Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
VM 508 final (2)
| Question | Answer |
|---|---|
| Anticoagulants MOA | Blocks vitamin K recycling, preventing the activation of factors II, VII, IX, X, leading to impaired clotting. Warfarin, Brodifacoum |
| Anticoagulants Clinical signs | Early signs (24-48 hrs): lethargy, dyspnea, bleeding gums, bloody feces. Advanced signs (3-5 days): hematomas, weak pulse, convulsions, sudden death. |
| Anticoagulants Diagnostics | Prolonged PT (after 24-36 hrs), elevated PTT later, chemical detection in liver/GI content. |
| Anticoagulants Treatment | Asymptomatic: Decontamination (emesis/AC), monitor PT/PTT. Symptomatic: Vitamin K1, transfusions, oxygen therapy, ICU care. |
| Bromethalin MOA | Uncouples oxidative phosphorylation in CNS mitochondria, causing brain edema and increased intracranial pressure. |
| Bromethalin Clinical signs | High dose (within 4-12 hrs): tremors, hyperexcitability, seizures. Low dose (1-5 days): hindlimb ataxia, CNS depression, coma (paralytic syndrome in cats). |
| Bromethalin Diagnostics | Detection of metabolites in fat, brain, liver, or baits. Radiographs, MRI for brain edema. |
| Bromethalin Treatment | Decontamination, seizure control (diazepam, methocarbamol), diuretics (mannitol), dexamethasone, supportive care. Poor prognosis. |
| Strychnine MOA | Blocks glycine receptors in the spinal cord, leading to uncontrolled reflex arc and muscle spasms. |
| Strychnine Clinical signs | Early signs (2 hrs): anxiety, tremors, tetanic seizures. Advanced signs: sawhorse stance, continuous seizures, death (due to exhaustion/hypoxia). |
| Strychnine Diagnostics | Detection of toxin in liver/urine, or postmortem stomach contents (green material). |
| Strychnine Treatment | Decontamination (if early), seizure control (pentobarbital, diazepam), oxygen support, IV fluids, muscle relaxants (methocarbamol). Poor prognosis. |
| Cholecalciferol (Vit D3) MOA | Increases calcium/phosphate absorption, leading to hypercalcemia, calcification of tissues (kidneys, liver, heart). |
| Cholecalciferol (Vit D3) Clinical signs | Early signs (12-36 hrs): vomiting, diarrhea, PU/PD. Advanced signs: hypercalcemia, renal failure, cardiac arrhythmias, death due to tissue calcification. |
| Cholecalciferol (Vit D3) Diagnostics | Hypercalcemia, hyperphosphatemia, postmortem examination for tissue calcification. CBC/Chem for calcium/phosphate levels. |
| Cholecalciferol (Vit D3) Treatment | Decontamination, IV saline, furosemide, steroids, monitor calcium levels. Poor prognosis if hypercalcemia is advanced. |
| Zinc Phosphide MOA | Converts to phosphine gas in the stomach, inhibiting cellular respiration (similar to cyanide), causing organ damage and CNS effects. |
| Zinc Phosphide Clinical signs | Signs (15 mins - 4 hrs): vomiting (garlic smell), tremors, seizures, recumbency, abdominal pain. Can lead to hepatic and renal damage. |
| Zinc Phosphide Diagnostics | Vomit/stomach contents for analysis (garlic smell). Handle samples carefully (risk to staff). |
| Zinc Phosphide Treatment | Antacids to neutralize stomach acid, methocarbamol for seizures, anticonvulsants, hepatoprotective agents, supportive care. |
| Metaldehyde MOA | Inhibits GABA receptors, leading to continuous excitatory activity in the CNS (used for snail and slug control). |
| Metaldehyde Clinical signs | Signs (within 3 hrs): vomiting, diarrhea, hyperthermia, ataxia, tachycardia, continuous convulsions. Death due to respiratory failure (within 4-24 hrs). |
| Metaldehyde Diagnostics | Metabolic acidosis, elevated CPK, myoglobinuria in CBC/Chem analysis. |
| Metaldehyde Treatment | Decontamination (if no seizures), control seizures (diazepam, methocarbamol), fluids, manage hyperthermia. |
| Which rodenticide poisonings are more easily managed with successful outcome and why? | Anticoagulant rodenticide poisoning is typically easier to manage with a more successful outcome, especially if caught early. This is because the mechanism of toxicity (vitamin K inhibition) can be countered effectively with vitamin K1 therapy, and clinical signs develop after a few days, allowing time for decontamination and treatment. Additionally, laboratory tests (PT/PTT) provide a reliable means of monitoring and guiding therapy, improving prognosis. |
