1
Q
When Zinc Phosphide Powder is Exposed to ____, It Liberates Phosphine Gas which is Toxic, Flammable and an Irritant
A
Acid
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
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
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 (
1
Q
Commonly used Molluscicide that is used to Kill Slugs and Snails
A
Metaldehyde
*Metaldehyde Exposure is Generally by Ingestion of Baits
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
2
Q
In which Toxicosis can you Microscopically see Peripheral Nerve and Optive Nerve Degeneration, Demyelination and Gliosis
A
Organic Arsenical Toxicosis
2
Q
True/False: Lead has the Potential to Cross the Blood Brain Barrier and the Placenta
A
True
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
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
4
Q
The Oral or Dermal LD50 of Pentachlorophenol in Domestic Animals is ____mg/kg
A
100-200 mg/kg
*Highly Toxic
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
4
Q
Most Toxic Form of Selenium
A
Organic Selenium in Plants
*Toxicity: Organic Selenium in Plants > Selenate = Selenite > Selenide > Synthetic Organoselenium Compounds
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
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
6
Q
Best Specimen for Laboratory Diagnosis of Inorganic Arsenic Toxicosis in a Live animal (Antemortem)
A
Urine
*Inorganic Arsenic gets concentrated in Urine
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
6
Q
A
Zinc
6
Q
Microscopic Lesions of which Toxicosis:
Yellow Birefringent Rosette-Shaped Calcium Oxalate Crystals in the Kindey or Urine
A
Ethylene Glycol Toxicosis
6
Q
Clinical Signs of which Toxicosis:
Narcotic Effects
CNS Depression
Ataxia
Possible Heinz Body Anemia (Cats)
A
Propylene Glycol
7
Q
Molybdenum Toxicity is most common in what Species
A
Cattle
*Most Common in Cattle, but can be seen in Sheep
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
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
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
8
**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
9
**Chronic Lead Exposure** may cause \_\_\_\_\_\_, _delays in Erythrocyte Maturation and Shortened Lifespan of the Erythrocytes_
**Anemia**
**\***_Abnormal Red Cell Maturation- Lead Toxicosis_
9
**A. Alcohol Dehydrogenase**
10
**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_
11
True/False: **Strychnine** is a CNS Inhibitory Toxin
**False**
**\***_Strychnine causes CNS Excitation_
12
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_
12
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_
12
Clinical Signs of which Toxicosis:
_**GI**- Vomiting, Anorexia, Abdominal Pain, Diarrhea_
_**Hematologic**- HEMOLYTIC ANEMIA, Icterus, Hemoglobinuria_
_**Renal**- Azotemia_
**Zinc Toxicity**
12
In **Ethylene Glycol** Toxicosis, ____ Acid binds to serum Calcium to form Insoluble _Calcium Oxalate Crystals_ and Hypocalcemia
**Oxalic Acid**
14
**B. The Chelator binds a metal and forms a complex that is excreted**
15
All Animals are Susceptible to **Strychnine**, However ____ are Most Frequently Poisoned and more Sensitive than Cats
**Dogs**
15
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**
16
Test used for Laboratory Diagnosis of **Ethylene Glycol** with these Characteristics:
**Catachem Ethylene Glycol Test**
17
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_
18
**Strychnine** is Readily Absorbed from the GI Tract, where ____ can Decrease Toxicity
**Vomiting**
19
True/False: Organic Pentavalent Arsenicals are LESS TOXIC than Inorganic Arsenic
**True**
_**\***Inorganic Arsenic is MORE TOXIC and Organic Arsenic_
20
**D. None of the Above**
**\***Most commonly we are not going to use any of them
21
**Molybdenum** is Excreted in ____ at Toxic Levels
**Milk**
**_\*Three Toxins that reach Toxic Levels in Milk- Molybdenum, Inorganic Arsenic, and Lead_**
22
Treatment For **Dipyridyl Herbicides (Paraquat)**
**Detoxification- Emetics, Activated Charcoal**
**Supportive Treatment- Fluid Therapy**
\*VERY BAD PROGNOSIS- No specific Antidotes
23
Chronic **Copper** Toxicosis is Mainly seen in Which Breed of Dog?
