Podcast
Questions and Answers
Which of the following K dependent clotting factors are involved in the coagulation process?
Which of the following K dependent clotting factors are involved in the coagulation process?
What is the primary mechanism of elimination for anticoagulant rodenticides?
What is the primary mechanism of elimination for anticoagulant rodenticides?
What clinical sign is not typically seen in the early stages of anticoagulant rodenticide toxicosis?
What clinical sign is not typically seen in the early stages of anticoagulant rodenticide toxicosis?
Which laboratory finding is indicative of an anticoagulant rodenticide toxicity?
Which laboratory finding is indicative of an anticoagulant rodenticide toxicity?
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What is the purpose of measuring PT in asymptomatic animals suspected of anticoagulant rodenticide exposure?
What is the purpose of measuring PT in asymptomatic animals suspected of anticoagulant rodenticide exposure?
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Which population of clinical signs has the highest reported percentage in anticoagulant rodenticide toxicity?
Which population of clinical signs has the highest reported percentage in anticoagulant rodenticide toxicity?
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Which anticoagulant rodenticide test is considered least sensitive and is typically assessed 3 days post-ingestion?
Which anticoagulant rodenticide test is considered least sensitive and is typically assessed 3 days post-ingestion?
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What is the recommended initial treatment for an asymptomatic animal with known anticoagulant rodenticide exposure?
What is the recommended initial treatment for an asymptomatic animal with known anticoagulant rodenticide exposure?
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What should be done for symptomatic animals with anticoagulant rodenticide exposure?
What should be done for symptomatic animals with anticoagulant rodenticide exposure?
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Which statement regarding the administration of Vitamin K1 in treating anticoagulant rodenticide exposure is incorrect?
Which statement regarding the administration of Vitamin K1 in treating anticoagulant rodenticide exposure is incorrect?
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Which of the following is a source of Acute Bovine Pulmonary Edema and Emphysema (ABPE)?
Which of the following is a source of Acute Bovine Pulmonary Edema and Emphysema (ABPE)?
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What is the mechanism through which paraquat acts as a respiratory toxicant?
What is the mechanism through which paraquat acts as a respiratory toxicant?
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What are the reactive intermediates produced by paraquat exposure in type 1 alveolar cells?
What are the reactive intermediates produced by paraquat exposure in type 1 alveolar cells?
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Which treatment is considered effective for paraquat toxicity?
Which treatment is considered effective for paraquat toxicity?
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Which plant is known to contain cyanogenic glycosides?
Which plant is known to contain cyanogenic glycosides?
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What is a common clinical syndrome associated with paraquat exposure?
What is a common clinical syndrome associated with paraquat exposure?
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Which of the following treatment options is NOT commonly effective during acute paraquat toxicity?
Which of the following treatment options is NOT commonly effective during acute paraquat toxicity?
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What type of cell death is primarily associated with the exposure to reactive intermediates due to paraquat?
What type of cell death is primarily associated with the exposure to reactive intermediates due to paraquat?
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What is the duration of action for Brodifacoum?
What is the duration of action for Brodifacoum?
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What is the therapeutic dosage for aspirin in dogs?
What is the therapeutic dosage for aspirin in dogs?
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What mechanism does aspirin use to exert its effects?
What mechanism does aspirin use to exert its effects?
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What is a recommended treatment approach for aspirin poisoning?
What is a recommended treatment approach for aspirin poisoning?
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What is the effect of aspirin on renal blood flow?
What is the effect of aspirin on renal blood flow?
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What is the target for monitoring post-aspirin treatment?
What is the target for monitoring post-aspirin treatment?
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Which compound is used as a GI protectant in treating aspirin toxicosis?
Which compound is used as a GI protectant in treating aspirin toxicosis?
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What is the primary clinical sign indicating first exposure to cyanogenic glycosides?
What is the primary clinical sign indicating first exposure to cyanogenic glycosides?
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Which compound forms a stable complex with cytochrome oxidase, inhibiting cellular respiration?
Which compound forms a stable complex with cytochrome oxidase, inhibiting cellular respiration?
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What is the mechanism of action for anticoagulant rodenticides?
What is the mechanism of action for anticoagulant rodenticides?
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What is the treatment goal for animals affected by cyanogenic glycosides?
What is the treatment goal for animals affected by cyanogenic glycosides?
