Quiz Flashcards
Why study toxicology?
Animal poison control center fields about 100,000 cases/year. Most cases do not result in serious toxicosis, you need to know when and how to treat.
How often are poisonings malicious?
It is very rare! only 1-2% are malicious. Most involve pesticides, drugs like aspirin and caffeine, ethylene glycol and cyanide.
What is a toxin/toxicant?
A compound that causes toxicity . Can be a synthetic or natural compounds.
Toxicology
The study of poisons. Is concerned with identification, treatment, and assessing risks of poisons. In a clinical, regulatory and environmental setting.
Xenobiotic
foreign substance
Antidote
Historically- remedy to counteract a poison. Current- any substance that prevents/relieves the effects of a toxicant.
What do some veterinarians call the universal antidote?
Activated charcoal.
But no antidote really works on all toxicants
Manmade chemicals
More than 50,000. Potential toxicants include pesticides, cleaning products, pharmaceuticals, industrial chemicals, etc,
Natural products
Toxic plants, at least 800 species with millions of compounds. Microbes, vitamins, and animal venoms. Don’t understand them all- like grapes
Are natural or synthetic poisonings worse?
Just depends on the situation
Additive compounds
Two compounds when together both have their full effect (1+1=2)
Antagonistic compounds
When one compound prevents the full action of another
Synergistic compounds
Two compounds that when together magnify each others effects (1+1=5)
What factors of toxicity are related to the chemical?
Chemical structure, affinity to molecules, the toxicants carrier.
What factors of toxicity are related to exposure?
Dose, route of entry, duration of exposure (acute, chronic, subacute)
What factors of toxicity are related to the subject?
species, age (young or old), health status, history (other medications they might be on), gender (might matter)
How does environment influence toxicosis?
Body temperature, outside temperature (where the microbes can survive), stomach pH.
Species differences
Differences in the capacity for biotransformation. Cats are deficient in glucuronidation. Dogs are deficient in acetylation. Pigs are deficient in sulfation. Pregnancy can also alter metabolism
Acute exposure
Single dose exposure or several doses within a 24 hour period. ex: snake venom, bottle of aspirin, rate poison
Sub-acute/subchronic exposure
Exposure over 7 to 90 days. ex: lawn pesticides
Chronic exposure
Protracted exposure (6 months- lifetime). ex: lead paint, well water
Dose-response relationship
Central concept of toxicology; assumes a cause and effect relationship and that response is proportional to dose
Toxicokinetics
Exposure and dose are NOT the same. Most important veterinary toxicants are absorbed by oral or dermal routes
ADME
Absorption, Distribution, Excretion and Metabolism
What does metabolism usually do?
It usually detoxifies a compound and increases its elimination
Bioactivation
Occasionally metabolism will increase the toxicity of a compound. ex: benzoapyrene, aflatoxin, acetaminophen
Mechanisms of toxicity
1) Delivery from site of exposure to target. 2) Reaction of the ultimate toxicant with the target molecule. 3) Cellular dysfunction and resultant toxicities. 4) Repair (apoptosis tissue regneration) or disrepair (tissue necrosis, fibrosis, cancer)
Cellular damage caused by toxicity
Can result from free radical damage, inhibition of energy production, disruption of enzyme function. ex: arsenic, acetaminophen
Organ system dysfunction by toxicity
Not associated with specific cellular injury, but lethal to intact organism. ex: insecticides, rodenticides
Top ten toxic foods for dogs
Alcohol, avocados, chocolate, coffee and caffeine, fruits with pits/seeds, grapes and raisins, macadamia nuts, onions and garlic, xylitol, yeast dough
Top ten toxins for dogs and cats
Prescription drugs, insecticides, organophosphates, OTC drugs, house hold products, human foods, veterinary medications, rodenticides, plants, lawn products
How important is it to take a history?
Pretty much the most important thing ever!
