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99 Cards in this Set
- Front
- Back
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Toxicant
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poison - chemical, not biological
Another term for poison. Any solid, liquid or gas that when introduced or applied to the body can interfere with biological processes of the cells |
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Toxin
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Poisons that originate form living organisms (ex zootoxins from animals, phytoxins from plants, bacterial toxins)
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LD50
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Leathal Dose 50% - the dose or a toxicant that will cause the death of 50% of the animals that recieve it
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LC50
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Lethal Concentration 50% - The concentration of a toxicant that will cause the death of 50% of the animals that recieve it.
Used when referring to toxicants in wateror sometimes feed. |
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MTD
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Minimal Toxic Dose or Maximal TOlerated Dose.
The dose at which some animals begin to show signs of toxicity |
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Acute Toxicity
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The effects of single or multiple doses durign the first 24 hours following dosing
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Chronic Toxicity
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The effects of single or multiple doses 90 days or longer after initial exposure
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Part per million
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1 pancake in a stack of pancakes a mile high
1 mg toxicant/kg other substance = 0.0001% |
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Factors that affect the response of an individual to a toxicant
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Dose
Absorption Distribution Metabolism Excretion |
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Small animal most often involved in accidental poisonings
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Labrador Retriever
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Small Animal most targeted for malicious poisonings
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Pit Bull
Chow Chow Boxer |
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Are poinsettias poisonous to small animals?
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They can cause dermal irritation, but usually are not fatal
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All toxic plants can cause what effects?
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GI irritation (nausea, vomiting, diarrhea)
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What is the toxin found in avocado and what is its mechanism of action?
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Persin - cardiotoxic
interferes with Na+/K+-ATPase enzymes in cardiac fibers. Increased intracellular Na/decreased intracellular K+ causes heart block. |
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Differentials for a dog presenting with a history of dyspnea, ascites, pleural and pericardial effusion, pulmonary edema, inc ALT and cardiac arrhythmias
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avocado poisoning
ionophore toxicosis (monensin) yew toxicosis vitamin E/Se defeciency cardiac glycoside toxicosis (oleander) Cardiomyopathy or infectious myocarditis |
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Differential for a budgie presenting with depression and mild tremors.
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avocado poisoning - can eb dead in 24-48 hours
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How do you treat an animal with avocado poisoning?
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treat for congestive heart failure (diuretics, antiarrhythmic drugs)
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what is the toxic product of the castor bean plant?
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ricin in all plant parts; seeds are most toxic
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mechanism of action of ricin
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it is cardiotoxic through inhibition of protein synthesis.
has a latent period |
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clinical signs of castor bean poisoning
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GI irritation, vomiting, diarrhea (sloughing of GIT)
hemorrhagic gastroenteritis, hypotension, hematemesis, abdominal pain increased hepatic enzymes, renal failure |
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Differentials for :
GI irritation, vomiting, diarrhea (sloughing of GIT) hemorrhagic gastroenteritis, hypotension, hematemesis, abdominal pain increased hepatic enzymes, renal failure |
Castor bean toxicosis
bacterial/viral diseases heavy metal poisoning (arsenic, lead, mercury, thallium, zinc phosphide) Antineoplastic drugs |
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Treatment for castor bean toxicosis
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Emesis, prevent absorption with activated charcoal, cathartics (Mg sulfate, sorbitol), symptomatic and supportive care
Diazepam or methocarbamol for seizures |
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Toxic substances in chocolate and their mechanism of action
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Caffeine
Theophylline and theobromine (methyl-xanthine type compounds) MOA - inhibit cyclic nucleotide phosphodiesterases and antagonize action of adenosine = RELEASE OF CATECHOLAMINES --> cerebral cortical stimulation, seizures, cardiac stimulation, smooth muscle relaxation, coronary dilation, diuresis |
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Differential for:
hyperactivity and vomiting progressing to tachycardia/bradycardia, hyperthermia, muscle tremors, clonic convulsions |
Methyl xyanthine-type compounds (chocolate)
other alkaloids (strichnine, nicotine, amphetamine) pesticides (organophosphate/carbamates, fluoroacetate) Tremorogenic mycotoxins, cardiac glycosides (garbage poisoning) |
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Treatment for chocolate poisoning
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Emesis, prevent absorption with activated charcoal, symptomatic/supportive care
- diazepam, atropine (bradycardia), lidocaine or propranolol (tachycardia) |
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Red flags in chocolate poisoning:
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- hyperactive
- panting more than normal - ingested baking chocolate |
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Mechanism of grape/raisin toxicity?
