Veterinary Pharma Toxicology

Question 1

What does LD50 refer to?
a. Dose that is lethal to 50% of a test sample
b.Dose that is lethal when the individual is exposed to 50% of the substance
c. Dose that is lethal at 50mg/kg
d.Dose that is lethal when 50% of the substance is ingested by the individual

Answer 1

Dose that is lethal to 50% of a test sample

Lethal dose-50 (LD50), also called median lethal dose (MLD), is the dose that is lethal to 50% of a test sample. It is an estimator of lethality and the most common expression used to rate the potency of toxicants.

Question 2

The minimum dose of a drug to produce the desired response is called:
a. Ceiling dose
b.Threshold dose
c. Both a and b
d.None

Answer 2

Threshold dose

Threshold dose is the exposure level below which the harmful or adverse effects of a substance are not seen in a population. This dose is also referred to as the no observed adverse effect level (NOAEL) or the no observed effect level (NOEL)1. However, for substances causing cancer (carcinogens), no safe level of exposure exists, since any exposure could result in cancer. Once threshold is crossed, adverse toxic response is observed 2.

Question 3

What is the duration of exposure for acute toxicosis/ toxicity?
a. Less than 4 hours
b.Less than 8 hours
c. Less than 24 hours
d.Around 24-48 hours

Answer 3

Less than 24 hours

Subacute toxicosis less than 1month
Subchronic toxicosis 1-3 months
Chronic toxicosis ~>3 months

Question 4

The liver and kidney are major target organs of toxicity because:
a. They both receive a high percentage of cardiac output.
b.They both have substantial xenobiotic (chemical) metabolizing capacity.
c. They both have transport systems that can concentrate xenobiotics.
d.All of the above

Answer 4

All of the above

Question 5

Deficiency of which element in the sow predisposes baby pigs to toxicosis by injectable iron preparations?
a. Copper
b.Zinc
c. Magnesium
d.Selenium

Answer 5

Selenium

in fatal cases of iron toxicosis, it has been speculated
that insufficient stores of antioxidants such as vitamin E and selenium can render affected piglets susceptible to the cytotoxic effects of increased reactive oxygen species (ROS) generated by iron at the cellular level

Question 6

Why are caged birds especially susceptible to fumes from chlorine bleach?
a. Dermal burns
b.Ocular irritation
c. Nasal irritation
d.Pulmonary irritation

Answer 6

Pulmonary irritation

Because of the countercurrent anatomy and physiology of the avian lung, caged birds are at increased risk of succumbing to fumes from bleaches and other cleaning agents

Question 7

Which of the following substances is not easily adsorbed by activated charcoal?
a. Iron
b.Ethanol
c. Methanol
d.All of the above

Answer 7

All of the above

Activated charcoal binds to the poison that is still in the digestive tract, preventing its absorption into the blood. However, it does not bind to alcohol, iron, and many household chemicals (corrosive acids/alkali) due to polarity

Question 8

The most susceptible species of animal for tetanus is?
a. Horse
b.Cattle
c. Hen
d.Elephant

Answer 8

Horse

Horses, lambs and humans are observed to be the most sensitive to the effects of tetanus toxin. Horses are readily exposed to the spores while grazing and their predilection for wounds such as lacerations and punctures make them prime candidates for acquiring tetanus.

Question 9

Which of the following is false regarding botulism toxin?
a. Botulism occurs via ingestion or wound contamination of spores or preformed toxin.
b.Preformed toxin sources are decaying carcasses.
c. For prevention, vaccination against C. botulism with toxoid can prevent clinical disease.
d.Clinical signs include “sawhorse stance,” muscle rigidity, erect ears, and a reluctance to eat due to “locked jaw.”

Answer 9

Clinical signs include “sawhorse stance,” muscle rigidity, erect ears, and a reluctance to eat due to “locked jaw.”

Botulism is characterized by flaccid muscle paralysis and includes progressive motor paralysis, disturbed vision, difficulty in chewing and swallowing, and generalized progressive paresis. Death is usually due to respiratory or cardiac paralysis. The toxin prevents release of acetylcholine at motor endplates (neuromuscular
junction), producing presynaptic neuromuscular blockade.

