Exam 2 Flashcards
When Zinc Phosphide Powder is Exposed to ____, It Liberates Phosphine Gas which is Toxic, Flammable and an Irritant
Acid
Which Synthetic Herbicide can cause these Clinical Signs in Ruminants?
Phenoxy Derivatives of Fatty Acids (2,4-D)
*Ulcers within the Oral Mucosa in Ruminants
*Depression and Muscle Weakness- Ruminants do not get Convulsions
Factors that _____ Pentachlorophenol Toxicity Include:
High Ambient Temperatures
Oily or Organic Solvent Vehicles
Hyperthyroidism
Increase
*Highly Lipid Soluble- Soluble in Oils and Organic Solutes
Factors Affecting Toxicity of _____
Ruminants are More Susceptible (Mainly Cattle)
Most Toxic of all NPN (NonProtein Nitrogen) Compounds
Adult Cattle are MORE sensative than Calfs
Fasting/Dehydration Increases Toxicity
Urea
*Adult Cattle are More Sensitive to Urea Toxicosis because the Calf is not a Ruminant yet- Very young Animals are Tolerant (
Commonly used Molluscicide that is used to Kill Slugs and Snails
Metaldehyde
*Metaldehyde Exposure is Generally by Ingestion of Baits
Treatment for Zinc Phosphide Toxicity
Decontamination- Emetics?? (Risk Versus Benefit Assessment), Antacids, Gastric Lavage
Supportive Therapy- Fluids, Oxygen, Antacids
*No Specific Antidote
In which Toxicosis can you Microscopically see Peripheral Nerve and Optive Nerve Degeneration, Demyelination and Gliosis
Organic Arsenical Toxicosis
True/False: Lead has the Potential to Cross the Blood Brain Barrier and the Placenta
True
Antidotal Treatment for Inorganic Arsenic Toxicosis
Dimercaprol (BAL)
*Only used if you confirm Inorganic Arsenic Toxicosis
*Alternative Antidote- Dimercaptosuccinic Acid- Safer Antidote but also Less Effective
Rodenticide that is a Grey-Black Powder with a “Dead Fish” Odor that is Stable in the Enviornment for 2 Weeks
Zinc Phosphide
The Oral or Dermal LD50 of Pentachlorophenol in Domestic Animals is ____mg/kg
100-200 mg/kg
*Highly Toxic
Treatment for Ionophore (Monensin) Toxicosis
Decontamination- Activated Charcoal/ Mineral Oil
Symptomatic Treatment- Fluids to Correct Hypovolemia
*No Specific Antidote
*The Damage in the Cardiac Muscle is going to Heal by Fibrous or Scar Tissue- Horses that survive may suffer Myocardial Scaring and Necrosis. If the Horse survives the Toxicosis, they can still die suddenly weeks or months later due to Heart Damage. Need to avoid STRESS in these Horses
Most Toxic Form of Selenium
Organic Selenium in Plants
*Toxicity: Organic Selenium in Plants > Selenate = Selenite > Selenide > Synthetic Organoselenium Compounds
Toxicant that Undergoes Lethal Synthesis and is Metabolized to Toxic Metabolites Mainly in the Liver
Ethylene Glycol
*Metabolites of Ethylene Glycol are Toxic
*Chart- The Red Metabolites are the Most Toxic
True/False: Emesis is the “go to” Treatment for Zinc Phosphide Toxicity
False
*Do Not Induce Emesis in Patients with Zinc Phosphide Toxicity- Emesis is Contraindicated because it is a Corrosive Substance
Side Note- Emesis may be used since there is No Specific Antidote for Zinc Phosphide Toxicity- Even though it is Technically Contraindicated
Best Specimen for Laboratory Diagnosis of Inorganic Arsenic Toxicosis in a Live animal (Antemortem)
Urine
*Inorganic Arsenic gets concentrated in Urine
True/False: Older Animals are more Sensitive than Younger Animals to Lead Toxicity
False
*Young Animals are More Sensitive than Adults- Greater Absorption and Immature BBB in Younger Animals. Lead is more likely to cross the Blood Brain Barrier in Younger Animals
Zinc
Microscopic Lesions of which Toxicosis:
Yellow Birefringent Rosette-Shaped Calcium Oxalate Crystals in the Kindey or Urine
Ethylene Glycol Toxicosis
Clinical Signs of which Toxicosis:
Narcotic Effects
CNS Depression
Ataxia
Possible Heinz Body Anemia (Cats)
Propylene Glycol
Molybdenum Toxicity is most common in what Species
Cattle
*Most Common in Cattle, but can be seen in Sheep
Clinical Signs of which Toxicosis:
Early Constipation and Thirst
Vomiting and Polyuria
Intermittent Convulsive Seizures (Not Elicited by External Stimuli)
Circling, Pivoting, Head Pressing
Blindness and Deafness
Inability to Eat or Drink
Water Deprivation-Sodium Ion Toxicosis
*Clinical Signs that we notice are mainly signs of Brain Damage
True/False: Emetics and Strong Cathartics are Contraindicated in Inorganic Arsenic Toxicosis
True
*Inorganic Arsenic causes GI Ulceration and Hermorrage- Emetics and Strong Cathartics are CONTRAINDICATED in these Cases
Best Specimens for Laboratory Diagnosis of Selenium Toxicosis
Acute Phase- Blood
Chronic Phase- Hair and Hoof
*Hoof specimen should be washed before Analysis
Ethylene Glycol is Oxidized by Alcohol Dehydrogenase to Glyocoaldehyde. Glycoaldehyde is Oxidized by Aldehyde Dehydrogenase to Glyoxylic Acid, which is Metablized to Toxic Metabolites such as _____, Glycine, Formic Acid and Hippuric Acid
Oxalic Acid
Chart- The Metabolites in Red are the Most Toxic
Chronic Lead Exposure may cause ______, delays in Erythrocyte Maturation and Shortened Lifespan of the Erythrocytes
Anemia
*Abnormal Red Cell Maturation- Lead Toxicosis
A. Alcohol Dehydrogenase
Dipyridyl Herbicides (Paraquat) is Unstabe and is Rapidly Inactivated in Light and ____
Soil
*Soil acts like an absorbant and Inactivates the Dipyridyl Herbicides- Paraquat binds strongly to soil
True/False: Strychnine is a CNS Inhibitory Toxin
False
*Strychnine causes CNS Excitation
Rodenticide that Condenses with Oxaloacetate to Fluorocitrate and Competes with Regular Citrate as a Substitute for Aconitase in the TCA Cycle
Fluoroacetate
*Slowing the TCA Cycle and Decreasing Cellular Respiration and Energy
Lesions of which Toxicosis:
GI Mucosal Edema and Hemorrhage with Sloughing and Perforation
Liver and Kidney Damage
Capillary Degeneration- Hemorrhage
Inorganic Arsenic
*HEMORRHAGE All over the Body- Capillary Damage
Clinical Signs of which Toxicosis:
GI- Vomiting, Anorexia, Abdominal Pain, Diarrhea
Hematologic- HEMOLYTIC ANEMIA, Icterus, Hemoglobinuria
Renal- Azotemia
Zinc Toxicity
In Ethylene Glycol Toxicosis, ____ Acid binds to serum Calcium to form Insoluble Calcium Oxalate Crystals and Hypocalcemia
Oxalic Acid
B. The Chelator binds a metal and forms a complex that is excreted
All Animals are Susceptible to Strychnine, However ____ are Most Frequently Poisoned and more Sensitive than Cats
Dogs
Type of Seleniferous Plant that Accumulates up to 25-100 ppm Selenium and Does Not Require Selenium to grow, but they can Accumulate it
Facultative Accumulators
Test used for Laboratory Diagnosis of Ethylene Glycol with these Characteristics:
Catachem Ethylene Glycol Test
True/False: Animals that are Preconditioned or Adapted to Nonprotein Nitrogens are more Tolerant of Urea
True
*The Toxic Amount of Urea is Significantly Different (2-3x’s) in Preconditioned Animals versus Non-Preconditioned Animals
*The Toxic Dose in Nonpreconditioned Cattle is 0.45g/kg. However, the Toxic dose in Preconditioned Cattle may be up to 4x’s that Amount
Strychnine is Readily Absorbed from the GI Tract, where ____ can Decrease Toxicity
Vomiting
True/False: Organic Pentavalent Arsenicals are LESS TOXIC than Inorganic Arsenic
True
*Inorganic Arsenic is MORE TOXIC and Organic Arsenic
D. None of the Above
*Most commonly we are not going to use any of them
Molybdenum is Excreted in ____ at Toxic Levels
Milk
*Three Toxins that reach Toxic Levels in Milk- Molybdenum, Inorganic Arsenic, and Lead
Treatment For Dipyridyl Herbicides (Paraquat)
Detoxification- Emetics, Activated Charcoal
Supportive Treatment- Fluid Therapy
*VERY BAD PROGNOSIS- No specific Antidotes
Chronic Copper Toxicosis is Mainly seen in Which Breed of Dog?
