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Toxicology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

When Zinc Phosphide Powder is Exposed to ____, It Liberates Phosphine Gas which is Toxic, Flammable and an Irritant

A

Acid

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1
Q

Which Synthetic Herbicide can cause these Clinical Signs in Ruminants?

A

Phenoxy Derivatives of Fatty Acids (2,4-D)

*Ulcers within the Oral Mucosa in Ruminants

*Depression and Muscle Weakness- Ruminants do not get Convulsions

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1
Q

Factors that _____ Pentachlorophenol Toxicity Include:

High Ambient Temperatures

Oily or Organic Solvent Vehicles

Hyperthyroidism

A

Increase

*Highly Lipid Soluble- Soluble in Oils and Organic Solutes

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1
Q

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

A

Urea

*Adult Cattle are More Sensitive to Urea Toxicosis because the Calf is not a Ruminant yet- Very young Animals are Tolerant (

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1
Q

Commonly used Molluscicide that is used to Kill Slugs and Snails

A

Metaldehyde

*Metaldehyde Exposure is Generally by Ingestion of Baits

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2
Q

Treatment for Zinc Phosphide Toxicity

A

Decontamination- Emetics?? (Risk Versus Benefit Assessment), Antacids, Gastric Lavage

Supportive Therapy- Fluids, Oxygen, Antacids

*No Specific Antidote

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2
Q

In which Toxicosis can you Microscopically see Peripheral Nerve and Optive Nerve Degeneration, Demyelination and Gliosis

A

Organic Arsenical Toxicosis

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2
Q

True/False: Lead has the Potential to Cross the Blood Brain Barrier and the Placenta

A

True

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3
Q

Antidotal Treatment for Inorganic Arsenic Toxicosis

A

Dimercaprol (BAL)

*Only used if you confirm Inorganic Arsenic Toxicosis

*Alternative Antidote- Dimercaptosuccinic Acid- Safer Antidote but also Less Effective

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4
Q

Rodenticide that is a Grey-Black Powder with a “Dead Fish” Odor that is Stable in the Enviornment for 2 Weeks

A

Zinc Phosphide

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4
Q

The Oral or Dermal LD50 of Pentachlorophenol in Domestic Animals is ____mg/kg

A

100-200 mg/kg

*Highly Toxic

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4
Q

Treatment for Ionophore (Monensin) Toxicosis

A

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

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4
Q

Most Toxic Form of Selenium

A

Organic Selenium in Plants

*Toxicity: Organic Selenium in Plants > Selenate = Selenite > Selenide > Synthetic Organoselenium Compounds

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4
Q

Toxicant that Undergoes Lethal Synthesis and is Metabolized to Toxic Metabolites Mainly in the Liver

A

Ethylene Glycol

*Metabolites of Ethylene Glycol are Toxic

*Chart- The Red Metabolites are the Most Toxic

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5
Q

True/False: Emesis is the “go to” Treatment for Zinc Phosphide Toxicity

A

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

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6
Q

Best Specimen for Laboratory Diagnosis of Inorganic Arsenic Toxicosis in a Live animal (Antemortem)

A

Urine

*Inorganic Arsenic gets concentrated in Urine

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6
Q

True/False: Older Animals are more Sensitive than Younger Animals to Lead Toxicity

A

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

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6
Q
A

Zinc

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6
Q

Microscopic Lesions of which Toxicosis:

Yellow Birefringent Rosette-Shaped Calcium Oxalate Crystals in the Kindey or Urine

A

Ethylene Glycol Toxicosis

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6
Q

Clinical Signs of which Toxicosis:

Narcotic Effects

CNS Depression

Ataxia

Possible Heinz Body Anemia (Cats)

A

Propylene Glycol

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7
Q

Molybdenum Toxicity is most common in what Species

A

Cattle

*Most Common in Cattle, but can be seen in Sheep

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8
Q

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

A

Water Deprivation-Sodium Ion Toxicosis

*Clinical Signs that we notice are mainly signs of Brain Damage

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8
Q

True/False: Emetics and Strong Cathartics are Contraindicated in Inorganic Arsenic Toxicosis

A

True

*Inorganic Arsenic causes GI Ulceration and Hermorrage- Emetics and Strong Cathartics are CONTRAINDICATED in these Cases

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8
Q

Best Specimens for Laboratory Diagnosis of Selenium Toxicosis

A

Acute Phase- Blood

Chronic Phase- Hair and Hoof

*Hoof specimen should be washed before Analysis

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8
Q

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

A

Oxalic Acid

Chart- The Metabolites in Red are the Most Toxic

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9
Q

Chronic Lead Exposure may cause ______, delays in Erythrocyte Maturation and Shortened Lifespan of the Erythrocytes

A

Anemia

*Abnormal Red Cell Maturation- Lead Toxicosis

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9
Q
A

A. Alcohol Dehydrogenase

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10
Q

Dipyridyl Herbicides (Paraquat) is Unstabe and is Rapidly Inactivated in Light and ____

A

Soil

*Soil acts like an absorbant and Inactivates the Dipyridyl Herbicides- Paraquat binds strongly to soil

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11
Q

True/False: Strychnine is a CNS Inhibitory Toxin

A

False

*Strychnine causes CNS Excitation

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12
Q

Rodenticide that Condenses with Oxaloacetate to Fluorocitrate and Competes with Regular Citrate as a Substitute for Aconitase in the TCA Cycle