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Not sure - suspect a mycotoxin
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Clinical signs of grape/raisin toxicosis
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oliguric/anuric renal failure, lethargy, some vomiting and diarrhea
elevated BUN and creatnine, hyperphosphatemia, hypercalcemia renal tubular necrosis |
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Clinical signs of chocolate poisoning
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1-2 hours post-exposure
hyperactivity, vomiting progression to tachycardia/bradycardia, hyperthermia, muscle tremors, clonic convulsions, death (6-24 hours after onset of chardiac arrhythmias). Heart rates can exceed 200bpm |
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what are the clinical signs of hops poisoning in dogs?
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malignant hyperthermia - tachycardia, tachypnea, abdominal pain, body temp >106 F, seizures, death (can occur within 6hrs of ingestion)
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Poisonous lilies?
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Asian, Easter, Japanese Show, Rubrum Tiger lilies
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Clinical signs of lily toxicosis
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Acute renal failure
cats are more sensitive |
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Differentials for acute renal failure, glucosuria, proteinuria, urinary casts
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lily poisoning
ethylene glycol poisoning oxalate-containing plants |
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Toxic substance in marijuana and its MOA
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psychoactive cannabinoids (THC) in leaves, flowers and seeds
MOA - THC acts on CNS (cholinergic, dopaminergic, GABA, serotonin receptors). Antiemetic effect (chemo patients) |
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Lethal dose of marijuana in dogs
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3gm/kg
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Clinical signs of marijuana poisoning in dogs
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onset 30-90 min after ingestion
hyperexcitability, depression, nystagmus, hypersalivation, hypothermia, mydriasis, hypotension, muscle weakness, ataxia |
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Plants that contain cardiac glycosides
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oleander - all parts contain oleandrin
rhododendron sp (azaleas) - leaves and flower nectar contain grayanotoxins (mad honey disease) |
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mechanism of action of oleander/rhododendron poisoning?
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digitalis-like toxins bind to Na+ channels leading to prolonged depolarization and excitation of neurons
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lethal dose of oleandrin or grayanotoxins
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as little as 3 mL/kg body weight
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How can you diagnose poisoning with cardiac glycoside containing plants?
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history of exposure
detection of grayanotoxins or oleandrin in stomach contents, biological specimens |
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how do you treat poisoning with cardiac glycoside containing plants?
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Emesis, activated charcoal, symptomatic and supportive care
Atropine for severe bradycardia; sodium channel blockers (quinidine or isoproterenol) for heart block |
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MOA of onion or garlic poisoning
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disulfides cause oxidative damage to hemoglobin (oxidizes sulfhydryl groups).
Causes methemoglobinemia and Heinz body anemia |
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Clinical signs of onion or garlic poisoning
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within 24 hours or up to 2 days post ingestion. Tachycardia, tachypnea, methemoglobinemia, HEMATURIA, hemoglobinuria
patients usually recover |
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Treatment of onion or garlic poisoning
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emesis, activated charcoal
N-acetylcysteine or SAMe (glutathione precursor) Severe cases - blood transfusion |
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Plants containing insoluble oxalates
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Philodendron, dieffenbachia (dumb cane), Jack-in-the-Pulpit
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MOA of insoluble oxalate-containing plants
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Calcium oxalate "needle-like" crystals cause GI irritation and pain, may cause release of histamine
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Clinical signs of philodendron (oxalate) poisoning
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Immediate pain and swelling of mouth, esophagus, stomach
can cause obstruction of airways, throat due to swelling |
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how do you treat oxalate-containing plant poisoning?
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emesis, antihisstamines, analgesics, eugenol (reduce tongue swelling)
GI protectants (sucralfate) |
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sources of nicotine poisoning
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tobacco products, insectisides
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MOA of nicotine poisoning
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mimics acetylcholine and stimulates post-synaptic nicotinic receptors of the CNS and at the neuromuscular junctions
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Clinical signs of nicotine poisoning
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vomiting, hyperexcitability, tremors, convulsions, inc peristalsis
High dose exposures - depression, descending paralysis |
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Why should you never use antacids to treat nicotine poisoning?