Known exposure
Owner saw or highly suspects that animal ingested a particular compound. Initial contact if often by phone
Unknown exposure
Animal presents with symptoms but no known cause. Much more difficult to diagnose and treat
what to evaluate for immediate life-threatening problems when toxic animals come in?
Cardiovascular function and output (HR), Respiratory (RR), Temperature, Having siezures (other CNS problems)? Hemorrhaging?
Who are candidates for intubation?
unconscious, paralyzed and severe respiratory distress patients
Ventilation may be needed if there is….
Hypoventalation and hypercapnia (PCO2 > 45 mmHg). Metabolic acidosis (pH 7.35). Hypoxia (PaO2
How do you prevent aspiration of vomitus?
Comes down to positioning. Head should be below the body. With large animals keep them on an incline with keeping head below the body
How do we control hyperactivity (seizures)?
Diazepam is the treatment of choice- repeat every 10 minutes for 2x the effect. Phenobarbital. Methocarbamol- skeletal muscle relaxation to control seizures
How do we treat depression?
Analeptics, Doxapram- increased respiratory rate
How do we treat tachycardia and arrhythmias?
Need to correct acid-base, electrolyte or fluid disorders. Lidocane or propranolol
How do we treat hypertension?
Nitroprusside via constant IV infusion. Hydralazine.
Fluid therapy to control cardiovascular function
Balanced electrolyte solution for shock and dehydration. Monitor urine output. Inotropic drugs like dobutamine
Stabilize the patient
Priority in animals that present with severe clinical signs. Potential diagnostic testing- EDTA tube, 2 serum tubes. Once patient is stable, perform a complete PE
Obtain a complete history
Most important and most overlooked part of diagnosing toxicity. Once patient is stable, question owner to narrow down causes of toxicity. 4 major themes: health history, clinical signs, environment, diet
History: health history
Ask about Vx history, any medications and suppliments, genetic diseases, ect.
History: current clinical history
How long has the problem been present? When was the animal observed first sick? If animal was found dead- when were they last seen healthy? What is the size of the herd?
History: clinical signs
Although you never want to diagnose based only on clinical signs because so many toxicities have the same signs. But it helps choose treatment because you know what organ system is effected. CNS, GI, Renal, Hepatic, Cardiac, Hematopoietic
History: environment
Type of environment in which the animal lives will greatly determine next line of questions to ask: indoor only, indoor/outdoor, fenced yard vs roaming.
History: diet
What are they eating? Method of feeding, moldy or spoiled food, drinking water source, water supply changes?
Formulate rule-out list
Popular list of differential diagnoses. Make sure not to have blinders on! Could be infection, metabolic, ect
Ancillary support
Ensure adequate urine output. Monitor respiratory, cardiac and neurological status. Manage clinical signs as they develop. Manage secondary hepatic or renal injury. Administer GI protectants and anti-emetics
Symptomatic care
Maintain body temperature- avoid heat lamps. Alleviate pain. Prevent irritation of skin and membranes with demulcents, milk, sucralfate
Decontamination measures
Only after animal has been fully stabilized. Two most common methods are emesis and activated charcoal, might consider cathartics.
Emesis
Prevents toxicant absorption! Given if you suspect oral exposure, should be done within 60 minutes of ingestion. Don’t use for very basic or acidic compounds, chronic exposures and minor toxicities. Always save the vomitus for analysis.
Emesis rule of thumb
Induce emesis if a toxic dose of a substance was ingested, no vomiting has occurred yet, and activated charcoal is not an option. There is little evidence that shows emesis improves the outcome in poisoned animals
Activated charcoal
Prevent toxicant absorption. The earlier you give the more effective it is. Give orally, can be mixed with baby food. Repeat dose every 5 hours. Don’t give to a sedated animal without airway protection- aspiration risk. Don’t give if toxican is a corrosive agent or non-polar.
Charcoal rule of thumb
Give if substance is known/thought to be absorbed, ingestion was very recent, undergoes enterohepatic circulation, the animal can tolerate it, there is no immediate need to administer oral medication. Have to wait at least 2 hrs between giving charcoal and a oral medication.