A

Fluoroacetate

*Slowing the TCA Cycle and Decreasing Cellular Respiration and Energy

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12
Q

Lesions of which Toxicosis:

GI Mucosal Edema and Hemorrhage with Sloughing and Perforation

Liver and Kidney Damage

Capillary Degeneration- Hemorrhage

A

Inorganic Arsenic

*HEMORRHAGE All over the Body- Capillary Damage

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12
Q

Clinical Signs of which Toxicosis:

GI- Vomiting, Anorexia, Abdominal Pain, Diarrhea

Hematologic- HEMOLYTIC ANEMIA, Icterus, Hemoglobinuria

Renal- Azotemia

A

Zinc Toxicity

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12
Q

In Ethylene Glycol Toxicosis, ____ Acid binds to serum Calcium to form Insoluble Calcium Oxalate Crystals and Hypocalcemia

A

Oxalic Acid

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14
Q
A

B. The Chelator binds a metal and forms a complex that is excreted

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15
Q

All Animals are Susceptible to Strychnine, However ____ are Most Frequently Poisoned and more Sensitive than Cats

A

Dogs

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15
Q

Type of Seleniferous Plant that Accumulates up to 25-100 ppm Selenium and Does Not Require Selenium to grow, but they can Accumulate it

A

Facultative Accumulators

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16
Q

Test used for Laboratory Diagnosis of Ethylene Glycol with these Characteristics:

A

Catachem Ethylene Glycol Test

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17
Q

True/False: Animals that are Preconditioned or Adapted to Nonprotein Nitrogens are more Tolerant of Urea

A

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

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18
Q

Strychnine is Readily Absorbed from the GI Tract, where ____ can Decrease Toxicity

A

Vomiting

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19
Q

True/False: Organic Pentavalent Arsenicals are LESS TOXIC than Inorganic Arsenic

A

True

*Inorganic Arsenic is MORE TOXIC and Organic Arsenic

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20
Q
A

D. None of the Above

*Most commonly we are not going to use any of them

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21
Q

Molybdenum is Excreted in ____ at Toxic Levels

A

Milk

*Three Toxins that reach Toxic Levels in Milk- Molybdenum, Inorganic Arsenic, and Lead

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22
Q

Treatment For Dipyridyl Herbicides (Paraquat)

A

Detoxification- Emetics, Activated Charcoal

Supportive Treatment- Fluid Therapy

*VERY BAD PROGNOSIS- No specific Antidotes

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23
Q

Chronic Copper Toxicosis is Mainly seen in Which Breed of Dog?

A

Bedlington Terrier

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24
Q

Treatment for Strychnine Toxicity

A

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

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24
Q

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

A

Pentachlorophenol

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25
Q

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

A

Iron Toxicity

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27
Q

Typically Poisonous Plants are Unpalatable to Animals, but ______ Improves the Palatability of some Poisonous Plants, which increases the Incidence of Poisoning

A

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

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28
Q

Chronic Copper Toxicosis is common in what Species?

A

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

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29
Q

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 ______

A

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

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29
Q

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

A

Dimercaptosuccinic Acid

*Can be Orally Administered, Does Not Enhance GI Absorption of Lead and is Less Nephrotoxic than other Chelators

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30
Q

Main Clinical Sign seen with Water Deprivation-Sodium Ion Toxicosis

A

Brain Damage

*Cerebral Edema and Neuronal Damage

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30
Q
A

B. Liver Failure

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31
Q

Three Oxidative forms of Selenium

A

Selenate (+6)

Selenite (+4)

Selenide (-2)- Least Toxic

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32
Q

Inorganic Arsenic Exists in Three Oxidative Forms. What are these Three Forms and which is the Most Toxic?

A

Elemental (Organic)

Trivalent (Aresenite)- Most Toxic

Pentavalent (Arsenate)

*Toxicity Ranking: Trivalent > Pentavalent > Elemental

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34
Q

Toxicosis that causes Oxidative Injury to RBC’s leading to Severe Intravascular Hemolysis

A

Zinc Toxicosis

*Big Clinical Sign- Hemolytic Anemia

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34
Q

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

A

Iron Toxicity

*With Oral Preparations you will see- GI Ulceration and Hemorrhagic Enteritis

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35
Q

True/False: Cats are Very Sensitive to Fluoroacetate Toxicity

A

False

*Dogs are Very Sensitive to Fluoroacetate- Dogs are More Likely to Ingest a Toxic Amount

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35
Q

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

A

Paraquat

*Caustic- in the Oral Cavity you will see Ulcers

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35
Q

_____ is Contraindicated in Early Treatment of Paraquat Toxicosis

A

Oxygen

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35
Q

Review of Ionophore (Monensin) Toxicity

A

*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

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36
Q

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?

