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377 Cards in this Set
- Front
- Back
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what is the first step when presented with a toxicosis case?
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stabilize the patient, be calm
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ABCs of stabilizing
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airway, breathing circulation
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preexisting conditions and diagnosis are determined
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after control of clinical signs
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when an owner calls with a toxicosis case, what instructions do you give them
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don’t waste time in transporting, bring container with you
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questions to ask in history
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time of onset, signs noted at home, owners suspicions, probable toxin/route of exposure
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many toxins lack a specific antidote, so ____________ may be lifesaving
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decreasing absorption
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goals of decontamination
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eliminate toxin, limit absorption, promote excretion, prevent reabsorption
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gastric decontamination includes
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emesis, gastric lavage, activated charcoal, cathartics/enema, whole bowel irrigation
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questions to ask re: gastric decontamination
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1) is the ingested toxin likely to cause significant effects. 2) is GID likely to change the outcome 3) do the risks outweigh the potential benefits?
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productive emesis requires
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food/liquid presence in the stomach
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when is emesis most effective?
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1 hour post ingestion
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emesis is contraindicated for
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corrosive materials, caustic materials, petroleum distillates, volatile materials
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emesis is contraindicated in patients with
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depressed mentation, decreased consciousness, lack of gag reflex, having or likely to have seizures, if the patient has already vomited
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centrally acting emetics
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apomorphine, ipecac, xylazine
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how can you reverse apomorphine?
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nalaxone
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which emetic is used in cats
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xylazine
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locally acting emetics
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hydrogen peroxide, ipecac
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indications for gastric lavage
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where the amount of toxin is potentially harmful. It was ingested within one hour of performing GL. Emesis cannot be achieved due to mentation/neuro signs
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contraindications for gastric lavage
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ingestion of a small amount of toxin or previous emesis (exception - snail bait). Ingestion of caustic/volatile substances
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risks for gastric lavage
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general anesthesia, aspiration, GIT trauma
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activated charcoal decreases absorption of many ingested toxins esp when given within
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two hours
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when will activated charcoal be beneficial greater than two hours post ingestion
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1- decreased gastric motility is present. 2- lg volume of toxin 3- toxins that undergo enterohepatic circulation 4- delayed release capsules
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significance of enterohepatic recirculation
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repeated doses of activated charcoal every 4 - 8 hours at half the original dose may be indicated. Metabolites are emptied in bile and reabsorbed into the small intestine. Allows for a persistent pharmacological effect
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name five toxins that activated charcoal is effective for
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organophosphates, insecticides, rodenticides, strychnine, ethylene glycol
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contraindications for activated charcoal
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abnormal mentation, hydrocarbon ingestion, GIT perforation
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saline cathartic
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sodium sulfate is efficient for bowel evacuation, preferable with activated charcoal
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sorbitol
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osmotic cathartic, available in activated charcoal preps
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colonic lavage
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aka high enema. Osmotic agents
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whole bowel irrigation
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through and through enema. Oral admin of large quantities of an iso-osmotic polyethylene glycol electrolyte solution. Irrigates entire GIT to prevent absorption
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when is WBI considered
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for large ingestions of sustained release drugs, iron tablets or illicit drugs
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contraindications for WBI
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GI perforation, gross hemorrhage, ileus, intractable vomiting, CV instability
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risks of WBI include
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electrolyte and fluid losses, abdominal pain, vomiting, aspiration, fatal aspiration and GI hemorrhage.
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absorbed toxins are generally excreted by
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kidneys
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urinary excretion may be manipulated
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with diuretics and drugs that alter urinary ph
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diuretics require
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maintenance of adequate renal function and hydration. Careful monitoring of fluid and electrolytes
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commonly used diuretics
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mannitol and furosemide
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alteration of urinary ph relies on physiochemical phenomenon that ionized compounds do not _________ and are not reabsorbed by the __________
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traverse cell membranes; renal tubules
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acid compounds and some barbiturates remain ionized in
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alkaline urine
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alkaline compounds remain ionized in
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acid urine
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name the urinary acidifier
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ammonium chloride, ethylenediamine dihydrochloride, physiologic saline
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urinary alkalinzer
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sodium bicarb
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supportive care
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control temp. maintain resp and CV function. Control acid base imbalances, control CNS disorders. Alleviate pain
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name three toxicants that cause seizures
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strychnine, tetanus, metaldehyde
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how to stop convulsions
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methocarbamol, diazepam, phenobarb, pentobarb
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which is preferred for strychnine?
