What two forms does cocaine come in?
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Hydrochloride salt
free base |
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What % of cocaine does crack contain?
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75-90%
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Where (in the body) can cocaine be absorbed?
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all mucosal surfaces
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Where is cocain metabolized? Excreted?
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metabolized in the liver
excreted in the urine |
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What is cocaine's mechanism of action?
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blocks reuptake of serotonin and NE
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What is an alkyloid?
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naturally occurring chemical compounds that contain basic nitrogen atoms.
Produced by many natural sources |
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Which toxins have we discussed that are considered alkyloids?
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Strychnine
Cocaine Caffeine Nicotine Morphine |
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What size of dose is required to see lethal effects of cocaine in dogs and cats?
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small doses
cat slightly more resistant than dog |
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What are the clinical signs of cocaine ingestion?
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Stimulatory effects
esp cardiac signs and hypertension |
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What treatment options should be implemented with cocaine ingestion?
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Control the seizures (diazepam, chloropromazine, barbituates)
Beta blockers for tachyarrythmias Fluids/electrolytes |
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Which drugs are considered psychotropic drugs?
|
serotonin
antidepressants SSRIs MOIs TCAs |
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What is serotonin's effect in the CNS? what is its common use?
|
inhibits excitatory neurotransmission in the CNS
Used as an anidepressant, for weight loss, anxiety, ADD |
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Describe Serotonin syndrome.
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when you have too much serotonin in the brain
leads to overstimulation of the serotonin receptors See a combo of CNS efffects, autonomic effects, NM effects |
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What are the CNS effects described in Serotonin Syndrome?
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dementia, disorientation, agitation, seizures
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What are the autonomic effects of serotonin syndrome?
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salivation, vomiting, diarrhea, hyperthermia, hyper/hypotension, mydriasis
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What are the Neuromuscular effects of serotonin syndrome?
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rigidity, hyperreflexia, ataxia, tremors,
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How should you handle a serotonin ingestion?
monitor or treat aggressively |
Serotonin syndrome is severe, and often life threatening.
It should be treated immediately and aggressively with close monitoring |
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What is the mechanism of action of L tryptophan?
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increased serotonin synthesis
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What is the mechanism of action of amphetamines and cocaine in regards to serotonin effects?
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increase serotonin release
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What are the autonomic effects of serotonin syndrome?
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salivation, vomiting, diarrhea, hyperthermia, hyper/hypotension, mydriasis
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What are the Neuromuscular effects of serotonin syndrome?
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rigidity, hyperreflexia, ataxia, tremors,
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How should you handle a serotonin ingestion?
monitor or treat aggressively |
Serotonin syndrome is severe, and often life threatening.
It should be treated immediately and aggressively with close monitoring |
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What is the mechanism of action of L tryptophan?
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increased serotonin synthesis
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What is the mechanism of action of amphetamines and cocaine in regards to serotonin effects?
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increase serotonin release and inhibit reuptake
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what is the mechanism of action of SSRIs and TCA in regards to serotonin?
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inhibit serotonin reuptake
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What is the mechanism of action of MAOIs in regards to serotonin?
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Increase serotonin release and inhibit serotonin breakdown
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What is the active ingredient of Griffonia simplicifolia?
|
5 HTP, which is converted to serotonin in the CNS
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What are some common SSRIs?
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Paxil, Prozac, Zoloft
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Which SSRI is most prone to be ingested by cats?
|
venlafaxine
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How long do the clinical signs of SSRI ingestion last?
|
days
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What are the expected clinical signs at low doses of SSRIs?
at high doses? |
Low dose-expect sedation
High dose-expect Serotonin syndrome signs |
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What are some commonly used MAOIs?
|
St. Johns Wort, Anipryl, Parnate, Nardil
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What NTs are likely to build up due to MAOI intake?
|
Serotonin, NE, Epi, Dopamine
accumute in the CNS |
|
|
Selegiline at its proper dose is used to treat ____ in dogs.
|
canine alzheimers
|
|
|
Selegiline at higher than its proper dose shows these clinical signs:
|
stereotypic behavior, dehydration, salivation, panting
|
|
|
What signs are associated with Serotonin Syndrome in dogs?
|
Seizures
Hyperthermia Diarrhea Depression Tremors Vomiting Ataxia Clinical Blindness |
|
|
What is a unique clinical sign associated with Serotonin Syndrome that is temporary?
|
Clinical Blindness
due to highly dilated pupils |
|
|
What is the speed of onset with Serotonin Syndrome?
|
rapid
|
|
|
What are the Tx options for Serotonin syndrome?
|
supportive care
Tx the seizures fluids to treat the hyperthermia and keep the animal hydrated |
|
|
What is an antidote for serotonin syndrome?
|
Cyproheptadine: a serotonin antagonist, but non-selective
|
|
|
What are the more lethal effects/signs of poor prognosis in serotonin syndrome?
|
DIC, rhabdomyaolysis, multiorgan failure
|
|
|
TCAs are antidepressants. What NT (s) are affected by their use?
|
serotonin, Dopamine, NE
|
|
|
What are some common TCAs?
|
clomipramine(Cloma calm), imipramine, doxepin, amitriptyline
|
|
|
What are some non-serotonin related SEs experienced with TCA use?
