Midterm Flashcards
Target organ and mechanism of botulism toxin?
Lower motor neurons - prevents release of acetylcholine at the presynaptic nerve terminal
Species differences in sensitivity to botulism toxin?
Horses > > > other mammals
Birds also highly sensitive
Main distinguishing clinical feature of botulism toxin?
Ascending lower motor neuron paralysis
Shaker foal syndrome
Key method for management of botulism?
Antitoxin - Helps to reduce circulating toxin PRIOR to binding to neurons, but does not reverse clinical signs
Target organ and mechanism of action of tetanospasmin?
CNS - prevents release of GABA and glycine resulting in uncontrolled muscle contraction
Target organ and mechanism of action of tetanolysin?
Wound site - local tissue necrosis and lysis of RBC
Differences in species sensitivity to tetanus?
Horses and small ruminants > other mammals > > > birds
Main distinguishing clinical features of tetanus?
Sawhorse stance and prolapsed third eyelid. Consciousness unaffected
Key method for management of tetanus?
Vaccination - core vaccine for horses and risk-based for cattle
Key clinical features of anthrax?
Sudden death and terminal hemorrhage from orofices
Target organ and mechanism of action of Microcystins (BGA)?
Liver - inhibition of protein phosphatases leading to cytoskeleton disruption, oxidative damage, and inhibition of glucose metabolism
Target organ and mechanism of action of Anatoxin-A (BGA)?
CNS - post-synaptic nicotinic acetylcholine agonist and acetylcholinesterase inhibitor
Key clinical features of anatoxin A (BGA)?
Peracute neuroexcitation, respiratory failure
Key methods for management of cyanobacterial toxins?
Decontamination often not possible, no antitoxin. Aggressive symptomatic and supportive care only
Target organ and mechanism of action of strychnine?
CNS - glycine antagonist at post-synaptic receptors in the SC and medulla –> uncontrolled stimulation of motor neurons
Key clinical features of strychnine?
Severe extensor rigidity, tonic-clonic seizures that are responsive to external stimuli
Management of strychnine?
Aggressive decontamination and supportive care
Species differences in sensitivity to bromethalin?
Cats > > other species > > > > guinea pigs
Target organ and mechanism of action of bromethalin?
Brain - loss of oncotic control and lipid peroxidation leading to cerebral edema
Key clinical features of HIGH DOSE bromethalin in dogs?
Convulsant syndrome - tremors, running fits, seizures, etc.
Key clinical features of LOW DOSE bromethalin in dogs (or any dose in cats)?
Paralytic syndrome - hindlimb paresis/ataxia and decreased proprioception
Abdominal distension in cats
Management of bromethalin poisoning?
No antidote; early decontamination is key. IVF diuresis is not helpful because of low renal excretion. Beware hypernatremia
Target organs and mechanism of fluoroacetate (compound 1080)?
CNS and heart - inhibition of key enzymes in the Krebs cycle
Species differences in sensitivity to fluoroacetate?
Dogs > other spp
Key clinical features of fluoroacetate poisoning?
Sudden death, CNS excitation, tachycardia and dyspnea
Management of fluoroacetate poisoning?
Antidote exists but is not readily available. Symptomatic and supportive care
Mechanism of action of warfarin (and other related rodenticides)?
Inhibition of vitamin K epoxide reductase –> prevention of recycling of vitamin K
Key clinical features of warfarin toxicity?
Hemorrhage, signs of anemia
Prolonged PT, followed by also PTT
Management of anticoagulant rodenticide poisoning?
Antidote - Vitamin K1 (ideally given with a fatty meal)
Decontamination and repeated assessment of PT. Blood/plasma transfusions (incl. autotransfusions) may be needed
Secondary poisoning with phosphide rodenticides?
Unlikely - only stable when stored in dry environments
Risk mainly to humans, associated with inhalation of phosphine gas
Mechanism of action of phosphide rodenticides?
Contact with stomach acid –> release of phosphine gas, which is highly irritating and causes oxidative damage to many tissues
Key clinical features of poisoning with phosphide rodenticides?