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pentobarbitol
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strychnine ADME
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metabolized in liver, excreted in urine. Blood, liver, kidney highest conc. Stomach contents highest at death
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Sources of strychnine
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Pesticides to control gophers, rats, coyotes
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Strychnine color
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Dyed red or green (blue green milo)
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Strychnine moA
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Antagonize glycine at post synaptic neuronal sites--> unchecked reflex stimulation --> rigidity
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Strychnine onset
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10-120 min
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Strychnine signs
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No vomiting. Anxiety, stiffness, violent tetanic seizures, rigid extension, hyperalert
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Strychnine diagnosis
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Food or bait in stomach, analysis of frozen liver/urine
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Strychnine tx
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Before convulsions- give emetic. Activated charcoal, Pentobarb to relax, ammonium chloride to acidify urine
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When is ammonium chloride contraindicated
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If animal is acidotic
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What produces tetanus toxin?
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Clostridium tetani
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Clostridium tetani etiology
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Gram pos spore forming bacillus (under anaerobic conditions)
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Tetanus incubation
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1-3 weeks
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Tetanus source
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Contaminated wounds with anaerobic conditions
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Usual port of entry of horses
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Deep puncture wounds
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Usual port of entry in cattle
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Via repro tract at parturition (retained placenta)
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Most common cause of tetanus in lambs
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Docking with elastic band
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Tetanus moa
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Blocks inhibitory synaptic input, esp at glycine mediated sites, by binding to the presynaptic membrane and blocking release of glycine --> spastic paralysis
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What species is most sens to tetanus toxin?
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Horses
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How does death occur from tetanus
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Rigidity of the muscles of respiration and assoc asphyxia
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Tetany is characterized by
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Sustained tonic contractions of muscle without twitching
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Tetany clinical signs
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Sawhorse stance, protrusion of third eyelid, rigidity, sardonic grin. Cats- pump handle tail. Horses- lockjaw of masseter muscles
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Tetanus tx
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Antitoxin (reduce uptake of toxin by nerves). Tetanus toxoid. Penicillin
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MetAldehyde source
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Slug and snail baits
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Species most affected by metaldehyde poisoning?
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Dogs
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Signs of metaldehyde in dogs
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Continuous convulsions
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Metaldehyde tx
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Methocarbamol
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Where is metaldehyde poisoning common?
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California, gulf coast
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the solution to pollution is always
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dilution
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definition of an alkaloid
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large group of nitrogenous basic substances (plants/ synthetic). Typically bitter. End in "ine"
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toxic principle of chocolate
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methylxanthines - theobromine, caffeine
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what type of chocolate is most toxic
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bitter, unsweeteneded chocolate (Bakers)
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caffeine LD 50 in the dog
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140mg/kg
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theobromine LD50 in the dog
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250-500mg/kg
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when can lcinical signs of toxicosis be seen?
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at 10-20% LD50
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chocolate toxicity MOA
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stimulates catecholamine release (Epi, norepi), competitively antagnoizes cellular adenosine rc (CNS stim, tachycard, vasoconstriction). Increased intracellular Ca conc
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diagnosing chocolate toxicity
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history - most owners know its been eaten (type/how much)
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clin signs of chocolate toxicity
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sugar high, V/D, diuresis, restlessness, hyperactivity, tachycardia, VPCs, tachypnea, tremors, seizures, hypokalemia
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tx of chocolat toxicity
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ABCs, eliminate and promote excretion (emesis, charcoal, saline cathartics, fluids, urinary catheterization. May need sedation
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tx for tachyarrhythmias
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lidocaine if indicated
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treatment for tremors/seizures
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diazepam, phenobarb
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where are CNS serotonergic neurons primarily located
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midline raphe nuclei
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serotonin effects on CNS
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wakefullness, food intake, thermoreg, behavior, emesis, nociception, motor tone, sexual behavior, perception
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serotonin effects on PNS
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regulate vascular tone, GI motility, platelets, wound healing, pain