| What is a typical presentation of dog with bromethalin poisoning? | Tremors and seizurs In cases of bromethalin poisoning, the clinical presentation varies depending on the dose ingested: High dose (within 4-12 hours): Dogs may exhibit rapid onset of tremors, hyperexcitability, and seizures. Low dose (within 1-5 days): The signs appear more slowly, with hindlimb ataxia, paresis, loss of deep pain perception, CNS depression, or coma. Paralytic syndrome is more common in cats. |
| Why does an animal presented to the clinic with zinc phosphide exposure present a risk to veterinary staff? | Zinc phosphide exposure presents a risk to veterinary staff because it releases phosphine gas in the stomach, which is highly toxic and can be harmful if inhaled. Vomiting by the animal can release this gas, which poses a risk similar to cyanide gas exposure. The staff must handle the animal and any vomit with extreme caution, using appropriate protective measures to avoid inhaling the gas. |
| What are the target systems for an animal exposed to a toxic vitamin D3 level? | Vitamin D3 (cholecalciferol) toxicity primarily affects the renal, cardiovascular, and gastrointestinal systems. It causes hypercalcemia and hyperphosphatemia, which lead to the calcification of tissues in the kidneys, heart, and GI tract. This can result in renal failure, cardiac dysfunction, and potentially death. |
| How does strychnine cause stiffness and seizures? | Strychnine works by blocking glycine receptors in the spinal cord, which normally function to inhibit reflexes. By competitively antagonizing these receptors, strychnine prevents the inhibitory effect of glycine on the reflex arc, leading to uncontrolled muscle spasms, rigidity, and tetanic seizures. This results in stiffness and convulsions, with death often occurring due to exhaustion or hypoxia. |
| The clinical presentations of strychnine and metaldehyde poisoning share similarities, as both cause seizures and muscle spasms. However, their underlying mechanisms differ: | Strychnine involves blocking glycine receptors, leading to continuous muscle contractions (tetanic seizures) and stiffness. The animal may assume a "sawhorse stance" with rigid muscles. Metaldehyde poisoning inhibits GABA receptors, resulting in the loss of inhibitory control in the CNS. > tremors, ataxia, and convulsions, with hyperthermia and tachycardia being prominent. |
| Between strychinine and metaldehyde, which one is more severe? | Both conditions can lead to death due to respiratory failure, but strychnine tends to cause more severe, sustained muscle contractions, while metaldehyde's hyperthermia and metabolic acidosis also contribute significantly to the fatality. |
| Where does ACh act as a NTMer? | Neuromuscular junctions Parasympathetic nervous system Sympathetic nervous system |
| Carbamates / Organophosphates (OPs) MOA | Binds and inhibits acetylcholinesterase (AchE), leading to buildup of acetylcholine (Ach). OPs = irreversible, carbamates = reversible. |
| Carbamates / Organophosphates (OPs) Clinical signs | SLUDGE-M signs: salivation, lacrimation, urination, defecation, GI upset, emesis, miosis, bradycardia, bronchospasm, bronchorrhea. |
| Carbamates / Organophosphates (OPs) Diagnostics | AchE inhibition can be confirmed through blood testing. (serum, plasma, or whole blood) |
| Carbamates / Organophosphates (OPs) Treatment | Atropine for carbomate toxicity, muscarinic antagonists for muscarinic signs. Decontamination (soap, emesis, AC if no seizures), seizure control. (Oxime cholinesterase reactivator is it is an OP: 2-PAM, protopam, pralidoxime chrloride. |
| Neonicotinoids MOA | Mimics Ach action but is not degraded by AchE, leading to persistent activation of nicotinic Ach receptors. |
| Neonicotinoids Clinical signs | Hyperexcitation, convulsions, paralysis, and insect death. |