A

Lead Toxicity

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37
Q

Which Rodenticide has These Clinical Signs:

Rapid Onset (Minutes to Hours)

Vomiting

Abdominal Pain

CNS Excitation

A

Zinc Phosphide

*Vomiting- Caused by GI Irritation

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37
Q

Ethylene Glycol Itself will cause Direct GI Irritation and CNS Depression. The Toxic Metabolites of Ethylene Glycol will Mainly cause Metabolic Acidosis and Acute _____

A

Renal Failure

*Ethylene Glycol Toxicosis- Acute Renal Failure

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38
Q

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

A

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

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38
Q

Toxicity caused by Ingestion of Antifreeze

A

Ethylene Glycol Toxicosis

*Sweet- Very Palatable to Animals

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39
Q

True/False: During the Treatment of any Toxicosis, Gastric Lavage and Emetics are Contraindicated in Patients with GI Ulceration and Hemorrhage

A

True

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40
Q

Mechanism of Action for which Molluscicide:

Decreases Brain GABA, Norepinephrine and Serotonin. Decreased GABA can lead to Seizures/CNS Excitement

A

Metaldehyde

*Causes CNS EXCITMENT- Seizures

*Metaldehyde also causes: GI Irritation, Metabolic Acidosis, and Hyperthermia

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41
Q

Treatment for Metaldehyde Toxicity

A

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

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42
Q

______ of Urine Enhances the Renal Excretion of Phenoxy Derivatives of Fatty Acids (2,4-D)

A

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

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44
Q

Selenium Toxicity is Reduced by High ____ Diets and Ingestion of other Elements that bind to Selenium such as Copper

A

Protein

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45
Q

Predominant Clinical Sign in Horses, Cattle, and Sheep with Fluoroacetate toxicity

A

Cardiac Signs- Heart Failure, Arrhythmias

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46
Q

Two Predominant Clinical Signs in Canines with Fluoroacetate Toxicity

A

CNS Stimulation- Running, Barking, Seizures

Gastrointestinal Signs- Vomiting, Diarrhea, Hyperirritability

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48
Q

Inorganic Arsenic binds to and Inhibits the ____ Group of many Enzyme Systems

A

-SH

*Inorganic Arsenic Binds and Inhibits the SH Groups of many Enzymes

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49
Q

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

A

D-Penicillamine

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50
Q

_____ are Contraindicated in Strychnine Toxicity because it will Increase Absorption of the Toxin

A

Antactids/Bicarbonate

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50
Q

Best Sample for Laboratory Diagnosis of Molybdenum Toxicosis in Live Cattle

A

Whole Blood

*Increased Molybdenum or Decreased Copper in the Blood

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51
Q

Dogs that Survive Acute Metaldehyde Toxicity may develop ____

A

Liver Failure

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52
Q
A

C. D-Penicillamine

*Most Useful Chelator for Copper Toxicity

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53
Q

Clinical Signs in Swine with which Toxicosis:

Incoordination/Ataxia

Recumbancy

Partial Paralysis

Animal will have GOOD Appetite

Possible Blindness

A

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

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54
Q

Clinical Signs of _____ in Horses:

Colic

Hyperventilation

Anorexia

Tachycardia/Tachyarrythmias

Cardiac Arrest- Sudden Death

A

Ionophore (Monensin) Toxicosis

*Ionophore Toxicosis in horses- Looks like the Horse is having a “Heart Attack”

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56
Q

Type of Seleniferous Plants that Accumulate 1-25 ppm Selenium and Accumulate Selenium Passively in Selenium Rich Soil

A

Passive Accumulators

*Passive Accumulators- Most common Source of Selenium Toxicity. They are More Palatable and Animals eat them more Frequently

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56
Q

Three Target Tissues of Lead Toxicity

A

CNS

GIT

Blood

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58
Q

Late Clinical Signs of which Toxicosis:

Oliguric Renal Failure

Vomiting

Anorexia

Lethargy

Anuria

A

Ethylene Glycol Toxicosis

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59
Q

The Acute Oral LD50 for Phenoxy Derivatives of Fatty Acids in Dogs is ____ mg/kg

A

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

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60
Q

Three General Characteristics of Heavy Metals

A

Very Potent- Small Amount to Poison the Animal

Poor Penetrators of Membranes

Very Small amount is Absorbed (10%)

*Most Heavy Metals have Specific Antidotes

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61
Q

True/False: Urea is the MOST TOXIC of the Nonprotein Nitrogen Compounds

A

True

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62
Q

The Most rapid Accumulation and Turnover of _____ occurs in the Pancreas and Liver, where some of these Patients may Develop Pancreatitis

A

Zinc

*Mainly accumulates in the Pancreas and Liver

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63
Q

______ of Red Blood cells can be seen in Dogs with Lead Toxicity and is likely due to accumulation of Ribosomal RNA Aggregates

A

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

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64
Q

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

A

Paraquat

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65
Q

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

A

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

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66
Q

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)

A

Phenoxy Derivatives of Fatty Acids (2,4-D)

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66
Q

Best Sample for Laboratory Diagnosis of Copper Toxicosis in Live Sheep

A

Serum or Whole Blood

*Elevated Copper Levels

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66
Q
A

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

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66
Q

Lab Diagnostics for which Toxicosis:

Increased Serum Osmolality

Increased Anion Gap (40-50mEq)

Low Urine Specific Gravity (

Azotemia

Calcium Oxalate Crystals in Urine

A

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

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68
Q

Serum and CSF Sodium Concentration Higher than _____mEq/L is Suggestive of Water Deprivation-Sodium Ion Toxicosis

A

160 mEq/L

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69
Q
A

Shorter

*Everything Progress more Quickly in Cats with Ethylene Glycol- Clinical Signs and Pharmacokinetics

*Clinical Signs Stages are shorter Durations in Cats

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70
Q

Treatment for Propylene Glycol

A

Decontamination- Emesis and activated Charcoal

Supportive Therapy- IV Fluids, Bicarbonate (Treat Acidosis)

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72
Q

Accumulation of Copper in the Liver is due to Imbalances between Copper, Molybdenum and _____

A

Sulfate

*Low Sulfate = Excess Copper in Blood that goes to the Liver

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72
Q

_____ Therapy is Indicated in Iron Toxicity only in Severe Toxicosis within 12 Hours of Ingestion

A

Chelation

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74
Q

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

A

Lead Toxicity

*Huge Number of Nucleated Red Blood Cells with No Reticulocytes (Non-Regenerative)- Lead Poisoning- KNOW THIS

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75
Q

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

A

Selenium

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77
Q

The Following Drugs are Microsomal Enzyme _____, and Contraindicated for Concurrent Administration with Inophores (Monensin):

A

Inhibitors

*When you use an Enzyme Inhibitor, the Ionophore concentration will go up and the Ionophore will become Toxic!