Question 10

A 1-year old Puspin accidentally ingested her ball toy. Which of the following emetic drugs are recommended for the vet to give to her?
a. 3% Hydrogen peroxide
b.Sodium chloride (table salt)
c. Apomorphine
d.Xylazine

Answer 10

Xylazine

Xylazine, an α2-agonist is indicated to induce emesis in cats. Since vomiting is mediated via α2 receptors in the CRTZ in cats, α2-agonists such as xylazine and dexmedetomidine hydrochloride can be used to induce emesis. Hydrogen peroxide (a) is not recommended for emesis in cats due to the risk of severe hemorrhagic esophagitis and gastritis. Sodium chloride (b) should not be used as salt toxicosis can easily occur in cases of overdose and can result in fatal cerebral edema. Apomorphine (c), a D2 receptor agonist is not effective in cats because it is the α2 receptors that need stimulating.

Question 11

All animals are susceptible to poisoning by ethylene glycol, but due
to its wide availability and common presence in homes, dogs and
cats are most often accidentally poisoned. Which of the following
common household solvents is the source of ethylene glycol toxicity for companion animals?
a.Antifreeze
b.Household bleach
c.Nail polish remover
d.Paint thinner

Answer 11

Antifreeze

Antifreeze is a solution of 95% ethylene glycol. The active ingredient of household bleach (B) is sodium hypochlorite in a dilute, approximately 5%, solution. Nail polish remover (C) is typically comprised of acetone. Paint thinner (D) has more than one formulation, but many are made of mineral spirits

Question 12

Clinical signs of ethylene glycol toxicity are dose- and time-dependent and are often multisystemic but nonspecific. Which of the following systems is NOT typically affected by ethylene glycol or its metabolites?
a.Central nervous system
b.Gastrointestinal system
c.Musculoskeletal system
d.Urinary system

Answer 12

Musculoskeletal system

The musculoskeletal system is not affected by ethylene glycol toxicosis. The central nervous system (A) is affected, and clinical signs are similar to those of alcohol intoxication. The lining of the GI system (B) is often irritated and results in vomiting. The urinary system (D), particularly renal tubular epithelium, is directly damaged by ethylene glycol metabolites, which can result in renal failure

Question 13

Which among the following lesions is a characteristic finding in EG intoxication?
a.Renal tubular epithelial necrosis
b.Renal tubular acidosis
c.Renal and perirenal edema
d.Polycystic kidneys

Answer 13

Renal tubular epithelial necrosis

Glycolic acid and oxalate are the metabolites thought to be most responsible for acute tubular necrosis associated with ethylene glycol ingestion. Oxalate also combines with calcium to form a soluble complex that is excreted via glomerular filtration. Calcium oxalate crystals form within the lumens of the renal tubules as water is reabsorbed from the glomerular filtrate and the pH decreases.

Question 14

Treatment of ethylene glycol toxicity aims to decrease absorption of ingested ethylene glycol, increase excretion of unmetabolized ethylene glycol, and correct metabolic acidosis that occurs with ethylene glycol metabolism. Which of the following is an appropriate part of the treatment regimen to address ethylene glycol toxicosis?
a.Give activated charcoal
b.Infuse intravenous fluids
c. Induce vomiting
d.Provide supplemental oxygen

Answer 14

Infuse intravenous fluids

Balanced crystalloid IV fluids (Lactated Ringer’s Solution/Plasma-Lyte A, twice the maintenance rate) are used to counteract the metabolic acidosis. Activated charcoal (A) is unlikely to reduce absorption of ethylene glycol, which is rapidly absorbed in the GI tract. Rapid absorption is also why induction of vomiting (C) is not likely to be effective; it also could lead to aspiration pneumonia. Supplemental oxygen (D) is not usually needed because the respiratory system is not directly affected

Question 15

What is NOT an antidote for ethylene glycol intoxication?
a.Ethanol
b.4-Methylpyrazole
c.Naloxone
d.Fomepizole

Answer 15

Naloxone

Naloxone is the antidote for opioid poisoning.

To prevent metabolism of ethylene glycol, the activity of alcohol dehydrogenase is decreased by direct inactivation or by competitive inhibition. In dogs, 4-methylpyrazole (4-MP, fomepizole) effectively inactivates alcohol dehydrogenase without the adverse effects of ethanol and is the treatment of choice. If 4-MP is not available, an ethanol regimen is recommended.