| Neonicotinoids Diagnostics | Based on clinical presentation. |
| Neonicotinoids Treatment | Dilution (water/milk), supportive care for convulsions. Low toxicity, symptomatic treatment generally enough. |
| Pyrethrins / Pyrethroids MOA | Slow the closing of sodium (Na) channels, leading to prolonged Na current and repetitive neuronal firing (Type 1) or depolarizing block (Type 2). |
| Pyrethrins / Pyrethroids Clinical signs | Type 1: Tremors and seizures. Type 2: Weakness, paralysis, depolarizing conduction block. |
| Pyrethrins / Pyrethroids Diagnostics | No specific diagnostic tests. History and clinical signs guide treatment. |
| Pyrethrins / Pyrethroids Treatment | Valium (diazepam) for tremors, IV fluids, bathing for dermal exposure, symptomatic care, supportive fluids. Gets metabolized rapidly. ILE may be useful! |
| Can you treat neonicotinoids with Atropine? | NO (Atropine is not useful here as it targets the muscarinic receptors and neonicotinoids are on the nicotinic recetors) |
| What species is especially sensitive to Pyrethrins? | Cats. Even casual contact can cause them clinical signs. Glucuronidation is a pathway of permethrin metabolism and this may be a possible explanation for their sensitivity since cats are deficient in glucuronidase transferase |
| Which class of insecticide could cause hyperexcitation of the insect nervous system? Carbamates Neonicotinoids Organophosphates Pyrethroids | All of the above |
| Semicarbazones / Oxadiazine MOA | Block voltage-gated Na channels, forcing them into an inactive state, preventing action potentials. |
| Semicarbazones / Oxadiazine Clinical signs | Paralysis, weakness, no axonal signaling. |
| Semicarbazones / Oxadiazine Diagnostics | No specific diagnostics. Clinical presentation and exposure history. |
| Semicarbazones / Oxadiazine Treatment | Supportive care. No specific treatment available. |
| Isoxazolines MOA | Antagonists of gated chloride channels (GABA and glutamate-gated Cl channels), leading to uncontrolled CNS activity in insects. |
| Isoxazolines Clinical signs | Hyperexcitation, uncontrolled CNS activity, death of fleas/ticks. |
| Isoxazolines Diagnostics | Based on exposure and symptoms. |
| Isoxazolines Treatment | Avoid in animals with seizures, supportive care for accidental ingestion, emesis, or activated charcoal if early. |
| Phenylpyrazoles MOA | Block GABA receptors (e.g., fipronil) or modulate glutamate-gated Cl channels (avermectins), leading to hyperpolarization and death in insects. |
| Phenylpyrazoles Clinical signs | Similar to isoxazolines: CNS hyperexcitation, paralysis, and insect death. |
| Phenylpyrazoles Diagnostics | No specific diagnostic tests, clinical presentation. |
| Phenylpyrazoles Treatment | Supportive care, induce emesis or AC for accidental exposures, symptomatic treatment as necessary. |
| Avermectins MOA | Agonists at glutamate-gated Cl channels, causing hyperpolarization and loss of CNS function in insects. |
| Avermectins Clinical Signs | CNS hyperexcitation in insects, not toxic to mammals at normal doses. |
| Avermectins Diagnostics | Clinical presentation for accidental overdoses. |
| Avermectins Treatment | Supportive care, symptomatic treatment if accidental ingestion occurs. |
| What is the primary clinical sign associated with xylitol toxicity in dogs? | Hypoglycemia initially > Liver toxicity after a few days (dose dependent) |
| Which of the following is the appropriate treatment for hypoglycemia caused by xylitol toxicity in dogs? | IV dextrose supplementation |
| What’s the #1 toxin reported to Pet Poison Helpline? | Chocolate Toxicity depends on the Theobromine content: Unsweetened > semi-sweet > dark > milk > white |
| Besides chocolate, what other common toxicants does the pet poison helpline handle? | Theobromine and caffeine Coffee or additional caffeine Macadamia nuts Grapes/raisins/currants (2nd) Xylitol (sugar free) (3rd) alcohol Marijuana |
| What is the most common toxicant for felines? | Lilies, second is chocolate. |