Severe GI distress, multi-organ damage (CV, lungs, CNS). Delayed onset liver/kidney failure is possible
Management of phosphide rodenticide poisoning?
Decontamination in well ventilated area
Neutralize stomach pH (zinc phosphide only)
Supportive care and antioxidants
Cholecalciferol mechanism of action?
Disruption of Ca/P homeostasis leading to hypercalcemia and dystrophic mineralization
Key clinical features of cholecalciferol poisoning?
Non-specific clinical signs. Hyperphosphatemia and hypercalcemia on bloodwork, and metastatic calcification (kidney, aorta, GIT, etc.)
Management of cholecalciferol poisoning?
Supportive care and monitoring
IVFT, prednisone, and furosemide to manage hypercalcemia
Cholestyramine to reduce enterohepatic recirculation
Context of exposure to organochlorine insecticides?
Banned in Canada due to environmental persistence, so poisonings are uncommon outside of access to old stockpiles
Target organ and mechanism of action of organochlorine insecticides?
CNS - interference with action potentials (Na/K flow) and NT (GABA inhibition) in the CNS leading to CNS excitation
Important toxicokinetics of organochlorine insecticides?
Highly lipophilic with a very long elimination half-life and enterohepatic recirculation
Key clinical features of organochlorine insecticide poisoning?
CNS excitation, agitation
Management of organochlorine insecticide poisoning?
No specific antidote. Anticonvulsants, methocarbamol, cholestyramine, and other forms of supportive care
Tissues to submit for pesticide screens?
Fat, liver, brain, gastric contents
Exposure to OP/carbamates?
Secondary poisoning possible from poisoned animals and insects, ingestion of ear tags, etc.
Target organ and mechanism of action of organophosphate/carbamate insecticides?
CNS/PNS - acetylcholinesterase inhibition leading to nicotinic and muscarinic overactivation
Key clinical signs of acute organophosphate/carbamate insecticide poisoning?
SLUDGE (salivation, lacrimation, urination, diarrhea, GI pain, emesis)
Tremors, weakness, ataxia, muscle stiffness, etc.
Altered mentation, respiratory depression
Two other syndromes caused by organoposphate/carbamate insecticides?
Intermediate syndrome - acute muscle weakness
OP-induced delayed polyneuropathy (OPIDPN) - degeneration of long motor nerves 1-4 weeks after exposure
Management of organophosphate/carbamate insecticides?
Antidote - atropine
Give low dose, check for mydriasis/tachycardia. If not present, diagnosis confirmed and give more atropine
Samples to submit for testing for OP/carbamate poisoning?
Heparinized whole blood or brain - check for AChE activity
Target organs and mechanism of action of chlorate herbicides?
Causes oxidative damage to RBCs and GIT
Key clinical signs associated with chlorate herbicide poisoning?
GI upset, hemolysis and signs of anemia
Management of chlorate herbicides?
Antidote - Methylene blue
IVFT and forced diuresis
Target organ and mechanism of paraquat herbicide poisoning?
Lungs - accumulation and oxidative damage in all cell types
Key clinical features of paraquat herbicide poisoning?
GI upset and blisters on immediate contact
Acute, severe respiratory distress, renal damage, liver damage
Target organ and mechanism of action of Metaldehyde molluscicide poisoning?
CNS - interference with inhibitory NT leading to CNS excitation
Key clinical features of metaldehyde poisoning?
CNS excitation - agitation, hyperesthesia, tremors…
Tachypnea and tachycardia, eventual resp failure
Stomach contents smell like apple cider vinegar
Management of metaldehyde poisoning?
Gastric lavage, anticonvulsants/muscle relaxants, active cooling. Beware the long half-life
Target organs and mechanism of action of NSAID toxicity?
GIT, kidney, CNS - decreased prostaglandin decreases blood flow, mucosal barrier, etc.
Cats tend to present with renal disease, dogs with GI disease
Key clinical signs of NSAID toxicity?
GI upset, PU/PD with renal papillary necrosis, right dorsal colitis in horses
CNS signs at very high doses
Management of NSAID poisoning?
Aggressive symptomatic and supportive care, ILE, therapeutic plasma exchange
Target organs and mechanism of acetaminophen poisoning?