|
antihistamine effects
anticholinergic effecs |
|
|
How are TCAs metabolized and excreted?
|
*Enterohepatic recirculation-prolongs its half life
|
|
|
What are the CV effects associated with TCAs?
|
tachycardia, bradycardia, hypotension, cardiac arrythmias
|
|
|
How do you treat a suspected TCA ingestion?
|
activated charcoal
emesis only if right after ingestion with vet supervision only manage the CNS and CV signs |
|
|
How long will the symptoms of TCA toxicosis persist?
|
long time (up to 72 hrs)
|
|
|
What is the correct treatment to manage the CV effects of a TCA ingestion?
|
Sodium bicarb: to overcome the sodium blockade
|
|
|
Can you use Atropine to counteract the CV effects of TCAs?
|
NO
|
|
|
Atropine is a good choice to treat the CV signs associated with TCAs. T or F?
|
F
|
|
|
You should not use Atropine to manage the CV effects of TCAs. T or F
|
T
|
|
|
Antidepressant toxicoses all show similar clinical signs. It is important to perform clinical testing to determine the specific agent ingested before starting treatment. T or F
|
F, treat the patient, not the poison
|
|
|
You treat antidepressant toxicosis the same regardless of which agent was ingested. T or F
|
T, symptomatic tx always
|
|
|
What is the preferred seizure tx for antidepressant toxicosis?
|
Benzodiazepines
|
|
|
What is responsible for producing mycotoxins?
|
fungi
|
|
|
What crops are likely to be contaminated with mycotoxins?
|
cereals, wheat, rice, corn, barley, oats
|
|
|
Which species do mycotoxin affected crops affect the most?
|
poultry and pigs
|
|
|
What is responsible for Staggers Syndrome?
|
Tremorgenic mycotoxins
|
|
|
What is the timeframe in which you are likely to see signs after mycooxin ingestion?
|
within 7 days after grazing
|
|
|
What is responsible for producing mycotoxins?
|
fungi
|
|
|
What crops are likely to be contaminated with mycotoxins?
|
cereals, wheat, rice, corn, barley, oats
|
|
|
Which species do mycotoxin affected crops affect the most?
|
poultry and pigs
|
|
|
What is responsible for Staggers Syndrome?
|
Tremorgenic mycotoxins
|
|
|
What is the timeframe in which you are likely to see signs after mycooxin ingestion?
|
within 7 days after grazing
|
|
|
What is responsible for producing mycotoxins?
|
fungi
|
|
|
What crops are likely to be contaminated with mycotoxins?
|
cereals, wheat, rice, corn, barley, oats
|
|
|
Which species do mycotoxin affected crops affect the most?
|
poultry and pigs
|
|
|
What is responsible for Staggers Syndrome?
|
Tremorgenic mycotoxins
|
|
|
What is the timeframe in which you are likely to see signs after mycooxin ingestion?
|
within 7 days after grazing
|
|
|
What are the clinical signs of Staggers syndrome?
|
fine muscle tremors of the head and neck that worsen with stimulation
wide based stance, exaggerated movements |
|
|
What are the 3 grass associated staggers syndromes?
|
Bermuda grass
Dallis grass Ryegrass |
|
|
What are the treatment options associated with Staggers syndrome?
|
supportive care
restrict from suspected pastures |
|
|
What is the definition of a tremorgenic mycotoxin?
|
Compounds produced by molds capable of inducing muscle tremors
Alkyloid compound |
|
|
Presence of mold in pasture indicates mycotoxin is present
T or F |
False
Presence of mold does not indcate presence of mycotoxin |
|
|
What are the important absorption, metabolism, and excretion properties of mycotoxins?
|
readily absorbed
enterohepatic recirculation is possible can penetrate the BBB |
|
|
What is the mechanism of action of mycotoxins?
|
inhibit glycine/GABA
may lead to increase in ACh |
|
|
What is the preffered drug for tremor control in most cases?
|
Methcarbamol
|
|
|
What is the poisonous substance in gophr and mole bait?
|
zinc phosphide
|
|
|
What conditions are expected to produce rapid degradation of zinc or aluminum phosphide?
|
damp and/or acidic
|
|
|
What is formed when zinc phosphide comes in contact with the stomach?
|
phosphine gas
which is then inhaled or absorbed through the stomach lining |
|
|
What is relay toxicosis?
|
when the poisoning effect is transfered from prey to predator
|
|
|
What are the deletorious effects of zinc phosphide?
|
it can shut down respiration and disrupt oxidative phosphorylation by blocking cytochrome C
|
|
|
How does zinc phosphide affect species that can vomit vs species that can't?
|
species that vomit will show a higher LD50
|
|
|
Which toxin is a common problem with relay toxicosis?
|
zinc phosphide
Mole/gopher poison |
|
|
What are the signs of phosphine gas formation/ingestion?
|
rapid onset of severe respiratory distress, vomiting
abdominal pain in horses and cattle ataxia and weakness tremors and seizures |
|
|
What are the two main species commonly affected by zinc phosphide?
|
horses and dogs
|
|
|
What is a distinctive feature that can be used to identify zinc phosphide ingestion?