Cathartics
Facilitate toxicant removal. Decrease GI transit time, increase movement of toxins, or charcoal-toxin complex, and decrease possible adsorption of the toxin. Use as a adjunct to activated charcoal therapy to reduce transit time
Mineral Oil
Type of Cathartic. Do not use with activated charcoal
Saline Cathartic
MgSO4 or Na2SO4. Can add to charcoal or use later
Corrosives, strong acids or bases toxicants
To prevent absorption use dilution instead of emesis (Dilute with milk, water or eggs)
Dermal Exposures
To prevent absorption bathe in liquid dish soup, rinse well
Lipid infusion
New treatment for preventing absorption. Off label use of intravenous lipids. Promising adjunct to conventional treatments.
Do most toxic agents have a specific antidote?
No they do not. If there is one, use it, but mostly treatment is symptomatic and supportive
Analytic testing
No one test will screen for all toxicants. Multiple tests to cover everything becomes costly. So have to narrow down to general type of agent involved.
Common toxins associated with an increased anion gap
> 30 mEq/L: suggests metabolic acidosis. Ethylene glycol, Ethanol, Iron, Methanol, Salicylates (aspirin), Strychnine
Common toxins associated with CNS depression
Ivermectin, cholinesterase inhibitors, organophosphate insecticides, carbamate insecticides, blue-green algae, slaframine, lead, locoweed, ethylene glycol
Common toxins associated with seizures
Bromethalin, chocolate, lead, organochlorine insecticides, pyrethrins/pyrethroids, syrchnine, water deprivation/sodium ion toxicosis, water hemlock.
4 parts to accurately diagnosing any toxicity
History, clinical signs, pathology/necropsy, chemical analysis
How do you prevent further exposures?
Change pasture, feed, water, ect. Remove baits, old pesticides. Bathe or flush for cutaneous or ocular exposures. Educate your clients!!
Chemicals that cause neurotoxicity
Both “all natural” and synthetic. Largest class of chemicals inducing toxicosis. Clinical signs can be grouped by peripheral vs. central and excitatory vs. depressive.
Organophosphate pesticides
Agricultural and residential use had increased since OCPs (degrade faster, used in flea collars, bug baits). Parathion, malathion, and chlorpyrifos. High water solubility and acute toxicity.
Prganophosphates mechanism of action
Irreversible inhibition of acetylcholine esterase activity. Cholinergic overstimulation within minutes to hours
Clinical signs of anti-esterase toxicity
May last 1-5 days- include respiratory distress and collapse. Muscarinic- SLUDGE-M. Nicotinic- muscle fasciculations. CNS.
Species specific clinical signs. Don’t forget- won’t always see textbook versions
Horses- colic and dehydration. Cattle- rumen stasis (no miosis). Cattle/sheep- severe depression. Dogs/cats- CNS stimulation-> convulsions. Cats- chlorpyrifos cause severe nicotinic signs
Diagnosing anticholinesterase toxicity
Correct history and clinical signs. Atropine challenge- administer, if normal signs of atropine are observed in 15 mins toxicity is NOT due to cholinesterase inhibitor. Decreased RBC AChE. May see pulmonary edema and petechial hemorrhage in GI mucosa
Treating anti-esterase toxicity
GI decontamination, bathing in exposure was dermal. Atropine sulfate for muscarinic signs (won’t stop nicotinic signs). Oximes can reactivate AChE. Diazepam or barbiturates for seizures. Time.
Pathology in dog with OP toxicity
Will see vacuolization of the brain
Organophosphate induced delayed neurotoxicity
OP compounds can produce significant inhibition of neuropathy target esterase can delay neuropathy. Characterized by axonal degeneration of long motor neurons. Hindlimb weakness and paralysis. No treatment
Ivermectin
Produced by Steptomyces avermitilis. Worm medication in cats/dogs. Anthelminthic in livestock. OD can cause ataxia and disorientation in any breed. In collies, shepherds and shelties smaller amounts can cause toxicity because BBB does not block ivermectin
Ivermectin mechanism of action
Increases GABA release, enhances GABA binding and is a direct GABA receptor agonist. Increased inhibitory input decreases ability to respond to other stimuli. Doses can cumulate
Ivermectin clinical signs
Onset is hours to 1 day. Ataxia, lethargy, mydriasis, coma, blindness, ect. Collies- recumbency and seizures. Respiratory distress typically precedes death.