**Bedlington Terrier**
24
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
24
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**
25
**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**
27
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_
28
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_
29
**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
29
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_
30
Main Clinical Sign seen with **Water Deprivation-Sodium Ion Toxicosis**
**Brain Damage**
_\*Cerebral Edema and Neuronal Damage_
30
**B. Liver Failure**
31
Three Oxidative forms of **Selenium**
**Selenate (+6)**
**Selenite (+4)**
**Selenide (-2)-** Least Toxic
32
**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
34
Toxicosis that causes _Oxidative Injury to RBC's leading to Severe **Intravascular Hemolysis**_
**Zinc Toxicosis**
_**\***Big Clinical Sign- Hemolytic Anemia_
34
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
35
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_
35
**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
35
\_\_\_\_\_ is Contraindicated in Early Treatment of **Paraquat** Toxicosis
**Oxygen**
35
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
36
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**
37
Which **Rodenticide** has These Clinical Signs:
_Rapid Onset (Minutes to Hours)_
_Vomiting_
_Abdominal Pain_
_CNS Excitation_
**Zinc Phosphide**
\*Vomiting- Caused by GI Irritation
37
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_
38
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_
38
Toxicity caused by Ingestion of **Antifreeze**
**Ethylene Glycol Toxicosis**
**\***Sweet- Very Palatable to Animals
39
True/False: During the Treatment of any Toxicosis, Gastric Lavage and Emetics are Contraindicated in Patients with **GI Ulceration and Hemorrhage**
**True**
40
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
41
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_
42
\_\_\_\_\_\_ 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_
44
**Selenium Toxicity** is _Reduced_ by High ____ Diets and Ingestion of other Elements that bind to Selenium such as Copper
**Protein**
45
Predominant Clinical Sign in Horses, Cattle, and Sheep with **Fluoroacetate** toxicity
**Cardiac Signs-** Heart Failure, Arrhythmias
46
Two Predominant Clinical Signs in _Canines_ with **Fluoroacetate** Toxicity
**CNS Stimulation-** Running, Barking, Seizures
**Gastrointestinal Signs-** Vomiting, Diarrhea, Hyperirritability
48
**Inorganic Arsenic** binds to and Inhibits the ____ Group of many Enzyme Systems
**-SH**
**\***_Inorganic Arsenic Binds and Inhibits the SH Groups of many Enzymes_
49
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**
50
\_\_\_\_\_ are **Contraindicated in Strychnine Toxicity** because it will Increase Absorption of the Toxin
**Antactids/Bicarbonate**
50
Best Sample for Laboratory Diagnosis of **Molybdenum Toxicosis** in Live Cattle
**Whole Blood**
**\***Increased Molybdenum or Decreased Copper in the Blood
51
Dogs that Survive **Acute Metaldehyde** Toxicity may develop \_\_\_\_
**Liver Failure**
52
**C. D-Penicillamine**
**\***Most Useful Chelator for Copper Toxicity
53
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_
54
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"
56
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_
56
Three Target Tissues of **Lead Toxicity**
**CNS**
**GIT**
**Blood**
58
Late Clinical Signs of which Toxicosis:
_Oliguric Renal Failure_
_Vomiting_
_Anorexia_
_Lethargy_
_Anuria_
**Ethylene Glycol Toxicosis**
59
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
60
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
61
True/False: **Urea** is the MOST TOXIC of the Nonprotein Nitrogen Compounds
**True**
62
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_
63
\_\_\_\_\_\_ 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_
64
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**
65
**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
66
_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)**
66
Best Sample for Laboratory Diagnosis of **Copper Toxicosis** in Live Sheep
**Serum or Whole Blood**
\*Elevated Copper Levels
66
**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_
66
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_
68
Serum and CSF **Sodium** Concentration Higher than \_\_\_\_\_mEq/L is Suggestive of **Water Deprivation-Sodium Ion Toxicosis**
**160 mEq/L**
69
**Shorter**
**\***Everything Progress more Quickly in Cats with Ethylene Glycol- Clinical Signs and Pharmacokinetics
\*Clinical Signs Stages are shorter Durations in Cats
70
Treatment for **Propylene Glycol**
**Decontamination- Emesis and activated Charcoal**
**Supportive Therapy- IV Fluids, Bicarbonate (Treat Acidosis)**
72