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What is a severe outcome for animals that ingest cyanogenic glycosides?
What is a severe outcome for animals that ingest cyanogenic glycosides?
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Which of the following describes a characteristic of 2nd generation anticoagulant rodenticides?
Which of the following describes a characteristic of 2nd generation anticoagulant rodenticides?
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Vicia sativa, commonly known as common vetch, primarily accumulates cyanogenic glycosides in which parts?
Vicia sativa, commonly known as common vetch, primarily accumulates cyanogenic glycosides in which parts?
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What is one of the first clinical signs that progress in cases of cyanogenic glycoside poisoning?
What is one of the first clinical signs that progress in cases of cyanogenic glycoside poisoning?
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Which of the following treatments can split the CN–Fe3+ bond in cyanide poisoning?
Which of the following treatments can split the CN–Fe3+ bond in cyanide poisoning?
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Flashcards
Respiratory Toxicants
Respiratory Toxicants
Substances causing damage to the respiratory system, affecting lungs and airflow.
Acute Bovine Pulmonary Edema & Emphysema (ABPE)
Acute Bovine Pulmonary Edema & Emphysema (ABPE)
A respiratory disease in cattle caused by toxic agents, leading to acute lung issues.
Sources of ABPE
Sources of ABPE
Common causes of ABPE include herbicides, feed types, and toxic plants.
Paraquat
Paraquat
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Reactive Oxygen Species (ROS)
Reactive Oxygen Species (ROS)
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Clinical syndrome of ABPE
Clinical syndrome of ABPE
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Treatment for ABPE
Treatment for ABPE
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Cyanogenic Glycosides
Cyanogenic Glycosides
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PT (Prothrombin Time)
PT (Prothrombin Time)
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Activated PTT (Partial Thromboplastin Time)
Activated PTT (Partial Thromboplastin Time)
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PIVKA
PIVKA
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Vitamin K1 Antidote
Vitamin K1 Antidote
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Symptomatic treatment
Symptomatic treatment
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K dependent clotting factors
K dependent clotting factors
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Toxicokinetics of anticoagulants
Toxicokinetics of anticoagulants
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Delayed onset of toxicosis
Delayed onset of toxicosis
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Common clinical signs
Common clinical signs
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Prolonged coagulation tests
Prolonged coagulation tests
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Common Vetch
Common Vetch
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Mechanism of Action
Mechanism of Action
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Clinical Signs of Cyanide Poisoning
Clinical Signs of Cyanide Poisoning
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Anticoagulant Rodenticides
Anticoagulant Rodenticides
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Warfarin
Warfarin
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Vitamin K and Clotting Factors
Vitamin K and Clotting Factors
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Symptoms of Cyanide Intoxication
Symptoms of Cyanide Intoxication
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Treatment for Cyanide Poisoning
Treatment for Cyanide Poisoning
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Conditions Favoring Intoxication
Conditions Favoring Intoxication
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Warfarin duration
Warfarin duration
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Aspirin dosage for dogs
Aspirin dosage for dogs
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Aspirin toxic dose for cats
Aspirin toxic dose for cats
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Aspirin mechanism of action
Aspirin mechanism of action
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Aspirin toxicokinetics
Aspirin toxicokinetics
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Aspirin toxicosis symptoms
Aspirin toxicosis symptoms
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Aspirin treatment for poisoning
Aspirin treatment for poisoning
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Aspirin laboratory findings
Aspirin laboratory findings
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Study Notes
Respiratory Toxicants
- Respiratory toxicants can originate from various sources, including air pollution, poor ventilation, food/feed/water, volatile compounds, mycotoxins, plants, pesticides, drugs, and many others.
- Exposure to respiratory toxicants can lead to various effects on the respiratory system, including asphyxiation, irritation, pulmonary edema, epithelial necrosis, emphysema, fibrosis, and more.
- Specific examples of respiratory toxicants mentioned include carbon monoxide, fluorocarbons, heavy metals, nitrogen oxides, smog, smoke, ammonia, carbon dioxide, carbon monoxide, hydrogen sulfide, methane, chlorine, formaldehyde, and more.
- Mycotoxins, ipomeanol, hydrocarbions fuels and solvents (paints and Teflon), Astragalus and Brassica (rape), 3-methyl indole, paraquat, ANTU, organophosphates, endotoxins (contaminants), and organic iodide were also listed as potential respiratory toxicants.