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78
Q

Main Sources of Which Toxicity:

Ingestion of Pennies

Galvanized Metals (Ex. Bars on Cages)

Batteries

A

Zinc Toxicity

*Subacute Toxicosis in dogs caused by ingestion of >/= 5 Pennies

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79
Q

Lesions associated with which Toxicosis:

Rapid Rigor Mortis

_Hyperkeratosis of the Skin and Villous like Hyperplasia of Urinary Bladder Mucosa (_Pathopneumonic)

A

Pentachlorophenol

*Urinary Bladder Hyperplasia is Pathopneumonic for this Disease in Chronic Cases

79
Q

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)

A

Ionized

Non-Ionized

*Too much Urea and Ammonia will Shift the Rumen pH to the Alkaline Side

79
Q

True/False: Ethylene Glycol can be detected in Blood and Urine Antimortem in Patients 1-6 Hours Post Ingestion

A

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

80
Q

Which Feed and Water Toxin has this Mechanism of Action:

A

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

81
Q

Most common Source of Lead Toxicosis in Animals

A

Lead-Based Paints

*A thumbnail size of lead based paint may contain 50-200 mg of Lead

82
Q

Normal Copper/Molybdenum Ratio

A

6:1

*Too Much Copper (Ex. 10:1) or No Molybdenum (Ex. 6:0) can cause Copper Toxicosis

83
Q

True/False: Diquat is LESS Toxic than Paraquat

A

True

*Diquat is Less Toxic and General Use

*Paraquat is More Toxic and Restricted Use

83
Q

Mainly see _____ Muscle Lesions in Horses with Ionophore (Monensin) Toxicity as well as Skeletal Muscle Lesions

A

Cardiac

85
Q

Specific Antedote for Copper Toxicosis

A

D-Penicillamine (Orally)

*Mainly only used in Human Medicine

86
Q

True/False: Antacids are Contraindicated in Zinc Phosphate Toxicity

A

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!!

88
Q

True/False: Organic Iron is less Irritant than Inorganic Iron and Ferrous Iron is Less Irritant than Ferric Iron

A

True

89
Q

Iron Levels in the Body are Controlled by Iron Absorption because most Animals lack a Mechanism for Efficient ____ of Iron

A

Excretion

90
Q

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

A

*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

91
Q

Treatment for Pentachlorophenol Toxicosis

A

Detoxification- Emetics or Gastric Lavage, Activated Charcoal

Supportive Therapy- Oxygen Therapy

*No specific Antidote

93
Q

Sources of which Toxicosis:

Oral Supplements (For Animals and Humans)

Parenteral Preparations (Ex. Piglets, Cats)

Mineral Fortified Fertilizers

A

Iron Toxicity

*Oral Iron Supplements- For Animals or Humans

94
Q

Most Common Places to Find Selenium Rich Soil

A
95
Q

Acute Clinical Signs of which Toxicosis:

A

Inorganic Arsenic

*GI SIGNS- severe Colic, Vomiting, Hemorrhagic Watery Diarrhea and eventually Death

97
Q

Clinical Signs of _______ Include:

Generally Nonspecific Signs

Mainly GI Irritation

Neuromuscular Signs- Ex. Seizures/Tremors in Dogs

A

Phenoxy Derivatives of Fatty Acids (2,4-D)

*GI and Neuromuscular Toxicosis

98
Q

Toxicity that is Very common and is the Second most Common Cause of Fatal Poisoning in Animals

A

Ethylene Glycol

*Mortality Rate- 59-70%

99
Q

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

A

True

*Organic Arsenicals- Mainly used in Swine and Poultry

101
Q

Best Sample for Laboratory Diagnosis of Ionophore (Monensin) Toxicosis

A

Feed

103
Q

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?

A

Posterior Paralysis

104
Q

Clinical Signs of _____ Toxicity

Severe Colic /Bloat

Rumen Stasis

Muscle Tremors

Salivation/Teeth Grinding

Convulsive Siezures

Death within 1-2 Hours

A

Urea

*Usually Die due to Respiratory Failure

105
Q

Mechanism of Action of which Fungicide?

A

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

107
Q

Treatment for Iron Toxicity

A

Decontamination- Emesis or Gastric Lavage (Before onset of Clinical Signs)

Supportive Treatment- IV Fluids

*Activated Charcoal is not effective- With any Heavy Metals

108
Q

Zinc Phosphide causes CNS _____, such as Compulsive Hypermotility (Mad Dog Running), Yelping, and Convulsions

A

Excitation

*Death within 3-48 Hours due to Tissue Anoxia

108
Q

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

A

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

109
Q

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

A

Stressed

*Onset of Clinical Signs is Sudden- Hemolytic Crisis

111
Q

All animals are susceptible to Dipyridyl Herbicides (Paraquat), Especially Dogs. The Oral LD50 Ranges from _____ mg/kg in cats, dogs, pigs ect.