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dopamine effects on CNS
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eating, sex, behavior, cognition, voluntary movement, sleep, mood, attention, memory, learning
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dopamine effects on PNS
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vasodilation (constriction at high doses with inc BP)
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can dopamine cross the BBB
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no
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norepi CNS effects
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attention, responses, fight or flight
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norepi PNS effects
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inc HR, release of glucose from energy stores, inc blood flow to skeletal muscle, increases brains oxygen supply
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effects of illicit drugs are from
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excessive serotonin/dopamine/norepi stimulation
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pathways to ultimate high
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incease synth from increased precursors, increased release from presynaptic neurons, decreased metabolism
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MOA for opioids and cocaine
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blockade of reuptake
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MOA for LSD
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stim of rc by agonists
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sympathomimetics
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stimulate release of norepi from stores in adrenergic nerve terminals. Directly stim alpha and beta adrenergic rc
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mentation changes assoc with illicit drugs
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agitation, confusion, disorientation, vocalization, excitement
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autonomc signs assoc with illicit drugs
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diarrhea, mydriasis, tachycardia, tachypnea, hypertension, fever
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neuromuscular signs assoc with illicit drugs
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hyperreflexia, myoclonus, tremors, rigidity, seizures, secondary hyperthermia, resp muscle compromise
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legal amphetamines
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ADHD, weight loss, narcolepsy drugs (ritalin, adderall, dexadrine, pseudoephedrine, ma huang)
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illegal amphetamiens
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methamphetamine, ecstasy/MDMA
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amphetamine metabolism / excretion
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liver / kidneys
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cocaine
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schedule 1, adulterated versions, hydrochloride salt
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cocaine metabolism / excretion
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liver / urine
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ddx for illicit drugs
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methylxanthines, metaldehyde, strychnine, OP, carbamates, TCA, tremorgenic mycotoxins, permethrin
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diagnosing illicit drugs
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can be difficult due to owners reluctance to give accurate history. Clinical presentation can be confusing. Collect blood, urine, stomach contents
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gold standard for illicit drug dx
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Gas chromatography / mass spectrometry
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tx for illicit drugs
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ABCS, decontaminate if safe (emesis), activated charcoal, manage seizures/tremors/hyperactivity, antagonize serotonin (cyproheptadine), acidify urine (ammonium chloride, ascorbic acid). Manage hyperthermia, manage CV abnormalities. Manage hyperextension/rigidity (methocarbamol). decrease stimulation
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tx cor cocaine induced hyperactivity
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naloxone
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concerns for patients from meth houses
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eval for injurty from volatile toxic ingredients. Resp distress/compromise, skin irritation/burns, ocular injury, oral cavity injury
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venlafaxine / effexor
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bicyclic antidepressant. Reuptake inhibitor of both serotonin and noradrenaline. Weakly inhbits dopamine reuptake
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decontamination from effexor
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emesis if asymptomatic and <1 hour. If extended release, pulse dose activated charcoal without a cathartic q4-6hours.
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treatment from effexor toxicity
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cyproheptadine, ace, high lipid solubility tx to decrease plasma levels
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lisdexamphentamine / vyvanse
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adhd, prodrug that is metabolized to dextroamphetamine. Extended release product.
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decontamination from vyvanse
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emesis if <1 hour, pulse dose activated charcoal, IV fluids, phenothiazines for hyperactivity/agitation, b-blockers for tachycardia. DIAZEPAM CONTRAINDCIATED, WORSENS DYSPHORIA
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4-aminopyridine (Avitrol, fampridine)
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utilized to control pest birds, tx of MS and lambert eaton mysasthenic syndrome. K channel blocker, and enhancing cholinergic transmission by increasing release of ACH and other neurotransmitters
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where is 4 aminopyridine common found
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in corn for birds to consume
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effects of 4 aminopyridine
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convulsions and death, depending on dosase, within 1 hour.
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4 aminopyridine dx
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GC/mass spec of stomach contents or bait
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4 aminopyridine tx
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emesis, activated charcoal, saline cathartic, diazepam to effect
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Bovine bonkers
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4 methyl imidazole
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What does 4MI form as a result of?
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Ammoniated feed
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Why are low quality forages ok when ammoniated?
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They contain low levels of soluble sugars
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Onset of 4MI toxicity
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Rapid OR weeks after start on treated hay
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Signs of bovine bonkers
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Hyperexcitability, wild running, circling, seizures, death. Seizures are intermittent.