| PPH consulting process. | When you call you give them the pet's information, medical conditions, and mediations, what the pet was exposed to and what dose, how long ago and route of exposure. They will do a risk assessment to determine the treatment. |
| Xylitol is commonly found in products like: | Sugar-free gum and mints Sugar-free candies and chocolates Baked goods Some peanut butter brands Toothpaste and mouthwash Dietary supplements and vitamins Medications like cough syrups. |
| Chocolate Toxicity (Theobromine and Caffeine): Mechanism | Chocolate contains theobromine (adenosine receptor blocker) and caffeine, which are methylxanthines. These cause stimulation of the CNS, cardiac muscle, and promote diuresis. |
| Chocolate Toxicity (Theobromine and Caffeine): Clinical signs | Vomiting, diarrhea, hyperactivity, increased heart rate, tremors, and potentially seizures. |
| Chocolate Toxicity (Theobromine and Caffeine): Diagnostic workup | Based on ingestion history, theobromine levels are not typically measured; diagnosis is clinical. Treatment involves decontamination (emesis/AC) and supportive care like IV fluids and seizure control (if necessary). |
| What tests can you perform to determine if there is liver toxicity due to xylithol toxicity? | ALT and AST. Would see elevated bilirubin. |
| What other word can clue you in that a product may have xylithol? | • 100% xylitol, “all xylitol” • Sugar free, “natural sweeteners” • “Birch sugar” or “wood sugar |
| Grapes/Raisins Toxicity Mechanism | The exact toxic component is unknown, but ingestion can cause acute kidney injury. |
| Grapes/Raisins Toxicity Clinical Signs | Vomiting, diarrhea, lethargy, and signs of kidney failure such as increased thirst and urination. |
| Grapes/Raisins Toxicity Diagnostic workup | Blood tests showing elevated creatinine and BUN, urinalysis showing proteinuria or casts. Treatment involves IV fluids, antiemetics, and renal function monitoring. |
| Xylithol Clinical presentation | Hypoglycemia (within 30 minutes to 1 hour): lethargy, weakness, vomiting, seizures, and collapse. Hepatic failure (within 12-72 hours): jaundice, vomiting, and coagulopathy. Hepatic necrosis. |
| Xylithol therapeutic approach | Immediate intervention with decontamination, including emesis (if early and asymptomatic) and activated charcoal. IV dextrose to manage hypoglycemia. Liver protectants like SAMe or N-acetylcysteine if hepatic failure is a concern. Monitoring of blood glucose and liver enzyme levels during treatment. |
| Spot-ons that are absorbed systemically into the blood stream are regulated by the | FDA (systemic absorption) |
| Spot-ons that remain on the skin to only treat external parasites (fleas, ticks, etc.) are generally regulated by the | EPA (topical) |
| Venom Proteins: Collagenase: | This enzyme breaks down collagen in connective tissues, leading to rapid tissue destruction around the bite area. The breakdown of structural proteins like collagen contributes to swelling, pain, and tissue damage. |
| Venom Proteins: Phospholipase A | A potent enzyme that causes hemolysis (destruction of red blood cells) and muscle toxicity. It disrupts cell membranes by breaking down phospholipids, which are essential to cell integrity, leading to cell lysis and muscle necrosis. |
| Venom Proteins: Proteases | These enzymes interfere with blood clotting by inhibiting coagulation factors, which can lead to excessive bleeding and systemic effects. This anticoagulant action allows venom to spread more rapidly and contributes to severe hemorrhagic effects in some cases. |
| Venom Polypeptides: | These are short chains of amino acids that can have various toxic effects depending on their structure and target sites in the body. In some venoms can also cause shock and widespread vascular damage, leading to a rapid systemic collapse in severe envenomations. |
| Venom Polypeptides: Cardiotoxic polypeptides: | They target the heart and can lead to irregular heart rhythms or even heart failure. |
| Venom Polypeptides: | These affect nerve cells, potentially causing paralysis, respiratory distress, and neurological symptoms. |
