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Questions and Answers
Which of the following plants is NOT a member of the Allium genus?
Which of the following plants is NOT a member of the Allium genus?
Which of the following is a common sign of hemolytic anemia caused by onion toxicity?
Which of the following is a common sign of hemolytic anemia caused by onion toxicity?
Which species is most resistant to onion toxicity?
Which species is most resistant to onion toxicity?
What is the primary mechanism of action for onion toxicity?
What is the primary mechanism of action for onion toxicity?
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Which of the following forms of onion is MOST toxic?
Which of the following forms of onion is MOST toxic?
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What is the primary source of zinc for monogastric animals?
What is the primary source of zinc for monogastric animals?
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What is the primary mechanism of zinc toxicity?
What is the primary mechanism of zinc toxicity?
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Which of the following is NOT a typical clinical sign of acute zinc toxicity?
Which of the following is NOT a typical clinical sign of acute zinc toxicity?
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Which of the following is a common treatment for zinc toxicity?
Which of the following is a common treatment for zinc toxicity?
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Which of the following is NOT a source of methylxanthines?
Which of the following is NOT a source of methylxanthines?
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Why are cats more susceptible to acetaminophen toxicity compared to dogs?
Why are cats more susceptible to acetaminophen toxicity compared to dogs?
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Which of the following is NOT a clinical presentation of acetaminophen toxicity in cats?
Which of the following is NOT a clinical presentation of acetaminophen toxicity in cats?
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Which of the following enzymes is primarily responsible for the detoxification of acetaminophen in dogs?
Which of the following enzymes is primarily responsible for the detoxification of acetaminophen in dogs?
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What is the primary mechanism by which acetaminophen causes toxicity in red blood cells?
What is the primary mechanism by which acetaminophen causes toxicity in red blood cells?
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Which of the following is a common antidote used in the treatment of acetaminophen toxicity?
Which of the following is a common antidote used in the treatment of acetaminophen toxicity?
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What is the primary target organ for acetaminophen toxicity in both dogs and cats?
What is the primary target organ for acetaminophen toxicity in both dogs and cats?
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What is the primary source of nitrates and nitrites found in the environment?
What is the primary source of nitrates and nitrites found in the environment?
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What is the primary mechanism by which nitrates and nitrites cause toxicity?
What is the primary mechanism by which nitrates and nitrites cause toxicity?
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Which of the following is NOT a clinical sign of nitrate/nitrite toxicity in cattle and other species?
Which of the following is NOT a clinical sign of nitrate/nitrite toxicity in cattle and other species?
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Which of the following is a common antidote used to treat nitrate/nitrite toxicity?
Which of the following is a common antidote used to treat nitrate/nitrite toxicity?
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Which of the following is the most effective method to prevent nitrate/nitrite toxicity in cattle?
Which of the following is the most effective method to prevent nitrate/nitrite toxicity in cattle?
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What is the role of ruminal microflora in nitrate/nitrite toxicity?
What is the role of ruminal microflora in nitrate/nitrite toxicity?
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What is the significance of the high nitrite levels found in the river water and animal tissue samples collected after the Neochim plant incident?
What is the significance of the high nitrite levels found in the river water and animal tissue samples collected after the Neochim plant incident?
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What is a likely contributing factor to the rapid death of the cows in the Neochim plant incident?
What is a likely contributing factor to the rapid death of the cows in the Neochim plant incident?
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Why is the use of nitrate-based fertilizers a concern for livestock producers?
Why is the use of nitrate-based fertilizers a concern for livestock producers?
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How can livestock producers reduce the risk of nitrate/nitrite toxicity?
How can livestock producers reduce the risk of nitrate/nitrite toxicity?
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Flashcards
Hemolytic Agents
Hemolytic Agents
Substances that cause hemolysis, or the destruction of red blood cells.
Onions
Onions
Plants of the Amaryllidaceae family that contain N-propyl disulfides, toxic to some animals.
N-propyl disulfides
N-propyl disulfides
Toxic compounds found in onions that lead to red blood cell oxidation.