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Species that is most sensitive to water deprivation
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Swine
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How are swine deprived of water
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Mechanical failure, neglect, overcrowding, animals fail to find water
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Source of sodium toxicosis in cattle
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Improperly mixed feeds, saline waters , brine from oil well drilling
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High salt consumption or water deprivation followed by unlimited access to water results in
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Cerebral edema and neuro signs
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Water deprivation MOA
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Na passively diffuses into CSF but requires active transport to be removed from the CSF. Sodium trapped in cns attracts water due to osmotic gradient --> cerebral edema
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Sign of water deprivation in swine
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Onset after 1-5d, wandering, circling, twitching snout, head pushing, pivoting around one foot, dog sitting
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Signs of water deprivation in cattle
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Head pressing, blindness, knuckling,
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Signs of sodium toxicosis in dogs
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Vomiting, GI signs
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Pathology of sodium toxicosis in swine (pathognomic lesion)
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Eosinophilic cuffs
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Diagnosing sodium toxicosis
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Serum and csf na levels of over 160meq/l. Brain levels often 2000-3000ppm
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Penitrem a
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Penicillum mycotoxins
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Sources of penitrem a
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Moldy fridge food, moldy nuts, moldy grains/mixed feeds
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Species to susceptible to penitrem a
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Bovine, canine, others
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The moa of penitrem a is similar to that of
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Strychnine/tetanus
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Signs assoc with penetrem a
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Low doses- fine muscle tremors. High dose- convulsions, death
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Treatment for penitrem a
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Activated charcoal, diazepam/pentobarb
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Name four staggers syndromes
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Ryegrass, dallis/paspalum, bermuda, corn
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Symptoms of staggers syndromes
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Hyperexcitability, tremors, stiff stilted gait, ataxia. Head tremors.
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In grass staggers, what type of plants are more hazardous
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Mature plants
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Dallis grass staggers has been assoc with
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Heavy ergot infection if dallis grass heads
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Major sign of paspalum staggers in sheep, cattle
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Legs move in unison - hopping
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Clinical signs of paspalum staggers in horses
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Mild excitability, spastic ataxia, hypermetria, tetany
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Corn staggers seen with ingestion of
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Corn silage
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Zinc phosphide
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Dull, greyish black powder used as rodenticide
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Alum phosphide is used as
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a grain fumigant for insect and rodent control
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Zinc and alum phosphide both degrade to ________ which is ______
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Reactive phosphine gas.... Toxic
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Stability of zinc phosphide
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Unstable in water or acid, stable for 2 weeks under average climactic conditions. Stable for long periods of time if kept dry
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Phosphine gas odor
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Garlic or rotten fish
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Two mechanisms of toxicity for phosphine gas
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Feeding directly on bait or relay toxicosis
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Signs of phosphine gas toxicity in dogs
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Tremors, salivation, running fits, ab pain, acetylene odor on breath
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What can phosphine gas seizures resemble?
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Strychnine convulsions
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Phosphine gas lesions
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Odor in stomach
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Diagnosing phosphine gas toxicity
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Frozen vomitus or gastric lavage fluid, frozen stomach contents
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Tx for phosphine gas toxicity
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Emesis
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Cicuta spp
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Water hemlock
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Water hemlock description
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Likes wet rich soil, ~6ft tall,
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Water hemlock toxin
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Cicutoxin
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Species susceptible to water hemlock
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Cattle
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Source of toxicosis in cattle
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From eating plant or drinking water in puddles with trampled plants
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Signs of water hemlock toxicity
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Peracute violent course, convulsions, violent seizures,
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Asclepias
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Milkweed
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Milkweed toxic principle
|
Galitoxin
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Which has higher toxicity- broad or narrow leaf?
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Narrow
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Main cause of fatalities from milkweeds
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Cardenolides (in western species of plant)
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A. Latifolia
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Broad leaf milkweed
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When does milkweed toxicity occur
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When good forage is inadequate
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What kind of signs do whorled milkweeds produce?
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Cns signs- convulsions, tremors, ataxia, tachyarrythmias
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What kind of signs do broad leafed milkweed have?
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Gi signs
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Milkweed toxicity treatment
|
Activated charcoal
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sources of lead in small animals
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lead paint, lead objects, plumbing materials, lead shot in tissues, oil well drilling, dumps
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ADME of lead
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ingestion most common. Can cross the placenta and enter milk.
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lead in cattle
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objects can settle in reticulum and allow absorption over an extended period of time
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clin path sign of lead toxicosis in dogs
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basophilic stippling
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enzymes inhibited by lead
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aminolevulinic acid synthetase (ALAS), aminolevulinic acid dehydratase (ALAD), coprogenase, heme synthetase,
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what affect does lead have on heme
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inhibits union with globin
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three causes of blindness in cattle
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lead, polio, water deprivation
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neuro signs of lead toxicosis
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blindness, circling, head pressing, ataxia, ear twitching, exaggerated blinking
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what kind of signs are seen in dogs with lead toxicosis
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GI signs
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what repro signs are seen with lead toxicosis?
|
crosses placenta, so can cause abortion. Also found in milk
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effects of lead on waterfowl
|
tenting of wings
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what sample is needed to test for lead?