Question 16

There are several types of rodenticides used as bait for targeted species. Unfortunately, they may be ingested by nontarget species such as pets, wildlife, or livestock and cause immediate or delayed illness or death. The most accurate way to identify the active ingredient of a rodenticide that caused a case of poisoning is by which of the following?
a.Brand and manufacturer
b.Clinical signs of affected animals
c. Color and shape of the bait
d.EPA/FPA registration number

Answer 16

EPA/FPA registration number

Question 17

A farm dog is brought to a veterinarian because of depression, limping, coughing, and pale mucous membranes. You suspect accidental poisoning. In speaking with the dog’s owner, he tells you he recently was trying to reduce the rodent population in his fields. Based on the clinical signs, what is the most likely rodenticide the dog has been exposed to?
a.Bromethalin
b.Strychnine
c.Warfarin
d.Zinc phosphide

Answer 17

Warfarin

Warfarin is an anticoagulant that leads to hemorrhage, but the bleeding may not be external. Pale mucous membranes raise concern for hemorrhage. Bromethalin (A) is a neurotoxin that may cause muscle tremors,
weakness, and seizures. Strychnine (B) leads to life-threatening tetanic seizures. Zinc phosphide (D) is converted to toxic phosgene gas in the stomach and often presents with vomiting.

Question 18

Many rodenticides have a delayed onset of clinical signs that are vague at first and may take days to appear. Which of the following rodenticides has a rapid onset and can lead to death within hours of ingestion?
a.Cholecalciferol
b.Strychnine
c.Warfarin
d.Zinc phosphide

Answer 18

Strychnine

Strychnine is rapidly absorbed in the small intestines, and tetanic seizures soon follow. Food in the stomach can slow this process somewhat. Cholecalciferol (A) toxicity causes electrolyte imbalances that take some time for clinical signs to show but can lead to organ failure in later stages if not treated. Warfarin (C) toxicity leads to hemorrhage that may not be apparent until stores of coagulation factors are exhausted. Zinc phosphide (D) is converted to phosgene gas in the acidic stomach environment. Food in the stomach may accelerate the conversion because it stimulates gastric acid secretion, but the onset of signs is considerably slower than those associated with strychnine poisoning.

Question 19

What is the antidote for anticoagulant rodenticides?
a.Tranexamic acid
b.Vitamin K1
c.Vitamin K3
d.Aspirin

Answer 19

Vitamin K1

Anticoagulant rodenticides mechanistically inhibit the enzyme vitamin K epoxide reductase, which is crucial in the recycling and production of vitamin K1, a necessary
component for clotting factors II, VII, IX, and X1. When the production of these clotting factors in the liver is inhibited, prothrombin cannot be adequately converted to thrombin, and coagulopathy results.

Question 20

The acronym SLUD stands for salivation, lacrimation, urination, and defecation, which are the clinical signs associated with muscarinic cholinergic overstimulation caused by certain toxins. Signs of SLUD are most consistent with exposure to which of the following classes of chemicals?
a.Carbamates
b.Chlorinated hydrocarbons
c.Metaldehyde
d.Pyrethroids

Answer 20

Carbamates

Carbamates (A) and organophosphates are insecticides and herbicides that inhibit acetylcholinesterase at nerve
synapses and neuromuscular junctions. These chemicals cause overstimulation of the parasympathetic nervous
system, resulting in SLUD signs in affected animals. Toxicities caused by chlorinated hydrocarbons (B), metaldehyde (C), and pyrethroid insecticides (D) typically result in neurologic signs, such as tremors, seizures, and ataxia.

Question 21

Cats are particularly sensitive to the effects of many insecticides. Which of the following insecticides is most appropriate for use in or around cats?
a. Benzene hexachloride
b.Carbophenothion
c. Imidacloprid
d.Permethrin

Answer 21

Imidacloprid

Imidacloprid (C) is a neonicotinoid insecticide that acts on acetylcholine receptors to inhibit cholinergic transmission in insects. It can be applied to cats and dogs to control fleas and lice. Benzene hexachloride (A) is a chlorinated hydrocarbon that is highly toxic to cats when used at concentrations that can control parasites. Carbophenothion (B) is used to control parasites on sheep, but a single dose is lethal to cats. Permethrin (D) is found in some brands of topical flea treatments for dogs, but it is highly toxic to cats.