Blood (cats) or liver (dogs/cats) - bioactivation results in depletion of cellular glutathione and oxidative damage
Key clinical signs of acetaminophen poisoning?
Early GI upset, depression, swelling
Later - signs of liver damage, hemolytic anemia
Management of acetaminophen poisoning?
Antidote - N-acetylcysteine
Decontamination and supportive care
Key clinical signs of metronidazole poisoning?
Vestibular signs (central)
Management of metronidazole poisoning?
Should stop on its own once metronidazole is discontinued
Target organ and mechanism of ivermectin poisoning?
CNS - potentiation of glutamate and GABA-gated chloride channels leading to CNS depression
Key clinical features of ivermectin poisoning?
CNS depression, mydriasis, blindness due to retinal edema
Management of ivermectin poisoning?
Nothing specific; symptomatic and supportive care. Animals will typically regain their sight slowly
Target organ and mechanism of action of pyrethroids?
CNS - prolonged Na channel opening leading to repetitive AP firing and CNS excitation
Which animals are most likely to be poisoned with pyrethroids and how?
Cats - via exposure to flea/tick meds (e.g. Advantix) for dogs
Key clinical features of pyrethroid poisoning?
GI upset, CNS excitation (tremors etc.), mydriasis, salivation
Management of pyrethroid poisoning?
Tremor control - methocarbamol
Dermal decontamination may be needed
Mechanism of antidepressant poisoning?
Overstimulation of serotonin, dopamine, and/or norepinephrine receptors affecting CNS and CV system
Main clinical features of serotonin syndrome?
GI upset
CNS excitation, mydriasis, tremors/seizures
Tachycardia/arrhythmias and hypertension
Management of poisoning with antidepressant medication?
Antidote to serotonin syndrome - cyproheptadine
Acepromazine for sedation
Supportive care
Mechanism of salbutamol poisoning?
Overstimulation of beta receptors (CV and CNS)
Main clinical features of salbutamol poisoning?
Tachypnea/dyspnea
Hypotension with reflex tachycardia and arrhythmias
CNS excitation
Hypokalemia
Management of salbutamol poisoning?
Decontamination not possible
Antidote - beta blockers
Correction of hypokalemia
Target organs and mechanism of action of cocaine/amphatamines?
Increased stimulation by NE, 5HT, and DA –> sympathomimetic toxidrome (CV and CNS)
Main target organs for opioids?
CNS, CV, respiratory, GI
Species differences in opioid poisoning between dogs and cats?
Dogs - depression/sedation, miosis, hypothermia
Cats - excitation, mydriasis, hyperthermia
Main cause of death from opioid poisoning?
Respiratory depression/failure
Antidote to opioids?
Naloxone
Mechanism of benzodiazepine poisoning?
Enhancement of GABA binding to CNS receptors –> CNS (and CV) depression
Most toxic benzodiazepine for cats?
Oral diazepam – causes fulminant liver failure
Management of benzodiazepine poisoning?
Antidote - flumazenil (short half-life)
Supportive care +/- IVLE
Mechanism of barbiturate toxicity?
Activation of GABA receptors, inhibition of glutamine receptors, and inhibition of NE/ACh release –> CNS depression
Main clinical features of barbiturate poisoning?
Weakness/hypothermia and CNS depression. Death due to respiratory/myocardial depression
Long-term use can cause hepatic cirrhosis
Target organs and mechanism of local anesthetic toxicity?
CNS and CV – blockage of voltage-gated sodium channels in nerves and myocardium
Key difference between lidocaine and bupivacaine poisoning?
Lidocaine is more neurotoxic (CNS signs first)
Bupivacaine is more cardiotoxic (CNS and CV signs at the same time)
Management of local anesthetic poisoning?
IVLE is considered an antidote
Mechanism of marijuana poisoning?
CNS - binding to CB1 (psychoactive) and CB2 (analgesic, anti-inflammatory) receptors
Key clinical features of marijuana poisoning?
Ataxia, hyperesthesia, mydriasis, urinary incontinence
Mechanism of xylazine poisoning?