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whole blood
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DDX for lead in dogs and cats
|
rabies, distemper, hepatitis, heavy metal toxicosis
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DDX for lead in ruminants
|
rabies, polioencephalomalacia, TEME, listeriosis
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name a chelation agent for lead
|
Succimer - DMSA mesodimercapto - succinic acid
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what should be given when treating for lead
|
Thiamine, meds to control seizures
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sources of mercury
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dental fillings, fungicides, fungicide treated seed grains,
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where can methyl mercury accumulate
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eggs and animal tissues, aquatic organisms
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main systems affected by mercury
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neuro, gI, renal, dermal
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what species is especially sensitive to environmental mercury?
|
felines
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major NPN source in use today
|
urea
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where is urea commonly found
|
feed supplements for mixing or blending, cubes, molasses-NPN combo
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what usually contains ammonia, ammonium salts or urea and may be accidentally ingested/
|
dry and liquid fertilizers
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most cases of ammonia poisoning occur as a result of
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mistakes in mixing or feeding supplements containing a high percentage of urea
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species susceptible to ammonia poisoning?
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all mammalian
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why are ruminants more susceptible to ammonia than monogastrics/
|
hydrolysis of urea to ammonia by rumen microorganisms
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predisposing factors for urea poisoning
|
failure to gradually adapt ruminants to diets containing NPN
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what does the rate of release of ammonia from urea depend on
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the amount of NPN ingested, the amount of urease present in the rumen and the ph of rumen contents
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what cycle does ammonia inhibit? What does this result in?
|
Krebs cycle. Compensatory increase in anaerobic glycolysis with resultant lactic acidemia (rumen alkalosis and blood acidosis)
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signs of ammonia poisoning
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rapid onset, frothy salivation, depression, teeth grinding, ab pain. Bloat/regurg of rumen contents. Sudden death
|
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lesions assoc with ammonia poisoning
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odor in rumen content and tissues, NO DEFINITIVE LESIONS. Animals bloat rapidly and may decompose more rapidly than normal due to heat
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diagnosing ammonia tx
|
clin signs, history, significant increases in PCV, rumen ph
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differentiate urea poisoning from acute grain overload
|
based on rumen PH
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a rumen ph of _____ is required to proper rumen motility
|
5.5-7.6
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treating a recumbent animal for ammonia poisoning
|
futile, they almost never respond
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best tx for cattle ammonia poisoning
|
cold water and vinegar
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ddx for urea poisoning
|
blue green milo, nitrate, urea, arsenic, bloat, herbicides
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what are fumonisins
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mycotoxins produced by fusarium moniliforme
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where are fumonisins primarily found
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corn
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what does infested corn look like?
|
grossly normal
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what climactic factors predispose to fungal growth
|
midsummer drought, early wet fall, fluctuant temps
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onset of fumonisin poisoning in horses
|
usually 14-21 d after a new batch of corn is fed, can be as early as 7 days
|
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signs of fumonesin poisoning in horses
|
neurotoxic syndrome, hepatotoxic syndrome
|
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hepatotoxic syndrome
|
5-10 days before death. Icterus, facial edema, elevated liver enzymes. Hepatoencephalopathy
|
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diagnosing fumonisin poisoning
|
ELISA screening test
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how much fumonisin is safe for horses to have?
|
less than 5ppm in the non roughage portion of the diet
|
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treating fumonisin poisoning
|
no known effective tx
|
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what plants causes chewing dz of horses
|
yellow star thistle and Russian napweed
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genus of yellow star thistle / Russian napweed
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centauria spp.
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toxic principle assoc with chewing dz
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unknown
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onset of chewing disease
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slow, gradual. Most from 30-90 d after grazing.
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signs of Russian napweed toxicity
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hypertonicity, upper lips pulled over teeth, traumatized lips, tongue lolling, non productive chewing movements (food never reaches pharynx)
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lesions assoc with chewing dz
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nigropallidoencephalomalacia
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what are the two locoweed genera
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astragalus and oxytropis
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are locoweeds perennials or annuals?
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perennials
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what is the significance of locoweed
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most economically significant genera of poisonous plants in the USA
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toxic principles of locoweeds
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miserotoxins --> yield 3-nitropropanol
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signs assoc with miserotoxins
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knuckling, goosestepping, resp distress,. Methemoglobin formation.