Ivermectin diagnosis
History of administration, brain concentration > 100ppb, measure GI content, liver, fat, feces. No diagnostic bloodwork or lesions
Ivermectin treatment
GI decontamination for recent exposures (charcoal- multiple times). Supportive care, barbiturate for convulsions. Prognosis depends of exposure dose, Should test dogs prior to administering them higher doses of ivermectin.
Bromethalin
Single dose rodenticide. Kills in 3-5 days. Parents and metabolite uncouple oxidative phosphorylation in CNS
Nicotine
Rodenticide. Usually stimulate then block nicotinic ACh receptor
Metaldehyde
Rodenticide. Sources: fuel for small heaters and molluscicides. Metabolism to acetaldehyde = CNS excitation
Mycotoxins
Fungal metabolites which cause pathological, physiological and/or biochemical alterations usually on several organ systems. Can affect all species.
Slaframine
Produced by black patch fungus. Seen in center, south eastern and southwestern USA. Is a ACh mimic, primarily acts as a muscarinic cholinergic agonist, especially in exocrine glands. Most common in horses and cattle.
Clinical signs of slaframine
Copious salivation is the primary sign, can be only sign. Bloat, diarrhea, frequent urination. May see feed refusal.
Slaframine diagnosis
Diagnose by consumption of clover, identification of black patch in clover. Have to differentiate from OPs and Botulism
Slaframine treatment
Remove source, maintain hydration and electrolytes. Can treat with atropine, rarely fatal- signs should cease within 48 hours.
Fumonisin
Metabolite of Fusarium spp. Found mostly on corn. Occurs in years of drought followed by wet weather. Presence of Fusarium spp is not indicative of fumonisin.
Fumonisin mechanism of action
Acts by inhibition of sphingosine-N-acetyltransferase causing increased levels of sphinganine (cytotoxic). Affects vascular endothelial cells-> stroke, hepatic injury, and pulmonary edema. Species susceptible- horses, swine, and rabbits.
Two diseases fumonisin toxicity causes
Equine leucoencephalomalacia (ELEM) and porcine pulmonary edema (PPE)
Porcine pulmonary edema
Clinical signs include inactivity, increased RR, and decreased HR. Develop lethal pulmonary edema within 4-7 days of consuming contaminated feed. Abdominal effort and open mouth breathing occurs within hours of death.
Diagnosis of PPE
Analysis of feed for fumonisin with clinical signs. Increase in serum and tissue sphingoid base. Increased liver enzymes, total bilirubin, bile acids and cholesterol. Post-mortem pathology shows pulmonary edema, hepatic lesions and necrosis.
Equine leukoencephalomalacia
Main target is brain and liver- acute onset of ataxia, drowsiness, hysteria that get progressively worse. Hepatoxicity- jaundice, encephalopathy, coma and convulsions are terminal. Near 100% mortality
ELEM diagnosis
Analysis of feed and clinical signs. Severe liver injury and lesions- increased cholesterol and liver enzymes. Post-mortem CNS necrosis and liquefaction
Treating fumonism toxicity
No treatment available. Isolate affected animals. Change feed. Pigs usually recover within 48 hrs.
Tremorgenic mycotoxins
Elicit intermittent/sustained tremors in vertebrates. Sources- food, garbage, compost. Clinica signs- dimished activity and immobility-> hyperexcitability.