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
72
\_\_\_\_\_ Therapy is Indicated in **Iron Toxicity** only in _Severe Toxicosis_ within 12 Hours of Ingestion
**Chelation**
74
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_
75
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**
77
The Following Drugs are Microsomal Enzyme \_\_\_\_\_, and Contraindicated for Concurrent Administration with I**nophores (Monensin):**
**Inhibitors**
_\*When you use an Enzyme Inhibitor, the Ionophore concentration will go up and the Ionophore will become Toxic!_
78
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
79
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_
79
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
79
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_
80
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_
81
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
82
Normal **Copper/Molybdenum** Ratio
**6:1**
**\***_Too Much Copper (Ex. 10:1) or No Molybdenum (Ex. 6:0) can cause Copper Toxicosis_
83
True/False: Diquat is LESS Toxic than Paraquat
**True**
_**\***Diquat is Less Toxic and General Use_
_\*Paraquat is More Toxic and Restricted Use_
83
Mainly see _____ Muscle Lesions in _Horses_ with **Ionophore (Monensin) Toxicity** as well as Skeletal Muscle Lesions
**Cardiac**
85
Specific Antedote for **Copper Toxicosis**
**D-Penicillamine (Orally)**
**\***Mainly only used in Human Medicine
86
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!!_
88
True/False: _Organic Iron is less Irritant than Inorganic Iron_ and _Ferrous Iron is Less Irritant than Ferric Iron_
**True**
89
**Iron Levels** in the Body are Controlled by _Iron Absorption_ because most Animals lack a Mechanism for Efficient ____ of Iron
**Excretion**
90
_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_
## Footnote
**_\*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
Treatment for **Pentachlorophenol** Toxicosis
**Detoxification- Emetics or Gastric Lavage, Activated Charcoal**
**Supportive Therapy- Oxygen Therapy**
_\*No specific Antidote_
93
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
94
Most Common Places to Find **Selenium Rich Soil**
95
_Acute_ Clinical Signs of which **Toxicosis:**
**Inorganic Arsenic**
**\*GI SIGNS-** _severe Colic, Vomiting, Hemorrhagic Watery Diarrhea and eventually Death_
97
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_
98
Toxicity that is Very common and is the _Second most Common Cause of Fatal Poisoning in Animals_
**Ethylene Glycol**
**\***Mortality Rate- 59-70%
99
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_
101
Best Sample for Laboratory Diagnosis of **Ionophore (Monensin) Toxicosis**
**Feed**
103
**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**
104
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
105
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_
107
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
108
**Zinc Phosphide** causes CNS \_\_\_\_\_, such as Compulsive Hypermotility **(Mad Dog Running**), Yelping, and Convulsions
**Excitation**
**\***_Death within 3-48 Hours due to Tissue Anoxia_
108
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_
109
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
111
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
112
What Characteristic of **Zinc Phosphide** Toxicity is Unique
**Severe Mucosal Hemorrhage/Irritation (Gastroenteritis)**
**"Dead Fish"/Garlic Odor**
114
Three Characteristics of **Urea Toxicity**
**GI (Rumen) Problems**
**Compulsive Seizures (CNS)**
**Neuromuscular**
115
**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_
115
Clinical Signs in **Swine** with which Toxicity:
_Hyperexcitability_
_Tremors_
_Collapse_
_Coma_
_Possible Death_
**Roxarsone** (Organic Arsenic)
**\***Roxarsone DOES NOT cause Peripheral Neurotoxicity in Swine
115
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
117
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_
118
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
120
Clinical Signs of **Subacute/Chronic** _____ Toxicity:
_Loss of Hair/Rough Hair Coat_
_Friable and Deformed Hooves_
_Lameness and Weakness_
**Chronic Selenium Toxicity**
121
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
123
**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
124
**Organic Arsenic** Toxicosis is a Peripheral _____ Toxicity
**Neural**
126
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
126
Characteristic Lesions of which Toxicosis:
_Icterus_
_Hemolysis_
_Methemoglobinemia_
_Yellow, Friable Liver_
_Gunmetal Kidneys (Enlarged and Hemorrhagic)_
**Copper Toxicosis**
127
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
127
**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
Most **Ethylene Glycol** Metabolites are Cytotoxic to ____ Tubular Epithelium