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selenium indicator plants are assoc with both
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acute and chronic poisoning
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chronic poising subtypes
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alkali dz and blind staggers
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alkali dz
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selenium accumulators. Signs include long hooves, separation of coronary band, rough hair, mane and tail loss.
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blind staggers
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possibly not due to selenium. Form of polioencephalomalacia
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true locoism is a result of ingestion of
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swainsonine
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locoism is characterized by
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emaciation, habituation, proprioception deficits, abortion, small/weak young, birth defects (BENT LEGS), hydrop,
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lesions assoc with swainsonine
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vacuolization of tissues
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high mountain dz
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right heart failure in cattle
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treating locoism
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no true tx. Remove plant.
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bromethalin
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single feeding rodenticide
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clinical signs of bromethalin toxicity
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depression, ataxia, tremors at low doses. Blindness, vomiting, headpressing. High dose -hyperexictability, running fits, generalized seizures, loss of bark, forelimb extensor rigidity
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species most sensitive to bromethalin
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cats
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bromethalin MOA
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uncouplers of oxidative phosphorylation, inhibit mitochondrial energy production
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DDX for bromethalin
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any number of neuro disorders
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tissue needed to dx bromethalin
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brain
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lesions assoc with bromethalin
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mild cerebral edema
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bromethalin tx
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charcoal. Mannitol. Steroids ineffective once clinical signs developed.
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buckeye /horse chestnut genus
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aesculus
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when does aesculus poisoning occur
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spring. Also in early fall/early winter
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what part of the plant is most dangerous?
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mature nuts
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species affected by aesculus poisoning
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cattle, sheep, hogs, chickens, horses
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early clinical signs assoc with aesculus
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incoordination, staggering, hyperesthesia
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lesions assoc with aesculus
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none on postmortem exam. Buckeyes appear bright red in rumen fluid
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what can polio be caused by
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sulfur toxicosis
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sources of sulfur
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corn gluten, molasses, water, forage, fertilizers, gypsum
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maximum total dietary conc of sulfur should be
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<2000 ppm
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maximum total dietary conc of sulfate in water should be
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<500ppm
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sulfur induced polioencephalomalacia occurs _______ of thiamine status
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independent
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what is polioencephalomalacia
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lesion in the brain - necrotizing destruction of cortical grey matter
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MOA of sulfur toxicosis
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hydrogen sulfide gas accumulates in the rumen gas cap. Interferes with cellular energy metabolism
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signs of sulfur toxicosis
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acute- blindness. Subacute- ataxia, crossed legs, tremors, circling. Diarrhea. Some calves may stop eating.
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lesions assoc with sulfur
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brain often fluoresces. Swelling ,edema, bulging on cut surfaces, herniation into foramen magnum,
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diagnosing sulfur toxicosis
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clinical signs, history, lesions. Feed/forage/water analysis
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DDX for sulfur
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lead, water deprivation, polio from other sources
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tx for sulfur
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thiamine. Remove from source.
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pteridium aquillinum
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brackenfern
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brackenfern toxic principles
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thiaminase (horses), bone marrow damage, ptaquiloside (cattle carcinogen). Cyanogenic glycoside.
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brackenfern toxicity in horses
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mostly neuro - bracken staggers. Emaciation
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radiomimetic dz
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brackenfern in sheep/cattle, affects bone marrow
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bovine enzootic hematuria
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bracken fern induced hematuria
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what kind of cancer can brackenfern cause
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bladder cancer in cattle
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ddx for brackenfern in cattle
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septicemia, anaplasma, moldy sweet clover, lepto
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brackenfern tx
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thiamine
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equisetum arvense
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horsetail
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toxic principle assoc with horsetail
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thiaminase (non ruminants). Still toxic when dried
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species susceptible to horse tail
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horses
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eupatorium rugosum
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white snakeroot
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white snakeroot habitat`
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open wooded, semi shaded areas
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toxic principle assoc with white snakeroot
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tremetol. Remains in dried plant. More of a problem in fall
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where is tremetol secreted rapidly?
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in the milk
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why is tremetol not considered a problem in modern dairies?
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dilution. NOT detoxified by pasteurization
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signs of white snakeroot in cattle
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cns depression
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signs of white snakeroot in horses
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CHF, wide legged stance, swelling of ventral neck, jug pulse, sweating, photosensitivity, tremors, hematuria
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cannabis sativa
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marijuana
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when is marijuana poisonous?