Tremorgenic mycotoxins mechanism of action
Release of neurotransmitters from synaptosomes in the CNS
Ammoniated feed toxicosis
Non-protein nitrogen sources are added to cattle feed. Found in high concentrations in some mineral licks. Species affected- bovine, caprine, ovine. Leads to excitability “bovine bonkers”
Ammonia toxicity/imidazoles clinical signs
Hyperexcitaility- rapid blinking, trembling, rapid RR, SLUD, tonic convulsions. Animals alternate between hyperexcitability and normal. Onset rapid- 15 mins to several hrs. Death within 24 hrs
Ammonia toxicosis diagnosis
History of exposure, clinical signs. Differentials- OP, cyanide, grain overload, meningitis. Analyse feed or blood/rumen for ammonia levels. Increased ammonia, glucose, BU, and decreased blood pH
Ammonia toxicosis treatment
Imidazole- no treatment, just feed removal, might need sedation. NPN- no treatment, water and vinegar by stomach tube
Strychnine
Seeds for Strychos-nux vomica. Often used as a malicious poison.
Strychnine mechanism of action
Rapidly absorbed and distributed to blood, liver and kidney. Rapid elimination. Competitive antagonist at postsynaptic glycine receptors. Glycine is an inhibitory transmitter, so antagonism results in stimulation of all muscles
Strychnine toxicity clinical signs
Rapid onset, begins with anxiety, restlessness, “grinning”, ears twitch. Proceeds to violent tetanic seizures. Sawhorse stance. Death from respiratory failure, exhaustion.
Strychnine toxicity diagnosing
Clinical signs, hyperthermia in dogs. Chemical analysis of bait, stomach contents or liver. Elevated CPK and LDH. Lactic acidosis, hyperkalemia and leukocytosis. Rule out- OP, tetanus, metaldehyde, Pb
Strychnine toxicity treatment
Need to control seizures and prevent asphyxiation. Given pentobarbital or methocarbamol. Gastric lavage, activated charcoal and forced diuresis. Ammonium chlorida to trap strychnine
Salt toxicity
Water deprivation (most common) or eating large amounts of salt. Most common is pigs.
Salt toxicity mechanism of action
Diffusion of sodium into CSF when plasma Na levels are high. When plasma Na level drop, sodium leaves CSF slowly, attracting water to maintain osmotic balance. Increases CSF volume and pressure.
Clinical signs of salt toxicity
Primarily CNS and includes salivation, increased thirst, abdominal pain and diarrhea. Cattle may be belligerent and uncoordinated
Diagnosis of salt toxicity
Na levels high especially in CSF. >2000ppm is diagnostic in swine and cattle. Differentiate from polio, lead, pesticides, encephalitis
Treatment of salt toxicity
Slow rehydration (over days). Serum sodium levels should be lowered at a slow rate. IV hyperosmotic fluids low in NA, loop diuretics- to prevent pulmonary edema
Pharmaceuticals
Neuroactive substances. Top- vicodin, synthyroid, zocor and lipitor, lisinopril. Clinical signs in animals can be similar to human toxicity
Alprazolam (Xanax)
Benzodiazeprine. ASPCA receives many calls about this.
Alprazolam mechanism of action and clinical signs
Acts on the CNS. Signs- ataxia, depression, vomiting, tremors, tachycardia, diarrhea, ptyalism, hypothermia. Appear with 30 minutes of ingestion, If there were especially high doses, may initially show CNS excitation
Alprazolam diagnosis and treatment
Dx- based on suspect and clinical signs. Tx- standard decontamination procedures, can use antagonist flumazenil. Need close monitoring. Fluids and medications to support respiratory function.
Zolpidem (Ambien) mechanism of action
Non-benzodiazepine hypnotic drug. Inhibits neuronal excitation by binding to the benzodiazepine omega-1 receptors
Zolpidem clinical signs
Rapid absorption from GI tract. Ataxia, vomiting, lethargy, disorientation, hyper-salivation, hyperactivity, panting. Signs usually resolve by 12 hours
Zolpidem diagnosis and treatment
Dx- suspect and clinical signs. Tx- supportive and symptomatic
Phenoxyacetic acid herbicides
Scott’s weed and feed, Silvex. Low toxicity in most animals, dogs are very susceptible. Affected animals usually exposed to concentrate or predisposed through kidney damage or genetics. MOA unknown.