Bedlington Terrier
Treatment for Strychnine Toxicity
Decontamination (Induce Emesis/Gastric Lavage)
Supportive Care- Fluid Therapy/Oxygen Support
*It may be too late for Decontamination (Emesis/Gastric Lavage) by the Time the Patient gets to you because Strychnine is Rapidly Absorbed
*Keep in a Quiet Place and Avoid External Stimuli
Properties of Which Fungicide Toxicosis:
Chlorinated Hydrocarbon Insecticide
Volatile and can give off Toxic Vapors in Toxic Concentrations especially in High Ambient Tempratures
Irritating to Mucous Membranes, Respiratory Tract and Skin
Pentachlorophenol
Acute ____ Toxicosis leads to these Stages of Clinical Signs:
Stage 1: Vomiting, Nausea, Diarrhea (GI Signs)
Stage 2: Apparent Recovery, GI Signs Resolve
Step 3: Vomiting, Diarrhea, Coagulation Disorders, DIC, Hepatic Failure, Cardiovascular Collapse (GI, Cardiovascular, and Liver Signs)
Stage 4: GI Obstruction secondary to Fibrosing Repair of the GI Damage
Iron Toxicity
Typically Poisonous Plants are Unpalatable to Animals, but ______ Improves the Palatability of some Poisonous Plants, which increases the Incidence of Poisoning
Phenoxy Derivatives of Fatty Acids (2,4-D)
*Phenoxy Derivatives Increase Plant Toxicity in Three Ways-
Increasing Accumulation of Nitrate
Increasing Accumulation of Cyanide
Improving Palatability of the Plant
Chronic Copper Toxicosis is common in what Species?
Sheep
*Copper Toxicity is more common in SHEEP but can be seen in Cattle
*Molybdenum Toxicity is more common in CATTLE but can be seen in sheep
Organic Arsenicals are mainly used as Feed Additives for Weight Gain in Swine and Poultry. In Swine we mainly use ______, while in Poultry we mainly use ______
Swine- Arsanilic Acid
Poultry- Roxarsone
*Even the Recommened Levels of Organic Arsenic in Debilitated, Dehydrated or Sick Animals may cause signs of Toxicity. Toxicity is Enhanced by Dehydration, Water Deprivation, and Renal Insufficiency
Chelating Agent used to Treat Lead Toxicity that can be administered Orally, alone or following Treatment with EDTA, that Does Not enhance GI Absorption of Lead and is Less Nephrotoxic than other Chelating Agents
Dimercaptosuccinic Acid
*Can be Orally Administered, Does Not Enhance GI Absorption of Lead and is Less Nephrotoxic than other Chelators
Main Clinical Sign seen with Water Deprivation-Sodium Ion Toxicosis
Brain Damage
*Cerebral Edema and Neuronal Damage
B. Liver Failure
Three Oxidative forms of Selenium
Selenate (+6)
Selenite (+4)
Selenide (-2)- Least Toxic
Inorganic Arsenic Exists in Three Oxidative Forms. What are these Three Forms and which is the Most Toxic?
Elemental (Organic)
Trivalent (Aresenite)- Most Toxic
Pentavalent (Arsenate)
*Toxicity Ranking: Trivalent > Pentavalent > Elemental
Toxicosis that causes Oxidative Injury to RBC’s leading to Severe Intravascular Hemolysis
Zinc Toxicosis
*Big Clinical Sign- Hemolytic Anemia
Which Toxicosis Primarily affects these three Organ Systems:
GIT- Vomiting, Diarrhea, Fluid and Electrolyte Loss
Liver- Liver Damage, Liver Failure
Cardiovascular System- Increased Vascular Permeability, Coagulopathy, DIC, Shock and Cardiovascular Collapse
Iron Toxicity
*With Oral Preparations you will see- GI Ulceration and Hemorrhagic Enteritis
True/False: Cats are Very Sensitive to Fluoroacetate Toxicity
False
*Dogs are Very Sensitive to Fluoroacetate- Dogs are More Likely to Ingest a Toxic Amount
Dipyridyl Herbicide that Produce Lesions mainly in the Respiratory Tract, such as Pulmonary Congestion Edema, Congestion, Hemorrhage, Fibrosis and Failure of the Lung to Collapse
Paraquat
*Caustic- in the Oral Cavity you will see Ulcers
_____ is Contraindicated in Early Treatment of Paraquat Toxicosis
Oxygen
Review of Ionophore (Monensin) Toxicity
*Influx of Sodium into the Cell. Increase in Intracellular Sodium is accompanied by an Increase in Intracellular Calcium. The Calcium is sequestered by the Mitochondria leading to Inhibition and Damage of the Mitochondria and Lack of ATP production and Muscle Necrosis
A Patient comes into the Clinic with Megaesophagus and Basophilic Stippling of Red Blood Cells, what should be at the top of your Differential List?