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when damaged by drying, heating, smoking or aging. NOT when fresh.
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are emetic drugs used to tx marijuana poisoning?
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only if prior to onset of sedation/ataxia
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does ivermectin cause seizures?
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NO
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how do you diagnose lead in a live animal
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PTT
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how do you diagnose lead in a dead animal?
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liver
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how do you diagnose polio in a live animal?
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feed/water analysis for sulfur
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how do you diagnose polio in a dead animal?
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brain
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how do you diagnose water deprivation in a live animal
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CSF, serum
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how do you diagnose water deprivation in a dead animal
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brain NA level
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What disease should you think of when you see blue green milo?
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strychnine
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What is the predominate clinical sign/distinguishing characteristic in strychnine seizures?
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powerful extensor rigidity
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genus of tetanus
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clostridium
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three most common toxins found in dogs in Oklahoma
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ethylene glycol, strychnine, anticoagulant rodenticides
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who was the father of modern toxicology?
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Paracelsus
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what is the toxic principle found in snail bait?
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metaldehyde
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what is the toxic principle in zinc phosphide?
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phosphine gas
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what is the toxic principle in bovine bonkers?
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4 methyl imidazole
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10. What type of feed do you start asking the owner about if you suspect their cow has bovine bonkers?
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ammoniated feed
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what is the key lesion in pigs that have died from water deprivation/
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eosinophilic cuffing
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what is the toxic principle of Avitrol?
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4-aminopyridine
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what is the tx of choice for metaldehyde poisoning?
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methocarbamol
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what are the three most common causes of blindness in calves?
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lead, polio, water deprivation
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what do you treat a lead poisoned cow with?
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Ca EDTA
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what is the best tx for lead toxicity in a dog?
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succimer
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what is the mycotoxin found in mold refigerator food/
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penitrem A
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what are the two toxic principles found in choclate
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caffeine and theobromine
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what kind of mercury accumulates in tissues and eggs
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methyl mercury
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what is the toxic principle of moldy corn dz
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fumonisin
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what is the max amount of fumonisin recommended by NRC that should be found in a horse's diet
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5 ppm
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what is the lesion in yellow star thistle
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nigropallidoenephalomalacia
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what causes a pump handle tail in cats?
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tetanus
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Which staggers syndrome is associated with ergot-infested seed heads?
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dallis grass staggers
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What causes flicking of the third eyelid in cattle?
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tetanus
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Which species is more sensitive to tetanus than a mouse, and why is this important?
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Horse; because you shouldn’t use the mouse inoculation test for a definitive diagnosis if the horse is more sensitive than the mouse, because if the levels are low the mouse will show a negative result but the tetanus could still be present in the horse.
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main dz assoc with ingestion of brackenfern
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urinary bladder cancer
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genus of water hemlock
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cicuda
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toxic principle of water hemlock
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cicutoxin
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primary clinical sign of water hemlock poisoning
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violent convulsions
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what causes alkali dz?
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selenium toxicosis
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How do you get selenium toxicosis in grazing animals?
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Ingestion of selenium-indicator locoweed
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What are the two genuses of locoweed?
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Astragalus and Oxytrophin
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What is the toxic principle of true locoism?
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wainsonine
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What organ does high mountain disease affect?
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Heart (causes right heart failure)
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what is the genus of buckeye?
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aesculus
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what is the genus of yellow star thistle?
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centauria
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what is the name of the cousin of yellow star thistle that is found in OK?
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russsian napweed
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What is the toxic principle of yellow start thistle?
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unknown
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Which rodenticide mainly mimics other poisons?
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bromethalin
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What is the genus of milkweed?
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aesclapias
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What is the toxic principle of milkweed?
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Galitoxin
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You necropsy a dog that was brought to you; upon opening the abdomen you smell garlic/rotten fish odor, as well as an acetylene-type smell. What is the most likely cause of death (the toxic principle)?
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phosphine gas
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You show up on a farm because the owner has a group of cattle that are trembling and falling over. As they start to move, they are hopping with both feet and staggering. What is the most likely disease you are faced with?
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Grass staggers (either Bermuda, dallis, rye, etc).
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You show up on a farm to see a dead cow and post it in the field. You suspect water deprivation. What is the BEST sample to send, and what are you testing for?
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Brain- sodium concentrations.
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A client calls because there are birds acting crazy, falling out of the sky, and flying into things. She thinks they have west nile, but you tell her that most likely the real agent causing the behavior is:
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avitrol - 4 aminipyridine
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What causes chewing disease in horses?
|
yellow star thistle
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What is the toxic principle of yellow star thistle?
|
unknown!