Alpha-2 agonist – sedation, analgesia
Management of xylazine poisoning?
Atipamezole, supportive care
Key clinical signs of lily poisoning in cats?
Early - vomiting, hypersalivation, anorexia
1-3 days - oliguric/anuric renal failure
Management of lily poisoning in cats?
Decontamination, IVFT for minimum 48hrs. Dialysis may be needed if anuria develops
Most common cardiac glycoside-containing houseplant and how to ID?
Oleander - small pink “double flowers”
(others: foxglove, lily of the valley, milkweed)
Mechanism of cardiac glycosides?
Inhibition of Na-K ATPase leading to increased Ca availability and dysrhythmias/increased vagal tone
Key clinical features of cardiac glycoside houseplant poisoning?
Lethargy and discomfort
GI upset
CV - either bradycardia or sinus tachycardia with runs of VTach and progression to atrial fibrillation
Poor perfusion - cold, dyspnea, sweating
CNS signs
Antidote for cardiac glycosides?
Anti-digoxin Fab antibody fragment
Mechanism of yew poisoning?
Heart - inhibition of sodium/calcium exchange in myocardium leading to acute heart failure
Key clinical features of yew poisoning?
Rapid onset – GI upset, signs of heart failure, CNS signs are possible
Management of yew poisoning?
Low stress handling and supportive care (anti-arrhythmics, fluids, etc.)
Target organs and mechanism of sago palm poisoning?
Liver/CNS/kidney
Bioactivation of cycasin to MAM –> mitochondrial damage, hepatic necrosis
Methylation of DNA/RNA –> inhibition of protein synthesis and hepatic necrosis
Key clinical features of sago palm poisoning?
Early - GI upset
2-3 days - acute hepatic necrosis
Examples of plants containing insoluble oxalates?
Peace lily, philodendron, monstera
Clinical features of ingestion of plants containing insoluble oxalates?
Rapid onset salivation, mouth pain, +/- GI upset (no systemic signs)
Other GI irritant plants?
Tulips/hyacinths (bulbs)
Mistletoe, poinsettia, holly
Mechanism of castor plant poisoning?
Ricin (toxin) inactivates ribosomes leading to cell death (incl. myocardial necrosis)
1-3 seeds can be lethal
Main barrier to treatment of castor plant poisoning?
Latency period of several hours up to multiple days
Key clinical features of castor plant poisoning?
Severe GI upset
Hypotension, hypovolemia, and arrhythmias
CNS depression
Liver/kidney damage
Prognosis is actually good with aggressive supportive care
Diagnosis of castor plant poisoning?
Ricinine can be detected in urine/blood
Mechanism of autumn crocus poisoning?
Colchicine is a microtubule inhibitor and anti-mitotic agent (P-GP substrate)
Clinical features of autumn crocus poisoning?
GI upset, CNS depression, cardiovascular depression, tachypnea, severe CNS signs, myelosuppression
Management of autumn crocus poisoning?
Supportive care (incl. mannitol for cerebral edema, prophylactic antibiotics, etc.)
Typical context in which an animal will develop “fog fever”?
Occurs 5-10 days after movement from dry to lush pastures; primarily affects beef cattle >2yrs
Mechanism of “fog fever” poisoning?
L-tryptophan is converted to 3-methylindole in the rumen, which damages type I pneumocytes and clara cells
Key clinical features of “fog fever”?
Expiratory grunt, dyspnea, wide-based stance with head lowered, death in 2-3 days
(most animals only mildly affected)
Postmortem findings of “fog fever”
Pulmonary edema and emphysema with necrotic alveoli, type II pneumocyte hyperplasia
Prevention of fog fever?
Limit use of lush pasture, feed hay before turnout, and supplement monensin
Context in which nitrate poisoning typically occurs?
Stubble fields (ingestion of lower stems), stressed crops, nitrate-accumulating weeds, young plants, green-feed oats/oat hay
Mechanism of nitrate poisoning?
RBCs - oxidation of hemoglobin causing methemoglobinemia and asphyxiation
Ruminants are more sensitive because of nitrite (NO2-) accumulation
Key clinical features of nitrate poisoning?