**Renal**
_**\***Ethylene Glycol toxicosis leads to ACUTE RENAL FAILURE_
130
Animals that are the Most Susceptible to **Water Deprivation-Sodium Ion Toxicosis**
**Pigs, Cattle, and Poultry**
131
**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
132
An _____ Environment Increases **Zinc** Release and Absorption from Metallic Objects
**Acidic**
133
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)
134
**Fluoroacetate** Toxicity _Antidotes_ are ____ Donors, which Compete with the Toxin to Reduce Conversion to Fluoroacetate
**Acetate**
**\***Ex. Glyceryl Monoacetate, Acetic Acid, Acetamide
136
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)_
137
**Urea's Toxicity** in Large Animals is due to the Production of \_\_\_\_\_
**Ammonia**
_**\***Lethal Synthesis- Ammonia is Toxic_
138
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
138
Toxicity where the source is Ingestion of **"Safe Antifreeze"**
**Propylene Glycol Toxicity**
**\***Propyele Glycol is Safer than Ethylene Glycol
139
**Lead** is Slowly stored in the \_\_\_\_\_, where it can stay for _several Years_
**Bone**
140
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**_
141
Most commonly used Chelating Agent used to Treat **Lead Toxicity**
**Calcium Disodium EDTA**
**\***Most Efficient Chelator for Binding Lead
142
**Ionophores (Monensin)** are Excreted mainly in \_\_\_\_
**Bile**
\*Horses do not have Gall Bladders
143
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_
144
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
146
Treatment for **Molybdenum Toxicosis**
**Copper Glycinate/Copper Sulfate**
**\***Need to Add Copper into the Diet
148
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_
149
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
150
Two Groups of **Synthetic Herbicides** that cause Poisoning in Pets
**Phenoxy Derivatives of Fatty Acids (2,4-D)**
**Dipyridyl Herbicides ( Ex. Paraquat)**
151
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_
152
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_
154
**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_
155
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
157
Treatment for **Ethylene Glycol** that has a Higher Affinity for Alcohol Dehydrogenase than Ethylene Glycol (Competitive Inhibition)
**Ethanol 20%**
**\***Causes CNS Depression
158
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_
159
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_
161
Lesions associated with which Toxicity:
_Hemorrhagic Gastroenteritis_
_Pulmonary Edema_
_Hepatic Necorsis_
_Abnormal Hooves_
_Hair Loss/Rough Hair_
**Selenium Toxicosis**
163
The Lethal dose of **Inorganic Arsenic** is \_\_\_\_mg/kg
**1-25mg/kg**
**\*Highly Toxic**
164
Pathopneumonic Lesion seen in _Pigs_ with **Water Deprivation-Sodium Ion Toxicosis**
**Eosinophilic Meningioencephalitis**
165
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
166
**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_
167
**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_
168
Chronic **Copper Poisoning** in Sheep is a _____ Crisis
**Hemolytic**
_**\***Most common Copper Poisoning is Chronic- Hemolytic Crisis_
170
One Part **Urea** Produces ____ Parts Protein
**Three (300%)**
171
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
172
**A. Renal System**
173
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**
175
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_
176
**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
178
**Arsenic** Increases Biliary Excretion of \_\_\_\_\_
**Selenium**
179
_Subacute_ Clinical Signs of Which **Toxicosis**
**Inorganic Arsenic**
_\*Subacute Toxicity- **GI Signs and Posterior Paralysis**_
180
_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
182
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
183
Treatment for **Acute Stage of Selenium Toxicosis**
**Decontamination- Saline Cathartics**
**Supportive Therapy- Oxygen and Treatment of Pulmonary Edema**
**\***No Specific Antedote
184
**Molybdenum Toxicosis** is Caused by Excess Molybdenum and/or ____ Deficiency
**Copper**
**\***Molybdenum Toxicosis is more Commonly due to Copper Deficiency
185
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**
186
Common Lesions of which Toxicosis:
_Gastric Ulcers_
_Liver Damage_
**_Pancreatitis_**
_Renal Tubular Casts_
**Zinc Toxicity**
187
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
188
Most Prominent Lesion associated with **Water Deprivation-Sodium Ion Toxicosis**
**Cerebral Edema**
189
Which **Rodenticide** should we Think:
_Seizures_
_Tremors_
**Strychnine**
190
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
191
If Chelation Therapy is Indicated in **Iron Toxcitiy**, which Chelating Agent will we use?