| Venom Serotonin: | An amine that is also a known inflammatory mediator. In venom, serotonin exacerbates pain and inflammation at the site of the bite or sting. It contributes to vasodilation (widening of blood vessels), which increases blood flow to the area, enhancing swelling and pain. |
| Venom Steroids: | These compounds, when present in venom, may play a role in modulating the immune response or causing inflammation. They can contribute to the general toxic effects, although their specific role in venom composition varies. |
| Hyaluronidase (often called a "spreading factor"): | This enzyme breaks down hyaluronic acid, a component of the extracellular matrix in connective tissues. By degrading this substance, hyaluronidase facilitates the spread of venom through tissues. This property allows venom components to penetrate tissues more effectively and rapidly, increasing the area affected by the venom and accelerating the onset of systemic effects. |
| ___________ are common in certain snake venoms (e.g., rattlesnakes), causing both local and systemic reactions that can be life-threatening without rapid intervention. | Hemorrhagic and neurotoxic factors |
| Venomous Animals | “Creatures that produce a poison in highly developed secretory gland which can be delivered during a stinging or biting act” |
| Poisonous Animals | Creatures with tissues (either part or entire tissue). No delivery system, rather those animals are toxic when eaten |
| Rattlesnake Venom | Species Source: Rattlesnakes (Crotalus spp.) Type of Toxin: Proteins (collagenase, phospholipase, proteases) Clinical Signs: Swelling, pain, hypotension, tachycardia, shock, respiratory distress Species Affected: Dogs, cats, horses, llamas Treatment: Antivenom, fluids, pain control, airway management, antibiotics |
| Bufo Toad Toxin | Species Source: Bufo toads (Florida, Hawaii) Type of Toxin: Cardiac glycosides (bufadienolides) Clinical Signs: Salivation, vomiting, ataxia, seizures, potential cardiac failure Species Affected: Dogs (mostly) Treatment: Rinse mouth, activated charcoal, propranolol, atropine |
| Blister Beetle Toxin | Species Source: Blister beetles (Epicauta spp.) Type of Toxin: Cantharidin Clinical Signs: Colic, anorexia, depression, oral ulcers, hypocalcemia, hematuria, shock, death Species Affected: Horses Treatment: Remove source, fluids, calcium, antibiotics, analgesics |
| Black Widow Venom | Species Source: Black widow spider (Latrodectus spp.) Type of Toxin: Neurotoxin (α-latrotoxin) Clinical Signs: Muscle pain, spasms, salivation, sweating, paralysis, death Species Affected: Dogs, cats, horses Treatment: Antivenom, fluids, muscle relaxants, pain management |
| Brown Recluse Venom | Species Source: Brown recluse spider (Loxosceles spp.) Type of Toxin: Proteases, hyaluronidase Clinical Signs: Edema, erythema, ulcerative wound, tissue necrosis Species Affected: Dogs, cats, humans Treatment: Wound management, pain control, antibiotics as needed |
| What components can be found in a venom? | Venoms often contain a mix of proteins, lipids, amines, steroids, serotonin, and glycosides. These components vary in their effects, potentially causing neurotoxicity, cardiotoxicity, hemolysis, and other severe reactions. Examples of venom components include collagenase (tissue destruction), phospholipase A (hemolytic and myotoxic effects), proteases (inhibit coagulation), and various polypeptides. |
| What should you do if an animal was bitten by a rattlesnake in the face/neck area? | Stay Calm: Minimize movement and keep the animal calm. Remove Collars: Prevent further constriction due to swelling. Veterinary Care ASAP: Rapid transport to a clinic is critical, and pre-arrangements for antivenom are recommended. Do Not: Avoid tourniquets, cold compresses, or attempts to suck out venom, as these can worsen the injury. |