Lead Toxicity
Which Rodenticide has These Clinical Signs:
Rapid Onset (Minutes to Hours)
Vomiting
Abdominal Pain
CNS Excitation
Zinc Phosphide
*Vomiting- Caused by GI Irritation
Ethylene Glycol Itself will cause Direct GI Irritation and CNS Depression. The Toxic Metabolites of Ethylene Glycol will Mainly cause Metabolic Acidosis and Acute _____
Renal Failure
*Ethylene Glycol Toxicosis- Acute Renal Failure
In the Subacute and Chronic Phase of Selenium Toxicosis there will be ______ Abnormalities. In the Acute Phase of Selenium Toxicosis there will mainly be ____ Signs and Respiratory Insufficiency
Hair and Hoof Abnormalities- Subacute and Chronic
GI Signs- Acute
*Subacute and Chronic Clinical Signs of Selenium Toxicity- Loss of Hair and Rough Hair Coat. Horses Loose Hair from the Mane and Tail. The Hooves will be Friable and Deformed
Toxicity caused by Ingestion of Antifreeze
Ethylene Glycol Toxicosis
*Sweet- Very Palatable to Animals
True/False: During the Treatment of any Toxicosis, Gastric Lavage and Emetics are Contraindicated in Patients with GI Ulceration and Hemorrhage
True
Mechanism of Action for which Molluscicide:
Decreases Brain GABA, Norepinephrine and Serotonin. Decreased GABA can lead to Seizures/CNS Excitement
Metaldehyde
*Causes CNS EXCITMENT- Seizures
*Metaldehyde also causes: GI Irritation, Metabolic Acidosis, and Hyperthermia
Treatment for Metaldehyde Toxicity
Decontamination- Emetics, Gastric Lavage, Activated Charcoal
Fluid Therapy- to Address Metabolic Acidosis
Seizure Treatment- Diazepam
*No Specific Antidote
*Prognosis for Metaldehyde Toxicity- Good if they Survive First 24 Hours
______ of Urine Enhances the Renal Excretion of Phenoxy Derivatives of Fatty Acids (2,4-D)
Alkalinization (Sodium Bicarbonate)
*Phenoxy Derivatives of Fatty Acids, are weak acids, therefore Alkalinization can be used to Enhance Renal Excretion- Sodium Bicarbonate IV is commonly used
Selenium Toxicity is Reduced by High ____ Diets and Ingestion of other Elements that bind to Selenium such as Copper
Protein
Predominant Clinical Sign in Horses, Cattle, and Sheep with Fluoroacetate toxicity
Cardiac Signs- Heart Failure, Arrhythmias
Two Predominant Clinical Signs in Canines with Fluoroacetate Toxicity
CNS Stimulation- Running, Barking, Seizures
Gastrointestinal Signs- Vomiting, Diarrhea, Hyperirritability
Inorganic Arsenic binds to and Inhibits the ____ Group of many Enzyme Systems
-SH
*Inorganic Arsenic Binds and Inhibits the SH Groups of many Enzymes
Chelating agent that is used to treat Lead Toxicity that is Given Orally, either Alone or following EDTA Therapy, that is less effective for Chelating Lead and has Potential Nephrotoxicity
D-Penicillamine
_____ are Contraindicated in Strychnine Toxicity because it will Increase Absorption of the Toxin
Antactids/Bicarbonate
Best Sample for Laboratory Diagnosis of Molybdenum Toxicosis in Live Cattle
Whole Blood
*Increased Molybdenum or Decreased Copper in the Blood
Dogs that Survive Acute Metaldehyde Toxicity may develop ____
Liver Failure
C. D-Penicillamine
*Most Useful Chelator for Copper Toxicity
Clinical Signs in Swine with which Toxicosis:
Incoordination/Ataxia
Recumbancy
Partial Paralysis
Animal will have GOOD Appetite
Possible Blindness
Arsanilic Acid (Organic Arsenical)
*Arsanilic Acid Toxicity in Swine causes Peripheral Neurotoxicity
*Swine will have GOOD Appetite- No Irritation of the GI Tract or Anorexia
Clinical Signs of _____ in Horses:
Colic
Hyperventilation
Anorexia
Tachycardia/Tachyarrythmias
Cardiac Arrest- Sudden Death
Ionophore (Monensin) Toxicosis
*Ionophore Toxicosis in horses- Looks like the Horse is having a “Heart Attack”
Type of Seleniferous Plants that Accumulate 1-25 ppm Selenium and Accumulate Selenium Passively in Selenium Rich Soil
Passive Accumulators
*Passive Accumulators- Most common Source of Selenium Toxicity. They are More Palatable and Animals eat them more Frequently
Three Target Tissues of Lead Toxicity
CNS
GIT
Blood
Late Clinical Signs of which Toxicosis:
Oliguric Renal Failure
Vomiting
Anorexia
Lethargy
Anuria
Ethylene Glycol Toxicosis
The Acute Oral LD50 for Phenoxy Derivatives of Fatty Acids in Dogs is ____ mg/kg
100mg/kg
* LD50
* LD50 1mg/kg- 50 mg/kg = Highly Toxic
*LD50 50mg/kg-500mg/kg= Moderately Toxic
*L50 0.5g/kg-5g/kg = Slightly Toxic
*LD50 >5g/kg = Non Toxic
Three General Characteristics of Heavy Metals
Very Potent- Small Amount to Poison the Animal
Poor Penetrators of Membranes
Very Small amount is Absorbed (10%)
*Most Heavy Metals have Specific Antidotes
True/False: Urea is the MOST TOXIC of the Nonprotein Nitrogen Compounds
True
The Most rapid Accumulation and Turnover of _____ occurs in the Pancreas and Liver, where some of these Patients may Develop Pancreatitis
Zinc
*Mainly accumulates in the Pancreas and Liver
______ of Red Blood cells can be seen in Dogs with Lead Toxicity and is likely due to accumulation of Ribosomal RNA Aggregates
Basophilic Stippling
*If a Patient has Basophilic Stippling, Lead Poisoning should be at the top of your differential list. However most dogs with Lead Poisoning do not get Basophilic Stippling
Mechanism of Action of Which Synthetic Herbicide:
Reduced by Nicotinamide-Adenine Dinucleotide Phosphate (NADPH) to Produce Singlet Oxygen. The Singlet Oxygen reacts with Lipids of the cell membranes to form Hydroperoxides. Production of Free Radicals leads to Membrane and Cellular Degeneration and Necrosis, especially Lung Tissue
Paraquat
Ionophores (Monensin) are Rapidly Metabolized by ____ Oxidative Demethylation Enzymes in the Liver. There is Slow Metabolism in Equines because they have the LOWEST Oxidative Demethylases compared to other Domestic Species
P-450
*P-450 = Liver Microsomal Enzymes
*Horses are Deficient in Oxidative Demethylases- may explain why horses are more sensitive than other species, along with the 100% Absorption in Equines
Sythetic Herbicide that Uncouples Oxidative Phosphorylation and Depresses Ribonuclease Synthesis leading to Irritation of the GI Mucosa and Damages the Skeletal Muscle in Dogs (Tremors/Seizures)
Phenoxy Derivatives of Fatty Acids (2,4-D)
Best Sample for Laboratory Diagnosis of Copper Toxicosis in Live Sheep
Serum or Whole Blood
*Elevated Copper Levels
B. Reticulocytosis
*Zinc is Characterized by a Regenerative Anemia, where Lead is a Non-Regenerative Anemia with no Reticulocytes
*Often see a Major Reticulocytosis with Zinc Toxicity due to Hemolytic Anemia
Lab Diagnostics for which Toxicosis:
Increased Serum Osmolality
Increased Anion Gap (40-50mEq)
Low Urine Specific Gravity (
Azotemia
Calcium Oxalate Crystals in Urine
Ethylene Glycol
*Normal Anion Gap is is 10-27 mEq. In patients with Ethylene Glycol Toxicosis the Anion Gap can be as High as 40-50mEq
*Azotemia- Increased Serum Creatinine and BUN between 24-48 Hours Post Ingestion- Damage has already been Done
Serum and CSF Sodium Concentration Higher than _____mEq/L is Suggestive of Water Deprivation-Sodium Ion Toxicosis
160 mEq/L
Shorter
*Everything Progress more Quickly in Cats with Ethylene Glycol- Clinical Signs and Pharmacokinetics
*Clinical Signs Stages are shorter Durations in Cats
Treatment for Propylene Glycol
Decontamination- Emesis and activated Charcoal
Supportive Therapy- IV Fluids, Bicarbonate (Treat Acidosis)
Accumulation of Copper in the Liver is due to Imbalances between Copper, Molybdenum and _____
Sulfate
*Low Sulfate = Excess Copper in Blood that goes to the Liver
_____ Therapy is Indicated in Iron Toxicity only in Severe Toxicosis within 12 Hours of Ingestion
Chelation
Hematology for which Toxicosis shows:
Non-Regenerative Anemia with Inappropriate Release of Large amounts of Nucleated Red Blood Cells (nRBC’s)
Basophilic Stiplling of Erythrocytes
Lead Toxicity
*Huge Number of Nucleated Red Blood Cells with No Reticulocytes (Non-Regenerative)- Lead Poisoning- KNOW THIS
These Six Disease are the Result of _____ Deficiency
White Muscle Disease / Nutritional Muscle Dystrophy- Lambs, Calves
Hepatosis Dietetica - Pigs
Exudative Diathesis - Chicks
Nutritional Pancreatic Atrophy - Chickens
Porcine Stress Syndrome- Pigs
Selenium
The Following Drugs are Microsomal Enzyme _____, and Contraindicated for Concurrent Administration with Inophores (Monensin):
Inhibitors
*When you use an Enzyme Inhibitor, the Ionophore concentration will go up and the Ionophore will become Toxic!