Sudden death, respiratory distress, chocolate-brown blood
Management of nitrate poisoning?
Antidote - methylene blue
Minimal handling, infuse cold water into rumen
Postmortem diagnosis of nitrate poisoning?
Send ocular fluid (from anterior chamber) for analysis. Can test feed, water
Cyanide-accumulating plants?
Sorghum spp.
Prunus spp. (cherry, apricot)
Linum spp. (linseed, flax)
Hydrangea, laurel, elderberry
Compounds released with plant stress; dissipates in cut forage (drying/baling)
Mechanism of cyanide poisoning?
Inactivation of hemoglobin and inhibition of ETC leading to systemic O2 and ATP deprivation
Ruminants most susceptible
Key clinical features of cyanide poisoning?
Sudden death, asphyxiation, bright cherry-red blood
Two antidote options for cyanide poisoning?
Sodium nitrate +/- sodium thiosulfate - promotes oxidation + excretion of affected Hb
Hydroxycobalamin - binds and inactivates cyanide
Distinguishing characteristic of water hemlock?
Spiked leaves with veins going to the inner corners
Multi-chambered root tuber thing
Tastes nice, so fucking toxic it’s unreal
Mechanism of water hemlock poisoning?
CNS - noncompetitive GABA antagonist –> acute neuroexcitation
Key clinical features of water hemlock poisoning?
Usually found dead with signs of a violent struggle
Acute, severe neuroexcitation with seizures and death due to respiratory failure
Mechanism of poison hemlock poisoning?
CNS - nicotinic acetylcholine agonist –> initial CNS excitation followed by depression
Key clinical features of poison hemlock poisoning?
Sublethal doses recover in 6-10hr
High dose - CNS stimulation followed by depression and paralysis, death from resp failure
Mechanism of larkspur poisoning?
Cattle only - nicotinic acetylcholine antagonist - neuromuscular blockade and paralysis
Key clinical features of larkspur poisoning?
Anticholinergic toxidrome - agitation, weakness, staggering gait, dyspnea
Eventual paralysis –> death from respiratory failure or bloat
Management of larkspur poisoning?
Antidote - neostigmine (nACh agonist)
Make sure to prevent/alleviate bloat by positioning animal in sternal
Plant culprit and mechanism of chewing disease?
Yellow star thistle - neurotoxic with chronic exposure affecting motor nerves of the head/pharynx –> equine nigropalladial encephalomalacia
Management/outcome of chewing disease?
Poor prognosis, some mildly-affected animals may be able to live with permanent impairment
Two main mechanisms of photosensitization?
Primary - ingestion of photoactive substance
Secondary - liver damage preventing metabolism of photoactive substances (phylloerythrin)
Plant culprits of primary photosensitivity?
St. John’s Wort, Buckwheat — symptoms 4-5d after ingestion
Plant culprits of secondary photosensitivity?
Dew poisoning (Alsike or red clover) - horse
Pyrrolizidine alkaloids - ragwort (Senecio)
Mechanism of pyrrolizidine alkaloid toxicity?
Inhibition fo hepatocellular mitosis –> megalocytes and extensive fibrosis
Plant culprit and mechanism of Slobbers?
Fungus found on red clover - acetylcholine agonist stimulates salivary glands (excellent prognosis)
Mechanism of red maple poisoning?
Oxidative damage to RBC –> anemia (methemoglobinemia) and renal failure
Black walnut intoxication in horses?
Skin contact with bedding –> reduced bloodflow to hoof causing laminitis
Plant culprit of seasonal pasture myopathy (non-exertional rhabdomyolysis?
Boxelder seeds - hypoglycin A blocks lipid metabolism leading to buildup/degeneration in postural, respiratory, and cardiac muscle
Mechanism of cocklebur poisoning?
Carboxyatractyloside in young (green) burs inhibits oxidative phosphorylation in the liver. Very poor prognosis
Plant cause of anticholinergic toxidrome in horses?
Jimsonweed - contains atropine/scopolamine –> multisystemic dose-dependent signs (including elevated blood glucose, for some reason)
Pretty good prognosis