|
rotten fish or garlic odor to the vomitus or breath
|
|
|
What is the best way to diagnose zinc phosphide poisoning?
|
Hx and clinical signs, characteristic Odor
no characteristic lesions path of stomach contents may be useful |
|
|
What are the treatment options for suspected zinc phosphide ingestion?
|
induce emesis
liquid antacids to increase the stomach pH activated charcoal Seizure control Monitor for acidosis |
|
|
What treatment is counterindicated when considering emetics with a suspected zinc phosphide ingestion?
|
NO hydrogen peroxide
|
|
|
When treating a zinc phosphide case, when must you be concerned with personal and staff safety?
|
when you can smell the distinctive odor of garlicky rotten fish, you ARE being exposed
|
|
|
What safety measures must be taken when treating a zinc phosphide toxicosis case?
|
Must tx in a well ventilated area.
|
|
|
What is the most common route of lead absorption?
|
oral
|
|
|
How does age affect lead absorption?
|
young have higher absorption rates
|
|
|
When you are testing for lead it is important to know that led is bound to ____.
|
>90% bound to RBCs
|
|
|
Which blood product is needed when doing lead testing?
|
whole blood anticoagulant...because lead is bound to RBCs
|
|
|
How is lead distributed throughout the body?
|
bone-long term storage (lead lines, bone remodeling might release bound lead)
crosses BBB can enter milk |
|
|
What are the signs of lead toxicity in dogs?
|
GI and NS effects
colic, tense abdomen, whining, vomiting, poor appetite, hyperthermia, behavioral changes, paresis and incoordination Hysteria and Grand mal seizures |
|
|
What infectious agent can be confused for lead toxicosis?
|
canine distemper
|
|
|
What are the clinical sign associated with acute lead toxicosis in cattle?
|
Mosly neurological signs
staggering, muscle tremors, head bobbing, eyelid snapping, jaw chomping, bellowing, apparent blindness, head pressing, clonic tonic seizures |
|
|
What are the clinical signs associated with subacute lead toxicity in cattle?
|
usually GI and neuro
anorexia, grinding teeth, kicking at abdomen, rumen atony, constipation then diarrhea, blindness, staggering, hypersalivation, depression and lethargy |
|
|
How does the presentation of clinical signs dffer between acute and subacute lead toxicosis in cattle?
|
Acute-mainly Neuro signs
Subacute-mixed neuro and GI signs |
|
|
How can you successfully diagnose lead disease?
|
clinical signs
basophilic stipling of RBCs, anemia, nRBCs whole blood lead levels erythrocyte ALA-D activity erythrocyte porphirin levels |
|
|
What are the gross lesions associated with lead poisoning?
|
ruminants show corical laminar necrosis
horses show axonal degradation cats and dogs show cerebral edema waterfowl are emaciated, and have pale streaking in heart, brain edema, renal and liver necrosis |
|
|
What are the appropriate treatment options for lead toxicosis?
|
decontamination
control seizures supportive care chelation |
|
|
What is the antidote for lead poisoning?
|
chelation
bind and enhance the elimination of metals |
|
|
What is the action of a chelator?
|
bind and enhance the elimination of a metal
|
|
|
What is the potentially harmful side effect of chelator use?
|
nephrotoxicity
|
|
|
Which chelator is most often used in the treatment of lead ingestion in small animals?
|
chemet, DMSA
|
|
|
Cuprimine (D Penicillamine) is used for the treatment of ___.
|
lead toxicosis and copper storage diseases
|
|
|
Succimer (DMSA, Chemet) is a ______ used to treat lead, arsenic and mercury toxicosis.
|
chelator
|
|
|
Which chelator is useful in treating lead, arsenic and mercury toxicosis?
|
DMSA, Chemet
|
|
|
Which chelator is the LEAST nephrotoxic?
|
DMSA, Chemet
|
|
|
Non Protein Nitrogen toxicosis is due to ____ or _____.
|
ammonia or urea
|
|
|
What is the definition of a NPN?
|
any nitrogen source that is not present in polypeptide form
|
|
|
What is a common source of NPNs?
|
ruminant nutrition additive
can be urea, biuret, ammonium salts, ammoniated salts, ammonium or urea rations |
|
|
What is the mechanism of action of NPNs?
|
NH3 depletes enzymes needed to run the Krebs cycle
result is acidosis and decreased ATP |
|
|
What factors might increase the susceptibility of a patient to NPN toxicosis?
|
improper feeding mix, feeding unaccustomed animals, low energy and plane of nutrition, givine free access to palatable urea concentrate, high ruminal pH
|
|
|
Non Protein Nitrogen toxicosis is due to ____ or _____.
|
ammonia or urea
|
|
|
What is the definition of a NPN?
|
any nitrogen source that is not present in polypeptide form
|
|
|
What is a common source of NPNs?
|
ruminant nutrition additive
can be urea, biuret, ammonium salts, ammoniated salts, ammonium or urea rations |
|
|
What is the mechanism of action of NPNs?
|
NH3 depletes enzymes needed to run the Krebs cycle
result is acidosis and decreased ATP |
|
|
What factors might increase the susceptibility of a patient to NPN toxicosis?