**Deferoxamine**
193
Treatment of Choice for **Ethylene Glycol Toxicosis**
**Fomepizole**
194
**Selenium Toxicosis** is a _____ Problem
**Poisonous Plant**
**\***Selenium Toxicosis is caused by Ingestion of Selenium Rich Plants
195
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**_
197
_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_
198
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**
200
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
202
Treatment for **Organic Arsenical** Toxicosis
**Supportive Therapy- Fluids and Water**
_\*No Specific Antedote_
204
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"
205
Arid ____ Soil of the Great Plains promotes Formation of **Selenate**
**Alkaline**
206
True/False: **Seleniferous Plants** have a Bad Odor and are Unpalatable
**True**
**\***Only eaten when other Forage is Unavailable
207
Which **Rodenticide** has These Effects:
_Slowing of TCA Cycle_
_Build up of Aconitase_
_Build up of Citrate_
**Fluoroacetate**
207
Most common **Nonprotein Nitrogen Toxicosis**
**Urea Toxicosis**
**\***Excess Urea in Feed as a Feed additive- Urea is commonly used as a feed additive
208
**Phenoxy Derivatives of Fatty Acids (2,4-D)** are Irritating to \_\_\_\_\_
**GI Mucosa**
209
Absorbed **Phosphine Gas** is Excreted by the \_\_\_\_
**Lungs**
210
Rodenticide Mainly used in _Livestock Protection Collars_ for Controlling Coyotes Preying on Sheep and Goats
**Fluoroacetate**
211
Clinical Signs in **Poultry** with which Toxicity:
_Incoordination_
_Ataxia_
**Roxarsone**
_\*Roxarsone DOES cause Peripheral Neurotoxicity in Poultry_
212
**Zinc Phosphide**
214
**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
215
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
216
Clinical Signs of which Toxicosis:
_Severe Diarrhea (Greenish)_
_Rough Hair Coat and Depigmentation of Hair around the Eyes_
_Weight Loss_
_Anemia_
_Osteoporosis_
**Molybdenum Toxicosis**
217
Rodenticide that Causes _Seizures that are Elicited by External Stimuli (Light, Sound, Touch)_
**Strychnine**
**\***_When Treating these patients you want Quiet, Calm, Dark Rooms_
219
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_
221
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
223
**Inorganic Arsenic** is a Toxicosis that mainly causes ____ effects
**GI**
_**\***GI Corrosion and Ulceration_
224
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_
225
Mechanism of Action for which Toxicosis:
_Copper Deficiency_
**Molybdenum Toxicosis**
226
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**
227
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
228
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
229
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_
230
Clinical Signs in **Poultry** with which Toxicosis:
_Anorexia_
_Depression_
_Coma_
_Death_
**Arsanilic Acid**
_**\***Arsanilic Acid DOES NOT cause Peripheral Neurotoxicity in Poultry_
231
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_
232
True/False: **Strychnine** is Often Given as _Malicious Baiting_ to Poison Animals
**True**
**\***Fast Onset and Short Term Toxin
233
**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
235
**Ionophores (Monensin)** can cause Sudden Death because they cause _____ Toxicity
**Cardiac**
236
**Acute (Early Signs) Clinical Signs** of which Toxicosis?
**Paraquat (Dipyridyl Herbicide)**
_\*Early Signs of Paraquat Toxicosis- GI Signs_
238
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_
239
Neuroparalytic Condition seen in _Swine_ with **Subacute Selenium Toxicosis**
**Porcine Focal Symmetrical Poliomyelomalacia**
240
Restricted use Pesticide that is Used to Control Gophers, Squirrels, Deer Mice, Moles ect.
**Strychnine**
**\***Underground Use- Used for Borrowing Animals
241
Two Predominant Clinical Signs in _Cats and Pigs_ with **Fluoroacetate** Toxicity
**CNS Signs-** Depression or Excitment
**Cardiac Signs-** Bradycardia, Arrhythmias
242
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_
243
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**
243
**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_
244
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)
245
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_
246
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_
248
Organ System that **Ethylene Glycol** is most Toxic
**Kidneys**
249
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**
250
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_
251
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_
252
Organ of the Body that is MOST SENSITIVE to **Inorganic Arsenic Toxicosis**
**Capillary Endothelial Cells**
_**\***Very Potent Capillary Poison- Inorganic Arsenic_
253
Most common form of **Copper Poisoning** in Veterinary Medicine
**Chronic Copper Poisoning**
**\***Only in Ruminants, Mainly Sheep
254
Animals that are Most Susceptible to **Inorganic Arsenic Toxicosis**
**Herbivores**
255
Animals that are the Most Susceptible to **Lead Toxicity**
**Cattle, Horses, Pets, Waterfowl, and Pet and Wild Birds**
256
**Selenium** acts as an _____ by prevention of Peroxide Accumulation through Reduction of Glutathione
**Antioxidant**
257
Use _____ Tubes for Chemical Analysis of **Zinc Toxicosis**
**Trace Element**
258
True/False: In the Gastric Environment some of the **Metaldehyde** Undergoes Hydroysis to Acetaldehyde. Both Metaldehyde and Acetaldehyde cross the Blood Brain Barrier
**True**
259
**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
260
**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_
261
Clinical Signs of **Acute** _____ Toxicosis:
_Respiratory Insufficiency_
_Pulmonary Edema and Hemorrhage_
_GI Signs_
**Acute Selenium Toxicosis**
\*Damage to Capillaries in the Thoracic Cavity
262
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**
Toxicology
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