A

25-75 mg/kg

*Highly Toxic- Caustic to Mucous Membranes

112
Q

What Characteristic of Zinc Phosphide Toxicity is Unique

A

Severe Mucosal Hemorrhage/Irritation (Gastroenteritis)

“Dead Fish”/Garlic Odor

114
Q

Three Characteristics of Urea Toxicity

A

GI (Rumen) Problems

Compulsive Seizures (CNS)

Neuromuscular

115
Q

Synthetic Herbicide that Alters the Metabolism of Plants which Increases their Toxicity by increasing accumulation of Nitrate and Cyanide

A

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

115
Q

Clinical Signs in Swine with which Toxicity:

Hyperexcitability

Tremors

Collapse

Coma

Possible Death

A

Roxarsone (Organic Arsenic)

*Roxarsone DOES NOT cause Peripheral Neurotoxicity in Swine

115
Q

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

A

Transferrin (Primary Transport Protein)

*Nomally Serum Transferrin Concentrations greatly Exceed Incoming Iron

117
Q

Source of Poinsoning for all Synthetic Herbicides (Phenoxy Derivatives and Dipyridyl)

A

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

118
Q

True/False: Acid Conditions Favor Dissolution of Lead

A

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

120
Q

Clinical Signs of Subacute/Chronic _____ Toxicity:

Loss of Hair/Rough Hair Coat

Friable and Deformed Hooves

Lameness and Weakness

A

Chronic Selenium Toxicity

121
Q

Two Dipyridyl Herbicides, which are Broad-Spectrum Dessicant contact Herbicides

A

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

123
Q

Fluoroacetate Toxicity can Lead to a Build up of ____ in the Blood Stream which can be Toxic and Lead to Anticoagulation effects

A

Citrate

*Build up of Citrate that is Not being Used

124
Q

Organic Arsenic Toxicosis is a Peripheral _____ Toxicity

A

Neural

126
Q

Elevated Enzymes that you will see in ____ Toxicosis

A

Ionophore (Monensin)

*Skeletal Muscle Damage- Increased CPK (Specific for Skeletal Muscle Damage)

*All of these Enzymes usually reflect TIssue Damage

126
Q

Characteristic Lesions of which Toxicosis:

Icterus

Hemolysis

Methemoglobinemia

Yellow, Friable Liver

Gunmetal Kidneys (Enlarged and Hemorrhagic)

A

Copper Toxicosis

127
Q

Treatment and Prevention for Chronic Copper Toxicosis in Sheep

A

Molybdenum

*Different Formulations available- Need to Add more Molybdenum to the Diet if Sheep Develop Copper Toxicosis

127
Q
A

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

129
Q

Most Ethylene Glycol Metabolites are Cytotoxic to ____ Tubular Epithelium

A

Renal

*Ethylene Glycol toxicosis leads to ACUTE RENAL FAILURE

130
Q

Animals that are the Most Susceptible to Water Deprivation-Sodium Ion Toxicosis

A

Pigs, Cattle, and Poultry

131
Q

Calcium, Zinc, or Protein Decreases GI Absorption of _____

A

Lead

*If the Patient is Deficient in these Minerals (Calcium, Zinc, or Protein), the Patient may absorb More Lead leading to Toxicosis

132
Q

An _____ Environment Increases Zinc Release and Absorption from Metallic Objects

A

Acidic

133
Q

Optimum Temperature and pH Optimum for Urease Activity

A

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)

134
Q

Fluoroacetate Toxicity Antidotes are ____ Donors, which Compete with the Toxin to Reduce Conversion to Fluoroacetate

A

Acetate

*Ex. Glyceryl Monoacetate, Acetic Acid, Acetamide

136
Q

Toxicity of Paraquat is _____ by:

Selenium-Vitamin E Deficiency

Depletion of Tissue Glutathione

Oxygen Therapy

A

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)

137
Q

Urea’s Toxicity in Large Animals is due to the Production of _____

A

Ammonia

*Lethal Synthesis- Ammonia is Toxic

138
Q

Prevention for Subacute and Chronic Selenium Toxicosis

A

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

138
Q

Toxicity where the source is Ingestion of “Safe Antifreeze”

A

Propylene Glycol Toxicity

*Propyele Glycol is Safer than Ethylene Glycol

139
Q

Lead is Slowly stored in the _____, where it can stay for several Years

A

Bone

140
Q

Test used for Laboratory Diagnosis of Ethylene Glycol with these Characteristics

A

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_

141
Q

Most commonly used Chelating Agent used to Treat Lead Toxicity

A

Calcium Disodium EDTA

*Most Efficient Chelator for Binding Lead

142
Q

Ionophores (Monensin) are Excreted mainly in ____

A

Bile

*Horses do not have Gall Bladders

143
Q

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

A

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

144
Q

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

A

Water Deprivation-Sodium Ion Toxicosis

*More commonly occurs due to Decreased Water Intake

146
Q

Treatment for Molybdenum Toxicosis

A

Copper Glycinate/Copper Sulfate

*Need to Add Copper into the Diet

148
Q

Three Feed and Water related Toxicants

A

Nonprotein Nitrogen (NPN)

Ionophore

Water-Deprivation-Sodium Salt

*These three are Feed Additives that are Problems in Large Animals

149
Q

Three Characteristics Signs of Monensin (Ionophore) Toxicity

A

GI Signs

Cardiac Signs

Skeletal Muscle Signs

*Monensin- One of the Toxins that causes sudden death due to Cardiac Toxicity

150
Q

Two Groups of Synthetic Herbicides that cause Poisoning in Pets

A

Phenoxy Derivatives of Fatty Acids (2,4-D)