|
improper feeding mix, feeding unaccustomed animals, low energy and plane of nutrition, givine free access to palatable urea concentrate, high ruminal pH
|
|
|
What are the clinical signs of NPN toxicosis?
|
onset 20 min to 4 hrs
uneasiness, tremors, dyspnea/achypnea, frequent urination or defecation, colic, bloat, regurg, ruminal atony, cardiac arrythmias, convulsions, death |
|
|
How effective is treatment of NPN toxicosis?
|
not very
unless caught early |
|
|
Which species is most likely to be affected by NPN toxicosis?
|
cattle
|
|
|
How would you diagnose NPN toxicosis?
|
rumen alkalosis/systemic acidosis
rumen ammonia > 80mg/dL whole blood or serum ammonia > 2 mg/dL feed analysis for NPN |
|
|
What is the cause of Bovine Bonkers?
|
ammonia Tx of forage
4 methyl imadazole |
|
|
What situations can lead to the development of 4 methyl imadazole in bovine feeds?
|
too much sugar
tx of higher quality hays high temps too much ammonia addded |
|
|
What does age have to do with Bovine Bonkers?
|
it goes in milk
often see the signs in calves not adults |
|
|
What are the common signs of Bovine Bonkers?
|
onset can be varied
trembling, ear twitching mydriasis ataxia wild running, excitability, seizures death |
|
|
How might you come to a Diagnosis of 4 methyl imadazole poisoning?
|
analysis of feed and Hx of exposure
|
|
|
What is the treatment for 4 methyl imadazole toxicosis?
|
remove suspect feed
seizure control sedation milk out dams |
|
|
What is the preferred seizure control drug for ammoniated feed toxicosis?
|
Acepromazine
|
|
|
Bovine Bonkers aka _____ is associated with 4 methyl imadazole.
|
Ammoniated feed toxicosis
|
|
|
T or F
ammoniated feed toxicosis may also be called Bovine Bonkers |
T
|
|
|
T or F
ammoniated feed toxicosis is due to NPNs in feed |
F
NPNs cause ammonia toxicosis |
|
|
T or F
Bovine Bonkers is associated with NPNs in feed? |
F
Bovine Bonkers is ammoniated feed toxicosis NPNs cause ammonia toxicosis |
|
|
How is lead excreted from the body?
|
unabsorbed lead is passed in the feces
Absorbed lead is passed in the urine accumulation can occur in the renal tubule epithelial cells |
|
|
What organ systems are primarily affected by lead ingestion?
|
Neuro, GI, hematologic, renal, and reproductive
|
|
|
Which essential ion does lead compete with?
|
Calcium
|
|
|
What neurologic effects does lead toxicosis cause?
|
acute encephalopathy
cognitive impairment demyelination of peripheral nerves |
|
|
What effects does lead have on the hematologic system?
|
shortened RBC lifespan
decreased energy metabolism in RBCs alteration of heme synthesis release of nRBCs |
|
|
How does lead affect the renal system?
|
accumulates in the renal tubule epithelial cells
leads to intranuclear inclusion bodies may be shed as a urine sediment |
|
|
How does lead affect the repro system?
|
leads to infertility in males and females and congenital anomalies
|
|
|
What are the 5 species most sensitive to lead toxicosis?
|
cattle, human, horse, dog, waterfowl
|
|
|
Is there an affect of age on lead ingestion?
|
young are more at risk b/c they have increased absorption and BBB is more permeable
|
|
|
T or F
Dietary deficiency can make an animal less sensitive to the effects of lead. |
False, more sensitive
|
|
|
What dietary deficiences might make an animalmore at risk to the effects of lead toxicosis?
|
Ca, Zinc, Fe, Vit D
|
|
|
What are fumonisins?
|
biotoxins produced by mold
|
|
|
What plant is most affected by fumonisins?
|
corn
|
|
|
Which species of mold produces fumonisins?
|
Fusarium spp
|
|
|
What weather conditions cause fumonisin damage to corn crops?
|
hot,dry weather
high humidity in storage |
|
|
T or F
All species that are experiencing fumonisin ingestion will metabolize it via enterohepatic recirculation? |
F, only swine
|
|
|
How are fumonisins excreted?
|
urine and feces
|
|
|
What is the general mechanism of action of fumonisins?
|
They are biologically similar to sphingosine, a constituent of sphingolipids in nerve tissue
Disrupt the synthesis of sphingosine |
|
|
What is the major fumonisin?
|
B1
|
|
|
What are the clinical signs of fumoninisin ingestion in swine?
|
PPE porcine pulmonary edema
also shows liver lesions Sphingosine acts as a second messenger and nhibits L type Ca channels in the myocardium leading ultimately to L sided HF and pulm edema |
|
|
What syndrome is experienced in horses that have come in contact with fumonisins?
|
Equine encephalomalacia
a lethal dz, necrosis of white matter in the brain |
|
|
Which two species tend to show some resistance to fumonisins deletorious effects?
|
poultry and cattle
|
|
|
How can you diagnose a suspected fumonisin toxicosis?
|
analyze the feed
also look at elevated blood or urine sphinganine to sphingosine ratio |
|
|
What are the treatment options for Fumonisin toxicosis?
|
none
|
|
|
Pyrethrins and Pyrethroids are safe insecticides. Which is synthetic and which is natural?