| Ponder about rattlesnake vaccine… would you promote it or not? | The rattlesnake vaccine, marketed by Red Rock Biologics, is available but considered controversial due to limited efficacy data. Veterinary treatment protocols are the same for vaccinated and unvaccinated animals, as antivenom is still required. UC Davis currently does not recommend the vaccine routinely, so it may be wise to weigh this decision based on local rattlesnake risk and discuss it with a veterinarian. The cost should also be a consideration. |
| Where would you find bufo toads? Are they venomous or poisonous? What do they have in common with oleander? | Location: Bufo toads are commonly found in Florida and Hawaii. Toxicity: These toads are poisonous, not venomous. They excrete toxins from glands as a defense, especially when mouthed by dogs. Commonality with Oleander: Both contain cardiac glycosides, which can lead to heart failure if ingested. Clinical signs include excessive drooling, vomiting, ataxia, and potentially seizures. |
| How would a horse be exposed to blister beetles and what would be the clinical signs? | Horses are exposed to blister beetles primarily through contaminated alfalfa hay. Clinical signs of cantharidin toxicosis include colic, depression, frequent urination, oral ulcers, elevated body temperature, and, in severe cases, shock or death. The beetle’s toxin irritates mucosal linings and can cause hypocalcemia and hematuria. |
| Describe the typical clinical presentation of an animal with a black widow and brown recluse spider bite. | Black Widow: Envenomation typically causes severe muscle pain and spasms, salivation, sweating, and potentially paralysis due to neurotoxic α-latrotoxin. It often leads to respiratory and circulatory distress if untreated. Brown Recluse: The bite results in localized tissue necrosis and an ulcerating wound due to proteolytic enzymes. Healing can be prolonged and difficult, often requiring weeks to months of care. |
| Which animals are susceptible to ionophores ? | Horses, cattle, and camelids are particularly sensitive, while poultry, sheep, swine, and dogs are also susceptible but at higher tolerances. |
| Target organs of ionophores | In horses, cattle, and camelids, ionophores primarily target the heart, causing cardiac damage. In sheep, swine, and dogs, ionophores mainly affect skeletal muscles, leading to muscle weakness. Poultry can experience both cardiac and skeletal muscle damage. |
| What is the reporting process for suspect feed contamination? | If there’s a suspicion of feed contamination, report through the FDA Safety Reporting Portal (link provided in slides) for issues with pet, livestock, or horse feed. It’s also recommended to communicate with veterinary colleagues, consult a toxicology lab, collect feed samples for analysis, document the incident, and inform regulatory agencies as needed. |
| What is a mycotoxin? | are toxic secondary metabolites produced by certain fungi (microfungi), which are harmful when ingested and can cause diseases similar to other toxicant exposures. They commonly contaminate feed and food. |
| What are the conditions that favor mycotoxin production? | Mycotoxin production is favored by warm temperatures (24–35°C) and high humidity (above 75%). These conditions promote fungal growth on crops and stored feed, particularly corn, cottonseed, and peanuts |
| What is the typical clinical presentation of an animal with aflatoxin toxicosis? | primarily affects the liver. In animals, this can lead to jaundice, anorexia, depression, diarrhea, and bleeding disorders. Dogs may exhibit gastrointestinal disturbances and hemorrhage, while cattle can have detectable aflatoxin metabolites in milk without visible clinical signs. |
| How would a dog be exposed to penitrem A? What would be the clinical signs? | Exposure: Penitrem A is a tremorgenic mycotoxin commonly found in moldy dairy products, walnuts, bread, and compost. Dogs can be exposed by ingesting moldy items in garbage or compost piles. Clinical Signs: Signs of penitrem A toxicity include tremors, hyperthermia, ataxia, and potentially seizures, with symptoms typically appearing within hours of ingestion. |