Dipyridyl Herbicides ( Ex. Paraquat)

151
Q

True/False: The Small Amount of Iron Normally Excreted in Urine does not Significantly Increase during Toxicosis, Prolonging Toxicosis

A

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

152
Q

Type of Seleniferous Plants that Accumulate up to 15,000 ppm Selenium and Require Selenium for Growth

A

Obligate Accumulators

*Normal Daily Requirement of Selenium- 0.1 ppm

154
Q

Paraquat is Distributed All over the Body and achieves High Concentration in the _____(10x’s)

A

Lung

*Paraquat Can cause Significant Lung Damage and Death- Paraquate causes Respiratory Insufficiency due to Lung Damage

155
Q

Early (Drunk) Clinical Signs of Which Toxicosis:

Nausea/Vomiting

Anorexia

CNS Depression

Ataxia

Incoordination

A

Ethylene Glycol

*Early Clinical Signs associated with Ethylene Glycol Itself- Animal Acts Drunk

157
Q

Treatment for Ethylene Glycol that has a Higher Affinity for Alcohol Dehydrogenase than Ethylene Glycol (Competitive Inhibition)

A

Ethanol 20%

*Causes CNS Depression

158
Q

Accumulation of Copper by Hepatocytes may cause _____ Damage. _____ may cause Sudden Loss of Copper from the Liver to the Blood

A

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

159
Q

Which Synthetic Herbicide Toxicity can cause these Clinical Signs in Canines

A

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

161
Q

Lesions associated with which Toxicity:

Hemorrhagic Gastroenteritis

Pulmonary Edema

Hepatic Necorsis

Abnormal Hooves

Hair Loss/Rough Hair

A

Selenium Toxicosis

163
Q

The Lethal dose of Inorganic Arsenic is ____mg/kg

A

1-25mg/kg

*Highly Toxic

164
Q

Pathopneumonic Lesion seen in Pigs with Water Deprivation-Sodium Ion Toxicosis

A

Eosinophilic Meningioencephalitis

165
Q

High Sodium in the Brain inhibits Anaerobic ____ resulting in Lack of Energy necessary for Active Transport of Sodium out of the Brain

A

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

166
Q

Fungicide that is used by Certified Applicators as a wood Perservative (no Longer found in Wood Perserving Solutions) that may cause Toxicity in Animals

A

Pentachlorophenol (PCP)

*Sources of Exposure- Vapors Penetrate Skin, Inhalation of Vapors (Especially in Barns with Poor Ventilation), Licking wood treated with Pentachlorophenol

167
Q

Propylene Glycol is Metabolized in the Liver by Alcohol Dehydrogenase to Lactaldehyde, which is Metabolized to _____

A

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

168
Q

Chronic Copper Poisoning in Sheep is a _____ Crisis

A

Hemolytic

*Most common Copper Poisoning is Chronic- Hemolytic Crisis

170
Q

One Part Urea Produces ____ Parts Protein

A

Three (300%)

171
Q

Animals that are most Suscpetible to Zinc Toxicity

A

Cattle, Sheep, Horses, Cats, Dogs, Ferrets, and Aviary/Birds

*A Lot of Species are Susceptible to Zinc Toxicosis

172
Q
A

A. Renal System

173
Q

What three Enzymes will be Elevated in Laboratory Diagonsis of Patients with Phenoxy Derivatives of Fatty Acids Toxicosis

A

ALP (Alkaline Phosphatase)- Tissue Damage

LDH (Lactate Dehydrogenase)- Tissue Damage

CPK (Creatine Phosphokinase)- Muscle Damage

175
Q

Treatment for Phenoxy Derivatives of Fatty Acids (2,4-D)

A

Detoxification/Supportive Therapy

*Detoxification- Wash the Skin with soap and water/Activated Charcoal

Supportive Therapy- Intravenous Fluids/ Antidiarrheals

*No Specific Antidote

176
Q

Organic Arsenical Toxicity causes _____ Toxicity in Swine who are Overdosed on Arsanilic Acid and Poultry who are Overdosed on Roxarsone

A

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

178
Q

Arsenic Increases Biliary Excretion of _____

A

Selenium

179
Q

Subacute Clinical Signs of Which Toxicosis

A

Inorganic Arsenic

*Subacute Toxicity- GI Signs and Posterior Paralysis

180
Q

Dietary Calcium, Copper, Iron, Phytate and Fiber will Decrease ____ Absorption in the GI Tract

A

Zinc

*These elements either bind the Zinc and prevent its Absorption or they compete with Zinc for Carrier Proteins and Decrease Zinc Absorption

182
Q

In Zinc Phosphide Toxicosis, Hydrolysis and Liberation of Phosphine Gas occurs at a pH of ___ or Lower

A

4

*Vomiting Decreases Toxicity- Less Zinc Phosphide in the Stomach to Produce Phosphine Gas

183
Q

Treatment for Acute Stage of Selenium Toxicosis

A

Decontamination- Saline Cathartics

Supportive Therapy- Oxygen and Treatment of Pulmonary Edema

*No Specific Antedote

184
Q

Molybdenum Toxicosis is Caused by Excess Molybdenum and/or ____ Deficiency

A

Copper

*Molybdenum Toxicosis is more Commonly due to Copper Deficiency

185
Q

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

A

Copper

186
Q

Common Lesions of which Toxicosis:

Gastric Ulcers

Liver Damage

Pancreatitis

Renal Tubular Casts

A

Zinc Toxicity

187
Q

Treatment for Lead Toxicity

A

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

188
Q

Most Prominent Lesion associated with Water Deprivation-Sodium Ion Toxicosis

A

Cerebral Edema

189
Q

Which Rodenticide should we Think:

Seizures

Tremors

A

Strychnine

190
Q

Clinical Signs of which Toxicosis:

Acute Neurotoxicosis and Hyperthermia- “Shake and Bake”

GI Irritation- Salivation, Vomiting, Diarrhea

CNS Stimulation- Tremors/Seizures

A

Metaldehyde

*Hyperthermia is More Pronounced

*Metaldehyde is also a GI Irritant so it will lead to Salivation, Vomiting and Diarrhea

191
Q

If Chelation Therapy is Indicated in Iron Toxcitiy, which Chelating Agent will we use?

A

Deferoxamine

193
Q

Treatment of Choice for Ethylene Glycol Toxicosis

A

Fomepizole

194
Q

Selenium Toxicosis is a _____ Problem

A

Poisonous Plant

*Selenium Toxicosis is caused by Ingestion of Selenium Rich Plants

195
Q

In Zinc Phosphide Toxicosis, Acute Toxicity is due to _____, while Chronic Toxicity may be due to Zinc Phosphide or Phosphine Gas

A

Phosphine Gas

*The Gas that is Produced will have the Greatest Toxicity- Acid (Ex. Gastric Acid) Enhances Toxicity

197
Q

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

A

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

198
Q

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

A

Lead Toxicity

200
Q

Treatment for Water Deprivation-Sodium Ion Toxicosis

A

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

202
Q

Treatment for Organic Arsenical Toxicosis

A

Supportive Therapy- Fluids and Water

*No Specific Antedote

204
Q

True/False: Post Mortem Examinations play an Important role in the Diagnosis of Urea

A

False

*There are no Characteristic Lesions associated with Urea Toxicity. The Body may Produce an “Ammonia Odor”

205
Q

Arid ____ Soil of the Great Plains promotes Formation of Selenate

A

Alkaline

206
Q

True/False: Seleniferous Plants have a Bad Odor and are Unpalatable

A

True

*Only eaten when other Forage is Unavailable

207
Q

Which Rodenticide has These Effects:

Slowing of TCA Cycle

Build up of Aconitase

Build up of Citrate

A

Fluoroacetate

207
Q

Most common Nonprotein Nitrogen Toxicosis

A

Urea Toxicosis

*Excess Urea in Feed as a Feed additive- Urea is commonly used as a feed additive

208
Q

Phenoxy Derivatives of Fatty Acids (2,4-D) are Irritating to _____

A

GI Mucosa

209
Q

Absorbed Phosphine Gas is Excreted by the ____

A

Lungs

210
Q

Rodenticide Mainly used in Livestock Protection Collars for Controlling Coyotes Preying on Sheep and Goats

A

Fluoroacetate

211
Q

Clinical Signs in Poultry with which Toxicity:

Incoordination

Ataxia

A

Roxarsone

*Roxarsone DOES cause Peripheral Neurotoxicity in Poultry

212
Q
A

Zinc Phosphide

214
Q

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?

A

Cattle and Dogs are the Most Susceptible

*Dogs and Cattle are most suscpetible because they will eat Anything

215
Q

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

A

C.

*Strychnine DOES Cross the Blood Brain Barrier- Important for Clincal Signs

216
Q

Clinical Signs of which Toxicosis:

Severe Diarrhea (Greenish)

Rough Hair Coat and Depigmentation of Hair around the Eyes

Weight Loss

Anemia

Osteoporosis

A

Molybdenum Toxicosis

217
Q

Rodenticide that Causes Seizures that are Elicited by External Stimuli (Light, Sound, Touch)

A

Strychnine

*When Treating these patients you want Quiet, Calm, Dark Rooms

219
Q

Non-Antidotal (Supportive) Treatment for Inorganic Arsenic Toxicosis

A

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

221
Q

Which Rodenticide has these Characteristics:

Direct Irritation of GI Mucosa

Toxicity Primarily due to pH

A

Zinc Phosphide

*Phosphine Gas is the Cause of Most of the Toxicity

223
Q

Inorganic Arsenic is a Toxicosis that mainly causes ____ effects

A

GI

*GI Corrosion and Ulceration

224
Q

Clinical Signs of which Toxicosis:

Hyperthermia

Tachycardia

Dyspnea

Cyanosis

Seizure

Collapse/Death

A

Pentachlorophenol

*Pentochlorophenol can cause signs of Respiratory Insufficiency and Hyperthermia. Also may cause seizures

225
Q

Mechanism of Action for which Toxicosis:

Copper Deficiency

A

Molybdenum Toxicosis

226
Q

Toxicity of Urea is due to Ammonia. Ammonia Inhibits the ____ Resulting in Lack of Energy and Decreased Cellular Respiration and Tissue Damage

A

Citric Acid Cycle

227
Q

Species that is the Most Sensitive to Monensin (Ionophore) Toxicosis

A

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

228
Q

Laboratory Diagnosis of which Toxicosis:

Significant Metabolic Acidosis

Hyperosmolarity

Increased Anion Gap (from Lactic Acid)

Heinz Body (Cats)