|
Pyrethrins are natural, from crysanthemum
Pyrethroids are synthetic |
|
|
What is the main use of pyrethrins a pyrethroids?
|
flea control on small animals
Fly control on large animals |
|
|
What is the MOA of pyrethrins?
|
bind to nerve cells near Na channels and slows channel opening and closing
leads to repetitive discharge and conductive blocks |
|
|
Which animals are most sensitive to pyrethrin use?
|
cold blooded animals
|
|
|
T or F
Tremors may be caused by TypeII pyrethroids and pyrethrins. |
F
Type I Pyrethroids and pyrethrins may cause tremors |
|
|
What topical flea med should not be used in cats?
|
Advantix
Spot on Type I pyrethroid |
|
|
What symptoms would you expect to see in a cat after a type I pyrethroid was applied?
|
tremors*, drooling, depression, anorexia, seizures
|
|
|
What is the most immediate treatment for a cat that had advantix recently applied topically?
|
wash with liquid dish soap
|
|
|
What medication is recommended for a cat with pyrethroid toxicosis?
|
Methcarbamol, after a bath in dish soap.
|
|
|
T or F
Because pyrethroid toxicosis cats may also be experiencing tachycardia, Atropine is a good choice as adjunctive treatment. |
F
NO Atropine in pyrethroid toxicosis cats!!! |
|
|
What is generally the prognosis of a cat that has been poisoned by pyrethroids?
|
good if no seizures
|
|
|
What is the most common way to diagnose pyrethroid toxicosis in cats?
|
Hx of exposure (plus tremors)
|
|
|
T or F
Pyrethroids and permethrins are generally considered unsafe products for flea control in small animals. |
F
they are very safe at proper doses |
|
|
Which plant is responsible for the majority of livestock economic losses in the US?
|
locoweeds
|
|
|
What are the three general syndromes due to locoweeds in cattle?
|
locosim due to the effects of the alkaloid swainsonin
respiratory problems and peripheral nerve degeneration due to nitropropanol glycoside compounds in the plants chronic selenium poisoning due to ingestion of selenium containing locoweed spp |
|
|
What are three compounds present in various locoweed spp that can cause deletorious effects in cattle?
|
swaisonin
nitropropanol glycoside selenium |
|
|
How long does it take after ingestion of locoweeds does it take animals to show clinical signs?
|
4-6 weeks
|
|
|
T or F
Animals will avoid locoweeds after first time ingestion. |
False
They can actually become addicted to it and seek it out |
|
|
What is the mechanism of action of swaisonine containing locoweeds?
|
inhibits alpha mannosidase leading to accumulation of oligosaccharides in the brain
Lysosomal storage dz |
|
|
What is the histological lesion expected with swainsonine toxicosis?
|
cytoplasmic vacuoles in all cells
lysosomal storage dz in the brain |
|
|
What causes cracker heels?
|
Nitropropanol glycoside containing locoweed ingestion
|
|
|
What are the clinical signs of swainsonine toxicosis?
|
depression, blindness, awkward gait, violent opr maniacal behavior, incoordination, vision and hearing impairment, infertility, cardiac failure, weight loss
|
|
|
What are the clinical signs expected with ingestion of nitrotoxin containing locoweeds?
|
weakness, ataxia, tremors, dazed and docile appearance
proprioceptive deficits, wheezing and roaring, cracker heels |
|
|
T or F
The clinical signs involved with locoweed chronic ingestion are completely reversible with proper treatment. |
F
Signs may be permanent |
|
|
What are the reproductive issues associated with chronic locoweed ingestion?
|
infertility, fetal loss, abortions, weak calves with high mortality
deformaties and crooked limbs |
|
|
What are the cardiac effects associated with locoweed ingestions?
|
R sided heart failure
high mt dz |
|
|
What is diagnostic for locoweed toxicosis?
|
ID of plant material in gut, swainsonine and nitrotoxins may be in serum, characteristic vacuolization of cytolplasm
|
|
|
What is the cause of Equine nigropallidal encephalomalacia?
|
Centaurea spp
yellow star thistle |
|
|
Which species is most commonly affected by yellow star thistle/Centaurea?
|
Horse
|
|
|
What is another name for Chewing disease in horses?
|
Equine nigropallidal encephalomalacia
|
|
|
What is the timeline for onset of action with Centaurea ingestion toxicosis?
|
horses must eat it for months before clinical signs ensue
|
|
|
What are the clinical signs of Centaurea ingestion?
|
Horses show an inability to prehend or swallow food or water
weight loss, dehydration, aspiration pneumonia |
|
|
T or F
Centaurea toxicosis in horses is fatal and irreversible. |
True
|
|
|
Bromethalin is found in ____.
|
rodenticides
|
|
|
T or F
Bromethalin, because it is a rodenticide, causes anticoagulation. |
F
it is a neurotoxin, not an anticoagulant |
|
|
What is important to remember about Bromethalin metabolism?
|
It is metabolized in the liver and its metabolite desmethylbromethalin is several times more toxic
|
|
|
Where does Bromethalin distribute in the body?
|
It is lipophilic: goes to the brain and fat
|
|
|
How is Bromethalin metabolized?