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they increase absorption of nicotine from the stomach
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differentials for vomiting, hyperexcitability, tremors, convulsions, inc peristalsis
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Nicotine
anticholinesterase insectisides (organophosphate/carbamates) depressants (high dose cases) |
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MOA of Yew toxicosis
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Japanese or English yew
Taxine alkaloids are Ca channel antagonists and cardioselective - inhibit depolarization in teh heart. HIGHLY TOXIC |
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Clinical signs of yew toxicosis
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most common in large animals
trembling, muscle weakness, dyspnea, arrhythmia, bradycardia, diastolic heartblock, DEATH (9/10 cases) |
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Treatment of yew toxicosis
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emesis or gastric lavage (rumenotomy), activated charcoal, IV fluids
atropine may be helpful for cardiodepressant effects of taxines |
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Differentails for sudden death in dogs with minimal lesions
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Organophosphate/carbamate insecticides
Strychnine Fluoroacetate (1080) Zinc phosphide Garbage poisoning Drugs of abuse (barbiturates, cocaine, amphetamines) |
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which must be activated by the liver - OPs or carbamates?
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OPs must be metabolized by CyP450 to be bioactive.
Carbamates are cholinesterase inhibitors as absorbed. |
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Which are more lipid soluble - OPs or carbamates? Why is this significant?
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OPs are more lipid soluble than carbamates and more readily cross the blood-brain-barrier.
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*What is the mechanism of toxicity for OPs and carbamates?
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Both inhibit AChE thereby inhibiting breakdown of Ach at cholinergic synapses
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Sites of action of Ach
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- sympathetic and parasympathetic ganglia
- btw PSNS post-gang neurons and effector organs (sm muscle, cardiac muscle, exocrine glands) - btw somatic motor neurons and skeletal muscle - cholinergic sites in CNS - AChE also present on RBCs |
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Overstimulation of muscarinic receptors gives what clinical signs?
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SLUDDE or DUMBELS
diarrhea, urination, miosis, bradycardia, emesis, lacrimation, salivation |
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at which receptors does atropine work?
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muscarinic Ach receptors
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where are muscarinic receptors found?
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between postganglionic ps neurons and effector organs
- smooth muscle - cardiac muscle - exocrine glands |
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where are nicotinic ACh receptors found?
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- btw pre- and post-ganglionic neurons in SNS and PSNS
- AND between somatic motor neurons and muscles |
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what is the effect of overstimulation of nicotinic receptors?
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produces muscular fasciculations and tremors initially, followed by flaccid paralysis.
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What is the effect of overstimulation of Ach receptors in the CNS?
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restlessness, anxiety, headaches, hyperactivity, seizures, mental depression
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what is AChE "aging" and does it occur with OPs or carbamates?
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If treatment is delayed, P's on the OPs attach to esteratic sites on AChE rendering it inactive with unbreakable bonds --> the enzyme remains unfunctional.
Carbamates can be hydrolyzed from the AChE binding site, so no aging occurs |
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how can the body recover form AChE aging if treatment is delayed?
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Synapse can regain function with production of new AChE.
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How does OP or carbamate poisoning eventually cause death?
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respiratory failure
- inhibition of central respiratory drive (medullary) - excessive bronchial secretion and bronchospasm (muscarinic) - depolarizing blockade at NMJ causing diaphragm and intercostal muscle paralysis (nicotinic) |
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which signs of OP/carbamate poisoning are seen first?
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muscarinic
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differentials for muscle tremors, salivation and vomiting, but lack of miosis
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with miosis - suspect carbamate/OP toxicosis
without miosis - - pyrethrin/pyrethroid toxicosis - amitraz toxicosis (mydriasis occurs) - tremorigenic mycotoxicosis - cationic surfactant/disinfectant toxicosis (oral and gastric irritation) - garbage poisoning (endotoxin intoxication) - primarily CNS depression |
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How do you diagnose carbamate/OP toxicosis?
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- history of exposure
- muscarinic signs preceding nicotinic signs - give atropine and look for anticholinergic signs (mydriasis, tachycardia) - Cholinesterase activity (brain or blood) - usually less than 25% of normal - high CPK or AST with some OPs - No definitive lesions at necropsy (rarely OPIDN) - Peseticide screen (vomitus, whole blood, suspected bait, stomach contents) |
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How do you treat carbamate/OP toxicicosis?