| What is the clinical presentation of fumonisin poisoning in horses and how does it differ from that in pigs? | causes Equine Leukoencephalomalacia (ELEM), characterized by rapid-onset neurological symptoms like depression, blindness, ataxia, facial paralysis, and coma. This condition is severe and often fatal. |
| What is the clinical presentation of fumonisin poisoning in pigs? | leads to Porcine Pulmonary Edema (PPE), a respiratory syndrome presenting as dyspnea, cyanosis, and weakness, often progressing to death within days of exposure. |
| Why are ergotism and fescue toxicosis identical in their clinical presentations? | Both ergotism and fescue toxicosis are caused by ergot alkaloids produced by fungi, which lead to vasoconstriction, prolactin inhibition, and neurological effects. Due to their similar mechanisms, they produce identical symptoms, including gangrene (fescue foot), hyperthermia (summer slump), and reproductive issues in mares. |
| Ionophores uses/source | Increase feed efficiency, weight gain; control bloat, coccidiosis |
| Ionophores Moa | Transport cations across cell membranes, disrupting gradients, depleting ATP, causing cell dysfunction and death |
| Ionophores target | Cardiac (horses, cattle); Skeletal muscle (sheep, swine); Polyneuropathy (cats) |
| Ionophores affected species | Horses, cattle, sheep, swine, dogs, cats, poultry |
| Ionophores Clinical signs | Anorexia, ataxia, dyspnea, weakness, shock, sudden death; sweating in horses; long-term: cardiac fibrosis, neurotoxicity |
| Ionophores Diagnostics | Feed history, analysis of ionophores in feed and biological specimens, ECG, elevated CPK, LDH, AST, troponin |
| Ionophores Therapeutic strategies | Activated charcoal, sorbitol cathartics, fluids, cardiac arrhythmia management, Vit E/selenium supplementation |
| Mycotoxins uses/source | Secondary fungal metabolites; produced in hot, humid conditions |
| Mycotoxins MOA | Not essential for fungal growth; ingested mycotoxins cause toxicity |
| Mycotoxins Target organs | Liver, CNS, respiratory |
| Mycotoxins affected species | All species; species and target organ vary by mycotoxin |
| Mycotoxins Clinical Signs | Varies by mycotoxin; liver and CNS effects common, can cause GI, renal, or respiratory signs |
| Mycotoxins Diagnostics | Detailed feed history, feed sample for mycotoxin analysis; hotspot distribution of mycotoxins |
| Mycotoxins Therapeutics | Supportive care based on clinical signs, liver protectants for liver-targeting mycotoxins |
| Aflatoxins source | Common in moldy grains (corn, peanuts); produced by Aspergillus spp. |
| Aflatoxins MOA | Metabolic activation in liver, binds to cellular components, causing hepatotoxicity and systemic effects |
| Aflatoxins target | Liver |
| Aflatoxins Affected species | All animals, primarily dogs, poultry, pigs, young animals |
| Aflatoxins Clinical signs | Liver disease (elevated GGT, AST, ALP), anemia, jaundice, anorexia, diarrhea; dogs: GI signs and hemorrhage |
| Aflatoxins Diagnostics | Feed and biological analysis for aflatoxins, liver function tests |
| Aflatoxins Therapeutics | Supportive care, liver protectants, Vitamin E, avoid feeding affected animals; avoid residues in cattle products |
| Penitrem A use | Moldy dairy products, walnuts, bread, compost. (Produced by penicillium) |
| Penitrem A Moa | CNS toxicant causing tremors |
| Penitrem A target system | CNS |
| Penitrem A affected species | mostly see cases in dogs |
| Penitrem A clinical signs | Tremors, hyperthermia due to tremors |
| Penitrem A diagnosed by | Feed history, clinical signs |
| Penitrem A therapeutics | Supportive care, anticonvulsants for tremors |
| Fumonisins source | Corn (moldy corn poisoning) |
| Fumonisins moa | Inhibits sphingolipid synthesis, causing cell dysfunction and death in specific organs |
| Fumonisins target systems | CNS (horses); lungs (swine); liver (all) |
| Fumonisins affected species | Horses, swine, humans |
| Fumonisins CS | Horses: ELEM - depression, blindness, ataxia, sweating, facial paralysis, coma; Swine: PPE - dyspnea, cyanosis, post-mortem lesions |