|
enterohepatic recirculation
5-6 day half life in dogs. |
|
|
What is Bromethalin's mechanism of action?
|
It uncouples oxidative phosphorylation in neurons
inhibits the ATPase pump decreased energy in neurons to maintain fluid balance and fluid buildup leads to vacuoles in myelin sheaths, which leads to decreased nerve conduction and paralysis |
|
|
What is the main histologic lesion associated with Bromethalin toxicity?
|
myelin sheath edema
|
|
|
Bromethalin has an associated pathoneumonic lesion:
|
spongy degeneration of CNS white matter in the brain and spinal cord
Vacuolization |
|
|
Which animal is most sensitive to Bromethalin toxicosis? dog or cat
|
cat, req's only half the dose for fatality
|
|
|
Which animal is considered resistant to bromethalin poisoning?
|
Guinea pig
|
|
|
What are the clinical signs associated with Bromethalin poisoning?
|
there are 2 syndromes
1. Acute/convulsant syndrome: 10-24 hrs post ingestion at or above lethal dose; mortality is 100%; agitation, depression, hyperesthenia, hind limb paresis, tremors, seizures, death 2. Chronic/paralytic syndrome: 1-5 days post exposure: ataxia, rear limb paresis, tremors, depression, recumbancy, decerebrate posture and seizures |
|
|
T or F
Bromethalin poisoning cannot be reversed. |
True
once animal shows clinical signs, there is no reversal |
|
|
T or F
There is an antidote for Bromethalin poisoning. |
F
|
|
|
What are the treatment options for Bromethalin poisoning?
|
aggressive emesis and activated charcoal may be used to decontaminate; formulated based on amt ingested
|
|
|
T or F
One dose of activated charcoal is useful in treating Bromethalin poisoning in a cat. |
F
it undergoes enterohepatic recirculation and req's multiple doses of activated charcoal in both the dog and the cat |
|
|
T or F
Treatment must be aggressive when treating a Guinea pig with Bromethalin poisoning. |
F
Guinea pigs are resistant |
|
|
What is problematic in a body shortage of Thiamin/TPP?
|
/Thiamin/TPP is a coenzyme in many energy transfer reactions
no TPP no ATP |
|
|
What clincal signs may be seen with a shortage of Thiamin/TPP?
|
weakness, weight loss, impaired feed utilization, seizures
|
|
|
What may be associated with a Thiamin/TPP shortage?
|
Ingestion of a thiaminase containing compound
|
|
|
Which plants contain thiaminase?
|
Bracken fern, Horse tail, scouring rush, raw fish, Nardoo
|
|
|
What is the toxic principle of bracken fern?
|
ptaquiloside
|
|
|
What regions are expected to have bracken fern growth?
|
It is distributed world wide
|
|
|
Which clinical syndrome is seen in sheep and cattle who have ingested bracken fern
|
Aplastic anemia in cattle and sheep
|
|
|
Which syndrome of bracken fern ingestion is associated with chronic exposure in cattle?
|
Enzootic bovine hematuria
chronic urinary tract neoplasia |
|
|
What are the clinical signs associated with bracken fern ingestion in horses?
|
anorexia, unthriftiness, weight loss, incoordination, wide stance, posterior paresis, convulsions, death
|
|
|
T or F
There are no treatment options for horses that have ingested bracken fern. It is fatal and irreversible. |
F
Thiamin injections, enough to overcome the thiaminase can reverse the signs. |
|
|
What are the clinical signs associated with scouring rush or horse tail ingestion?
|
it is a thiaminase containing plant
so weakness, weight loss, paresis, convulsion, similar to bracken fern |
|
|
What is beri beri?
|
thiamin deficiency due to ingestion of Nardoo, a thiaminase containing plant in Australia
must heat it to inactivate thiaminase |
|
|
T or F
Heating a thiaminase containing plant or fish can deactivate the thiaminase. |
T
|
|
|
What is the toxic compound contained in marijuana?
|
THC
|
|
|
What conditions can increase the toxicity of marijuana?
|
heating, drying, aging, and smoking
|
|
|
How does marijuana enter the body?
|
easil;y absorbed through inhalation or orally
|
|
|
T or F
Marijuana is often fatal if ingested by dogs and cats. |
F
it has a very wide margin of safety |
|
|
What is the onset of action and duration of action for marijuana?
|
30-60 minutes onset
duration less than 72 hrs |
|
|
What are the clinical signs of marijuana toxicosis?
|
euphoria followed by depression
ataxia, dilated pupils, nystagmus, bradycardia, hypothermia, lethargy, recumbency, dribbling urine, vocalization |
|
|
How is marijuana toxicosis ID'd in small animals?
|
usually Hx and clinical signs are enough
can use GCMS test to detect THC metabolites in urine |
|
|
What are the four opiod receptors?
|
mu, kappa, delta, sigma
|
|
|
What is the specific reversal agent of opiods?
|
Naloxone
it will NOT reverse the vomiting, only the CNS and respiratory effects |
|
|
What is Naloxone's mechanism of action?
|
it is a mu antagonist.
|
|
|
What are the common clinical signs associated with opiods?
|
CNS depression, ataxia, flaccidity, respiratory depression, bradycardia, hypotension, vomiting and decreased gut motility
|
|
|
How would you treat an animal with suspected opiod ingestion?