Affected Species
Affected Species
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Mechanism of Action
Mechanism of Action
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Clinical signs of poisoning
Clinical signs of poisoning
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Zinc toxicity
Zinc toxicity
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Methylxanthines
Methylxanthines
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Symptoms of Methylxanthine ingestion
Symptoms of Methylxanthine ingestion
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Treatment for Toxicity
Treatment for Toxicity
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Methemoglobin
Methemoglobin
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Acetaminophen (APAP)
Acetaminophen (APAP)
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Toxicity in Dogs
Toxicity in Dogs
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Toxicity in Cats
Toxicity in Cats
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Mechanism of Acetaminophen Toxicity
Mechanism of Acetaminophen Toxicity
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Clinical Signs of Acetaminophen Toxicity
Clinical Signs of Acetaminophen Toxicity
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Nitrates
Nitrates
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Nitrates and Methemoglobinemia
Nitrates and Methemoglobinemia
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Toxicity Threshold for Nitrates
Toxicity Threshold for Nitrates
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Acute Clinical Signs of Nitrate Toxicity
Acute Clinical Signs of Nitrate Toxicity
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Diagnosis for Nitrate Toxicity
Diagnosis for Nitrate Toxicity
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Treatment for Methemoglobinemia
Treatment for Methemoglobinemia
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Neochim Incident Summary
Neochim Incident Summary
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Prevention of Nitrate Toxicity
Prevention of Nitrate Toxicity
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Acetaminophen Antidote
Acetaminophen Antidote
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Study Notes
RBC Oxidants
- Methemoglobin producers include acetaminophen and nitrates.
- Hemolytic agents include onions and zinc.
Acetaminophen
- Acetaminophen is an over-the-counter analgesic and antipyretic.
- Common forms include Tylenol(325, 500, 625 mg tablets) and combination drugs.
- Prescription medications like Lortab (500-750 mg) and Vicodin contain acetaminophen.
- Toxicity ranges from 100-900 mg/kg in dogs and humans.
- In cats, lower doses (40-60 mg/kg) can be fatal, with reported deaths at 10 mg/kg.
- Acetaminophen affects RBC hemoglobin.
Acetaminophen Toxicokinetics
- Absorption is rapid.
- Phase II conjugation: Dogs metabolize 50-75% to glucuronide, while cats metabolize less than 3%.
- Phase I oxidation involves the breakdown and conversion of the compound.
- Deacetylation is a crucial step in the metabolism of acetaminophen.
- Excretion occurs primarily through urine.
Acetaminophen Liver Target
- The liver is the primary target for acetaminophen toxicity.
- Dogs and cats' RBCs are affected
- Dogs lack NAT 1,2.
- Cats NAT1 is slow.
- The breakdown process produces a toxic metabolite (NAPQI).
Acetaminophen Mechanism
- Redox cycling of para-aminophenol (PAP) oxidizes Hb to MetHb.
- Reduced activity of reductase enzyme.
- Depletion of glutathione (GSH) occurs.
Acetaminophen Clinical Presentation (Cats & Dogs)
- Clinical signs appear within 3-12 hours.
- Decreased oxygen transport and hemolytic anemia are common.
- Signs like cyanosis, dark mucous membranes, dyspnea, tachypnea, hypothermia, tachycardia, hematuria, and edema are observed.
- In cases of cats, face and front paw swelling are common symptoms
- Death can occur.
- Diagnostics include chocolate brown blood, methemoglobinemia, Heinz bodies, and elevated liver enzyme levels
Acetaminophen Treatment
- Treatment options include blood transfusion, oxygen therapy, emesis and activated charcoal with sorbitol, and administration of N-acetylcysteine (Mucomyst, Acetadote) within 8 hours post-ingestion.
- Other supportive therapies include sodium sulfate, ascorbic acid, cimetidine (cytP450 inhibitor), SAMe (s-adenosyl-l-methionine), and silymarin.
Nitrates/Nitrites
- These compounds are found in soil, plants, water, stems, stalks, hay, forage (alfalfa, fescue, sorghum, sudan grass, corn, soybeans), and many poisonous plants, as well as in fertilizers and phenoxy herbicides like 2,4-D.