Main Sources of Which Toxicity:
Ingestion of Pennies
Galvanized Metals (Ex. Bars on Cages)
Batteries
Zinc Toxicity
*Subacute Toxicosis in dogs caused by ingestion of >/= 5 Pennies
Lesions associated with which Toxicosis:
Rapid Rigor Mortis
_Hyperkeratosis of the Skin and Villous like Hyperplasia of Urinary Bladder Mucosa (_Pathopneumonic)
Pentachlorophenol
*Urinary Bladder Hyperplasia is Pathopneumonic for this Disease in Chronic Cases
Ammonia produced in the Rumen at Normal pH (6.5) is in the ____ Form, which is Not Absorbed. Too much Urea or Ammonia results in Elevations in Rumen pH (8.0) and Ammonia will be in the _____ Form and more Readily Absorbed (Toxicosis)
Ionized
Non-Ionized
*Too much Urea and Ammonia will Shift the Rumen pH to the Alkaline Side
True/False: Ethylene Glycol can be detected in Blood and Urine Antimortem in Patients 1-6 Hours Post Ingestion
True
*Tend to Use Blood Sample for Ethylene Glycol Lab Diagnosis
*After 6 Hours More Ethylene Glycol is being Transformed into Metabolites, and is no longer detectable in serum or Urine by 48 Hours Post Ingestion
Which Feed and Water Toxin has this Mechanism of Action:
Ionophore (Monensin) Toxicosis
*Myocardium is the Main source of Energy- Monensin causes Cardiac Toxicity
*Sequestration of Calcium in the Mitochondria, leading to Inhibition of Mitochondria and Decreases in ATP and Energy- Causes cell damage all over the Body- Especially the HEART and SKELETAL MUSCLE
Most common Source of Lead Toxicosis in Animals
Lead-Based Paints
*A thumbnail size of lead based paint may contain 50-200 mg of Lead
Normal Copper/Molybdenum Ratio
6:1
*Too Much Copper (Ex. 10:1) or No Molybdenum (Ex. 6:0) can cause Copper Toxicosis
True/False: Diquat is LESS Toxic than Paraquat
True
*Diquat is Less Toxic and General Use
*Paraquat is More Toxic and Restricted Use
Mainly see _____ Muscle Lesions in Horses with Ionophore (Monensin) Toxicity as well as Skeletal Muscle Lesions
Cardiac
Specific Antedote for Copper Toxicosis
D-Penicillamine (Orally)
*Mainly only used in Human Medicine
True/False: Antacids are Contraindicated in Zinc Phosphate Toxicity
False
Antacids are Good for Treatment of Zinc Phosphide Toxicity- Antacids Raise the Gastric pH Level above 4 Decreasing the Amount of Phosphine Gas and Lowering Toxicity!!
True/False: Organic Iron is less Irritant than Inorganic Iron and Ferrous Iron is Less Irritant than Ferric Iron
True
Iron Levels in the Body are Controlled by Iron Absorption because most Animals lack a Mechanism for Efficient ____ of Iron
Excretion
Review of Urea Toxicosis:
*Urea is the most economical Nonprotein Nitrogen feed Additive in Large Animal, but it is also the most Toxic
*The Rumen Microflora with Enzyme Urease, convert Urea to Ammonia + Carbon Dioxide. The Ammonia Aminates Ketoacids from Soluble Carbohydrates (CHO). For Urea or Ammonia to make protein, you need Carbohydrates. The Ketoacids form Amino Acids by the Rumen Microflora. The Amino Acids form Microbial Protein. When these bacteria Die, they become a souce of Animal Protein
*Urea is given as a feed Additive in Large animals because it is a cheap way of creating protein via the Rumen Microflora
*The Converstion of Urea to Ammonia Favors Warm Temperatures (49 Degrees Celcius) and Alkaline Environments
*Cold or Frozen water can be used to Inhibit the Reaction of Urea to Ammonia within the Rumen. Acidic Acid can be Given to Prevent the Reaction as well
Treatment for Pentachlorophenol Toxicosis
Detoxification- Emetics or Gastric Lavage, Activated Charcoal
Supportive Therapy- Oxygen Therapy
*No specific Antidote
Sources of which Toxicosis:
Oral Supplements (For Animals and Humans)
Parenteral Preparations (Ex. Piglets, Cats)
Mineral Fortified Fertilizers
Iron Toxicity
*Oral Iron Supplements- For Animals or Humans
Most Common Places to Find Selenium Rich Soil
Acute Clinical Signs of which Toxicosis:
Inorganic Arsenic
*GI SIGNS- severe Colic, Vomiting, Hemorrhagic Watery Diarrhea and eventually Death
Clinical Signs of _______ Include:
Generally Nonspecific Signs
Mainly GI Irritation
Neuromuscular Signs- Ex. Seizures/Tremors in Dogs
Phenoxy Derivatives of Fatty Acids (2,4-D)
*GI and Neuromuscular Toxicosis
Toxicity that is Very common and is the Second most Common Cause of Fatal Poisoning in Animals
Ethylene Glycol
*Mortality Rate- 59-70%
True/False: Organic Arsenicals are used as Feed Additives to Improve Weight Gain and Feed efficiency and to Control Enteric Infection in Swine and Poultry
True
*Organic Arsenicals- Mainly used in Swine and Poultry
Best Sample for Laboratory Diagnosis of Ionophore (Monensin) Toxicosis
Feed
Inorganic Arsenic is a classified as a Corrosive GI Toxicant, that has a Peracute, Acute, or Subacute Toxicity. If Toxicity is Peracute or Acute the Patient will just experience GI Signs. In addition to GI Signs, what other Pathology will Patients with Subacute toxicity Experience?
Posterior Paralysis
Clinical Signs of _____ Toxicity
Severe Colic /Bloat
Rumen Stasis
Muscle Tremors
Salivation/Teeth Grinding
Convulsive Siezures
Death within 1-2 Hours
Urea
*Usually Die due to Respiratory Failure
Mechanism of Action of which Fungicide?