|
decontaminate with emesis or activated charcoal
respiratory support naloxone |
|
|
What is the mechanism of action for barbituates?
|
enhance inhibitory effects of GABA, inhibit glutamate
|
|
|
T or F
Benzodiazepines are metabolized in the liver. They produce inactive metabolites that are easily excreted. |
F
active metabolites produced in the liver Biotransformation! |
|
|
What is the mechanism of action for benzodiazepines?
|
enhance inhibitory effects of GABA
|
|
|
What is a reversal agent used for benzodiazepines?
|
Flumazenil
|
|
|
Flumazenil is a reversal agent for benzodiazepines. What is a potential SE?
|
seizures
|
|
|
T or F
Diazepam has a wide margin of safety in both dogs and cats. |
F
idiosynchratic liver failure in cats given oral diazepam |
|
|
T or F
Zolepidem is given as an antiinsomia agent. Its mechanism of action and margin of safety are similar to benzodiazepines. |
F
it has a smaller margin of safety |
|
|
What are the forms of alcohol?
|
ethanol, isopropanol, methanol
|
|
|
What metabolite of alcohol actually causes a hangover?
|
acetylaldehyde
|
|
|
What are the clinical signs of alcohol ingestion?
|
CNS depression, hypothermia, hypoglycemia, hypotension, abdominal pain, metabolic acidosis
|
|
|
Bread dough is dangerous because it contains _____.
|
alcohol
and it leads to gastric distension which makes it worse |
|
|
How should you treat an animal that has ingested bread dough?
|
cold water gastric lavage
possible gastrotomy manage alcohol toxicosis |
|
|
What are the severe effects of methanol in primates?
|
blindness and neural necrosis
|
|
|
T or F
Methanol is a serious toxicosis in all spp. |
F
only primates |
|
|
Which animal is extremely sensitive to avermectins?
|
chelonians
|
|
|
Why do collies show a breed sensitivity to ivermectin?
|
they lack a p glycoprotein
|
|
|
What are the clinical signs of avermectin toxicosis?
|
depression, weakness, ataxia, recumbency, coma
tremors, seizures, transient blindness bradycardia, hypothermia/hyperthermia |
|
|
T or F
Recovery from avermectin toxicosis is unlikely? |
F
may take several weeks, but recovery is possible with good supportive care |
|
|
What clinical signs might be present in a dog that has ingested moxidectin?
|
coma if PO
|
|
|
What is a common source in which dogs might ingest moxidectin?
|
equine horse dewormer
|
|
|
What is the preferred treatment if an animal is experiencing amitraz toxicosis?
|
Alpha 2 antagonists
Yohimbine! or atipamezole |
|
|
T or F
Atropine is the preffered treatment option to treat the clinical signs of amitraz toxicosis. |
F
Atropine is contraindicated |
|
|
Why are cats affected by cirtus oils?
|
they can't glucoronidate..lack the enzyme
|
|
|
What are the clinical signs in cats that have ingested potpourri oils?
|
ataxia, depression, weakness, hypothermia, recumbency,seizures
|
|
|
T or F
If a cat has ingested citrus oil it is a good idea to induce vomiting for decontamination. |
F
emesis is contraindicated because citrus oil can be aspirated |
|
|
What is the active ingredient in white snake root?
|
Tremetol
|
|
|
T or F
Tremetol is active and hepatic metabolism deactivates it. |
F
Biotransformation into active metabolites occurs in the liver |
|
|
What is the onset of action for white snake root toxicosis?
|
must be ingested for several days before clinical signs occur
|
|
|
What lesions are likely seen in horses with Tremetol ingestion?
|
cardiac lesions
degeneration and necrosis of cardiac muscle myoglobinuria, degeneration of renal tubules liver, kidneys, spleen, lungs congested |
|
|
T or F
If you suspect white snake root ingestion in horses, aggressive treatment is prefferred. |
F
hands off, monitor |
|
|
What are the clinical signs with white snake root/Tremetol toxicosis?
|
profuse sweating, increased pulse and resp rate, cardiac arrhythmias
|
|
|
What plants are known to contain atropine?
|
Atropa belladonna
deadly nightshade |
|
|
Which receptor does atropine affect?
|
competitive antagonist at ACh muscarinic receptors
|
|
|
What are the clinical signs of Atropine toxicosis?
|
Basically, it inhibits the parasympathetic NS
tachycardia, urinary retention, dry mouth, ileus, mydriasis, delirium , seizures, excitement |
|
|
What is the treatment protocols for Atropine OD?
|
decontaminate, indice vomiting
propanolol to slow the heart rate Physiostigmine to bind the AChesterase, penetrate the CNS |
|
|
There is a pneumonic for Atropine signs that sums up the main signs as:
|
Red as a beet
Dry as a bone Blind as a bat Mad as a hatter anticholinergics! |
|
|
What is the mechanism of action for muscarinic mushrooms?
|
muscarine binds the muscarinic ACh receptors in the parasympathetic NS and are not readily degraded, leading to persistent stimulation
SLUD effects |
|
|
T or F
Muscarinic mushrooms stimulate the sympathetic NS. |
F
parasympathetic |
|
|
What are the clinical signs of muscarinic mushroom ingestion?