Nitrate/Nitrite Mechanism of Action
- Ruminal microflora converts nitrate to nitrite.
- Nitrite then oxidizes hemoglobin to methemoglobin.
Nitrate/Nitrite Toxicity
- Toxicity levels vary based on the type and amount of nitrates/nitrites consumed.
- Over 10,000 ppm dry weight is considered toxic.
- Levels between 5000-10,000 ppm is dangerous to pregnant animals.
- Less than 1,000 ppm in water is considered safe.
Nitrate/Nitrite Clinical Presentation (Acute)
- Signs appear 1-4 hours after excessive ingestion.
- Symptoms include respiratory distress, exercise intolerance, cyanosis, tachypnea, gasping, ataxia, tachycardia, seizures, GI distress, salivation, and diarrhea.
- Death is possible within 6-24 hours.
Nitrate/Nitrite Diagnostics
- Discolored blood and tissues.
- Presence of methemoglobinemia is identified by diagnostic testing.
- Animals that died beyond a few hours may not show evidence of the condition.
- Nitrate/nitrite testing can be performed on blood, urine, ocular fluid, hay, and water.
Nitrate/Nitrite Treatment
- The primary goal is to reduce methemoglobin levels.
- Methylene blue is a common antidote.
Nitrate/Nitrite Prevention
- Strategies for preventing nitrate/nitrite toxicity include appropriate testing, adaptation, dilution, and ensiling of feed sources.
Onions and Their Toxins
- Onions, along with related plants like garlic and shallots in the Amaryllidaceae family, contain N-propyl disulfides which are potent toxins.
- Toxicity varies based on plant type, growing conditions, processing, and the species of animal.
- Areas with higher sulfur content in the soil tend to have more toxic levels.
- Reported incidents show that poisoning is associated with raw, cooked, dried, or powdered onion consumption.
Onions and Friends Clinical Signs
- Hemolytic anemia. Symptoms can range from acute to delayed onset.
Onions and Friends Treatment
- Treatment for onion toxicity involves blood transfusion, fluids, GI decontamination, and monitoring of hematocrit for several days
Zinc
- Zinc is an essential nutrient found in pennies, skin ointments, galvanized metals (bolts, nails), and paints (at 55%).
- Dietary excess is possible in cases of monogastrics such as dogs, pigs and birds.
Zinc Toxicokinetics
- Absorption primarily occurs in the upper small intestine, where dietary zinc deficiency can increase absorption.
- Zinc's absorption is enhanced in acidic conditions.
- Distribution occurs through transport proteins to various tissues, with accumulation occurring in the liver, which releases zinc back into circulation.
- Excretion routes include feces (bile and pancreatic fluids), and the GI mucosa.
Zinc Mechanism and Toxicosis
- Oxidative damage, Heinz bodies, and RBC hemolysis can occur.
- Acute toxicoses can also lead to gastroenteritis, hemolytic anemia, icterus, tachycardia, and hemoglobinuria, potentially causing renal failure. Treatment includes appropriate fluids and transfusions, removal of the contaminant source, antacids, H2 antagonists, and chelation with Ca++ and Na2EDTA.
Methylxanthines
- Methylxanthines are plant alkaloids found in chocolate, coffee, tea, cola.
- Other sources include cocoa bean shell mulch and human/veterinary medications.
- Common methylxanthines include theobromine, caffeine, and theophylline.
- Some sources include chocolate.
- The relative amount of theobromine and caffeine in various chocolate forms are described in table form in the source material.
Methylxanthines Dogs (Cats)
- LD50 values (for causing death in 50% of test animals) for methylxanthines in dogs and cats range between 80-200 mg/kg.
- Mild signs of methylxanthine poisoning may appear at 20 mg/kg.
- Severe signs appear between 40-50 mg/kg.
- Seizures may appear at 60 mg/kg.
- 1 oz of milk chocolate per pound of body weight.
- Less than 0.1 ounce of baker's chocolate per pound of body weight.
Methylxanthines Toxicokinetics
- Methylxanthines are readily absorbed and widely distributed.