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What is the primary lesion found in chewing disease?
|
nigropallidoenephalomalacia
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What does activated charcoal do?
|
adsorbs toxins
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You have a dog that presents with seizures, SLUDDE, and dies quickly. The owner hands you something that he thinks the dog could have gotten into; it looks like little poppyseeds. What type of compound is it most likely going to be?
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carbamate
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What is the antidote for carbamates and OP’s in an emergency situation?
|
atropine
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If you have a cat that presents damp, and is shivering, salivating, shaking, and starts seizuring, what is the first thing you need to do?
|
wash it off
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Name 4 toxins that cause CNS depression:
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White snakeroot, Marijuana, Amitraz, Ivermectin
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If you show up to a LOT of cows because they suddenly died, would the following diseases be on your differential list? Water deprivation? Dallis grass? Aluminum phosphide? Water hemlock? High fumonisin in feed? Locoweed? Urea lick tanks? sulfates? white snakeroot?
|
water deprivation - Y. dallis grass- N. alum phosphide - Y. water hemlock -Y. high fumonisin -N. locoweed -N. Urea lck tanks - Y (if no previous exposure). Sulfates - N. white snakeroot -N
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|
|
genus of the mold in fumonisin
|
fusarium
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|
|
fumonisin lesion in horses
|
leukoencephalomalacia
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If an owner brings in a sick dog and keeps saying it has been eating grass, and right in front of you the dog has a seizure, what are some things that can cause seizures, and what will the seizures look like for each?
|
"Strychnine – Powerful extensor rigidty. Treat with pentobarbital. b. Bromethalin – Same kind of seizures as strychnine but may also be head pressing and acting blind when not having a seizures because of cerebral edemGummy worm. c. Zinc phosphide (or aluminum) – typical seizures but on post mortem should smell garlic/fish/acetylene.
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A dog presents because he keeps vomiting repeatedly. Name some differentials:
|
chocolate, lead - chronic vomiting (more GI signs in dogs)
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|
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Pet birds, ADR, off feed, diarrhea:
|
lead poisoning
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Elephant had a seizure, died. All 4 legs were sticking out straight. What could it be?
|
strychnine
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Group of cattle, but only calves are having clinical signs of staggering, blindness:
|
sulfur, white snakeroot
|
|
|
Group of cattle, only lactating cows are dying:
|
water deprivation
|
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If a dog ate a bunch of lead paint chips, what would you see on a blood smear (cytology)?
|
Nucleated RBCs and basophilic stippling
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|
|
Big lesion seen in locoweed across different types of tissues:
|
vacuolization
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|
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If cows that have been eating locoweed have enlarged hearts, what is the named of the disease?
|
high mountain disease
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If someone has “gyp water” on their place, what disease do you think about?
|
Polio in calves because gyp has sulfate
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Geese, cut them open have little gray balls:
|
lead
|
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|
Geese with little poppyseeds:
|
aldecarb (carbanamate stuff)
|
|
|
Geese with bluegreen milo:
|
strychnine
|
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|
Dog comes in, just ate a bunch of no-doz, what do you do?
|
Emetics: apomorphine, hydrogen peroxide, xylazine
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|
|
Activated charcoal is a very good method for adsorbing toxins, but does NOT work in what type of toxicosis?
|
acid base disorders
|
|
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Name 5 things inhibited by lead in the body:
|
ALAS, ALAD, coprogenase, heme synthesis, and union of heme with globin
|
|
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In waterfowl such as ducks, when they have lead poisoning what are two clinical signs you can see?
|
Tenting of wings and stained vent
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For large animals and small animals, what is the KEY treatment/antidote for lead toxicosis?
|
LA - Ca EDTA, SA - succimur
|
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An animal comes in showing neurologic signs and you suspect lead. What is the first treatment?
|
Give Thiamine to relieve neurologic signs
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|
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cattle predominate clinical sign of lead toxicosis:
|
neuro (blindness, circling)
|
|
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dog predominate clinical sign of lead toxicosis:
|
GI - V/D
|
|
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horse predominate clinical sign of lead toxicosis:
|
laryngeal paralysis, heave lines
|
|
|
psittacine birds predominate clinical sign of lead toxicosis:
|
ADR, off feed, diarrhea
|
|
|
waterfowl predominate clinical sign of lead toxicosis:
|
tenting of wings, stained vents
|