Acute Bovine Pulmonary Edema & Emphysema (ABPE)
- ABPE is a respiratory condition.
- Sources of ABPE include herbicides (like paraquat), lush pastures, moldy sweet potatoes, peanut vine hay, and soybeans. Additionally, the perilla mint plant is listed as a toxic plant that can cause ABPE.
- The general mechanism of ABPE involves the toxicant, or a metabolite of it, affecting type 1 alveolar cells and endothelial cells, generating reactive oxygen species (ROS). This, in turn, leads to cell death.
- Paraquat has a 10x affinity for alveolar cells, undergoing reduction/oxidation cycles, and produces hydrogen peroxide, superoxide anion, and hydroxyl radical; all agents that lead to cell death.
- Exposure to plants like perilla mint, moldy sweet potatoes and lush pastures, can result in the production of L-tryptophan, which is metabolized into 3-methyl indole in the rumen. These are then transported to the lungs and contribute to the development of reactive intermediates, leading to ABPE.
Cyanogenic Glycoside-Containing Plants
- Cyanogenic glycosides are present in various plants.
- Toxic plants include black cherry, choke cherry, hydrangeas, flowering quince, crabapple, Johnson grass (and other Sorghum spp.), common vetch.
- Cyanogenic glycosides, especially in these plants, transform into hydrogen cyanide (HCN) during consumption or when the plant experiences stress factors like frost.
- The transformation of glycosides into HCN occurs in the rumen of ruminants, therefore making ruminants more susceptible.
- HCN is rapidly absorbed throughout the gut and dispersed throughout the bloodstream.
Cyanogenic Glycosides: Mechanism of Action
- Cyanide (CN−) forms a stable complex with iron (Fe3+) in cytochrome oxidase, a critical component of the electron transport chain (ETC).
- This complex formation prevents the conversion of Fe3+ to Fe2+
- Disruption of this process inhibits electron transport and cellular respiration.
- The body can still look oxygenated (appear cherry red) but cells can't use the oxygen for metabolism.
Cyanogenic Glycosides: Clinical Syndromes
- Death can happen after only minutes in some cases of cyanide poisoning or can be dependent on the dose.
- Animals that survive beyond 120-minute exposure to cyanide commonly recovered.
- Initial clinical signs encompass salivation, rapid breathing, marked dyspnea, weakness, muscle fasciculation, urination, defecation and staggering, tachycardia and mydriasis.
- Terminal signs include lateral recumbency, convulsions, and cyanosis accompanied by death due to respiratory paralysis.
Cyanogenic Glycosides: Treatment
- Removal of the source or the food causing the poisoning is crucial.
- Treatment differs depending on the size of the animal.
- For small animals, the goal is forming a decoy receptor, utilizing hydroxycobalamine as a treatment method, and allowing body to eliminate in urine.
- Larger animals treatment involves using amyl and/or sodium nitrite to split CN-Fe3+ bond for elimination of cyanide from the system.
One Health Perspective
- Pets and humans share environments making them vulnerable to exposure of same toxins such as the contaminated air from LA wildfire study (2025), with examples of CO, NOx, Pb, chlorine, PAHs, and PM 2.5.
- Sled dogs in Alaska wildfire study (2021) experienced adverse effects of particulate matter due to similar environmental factors.
Cardiovascular and Blood System Toxicants: Anticoagulant Rodenticides
- Anticoagulant rodenticides are toxic substances aimed to kill rodents.
- Examples include rodenticides and aspirin.
- Hemorrhagic syndrome is an effect that can occur after exposure to rodenticides like sweet clover hay and silage.
- Some rodenticides are fungal metabolites like coumarin, 4-hydroxycourmarin (Dicumarol). Other examples include synthetic dicumarol analogs, such as Warfarin.
- Rodenticides come in different forms such as bait blocks, grain mixes, and tracking powders.
Anticoagulant Rodenticides: 1st/2nd Generation
- First-generation rodenticides (1940s) feature low potency, multiple doses, and the potential for aversion.
- Rodenticides are rapidly excreted.
- Second-generation rodenticides (1970s) showcase higher potency, single doses, potentially longer retention, and the risk of "relay toxicosis."
- Warfarin, Dicoumarol, and Pindone fall under first generation rodenticides, while Brodifacoum, Bromadiolone, and Diphacinone belong to the second generation.