|
salivation, lacrimation, urination, defecation
|
|
|
Which species has naturally occurring Atropinase?
|
Rabbits
|
|
|
What is the treatment of choice for muscarinic mushroom ingestion?
|
Atropine
it antagonizes the parasympathetic NS |
|
|
T or F
Muscarinic mushroom ingestion is generally fatal. |
F
|
|
|
What clinical signs are associated with solanine ingestion?
|
Gi irritation
|
|
|
What are the common sources of solanidine?
|
green potatoes and tomatoes
|
|
|
What is the common source of slaframine?
|
red clover infected with Rhizoctonia leguminicola
|
|
|
What is slaframine's mechanism of action?
|
it is a cholinergic agonist
mimics ACh Stimulatory effects |
|
|
What is a common clinical signs in horses that have ingested contaminated red clover?
|
major saliva production
|
|
|
Which species is contaminated red clover actually fatal?
|
pigs
|
|
|
T or F
Red clovers active ingredient must be activated through biotransformation. |
T
in the liver |
|
|
T or F
The clinical signs associated with red clover are generally short lived |
F
long acting, up to 96 hrs |
|
|
T or F
Atropine is an ineffective treatment option for red clover toxicosis. |
T, only good if given before exposure
|
|
|
T or F
Treatment for red clover toxicosis needs to be rapid and aggressive |
F
signs usually resolve on their own once you remove contaminated forage |
|
|
T or F
Most OPs are poorly absorbed, orally, but good for dermal and inhalation. |
F
they are absorbed well by oral, dermal, and inhalation |
|
|
T or F
OPs replaced Organochlorines. This led to less worker deaths. |
F
more worker deaths resulted |
|
|
How do toxicoses by OPs generally occur?
|
spillage and improper storage
miscalculation of concentration retreating too frequently ignoring label precautions |
|
|
What is the general mechanism of action of OPs?
|
cholinesterase inhibitors
bind and inhibit AChesterase leads to ACh build up excitation results |
|
|
What are the sources of body cholinesterase?
|
RBCs
brain smooth m, glands, cardiac m (muscarinic receptors) autonomic ganglia (nicotinic receptors) skeletal m (nicotinic receptors) |
|
|
T or F
Cats have higher levels of cholinesterase. |
F
have pseudocholinesterase, b/c they have low levels of cholinesterase |
|
|
How do OPs affect the esteratic site of AChE?
|
phosphorylate, irreversible
|
|
|
How do carbmates affect he esteratic site of AChE?
|
carbamylate it, reversible
|
|
|
What agent cn be used to "treat" OP toxicity?
|
2 PAM
|
|
|
What are the speeds of reaction for both OPs and carbamates?
|
OPs -- slow reactivity
Carbamate is rapid |
|
|
What is "aging" of OPs?
|
chemical change that strengthens the bond to AChE enzyme, loss of alkyl or alkoxyl group
occurs after phosphorylation now 2 PAM is not effective Warfare agents age rapidly |
|
|
What is OP induced delayed neuropathy?
|
develops 7-21 days after exposure
ataxia, weakness, CP deficits, hind limbs affected first inhibition of Neurotoxic esterase |
|
|
What are the clinical signs of OPs or carbamate ingestion?
|
hypersalivation, GI upset, tremors, dyspnea, seizures
|
|
|
How specific diagnostic test can you use diagnose OP exposure in cats?
|
Whole blood AChE
|
|
|
How can you diagnose an OP/carbamate exposure?
|
chemical analysis for insecticide
clinical signs and Hx depressed cholinesterase activity submit brain and retina |
|
|
How can you treat an animal that has been exposed to OP/carbamate?
|
bathe with dish detergent
emesis, activated charcoal, cathartic atropine may be used for muscarinic effects 2 PAM for nicotinic effects, not if aging has occured supportive care |
|
|
Why would you use a test dose of Atropine when you suspect OP/carbamate exposure?
|
If you give Atropine to the patient, and it responds...then not an antcholinesterase type compound as culprit
|
|
|
Chlorpyrifos most commonly affects these species:
|
cats
and bulls |
|
|
T or F
Chlorpyrifos has strong nicotonic and muscarinc effects? |
F
mostly only nicotinic effects |
|
|
T or F
Tetrachlorvinophos has a very small LD50 and commonly affects cats. |
F
very high dose needed for lethal effects |
|
|
Which "hot" OP may be mixed with blood and bone meal and fertilizer?
|
Dislfoton
|
|
|
Which OP/Carbamate only shows mild GI upset when ingested?
|
Diazinon
|
|
|
Which "hot" carbamate is used in fly baits and can show rapid onset and death with ingestion?
|
Methomyl
|
|
|
Which "hot" carbamate is considered illegal and produces extremely rapid death and has a small LD50?
|
Aldicarb
Tres Pasitos Chinese chalk |
|
|
ἐκκλησία, ἡ
|
church; assembly
|
|
|
What is the name of the only naturally occurring OP?
|
anatoxin a produced by blue green algae
|
|
|
T or F
Atropine and 2 PAM are very effective treatment options for anatoxin a ad a(s) exposure. |
F
not used at all |