Pentachlorophenol
*Uncoupler of Oxidative Phosphorylation which Blocks energy Production. Oxygen demand is more than oxygen supply. “Animal cooks in its own heat”
*Pentachlorophenol causes OVERHEATING, metabolic acidosis and dehydration
Treatment for Iron Toxicity
Decontamination- Emesis or Gastric Lavage (Before onset of Clinical Signs)
Supportive Treatment- IV Fluids
*Activated Charcoal is not effective- With any Heavy Metals
Zinc Phosphide causes CNS _____, such as Compulsive Hypermotility (Mad Dog Running), Yelping, and Convulsions
Excitation
*Death within 3-48 Hours due to Tissue Anoxia
Mechanism of Action for which Toxicosis:
Binds with SH and other Nucleophilic Groups Disrupting Hemoglobin Synthesis
Competes with Calcium Ions and alters calcium movement Across Membranes
Lead
*Exact Mechanism of Action for Lead is mainly Unknown
*Important in Clinical Signs- Disrupts Heme Synthesis
*Competes with Calcium- Tend to see changes in Endothelial Cells and Fluid Balance within the Cells
A Large Level of Copper can Accumulate in the Liver without causing Clinical Signs. As soon as the Sheep becomes ____, the Liver will Release the Copper and cause a Hemolytic Crisis
Stressed
*Onset of Clinical Signs is Sudden- Hemolytic Crisis
All animals are susceptible to Dipyridyl Herbicides (Paraquat), Especially Dogs. The Oral LD50 Ranges from _____ mg/kg in cats, dogs, pigs ect.
25-75 mg/kg
*Highly Toxic- Caustic to Mucous Membranes
What Characteristic of Zinc Phosphide Toxicity is Unique
Severe Mucosal Hemorrhage/Irritation (Gastroenteritis)
“Dead Fish”/Garlic Odor
Three Characteristics of Urea Toxicity
GI (Rumen) Problems
Compulsive Seizures (CNS)
Neuromuscular
Synthetic Herbicide that Alters the Metabolism of Plants which Increases their Toxicity by increasing accumulation of Nitrate and Cyanide
Phenoxy Derivatives of Fatty Acids (2,4-D)
*Important Characteristic- Not only can they cause Toxicosis but they can Increase Toxicity of other Toxicants- Especially Poisoning Plants. Phenoxy Derivatives can alter the metabolism of Plants, which Increases the accumulation of Nitrate leading to Nitrate Poisoning
*Spraying plants with Phenoxy Derivatives causes the Plants to accumulate more Nitrate and Cyanide and increase the plants Toxicity
Clinical Signs in Swine with which Toxicity:
Hyperexcitability
Tremors
Collapse
Coma
Possible Death
Roxarsone (Organic Arsenic)
*Roxarsone DOES NOT cause Peripheral Neurotoxicity in Swine
Ferrous Iron is Absorbed from the Small Intestine using an Energy Dependent Carrier Mechanism. Absorbed Ferrous Iron is Oxidized to Ferric Iron. Ferric Iron binds to _____ in Plasma and is Distributed throughout the Body
Transferrin (Primary Transport Protein)
*Nomally Serum Transferrin Concentrations greatly Exceed Incoming Iron
Source of Poinsoning for all Synthetic Herbicides (Phenoxy Derivatives and Dipyridyl)
Accidental Ingestion of High Concentrations or Sprays
*Ex. Grazing Freshly Sprayed Pastures/Access to Freshly sprayed Lawns
*Generally, Sprayed Forages in the Recommended Concentration do no cause Poisoning
True/False: Acid Conditions Favor Dissolution of Lead
True
*Lead within the GI Tract will Dissolve due to the Acidic Environment leading to Higher Systemic Absorption and Toxicosis. This is why Ingestion of Lead is More Toxic than being Shot with a Lead Bullet
Clinical Signs of Subacute/Chronic _____ Toxicity:
Loss of Hair/Rough Hair Coat
Friable and Deformed Hooves
Lameness and Weakness
Chronic Selenium Toxicity
Two Dipyridyl Herbicides, which are Broad-Spectrum Dessicant contact Herbicides
Paraquat- Restricted Use Product (RUP)
Diquat- Generally Used Product (GUP)
*Diquat is General Use and can be purchased from anywhere- Therefore the Lecture is Focused on Paraquat because it is much more likely to cause toxicity
Fluoroacetate Toxicity can Lead to a Build up of ____ in the Blood Stream which can be Toxic and Lead to Anticoagulation effects
Citrate
*Build up of Citrate that is Not being Used
Organic Arsenic Toxicosis is a Peripheral _____ Toxicity
Neural
Elevated Enzymes that you will see in ____ Toxicosis
Ionophore (Monensin)
*Skeletal Muscle Damage- Increased CPK (Specific for Skeletal Muscle Damage)
*All of these Enzymes usually reflect TIssue Damage
Characteristic Lesions of which Toxicosis:
Icterus
Hemolysis
Methemoglobinemia
Yellow, Friable Liver
Gunmetal Kidneys (Enlarged and Hemorrhagic)
Copper Toxicosis
Treatment and Prevention for Chronic Copper Toxicosis in Sheep
Molybdenum
*Different Formulations available- Need to Add more Molybdenum to the Diet if Sheep Develop Copper Toxicosis
Whole Blood
*Lead is 99% Bound to Erythrocyte Membranes
*Blood Lead more than 0.4ppm along with Clinical Signs is considered Diagnostic. Blood Levels may not Correlate with Clinical Signs
Most Ethylene Glycol Metabolites are Cytotoxic to ____ Tubular Epithelium
Renal
*Ethylene Glycol toxicosis leads to ACUTE RENAL FAILURE
Animals that are the Most Susceptible to Water Deprivation-Sodium Ion Toxicosis
Pigs, Cattle, and Poultry
Calcium, Zinc, or Protein Decreases GI Absorption of _____
Lead
*If the Patient is Deficient in these Minerals (Calcium, Zinc, or Protein), the Patient may absorb More Lead leading to Toxicosis
An _____ Environment Increases Zinc Release and Absorption from Metallic Objects
Acidic
Optimum Temperature and pH Optimum for Urease Activity
Temperature Optimum- 49 Degrees Celsius
pH Optimum- 7.7-8.0 (Alkaline)
*These Temperature and pH optimums will lead to Faster converstion of Urea to Ammonia (Toxic)
Fluoroacetate Toxicity Antidotes are ____ Donors, which Compete with the Toxin to Reduce Conversion to Fluoroacetate
Acetate
*Ex. Glyceryl Monoacetate, Acetic Acid, Acetamide
Toxicity of Paraquat is _____ by:
Selenium-Vitamin E Deficiency
Depletion of Tissue Glutathione
Oxygen Therapy
Enhanced
*Usually Paraquat causes Respiratory Insufficiency Signs- Giving Oxygen can INCREASE the Damage of Paraquat
*Generally, with Paraquat Poisoning, you shouldn’t use Oxygen Therapy (Unless Absolutely Necessary)
Urea’s Toxicity in Large Animals is due to the Production of _____
Ammonia
*Lethal Synthesis- Ammonia is Toxic
Prevention for Subacute and Chronic Selenium Toxicosis
Soil and Forage should be tested Regularly for Selenium Levels
Remove animals from Seleniferous Areas
Addition of Copper to the Diet or High Protein Diet
*There is No Treatment for Subacute/Chronic Selenium Toxicosis, but it can be Prevented
Toxicity where the source is Ingestion of “Safe Antifreeze”
Propylene Glycol Toxicity
*Propyele Glycol is Safer than Ethylene Glycol
Lead is Slowly stored in the _____, where it can stay for several Years
Bone
Test used for Laboratory Diagnosis of Ethylene Glycol with these Characteristics
Kacey EG Test
*False Positives can occur from other Substances- Propylene Glycol, Mannitol, Sorbitol, and Ethanol
_*Ethanol Interferes with the Kacey EG Test and can give a False Positive_
Most commonly used Chelating Agent used to Treat Lead Toxicity
Calcium Disodium EDTA
*Most Efficient Chelator for Binding Lead
Ionophores (Monensin) are Excreted mainly in ____
Bile
*Horses do not have Gall Bladders
Sources of ______ Toxicosis:
Eating Feeds that Contain more than Recommended Levels for Chickens, Cattle, and Swine
Eating Feeds with Added Ionophores, accidentally or Intentionally, in Horses, Sheep, and Dogs (Non Target Species)
Malicous Poisoning in Horses
Monensin (Ionophore) Toxicosis
*Most common Source of Toxicosis occurs is Non-Target Species, Mainly Equines- We don’t use Ionophores in Horses. Accidental Ingestion of Large amounts of Monensin (Ionophores) in Equines leads to Toxicosis
Toxicity that Causes Excess Sodium and Water Deprivation, caused by:
Feeding Brine, Whey, or Garbage
Ingestion of Salt Licks or Ice Melts
Drinking water containing Salt
Frozen Water/ Lack of Water
Water Deprivation-Sodium Ion Toxicosis
*More commonly occurs due to Decreased Water Intake
Treatment for Molybdenum Toxicosis
Copper Glycinate/Copper Sulfate
*Need to Add Copper into the Diet
Three Feed and Water related Toxicants
Nonprotein Nitrogen (NPN)
Ionophore
Water-Deprivation-Sodium Salt
*These three are Feed Additives that are Problems in Large Animals
Three Characteristics Signs of Monensin (Ionophore) Toxicity
GI Signs
Cardiac Signs
Skeletal Muscle Signs
*Monensin- One of the Toxins that causes sudden death due to Cardiac Toxicity
Two Groups of Synthetic Herbicides that cause Poisoning in Pets
Phenoxy Derivatives of Fatty Acids (2,4-D)
Dipyridyl Herbicides ( Ex. Paraquat)
True/False: The Small Amount of Iron Normally Excreted in Urine does not Significantly Increase during Toxicosis, Prolonging Toxicosis
True
*Even if there is an Overwhelming amount of Iron in the body, there isn’t Significant increase in Urine Excretion of Iron
*Toxicokinetics- Overwhelming our Storage Capacity, Resulting in Free Iron in the Blood stream and no Efficient way to Excete it
Type of Seleniferous Plants that Accumulate up to 15,000 ppm Selenium and Require Selenium for Growth
Obligate Accumulators
*Normal Daily Requirement of Selenium- 0.1 ppm
Paraquat is Distributed All over the Body and achieves High Concentration in the _____(10x’s)
Lung
*Paraquat Can cause Significant Lung Damage and Death- Paraquate causes Respiratory Insufficiency due to Lung Damage
Early (Drunk) Clinical Signs of Which Toxicosis:
Nausea/Vomiting
Anorexia
CNS Depression
Ataxia
Incoordination
Ethylene Glycol
*Early Clinical Signs associated with Ethylene Glycol Itself- Animal Acts Drunk
Treatment for Ethylene Glycol that has a Higher Affinity for Alcohol Dehydrogenase than Ethylene Glycol (Competitive Inhibition)
Ethanol 20%
*Causes CNS Depression
Accumulation of Copper by Hepatocytes may cause _____ Damage. _____ may cause Sudden Loss of Copper from the Liver to the Blood
Liver
Stress
*Liver- Organ that Stores Copper. Chronic Copper Toxicity leads to LIVER DAMAGE
*Side Note- Liver Damage (Not due to Copper) can cause Copper Accumulation in the Liver, which leads to Secondary Copper Toxicosis. Copper Poisoning can lead to Liver Damage and Liver Damage can lead to Copper Poisoning
Which Synthetic Herbicide Toxicity can cause these Clinical Signs in Canines
Phenoxy Derivatives of Fatty Acids (2,4-D)
*Myotonia- Damage in the Skeletal Muscle of Canines- leading to Weakness, Posterior Paresis and Ataxia
*At High doses (ONLY IN DOGS)- Opisthatanos (Tetanic Spasms) and Posterior Paralysis in Addition ot GI Signs
Lesions associated with which Toxicity:
Hemorrhagic Gastroenteritis
Pulmonary Edema
Hepatic Necorsis
Abnormal Hooves
Hair Loss/Rough Hair
Selenium Toxicosis
The Lethal dose of Inorganic Arsenic is ____mg/kg
1-25mg/kg
*Highly Toxic
Pathopneumonic Lesion seen in Pigs with Water Deprivation-Sodium Ion Toxicosis
Eosinophilic Meningioencephalitis
High Sodium in the Brain inhibits Anaerobic ____ resulting in Lack of Energy necessary for Active Transport of Sodium out of the Brain
Glycolysis
*The Movment of Sodium from the Brain back into the Plasma requires Active Transport. High Sodium Concentrations in the Brain results in lack of Energy for Active Transport and Sodium becomes Trapped in the Brain- The trapping of Sodium in the Brain will pull water with it which can cause CEREBRAL EDEMA and Neuronal Damage
Fungicide that is used by Certified Applicators as a wood Perservative (no Longer found in Wood Perserving Solutions) that may cause Toxicity in Animals
Pentachlorophenol (PCP)
*Sources of Exposure- Vapors Penetrate Skin, Inhalation of Vapors (Especially in Barns with Poor Ventilation), Licking wood treated with Pentachlorophenol
Propylene Glycol is Metabolized in the Liver by Alcohol Dehydrogenase to Lactaldehyde, which is Metabolized to _____
Lactic Acid
*D-Lacatic Acid Accumulates and can cause Lactic Acidosis
*Propylene Glycol is NOT Metabolized to Toxic Metabolites. It is Metabolized to Lactic Acid that Accumulates- D-Lactic Acid may cause Encephalopathy
Chronic Copper Poisoning in Sheep is a _____ Crisis
Hemolytic
*Most common Copper Poisoning is Chronic- Hemolytic Crisis
One Part Urea Produces ____ Parts Protein
Three (300%)
Animals that are most Suscpetible to Zinc Toxicity
Cattle, Sheep, Horses, Cats, Dogs, Ferrets, and Aviary/Birds
*A Lot of Species are Susceptible to Zinc Toxicosis
A. Renal System
What three Enzymes will be Elevated in Laboratory Diagonsis of Patients with Phenoxy Derivatives of Fatty Acids Toxicosis
ALP (Alkaline Phosphatase)- Tissue Damage
LDH (Lactate Dehydrogenase)- Tissue Damage
CPK (Creatine Phosphokinase)- Muscle Damage
Treatment for Phenoxy Derivatives of Fatty Acids (2,4-D)
Detoxification/Supportive Therapy
*Detoxification- Wash the Skin with soap and water/Activated Charcoal
Supportive Therapy- Intravenous Fluids/ Antidiarrheals
*No Specific Antidote
Organic Arsenical Toxicity causes _____ Toxicity in Swine who are Overdosed on Arsanilic Acid and Poultry who are Overdosed on Roxarsone
Peripheral Neural (Locomotor Signs, Ataxia, and Paralysis)
*Only causes Peripheral Neural Toxicity in the Target Species-
Arsanilic Acid causes Neural Toxicity in Swine
Roxarsone causes Neural Toxicity in Poultry
*If you switch the Species (Ex. Roxarsone Toxicity in Swine) you will see different Clinical Signs because Swine are not the Target Species for Roxarsone
Arsenic Increases Biliary Excretion of _____
Selenium
Subacute Clinical Signs of Which Toxicosis
Inorganic Arsenic
*Subacute Toxicity- GI Signs and Posterior Paralysis
Dietary Calcium, Copper, Iron, Phytate and Fiber will Decrease ____ Absorption in the GI Tract
Zinc
*These elements either bind the Zinc and prevent its Absorption or they compete with Zinc for Carrier Proteins and Decrease Zinc Absorption
In Zinc Phosphide Toxicosis, Hydrolysis and Liberation of Phosphine Gas occurs at a pH of ___ or Lower
4
*Vomiting Decreases Toxicity- Less Zinc Phosphide in the Stomach to Produce Phosphine Gas
Treatment for Acute Stage of Selenium Toxicosis
Decontamination- Saline Cathartics
Supportive Therapy- Oxygen and Treatment of Pulmonary Edema
*No Specific Antedote
Molybdenum Toxicosis is Caused by Excess Molybdenum and/or ____ Deficiency
Copper
*Molybdenum Toxicosis is more Commonly due to Copper Deficiency
Mechanism of Action of which Toxin:
Accumlation in the Liver causing Liver Degerenation and Necrosis
Release from the Liver and Excess in the Blood causes Oxidation of Erythrocyte Membranes increasing their Fragility Resulting in a Hemolytic Crisis
Copper
Common Lesions of which Toxicosis:
Gastric Ulcers
Liver Damage
Pancreatitis
Renal Tubular Casts
Zinc Toxicity
Treatment for Lead Toxicity
Stabilize Patient- Fluid/electrolyte Therapy
Decontamination- Remove any lead from the Gut BEFORE Chelation (Chelation may Enhance Absorption Further)
*Activated Charcoal is not Recommended- does not absorb Heavy Metals well
Most Prominent Lesion associated with Water Deprivation-Sodium Ion Toxicosis
Cerebral Edema
Which Rodenticide should we Think:
Seizures
Tremors
Strychnine
Clinical Signs of which Toxicosis:
Acute Neurotoxicosis and Hyperthermia- “Shake and Bake”
GI Irritation- Salivation, Vomiting, Diarrhea
CNS Stimulation- Tremors/Seizures
Metaldehyde
*Hyperthermia is More Pronounced
*Metaldehyde is also a GI Irritant so it will lead to Salivation, Vomiting and Diarrhea
If Chelation Therapy is Indicated in Iron Toxcitiy, which Chelating Agent will we use?