Phenoxyacetic acid clinical signs
GI effects (sometimes only sign in dogs). Muscle affects- rigid muscles, ataxia, seizures, rumen atony, myotonia with serious toxicosis. Renal tubular degeneration, hepatic necrosis.
Phenoxyacetic acid diagnosis
Oral and GI ulcers, enteritis, rumen stasis, congestion of kidney/liver, hyperemia of lymph nodes. Chemical analysis of serum, urine.
Phenoxyacetic acid treatment
Emesis, lavage or bath decontamination. Activated charcoal/cathartic. Ion trapping to enhance excretion. Prognosis good for treated animals
Ergot alkaloids
Produce in grains by Claviceps purpurea. Alkaloids are dopamine serotonin agonists which produce hallucinations. Lead to decreased prolactin secretion. Smooth muscle contractions- uterus and peripheral vasculature- causes abortion and ischemia
Ergot clinical signs
Reduced feed intake and weight gain, heat intolerance and retain winter coat. Necrotizing ergotism- lameness, gangrene of extremities. Fat necrosis, poor reproductive performance
Clinical signs of ergotism in horses and pigs
Horses- abortion, weak foals, prolonged gestation. Pigs- causes infertility and early parturition, decreased milk production.
Ergotism diagnosis and treatment
Evidence of sclerotia in feed, fescue in forage. Treat by removing source, prevent secondary infections. Metoclopromide and domperidone increase prolactin secretion and normalize gestation in mares.
Inophores
Compounds that form lipid soluble complexes with cations. Used as antibiotics. Used to improve milk production in dairy cattle
Inophores mechanism of action
Act by increasing Na and Ca, leads to mitochondrial swelling and cell death, especially in muscle. Usually a feed-mixing error. Horses are most susceptible. Poultry are the least sensitive
Inophores clinical signs
Occur 12-72 hrs after ingestion. Anorexia, colic, sweating, in-coordinated, and weak (horses). Unlikely but poultry- down with legs and wings out, dogs- posterior paresis, cats- polyneuropathy from salinomycin.
Inophores diagnosis
Increased muscle enzymes and myoglobinuria. Elevated liver values. Decreased K and Ca (horses). Chemical analysis of feeds, liver (not blood). Differentiate from other colic, Vit E and Se deficiency, white snakeroot, botulism
Inophores treatment
No specific treatment or antidote. Feed change must be made immediately until all diagnostic procedures are completed. Supportive therapy. Animals may die later due to exercise intolerance
Tetanus (clostridium tetani)
Mostly affects cattle. Spores in a puncture wounds, can be ingested. Toxins acts by blocking release of GABA and glycine. Results in overstimulation of muscles leading to stiffness and tetany
Tetanus clinical signs
Stiffness and reluctance to move, twitching and tremors, lockjaw, unsteady gait, stiff tail, bloat-> collapse, spasm, death
Tetanus treatment
Antitoxin is available- only works very early on. Supportive therapy, prognosis is very poor.