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- bathe with soap and water if topical
- activated charcoal - works if ingested or topical - supportive care (body temp,electrolytes, acid-base, fluids) - atropine for muscarinic signs - methocarbamol for seizures - 2-PAM within 24-36 hrs for nicotinic and muscarinic signs (ineffective with carbamates, but not contraindicated) |
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treatment of seizures associated with OP/carbamate toxicosis
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methocarbamol
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treatment of muscarinic signs
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atropine
1/4 IV (0.1-0.5 mg/kg) 3/4 IM or SQ |
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This drug helps alleviate nicotinic and muscarinic signs of OP toxicosis, but not carbamate.
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2-PAM (Protopam chloride or pralidosime chloride)
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How does 2-PAM work and why would you use it?
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if given within 24-26 hrs of OP poisoning, it reactivates AChE by binding to the phosphate moeity in the esteratic site, releasing the OP moiety from the enzyme.
Use it to help allieviate nicotinic and muscarinic signs of OP toxicosis. Not effective on carbamates. |
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what is "Intermediate Syndrome"?
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May follow acute OP/carbamate crisis or result from prolonged exposure.
Long-term accumulation of ACh at muscarinic receptors induced tolerance, so intermediate syndrome lacks more dramatic muscarinic signs. Nicotinic receptors do not develop tolerance, so nicotinic signs predominate. |
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Which insecticies are implicated in Intermediate Syndrome?
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lipophilic insecticides with longer half-lives
-chlorpyrifos in cats -carbaryl in swine -disulfoton in dogs |
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what is OPIDN?
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organophosphate induced delayed neuropathy
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What causes OPIDN?
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OPs block other esterases, including neuropathy target esterases (NTE). NTE inhibition causes loss of myelin and axons in spinal cord 2-3 weeks post-exposure.
Chlorinated OPs (chlorpyrifos) especially bind to NTEs. |
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Signs of OPIDN
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weakness, ataia/conscious proprioception deficits, esp in hindlimbs due to distal axonal degeneration of CNS and PNS
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Differences between carbamate and OP poisoning
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Carbamates
- can be more toxic than OPs - readily absorb through skin and can cross BBB - AChE-carbamate complex doesn't "age" - 2-PAM not used for carbamate toxicosis, but not contraindicated. |
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examples of organochlorines
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endosulfan
methoxychlor paradichlorobenzene |
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Clinical signs of organochlorine poisoning
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Overstimulation of CNS
- apprehension, incoordination, muscle fasiculations progressing to convulsive seizures (without PS-mimetic signs) |
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Which animals are most sensitive to organochlorines?
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cats are VERY sensitive to lindane
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What is the major elimination route of OCs?
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Milk - passively transported from blood to mammary cell lipid.
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How would you treat OC poisoning?
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- oral exposure - activated charcoal, mineral oil
- symptomatic and supportive care - muscle relaxants (methocarbamol), barbiturates, diazepam - there is no specific antidote or treatment |
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what is the toxin in death cap mushroom?
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amatoxins and phalloidin
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what organs does death cap mushroom affect?
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GIT, kidney, liver
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what are the phases of amatoxin poisoning?
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1 - latency
2 - GI sighs 3 - Latency 4 - massive liver and kidney failure, coagulopathies |
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how do you diagnose mushroom poisoning?
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ID mushroom or toxins in vomitus
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how do you treat mushroom poisoning?
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GI decontamination, symptomatic and supportive care
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which bacteria are responsible for garbage poisoning?
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tremorogenic mycotoxins - Penicillium crustosum/roquefortii
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clinical signs of garbage poisoning
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30 min to 3 hours post ingestion
panting, hypersalivation, muscle tremors, hyperresponsiveness to external stimuli -- seizures and death |
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treatment for garbage poisoning
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decontamination, symptomatic/supportive treatment, anticonvulsants
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sources of tremorigenic mycotoxins
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ingestion of feed, moldy English walnuts, moldy cream cheese, compost by dogs
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Differentials for garbage poisoning
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strychnine
methylxanthines nicotine anticholinesterase pesticides |