Deferoxamine
Treatment of Choice for Ethylene Glycol Toxicosis
Fomepizole
Selenium Toxicosis is a _____ Problem
Poisonous Plant
*Selenium Toxicosis is caused by Ingestion of Selenium Rich Plants
In Zinc Phosphide Toxicosis, Acute Toxicity is due to _____, while Chronic Toxicity may be due to Zinc Phosphide or Phosphine Gas
Phosphine Gas
*The Gas that is Produced will have the Greatest Toxicity- Acid (Ex. Gastric Acid) Enhances Toxicity
Mechanism of Action for which Toxicosis:
The Trivalent Binds to and Inhibits 2-SH Groups of Lipoic Acid. Lipoid Acid is Essential Cofactor for the enzymatic Decarboxylation of Keto Acids.
Inhibition of Lipoic Acid inhibits Glycolysis and Citric Acid Cycle as well as Oxidative Enzymes and Inactivates Glutathione
The Pentavalent Uncouples Oxidative Phosphorylation
Inorganic Arsenic
*Tissues rich in Oxidative Enzymes such as Intestines, Liver, and Kidney are more Sensitive to Inorganic Arsenic- Damage cause by Lack of Energy and Irriation/Corrosion
Clinical Signs of which Toxicity:
GIT- Anorexia, Vomiting, Diarrhea or Constipation
CNS- Hyperexcitability, Seizures, Anxiety, Pharyngeal Paralysis (Roaring) in Horses, CNS Depression with Chronic Toxicosis
Hematologic- Mild/Moderate Anemia
Lead Toxicity
Treatment for Water Deprivation-Sodium Ion Toxicosis
Giving Small Amounts of Fresh Water gradually Over 2-3 Days
*If the animal is able to drink- 50% Recover
*Giving Water in large amounts may kill the animal by aggrevating Cerebral Edema
Treatment for Organic Arsenical Toxicosis
Supportive Therapy- Fluids and Water
*No Specific Antedote
True/False: Post Mortem Examinations play an Important role in the Diagnosis of Urea
False
*There are no Characteristic Lesions associated with Urea Toxicity. The Body may Produce an “Ammonia Odor”
Arid ____ Soil of the Great Plains promotes Formation of Selenate
Alkaline
True/False: Seleniferous Plants have a Bad Odor and are Unpalatable
True
*Only eaten when other Forage is Unavailable
Which Rodenticide has These Effects:
Slowing of TCA Cycle
Build up of Aconitase
Build up of Citrate
Fluoroacetate
Most common Nonprotein Nitrogen Toxicosis
Urea Toxicosis
*Excess Urea in Feed as a Feed additive- Urea is commonly used as a feed additive
Phenoxy Derivatives of Fatty Acids (2,4-D) are Irritating to _____
GI Mucosa
Absorbed Phosphine Gas is Excreted by the ____
Lungs
Rodenticide Mainly used in Livestock Protection Collars for Controlling Coyotes Preying on Sheep and Goats
Fluoroacetate
Clinical Signs in Poultry with which Toxicity:
Incoordination
Ataxia
Roxarsone
*Roxarsone DOES cause Peripheral Neurotoxicity in Poultry
Zinc Phosphide
Phenoxy Derivatives of Fatty Acids Toxicity is Normally Acute, but Toxicity mainly depends on the Species and Duration of Exposure. Which Two Species are More Susceptible to Toxicity?
Cattle and Dogs are the Most Susceptible
*Dogs and Cattle are most suscpetible because they will eat Anything
Which of the Following is Incorrect for Strychnine:
A. Does Not Accumulate in Tissue
B. Not Highly Protein Bound
C. Does Not Cross the Blood Brain Barrier
C.
*Strychnine DOES Cross the Blood Brain Barrier- Important for Clincal Signs
Clinical Signs of which Toxicosis:
Severe Diarrhea (Greenish)
Rough Hair Coat and Depigmentation of Hair around the Eyes
Weight Loss
Anemia
Osteoporosis
Molybdenum Toxicosis
Rodenticide that Causes Seizures that are Elicited by External Stimuli (Light, Sound, Touch)
Strychnine
*When Treating these patients you want Quiet, Calm, Dark Rooms
Non-Antidotal (Supportive) Treatment for Inorganic Arsenic Toxicosis
Emergency and Supportive Treatment- Fluids and Electrolytes and possible Blood Transfusion
Decontamination- Gastric Lavage, Mineral Oil, Activated Charcoal
*These Patients Die Quickly from Hypovolemic Shock
*If there is Hemorrhage and Ulcuration in the GI Tract, Gastric Lavage and Emetics are CONTRAINDICATED
Which Rodenticide has these Characteristics:
Direct Irritation of GI Mucosa
Toxicity Primarily due to pH
Zinc Phosphide
*Phosphine Gas is the Cause of Most of the Toxicity
Inorganic Arsenic is a Toxicosis that mainly causes ____ effects
GI
*GI Corrosion and Ulceration
Clinical Signs of which Toxicosis:
Hyperthermia
Tachycardia
Dyspnea
Cyanosis
Seizure
Collapse/Death
Pentachlorophenol
*Pentochlorophenol can cause signs of Respiratory Insufficiency and Hyperthermia. Also may cause seizures
Mechanism of Action for which Toxicosis:
Copper Deficiency
Molybdenum Toxicosis
Toxicity of Urea is due to Ammonia. Ammonia Inhibits the ____ Resulting in Lack of Energy and Decreased Cellular Respiration and Tissue Damage
Citric Acid Cycle
Species that is the Most Sensitive to Monensin (Ionophore) Toxicosis
Equines
*Even though they are the most sensitive species, if they ingest the recommended levels for Cattle, Horses will not be Poisoned
*While Ruminants will only Absorb 50% of Ionophores (Monensin), Equines will absorb 100%- High Concentration Absorbtion in Horses
Laboratory Diagnosis of which Toxicosis:
Significant Metabolic Acidosis
Hyperosmolarity
Increased Anion Gap (from Lactic Acid)
Heinz Body (Cats)
Propylene Glycol
*Significant Metabolic Acidosis caused by Build up of Lactic Acid
Most Cases of Ionophore Toxicosis, are due to _____, which is approved for use in Dairy Cattle to Improve Efficiency of Milk Production
Monensin
*Monensin- Common Ionophore that leads to Toxicosis
*Ionophores are mainly used as Growth Promotor Feed Additives. They can also be used to Prevent Coccidial Infections in Cattle, Poultry and Goats. Ionophores are only used to PREVENT Coccidosis, not for Treatment
Clinical Signs in Poultry with which Toxicosis:
Anorexia
Depression
Coma
Death
Arsanilic Acid
*Arsanilic Acid DOES NOT cause Peripheral Neurotoxicity in Poultry
True/False: Phenoxy Derivatives of Fatty Acids (2,4-D) is Readily Absorbed from the GI Tract or by Inhalation
True
*Phenoxy Derivatives of Fatty Acids (2,4-D) are Metabolized mainly be Hydrolysis and Excreted mainly unchanged in Urine by Tubular Secretion
True/False: Strychnine is Often Given as Malicious Baiting to Poison Animals
True
*Fast Onset and Short Term Toxin
Clinical Signs of Which Toxicosis causes SUDDEN ONSET of:
Weakeness
Anorexia
Pale Mucous Membranes
Icterus
Hemoglobinuria
Fever/Shock
Copper
*Pale Mucous Membranes, Weakness, Hemoglobinuria- Hemolytic Shock
*Icterus- Liver Damage
*While the Toxicity was Chronic over Several Weeks, the Onset of Clinical Signs is Sudden for Copper Toxicosis
Ionophores (Monensin) can cause Sudden Death because they cause _____ Toxicity
Cardiac
Acute (Early Signs) Clinical Signs of which Toxicosis?