A

Propylene Glycol

*Significant Metabolic Acidosis caused by Build up of Lactic Acid

229
Q

Most Cases of Ionophore Toxicosis, are due to _____, which is approved for use in Dairy Cattle to Improve Efficiency of Milk Production

A

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

230
Q

Clinical Signs in Poultry with which Toxicosis:

Anorexia

Depression

Coma

Death

A

Arsanilic Acid

*Arsanilic Acid DOES NOT cause Peripheral Neurotoxicity in Poultry

231
Q

True/False: Phenoxy Derivatives of Fatty Acids (2,4-D) is Readily Absorbed from the GI Tract or by Inhalation

A

True

*Phenoxy Derivatives of Fatty Acids (2,4-D) are Metabolized mainly be Hydrolysis and Excreted mainly unchanged in Urine by Tubular Secretion

232
Q

True/False: Strychnine is Often Given as Malicious Baiting to Poison Animals

A

True

*Fast Onset and Short Term Toxin

233
Q

Clinical Signs of Which Toxicosis causes SUDDEN ONSET of:

Weakeness

Anorexia

Pale Mucous Membranes

Icterus

Hemoglobinuria

Fever/Shock

A

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

235
Q

Ionophores (Monensin) can cause Sudden Death because they cause _____ Toxicity

A

Cardiac

236
Q

Acute (Early Signs) Clinical Signs of which Toxicosis?

A

Paraquat (Dipyridyl Herbicide)

*Early Signs of Paraquat Toxicosis- GI Signs

238
Q

Treatment for Urea Poisoning

A

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

239
Q

Neuroparalytic Condition seen in Swine with Subacute Selenium Toxicosis

A

Porcine Focal Symmetrical Poliomyelomalacia

240
Q

Restricted use Pesticide that is Used to Control Gophers, Squirrels, Deer Mice, Moles ect.

A

Strychnine

*Underground Use- Used for Borrowing Animals

241
Q

Two Predominant Clinical Signs in Cats and Pigs with Fluoroacetate Toxicity

A

CNS Signs- Depression or Excitment

Cardiac Signs- Bradycardia, Arrhythmias

242
Q

Clinical Signs of ____ Toxicity Include:

Panting/Vomiting

Stiffness/Muscle Twitching

Tonic Seizures

Sardonic Grin

A

Strychnine

*Rapid Onset and Rapid Death (10 min- 2 Hours)

*Death is Caused by Respiratory Failure

243
Q

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

A

Strychnine

*Glycine- Inhibitory Neurotransmitter in the Spinal Cord

*Strychnine Blocks Glycine = CNS Excitatory Toxin

243
Q

Delayed Clinical Signs of Which Toxicosis?

A

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

244
Q

Three Important Concepts about the Converstion of Urea to Ammonia within the Rumen

A

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)

245
Q

True/False: Zinc Phosphide Specimens should be Placed in an Airtight Container and Frozen ASAP

A

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

246
Q

Mechanism of Action for which Toxicosis:

Irritation of GI Mucosa

Dramatic Depletion of Tissue Glutathione

Decreased ATP

Abnormal Proteins

A

Selenium Toxicosis

*Selenium Replaces Sulfur in Amino Acids causing Abnormal Proteins- leads to Hoof and Hair Abnormalities

248
Q

Organ System that Ethylene Glycol is most Toxic

A

Kidneys

249
Q

Restricted Use Rodenticide available as Grain and Tracking Powder. Exposure is Due to Ingestion of Baits that has Also been Reported as Malicous Poisoning

A

Zinc Phosphide

250
Q

Treatment for Zinc Toxicity

A

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

251
Q

Two Common Sources of Selenium Toxicosis

A

Cattle, Sheep, and Horses Grazing Seleniferous Plants

Swine and Poultry eating Grains grown on Selenium Rich Soil

*Seleniferous- Plants Rich in Selenium

252
Q

Organ of the Body that is MOST SENSITIVE to Inorganic Arsenic Toxicosis

A

Capillary Endothelial Cells

*Very Potent Capillary Poison- Inorganic Arsenic

253
Q

Most common form of Copper Poisoning in Veterinary Medicine

A

Chronic Copper Poisoning

*Only in Ruminants, Mainly Sheep

254
Q

Animals that are Most Susceptible to Inorganic Arsenic Toxicosis

A

Herbivores

255
Q

Animals that are the Most Susceptible to Lead Toxicity

A

Cattle, Horses, Pets, Waterfowl, and Pet and Wild Birds

256
Q

Selenium acts as an _____ by prevention of Peroxide Accumulation through Reduction of Glutathione

A

Antioxidant

257
Q

Use _____ Tubes for Chemical Analysis of Zinc Toxicosis

A

Trace Element

258
Q

True/False: In the Gastric Environment some of the Metaldehyde Undergoes Hydroysis to Acetaldehyde. Both Metaldehyde and Acetaldehyde cross the Blood Brain Barrier

A

True

259
Q

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 _____

A

Trivalent

*More Toxic

260
Q

Copper Toxicosis is in Sheep, is either caused by Excess Copper and/or _____ Deficiency

A

Molybdenum

*Excess Copper in Feed or Deficiency of Molybdenum in Sheep can cause Copper Toxicosis

261
Q

Clinical Signs of Acute _____ Toxicosis:

Respiratory Insufficiency

Pulmonary Edema and Hemorrhage

GI Signs

A

Acute Selenium Toxicosis

*Damage to Capillaries in the Thoracic Cavity

262
Q

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

A

Hypertonicity

Toxicology (5 decks)

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