Anticoagulant Rodenticides: Vitamin K
- Vitamin K is a lipid-soluble vitamin vital for activation of clotting factors.
- Anticoagulant rodenticides antagonize vitamin K, impacting blood coagulation.
- Toxicity from rodenticides can cause delayed onset; clinical signs may not become evident until clotting factors are used up.
- Examples of clinical effects due to rodenticides include cerebral, thoracic, and pericardial hemorrhage, and swelling of joints accompanied by edema.
Anticoagulant Rodenticides: Toxicokinetics
- Rodenticide absorption is slow but complete (approximately 90%).
- Peak plasma levels usually occur within 12 hours after exposure.
- Rodenticide distribution involves binding to plasma proteins and retention within the liver.
- Elimination involves metabolism by cytochrome P450 oxidases and excretion in the urine.
Anticoagulant Rodenticides: Clinical signs and labs
- Clinical signs of rodenticides exposure include cutaneous hematomas, epistaxis, dark tarry stools, and bloody vomit, dyspnea, paleness of mucous membranes, exercise intolerance, anorexia, weakness, ataxia, spontaneous hemorrhaging, and swelling of joints
- Labs that are useful in diagnosis include PT (2-6x longer), activated PTT, activated coagulation time (2-10x longer). These tests assess clotting times and can help detect if excessive clotting factors are being used up from a poisoning event.
- PIVKA (proteins induced in Vitamin K absence/antagonism) tests can aid diagnosis in a more specific manner.
Anticoagulant Rodenticides: Treatment
- For asymptomatic animals, GI decontamination, PT baseline measurement, and oral vitamin K treatment are often sufficient.
- For symptomatic animals, whole blood or plasma transfusion is indicated to improve health.
- In cases of dyspnea, thoracentesis may be performed.
- Vitamin K₁ therapy may be administered subcutaneously.
Anticoagulant Rodenticides: Stabilization and Duration
- Stabilize symptomatic animals with appropriate treatment to meet their needs.
- Duration of treatment depends on the specific rodenticide and can range from 14 days for warfarin to 30 days for Brodifacoum and Diphacinone.
- Routine PT(prothrombin time) values are taken weekly until it returns back to normal levels.
Anticoagulant Rodenticides: Contraindications
- Wide spectrum antibiotics, decrease Vitamin K absorption from sulfonamides and corticosteroids need to be monitored and avoided or taken with extra caution when treating.
Aspirin (NSAIDs)
- Aspirin is a salicylate and NSAID (non-steroidal anti-inflammatory drug).
- Original aspirin is available as 81, 325, and 500 mg tablets.
- Other products containing aspirin include Alka-Seltzer and arthritis creams.
- Aspirin is also found in Pepto-Bismol, Kaopectate, and canine formulations.
- Aspirin is frequently present in pet stores in 100 and 325 mg forms.
- Typical therapeutic dosage for cats to dogs ranges from 10-25 mg/kg/day to 25-35 mg/kg/day, respectively.
- Aspirin toxicity in cats and dogs typically range from 80-120 mg/kg, taken for extended periods of 10 to 12 days.
Aspirin: Toxicokinetics
- Aspirin is absorbed via passive diffusion from the stomach and intestines.
- Biotransformation of aspirin occurs primarily via acetylation of enzyme COX-1 and COX-2 to prevent the formation of prostaglandins or the formation of thromboxanes.
- Excretion primarily occurs via renal pathways.
- Cats can exhibit increased half-life compared to other species.
Aspirin: Toxicosis
- Symptoms of lower-dose aspirin toxicity include gastroenteritis, nausea, vomiting, and GI bleeding, while moderate to high doses will induce vomiting, elevated respiration, depression, lethargy, dehydration, and/or hyperthermia.
- Diagnosis can be performed using lab tests like blood tests.
Aspirin: Treatment
- Treatment for aspirin toxicity involves stabilizing the patient, providing blood transfusions, fluids (such as sodium bicarbonate), decontamination (using emesis, activated charcoal or cathartic), urine alkalinization, and GI protectants.
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Description
Explore the various sources and effects of respiratory toxicants in this quiz. You will learn about specific examples, such as carbon monoxide and heavy metals, and their impact on the respiratory system. Additionally, the quiz will cover Acute Bovine Pulmonary Edema and Emphysema (ABPE) and its significance.