Paraquat (Dipyridyl Herbicide)
*Early Signs of Paraquat Toxicosis- GI Signs
Treatment for Urea Poisoning
Cold Water and 5% Acetic Acid (or Vinegar) Relieve Bloat
*Treatment should occur every 4-6 Hours over a 48 Hour Period
*Good Prognosis if the Kidneys are still working and the Animal is still Urinating
Neuroparalytic Condition seen in Swine with Subacute Selenium Toxicosis
Porcine Focal Symmetrical Poliomyelomalacia
Restricted use Pesticide that is Used to Control Gophers, Squirrels, Deer Mice, Moles ect.
Strychnine
*Underground Use- Used for Borrowing Animals
Two Predominant Clinical Signs in Cats and Pigs with Fluoroacetate Toxicity
CNS Signs- Depression or Excitment
Cardiac Signs- Bradycardia, Arrhythmias
Clinical Signs of ____ Toxicity Include:
Panting/Vomiting
Stiffness/Muscle Twitching
Tonic Seizures
Sardonic Grin
Strychnine
*Rapid Onset and Rapid Death (10 min- 2 Hours)
*Death is Caused by Respiratory Failure
Rodenticide that Blocks Post-Synaptic Effect of Glycine in the Spinal Cord that Leads to:
Highly Exaggerated Reflex Arcs
Muscle Spasms
Severe Extensor Rigidity
Tonic Seizures
Strychnine
*Glycine- Inhibitory Neurotransmitter in the Spinal Cord
*Strychnine Blocks Glycine = CNS Excitatory Toxin
Delayed Clinical Signs of Which Toxicosis?
Paraquat
*GI signs subside and Respiratory Insufficiency Takes over- Occurs 2-3 Days after Paraquat Exposure
*Subacute or Chronic Paraquat Toxicosis can lead to Pulmonary Fibrosis
Three Important Concepts about the Converstion of Urea to Ammonia within the Rumen
The Reaction is Fast- Fast Onset, Duration, and Death
The pH is Alkaline- Favors Alkaline Environments (pH > 7.45)
The Temperature is High (49 Degrees Celsius)
True/False: Zinc Phosphide Specimens should be Placed in an Airtight Container and Frozen ASAP
True
*Don’t want to be Exposed to Phosphine Gas- Liberated Phosphine Gas is a Potential Hazard!!!!
*Live Patient will Be Breathing out Phosphine Gas!!- If you Suspect Zinc Phosphide Toxicity you want to Ventilate the Patient to make sure you and your staff are not breathing in Phosphine Gas
Mechanism of Action for which Toxicosis:
Irritation of GI Mucosa
Dramatic Depletion of Tissue Glutathione
Decreased ATP
Abnormal Proteins
Selenium Toxicosis
*Selenium Replaces Sulfur in Amino Acids causing Abnormal Proteins- leads to Hoof and Hair Abnormalities
Organ System that Ethylene Glycol is most Toxic
Kidneys
Restricted Use Rodenticide available as Grain and Tracking Powder. Exposure is Due to Ingestion of Baits that has Also been Reported as Malicous Poisoning
Zinc Phosphide
Treatment for Zinc Toxicity
Decontamination- Remove Zinc Foreign Bodies, Cathartics
Supportive Care- Blood Transfusion, Oxygen Therapy, Fluid Therapy
*In canines, once you remove the Zinc Foreign Body, the zinc levels fall very quickly and usually Chelation is not Needed. However, if you perform Chelation, Calcium Disodium EDTA is Best
Two Common Sources of Selenium Toxicosis
Cattle, Sheep, and Horses Grazing Seleniferous Plants
Swine and Poultry eating Grains grown on Selenium Rich Soil
*Seleniferous- Plants Rich in Selenium
Organ of the Body that is MOST SENSITIVE to Inorganic Arsenic Toxicosis
Capillary Endothelial Cells
*Very Potent Capillary Poison- Inorganic Arsenic
Most common form of Copper Poisoning in Veterinary Medicine
Chronic Copper Poisoning
*Only in Ruminants, Mainly Sheep
Animals that are Most Susceptible to Inorganic Arsenic Toxicosis
Herbivores
Animals that are the Most Susceptible to Lead Toxicity
Cattle, Horses, Pets, Waterfowl, and Pet and Wild Birds
Selenium acts as an _____ by prevention of Peroxide Accumulation through Reduction of Glutathione
Antioxidant
Use _____ Tubes for Chemical Analysis of Zinc Toxicosis
Trace Element
True/False: In the Gastric Environment some of the Metaldehyde Undergoes Hydroysis to Acetaldehyde. Both Metaldehyde and Acetaldehyde cross the Blood Brain Barrier
True
Inorganic Arsenic is Distributed all over the body and achieves high Concentrations in Liver and Kidney, and also Hair, Hoof, Nails and Skin. Pentavalent is Reduced in the Liver to _____
Trivalent
*More Toxic
Copper Toxicosis is in Sheep, is either caused by Excess Copper and/or _____ Deficiency
Molybdenum
*Excess Copper in Feed or Deficiency of Molybdenum in Sheep can cause Copper Toxicosis
Clinical Signs of Acute _____ Toxicosis:
Respiratory Insufficiency
Pulmonary Edema and Hemorrhage
GI Signs
Acute Selenium Toxicosis
*Damage to Capillaries in the Thoracic Cavity
Excess Absorbed Sodium Following Large Dietary Intake is rapidly excreted in Urine as long as there is Enought Water. Excess Sodium and Water Deprivation results in _____ of the Blood and toxicosis
Hypertonicity