- They are transferred through the placenta.
- Elimination occurs through biotransformation which leads to inactive metabolites.
- Metabolites are excreted in bile, urine, and through reabsorption from the bladder, and also in milk.
- Relevant half-life times are given in reference tables.
Methylxanthines Mechanism of Action
- Methylxanthines act as competitive antagonists of adenosine receptors, influencing ATP-energy transfer, cAMP signal transduction, and inhibitory neurotransmitter functions.
- They affect adenosine's actions in the CNS, cardiovascular system, and kidneys.
- They inhibit phosphodiesterase (noncompetitive). This impacts the regulation of cAMP levels, which stimulates adenylate cyclase, leading to increased cyclic AMP (cAMP).
###Methylxanthines Clinical Presentation
- Signs typically appear within 1-12 hours of ingestion and include polydypsia, vomiting, bloating, diarrhea, hyperactivity, polyuria, tremors, seizures, ataxia, tachycardia, arrhythmias, tachypnea, cyanosis, hypertension, hyperthermia, and coma.
- Death due to cardiac failure is possible, but rare.
Methylxanthines Treatment
- Treatment often involves stabilizing the animal's condition by addressing tremors, seizures, with medications like methocarbamol or diazepam, controlling arrhythmias, and providing GI decontamination (emetics, gastric lavage, and activated charcoal, with 1 X cathartic used).
- Severe cases could take 72 hours or longer to resolve.
CNS/Cardiovascular Toxicants
- Prescription drugs (e.g., Amitriptyline, Nortriptyline, Imipramine and Norpramin, Tofranil) and street drugs can be toxic.
- Minimum lethal doses (LD) are important in relation to toxicity.
TCAs
- TCAs are also a type of antidepressant, with a minimum LD of less than 15 mg/kg.
- TCAs are lipophilic and rapidly absorbed and widely distributed, reaching their peak plasma levels within 2 hours.
- Hepatic metabolism and excretion in urine is how the body processes it.
- TCAs have active metabolites that can recirculate through enterohepatic circulation.
###TCAs Mechanism of Action
- TCAs affect various receptors, including blocking the reuptake of dopamine, norepinephrine, and serotonin (5-HT). and having anticholinergic and antihistaminergic effects.
- They also have significant anti-adrenergic properties.
###TCAs Clinical Presentation
- Symptoms may include lethargy, ataxia, rapid progression to tachycardia, mydriasis, vomiting, hypotension, cardiac arrhythmias, dyspnea, pulmonary edema, seizures, hyperthermia, and coma.
TCAs Treatment
- No specific antidotes exist for TCA toxicity.
- Treatment primarily focuses on supporting vital signs, addressing hypotension with fluids, and managing seizures with diazepam, with GI decontamination (omitting emesis, then gastric lavage, charcoal, and a cathartic)
Amphetamines
- These central nervous system (CNS) stimulants are commonly used recreationally and have possible medical purposes, but they are also prescribed.
- They are alkaline, and readily absorbed from the GI tract, reaching peak plasma levels within 2-3 hours.
- Amphetamines are widely distributed through the body, metabolized in the liver, and excreted in the urine.
- Amphetamines block norepinephrine and dopamine (NE/DA) reuptake.
Amphetamines Clinical Presentation
- Amphetamine toxicity often manifests with rapid onset (1-2 hours) of signs like hyperexcitability, agitation, mydriasis, tremors, hyperreflexia, rapid breathing, tachycardia, hypertension, cardiac arrhythmias, and infrequent seizures.
Amphetamines Treatment
- Treatment involves stabilization of the animal's condition.
- Hyperactivity is controlled with medications like diazepam and barbiturates.
- Cardiac arrhythmias are also treated.
- GI decontamination using emetics, lavage, and activated charcoal, along with use of a cathartic, is essential.
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Description
Test your knowledge on veterinary toxicology with this quiz focused on various plant and metal toxicities, including onions, zinc, and acetaminophen. Answer questions about signs of toxicity, mechanisms of action, and treatment options for different species. Perfect for veterinary students or animal health professionals!