Common respiratory toxins: ventilatory muscle paralysis
Botulism, tetanus, snake venom, OP insecticides, strychnine
Common respiratory toxins: respiratory center depression
Barbiturates, opiodes, ethylene glycol, hypnotics, sedatives, tricyclic antidepressants, crude oil
Anticoagulant & anticoagulant rodenticides mechanisms of actions
Inhibits Vit K epoxide reductase. Prevents formation of Vit K dependent clotting factors (II, VII, IX, X)
Anticoagulant & anticoagulant rodenticide toxicity clinical signs
Delayed onset of clinical signs (3-5 days) as clotting factors are consumed. Depression, anorexia, anemia, dyspnea, nosebleeds, bleeding gums, bloody feces. Hemorrhage into chest/abdomen and hematoma. Prolonged bleeding from injection sites noted
Anticoagulant & anticoagulant rodenticide toxicity diagnosis
History of exposure, evidence of a coagulopathy and response to vitamin K therapy. Hematological tests: increased PT/PTT
Anticoagulant & anticoagulant rodenticide toxicity treatment
If it has been within the last few hours- emetic, adsorbent, cathartic therapy. Vitamin K administration. Therapy for 10-14 days for warfarin, 30 days for second generation compounds. Severe cases may require a transfusion
Nitrate toxicosis
Found in fertilizers, many plants, contamination of water. Converted to nitrite- nitrite anion causes vasodilation and oxidized ferrous iron in hemoglobin to the ferric state forming methemoglobin. Results in oxygen starvation of tissues
Nitrate toxicosis clinical signs and diagnosis
Levels of metHb. Diagnosis by nitrate levels in feed or water. In suspected nitrate deaths save eye for analysis of nitrate.
Nitrate toxicosis treatment
IV or aqueous solution of methylene blue- good for ruminants, urine becomes dark green. Use ascorbic acid in cats and horses. Educate farms about nitrate accumulation
Cardiac glycosides
Contain glycosides- inhibit the sodium-potassium ATPase pump through competition with potassium for binding sites
Cardiac glycoside toxicity clinical signs and diagnosis
Clinical signs can occur from 1 hr to weeks after ingestion, depending on plant species. Trembling, staggering and dyspnea. Increased Ca and Na. Racing HR, arrhythmia, weak pulse. Dx- based on history, suspect, clinical signs, and analysis of vomit
Cardiac glycoside toxicity treatment
GI decontamination (if recently eaten), treat arrhythmia with propanolol, treat hyperkalemia if needed, use digoxin immune Fab fragments if propranolol ineffective.
Cyanide toxicity
Usually a problem with consumption of wilted leaves and seeds of wild cherry, ect. Also found in fertilizers, pesticides/rodenticides, fumigants, combustion.
Cyanide toxicity mechanism of action
Not toxic when dry, as hydrogen cyanide is volatile. Mechanism of toxicity is inhibition of cytochrome oxidase
Cyanide toxicity clinical signs
Generally occur within 15 mins to a few hrs after consumption. Classic symptom is cherry red blood that is slow to clot. Stomach contents smell like almonds. Sudden death, dyspnea, weakness, tremors.
Cyanide toxicity diagnosis
Made by history of ingestion and unclotted red blood. As well as analysis of frozen stomach contents
Cyanide toxicity treatment
Two steps: 1) Induce methemoglobin formation with sodium nitrite to bind cyanide. 2) Give sodium thiosulfate to increase formation of thiocyanate by rhodanese. Thiocyanate in non-toxic and elminated. If necessary, treat metHb with methylene blue
Methylxanthines
Caffeine, theobromine, theophylline, chocolate, medications. Most common around the holidays (chocolate). Unsweetened baking chocolate is especially toxic. Caffeine tablets and cocoa bean mulch are also a common problem in horses
Methylxanthine mechanism of action
Competitive antagonist of adenosine receptors; causes CNS stimulation, vasoconstriction and tachycardia. Prevents Ca reuptake leading to increased skeletal and cardiac muscle contractility. Inhibits phosphodiesterase, increases cyclic AMP and GMP concentrations
Methylxanthine toxicity clinical signs
Vomiting, diarrhea, diuresis, hyperactivity, “bounce”, panting, tachycardia, hypertension, ataxia, tremors, seizures, coma. Death is from arrhythmias or respiratory failure
Methylxantine toxicity diagnosis
Chemical analysis of stomach contents, plasma, serum, urine or liver. Theobromine can be detected in serum for 3-4 days after ingestion (long half-life)
Methylxantine toxicity treatment
GI decontamination (induction of emesis, repeated admin of charcoal). Monitor EKG (treat arrhythmias with lidocaine-not cats!). Treat seizures with diazepam or barbiturates, maintain respiration, fluid diuresis may increase excretion