| Fumonisins diagnosis | Analysis of corn feed, clinical signs, histopathology of brain necrosis (horses) and lungs (swine) |
| Fumonisins therapeutics | Supportive care, early intervention critical for horses (poor prognosis for CNS signs) |
| Ergot/Fescue source | Found on grains (wheat, rye, barley, oats) and fescue grass |
| Ergot/Fescue moa | Potent vasoconstriction, D2 dopamine receptor stimulation in CNS |
| Ergot/Fescue target systems | CNS, cardiovascular |
| Ergot/Fescue affected species | Cattle, sheep, horses (particularly mares) |
| Ergot/Fescue CS | Fescue foot (ischemic necrosis), summer slump, hyperthermia, prolonged gestation, dystocia, immunosuppression |
| Ergot/Fescue diagnosis | Feed and environmental history, clinical signs, necropsy findings in severe cases |
| Ergot/Fescue therapeutics | Symptomatic care, avoid grazing in affected areas, manage heat stress, monitor pregnant mares for dystocia complications. Domperidone for mares. |
| Select all correct answers. Bromethalin poisoning is characterized by: A. Tremors, seizures and running fits in dogs. B. Ataxia, paresis and coma in cats. C. Epistaxis, melena, and hematemesis in dogs. D. Lethargy and PU/PD in cats. E. Salivation and gagging in dogs. | A and B |
| The target tissue of horses and cattle with monensin intoxication is cardiac muscle. In swine and dogs, the primary clinical syndrome induced by ionophores reflects which of the following? A. Neuromuscular dysfunction B. Sudden death without prior clinical signs C. Coagulation dysfunction D. Hepatic failure E. Renal failure | A |
| What mycotoxin?: A horse shows blindness, ataxia and seizures | Fumonisin, Corn |
| What mycotoxin?: A dog is anorexic, weak, and has diarrhea | Aflatoxins, Corn |
| What mycotoxin?: A dog with tremors after getting into a garbage pile | Penitrem A |
| What mycotoxin?: It is freezing cold for several days and cows have developed gangrenous lesions on their feet. | Ergot alkaloids, Rye |
| What mycotoxin?: A mare is overdue (380 days of gestation) | Ergot alkaloids, Rye |
| Methylxanthines competitively antagonize which one of the following receptor or receptor types? | Adenosine |
| Which one of the following abnormalities would be of most concern in an animal that has been intoxicated by cholecalciferol and therefore would be the focus of your initial case management? Hyperkalemia High BUN/creatinine Metastatic tissue calcification Oliguria Hypercalcemia | Hypercalcemia |
| The mechanism by which strychnine causes nervous system stimulation is: | via glycine receptor antagonism |
| Moa for Neonicotinoids | Acetylcholine Receptor Stimulation |
| Moa for Organophosphates / Carbamates | Acetylcholinesterase Inhibition |
| Moa for Pyrethrins / Pyrethroids | Voltage-gated Sodium Channel Modulation |
| Moa for Phenylpyrazoles | GABA Receptor Blockage |
| Neonicotinoids are widely used insecticides in veterinary and agricultural practices. Which of the following best describes the mechanism of action of neonicotinoids? | They mimic acetylcholine and bind to nicotinic acetylcholine receptors in insects. |
| Pyrethroid, semicarbazone and oxadiazine insecticides target voltage-gated sodium channels. What symptoms or clinical signs would you expect with overexposure to these insecticides? | Tremors, seizures, paralysis |
| Carbamates are a class of insecticides that inhibit acetylcholinesterase. Which of the following is the most appropriate treatment for overexposure to carbamates? Administration of activated charcoal and supportive care Administration of atropine and supportive care Administration of naloxone and supportive care Administration of vitamin K and fresh frozen plasma | Administration of atropine and supportive care |
| Pyrethrins are widely used insecticides in veterinary medicine. Which of the following statements best describes the species selectivity of pyrethrins and their clinical relevance to cats? Pyrethrins are: | more toxic to cats than to other mammals because cats have a limited ability to metabolize these compounds. |
Created by:
awahay