Question 22

Metaldehyde is the active ingredient in molluscicides, which are used to control snails and slugs. It is primarily used in humid, coastal regions where these mollusks are more common. Which of the following medications is most appropriate for treatment of metaldehyde poisoning in dogs?
a. 4-methylpyrazole
b.Diazepam
c. Phenobarbital
d.Vitamin K1

Answer 22

Diazepam

There is no specific treatment for metaldehyde poisoning, although aggressive symptomatic treatment during the first 24 hours may allow for a full recovery in most patients within 2–3 days. Diazepam (2–5 mg/kg, IV, to effect) may be given to control neurologic signs such as seizures

Question 23

Consumption of the fruit, seed, stem, or leaves of avocados can cause toxicity in animals. Ingestion of sufficient quantities of avocado fruit is most likely to cause myocardial necrosis in which of the following species?
a. Cats
b.Chickens
c. Cockatiels
d.Dogs

Answer 23

Cockatiels

Birds, horses, cattle, goats, sheep, rabbits, small mammals, and fish are all susceptible to myocardial necrosis after ingesting avocado. Caged birds, such as cockatiels (C) and budgerigars, are more sensitive to the toxicity than chickens (B). Cats (A) and dogs (D) may experience gastrointestinal upset upon ingestion of avocado fruit, and the seed can cause gastrointestinal obstructions.

Question 24

What is the most toxic part of the avocado plant?
a. Fruit
b.Leaves
c. Stem
d.Seed

Answer 24

Leaves

Ingestion of fruit, leaves, stems, and seeds of avocado has been associated with toxicosis in animals; leaves are the most toxic part containing the most persin. Avocado plant ingestion causes necrosis and hemorrhage of mammary gland epithelium in lactating mammals and myocardial necrosis in birds and mammals.

Question 25

Although many species are susceptible to chocolate toxicosis, it is most common in dogs. Ingestion of chocolate can result in gastrointestinal upset at lower doses and cardiac arrhythmias, neurologic dysfunction, and death at higher doses. One of the toxic ingredients in chocolate is caffeine. Which of the following is the other toxic component of chocolate?
a. Bromethalin
b.N-propyl disulfide
c. Sugar
d.Theobromine

Answer 25

Theobromine

Caffeine and theobromine are methylxanthines that cause cardiotoxic and neurotoxic effects. The concentrations of theobromine and caffeine differ based on the type of chocolate: cocoa powder contains the most (~800 mg/oz), whereas white chocolate contains insignificant amounts. Cocoa bean hulls also contain methylxanthines and can cause death in livestock. Bromethalin (A) is a neurotoxin found in some rodenticides. N-propyl disulfide (B) is an oxidant found in onions that can cause hemolytic anemia in dogs, cattle, horses, sheep, and goats. Sugar (C) is not a toxic ingredient of chocolate.

Question 26

Ingestion of xylitol, a sugar substitute that can be found in gum, candy, baked goods, and liquid medications, can cause toxicity in dogs. Which of the following is most likely to occur in dogs after the consumption of xylitol?
a. Hypercalcemia
b.Hyperglycemia
c. Hypocalcemia
d.Hypoglycemia

Answer 26

Hypoglycemia

Profound hypoglycemia (D) can occur in dogs that ingest xylitol due to a dose-dependent release of endogenous insulin. Hepatic insufficiency or failure can also occur. Patients that have ingested more than 75 mg/kg of xylitol require hospitalization and blood glucose monitoring. Hypercalcemia (A), hyperglycemia (B), and hypocalcemia (C) are not typically associated with xylitol toxicity.

Question 27

A dog living in a bakeshop accidentally ingested raw bread dough. Soon, he started attempting to vomit, to no avail. Which of the following WILL NOT help in treating this intoxication?
a. Attempting emesis with hydrogen peroxide
b.Initiating IV fluid therapy
c. Gastric lavage with warm water
d.Surgical removal

Answer 27

Gastric lavage with warm water

Warm water will cause further fermentation of the dough, leading to consequent ethanol intoxication. Cold water introduced into the stomach may slow the rate of yeast
fermentation and help in dough removal.

Question 28

Coumaphos, dichlorvos, fenthion and malathion among others are widely used pesticides with low toxicity. They are easily destroyed by sunlight, water, microbes, alkalis, metals, and so on, leaving minimal environmental residue. However, they have considerable toxicity for mammals if consumed directly. What is the antidote for this type of toxicity?
a. Atropine + 2-pralidoxime
b.Atipamezole
c. Diazepam
d.Atropine

Answer 28

Atropine + 2-pralidoxime

Coumaphos, dichlorvos, fenthion and malathion are examples of organophosphates. Three categories of drugs are used to treat OP poisoning: (1) Muscarinic receptor–blocking agents, (2) Cholinesterase reactivators, and (3) Emetics, cathartics, and adsorbents to decrease
further absorption. Atropine sulfate blocks the central and peripheral muscarinic receptor–associated effects of OPs. An improved treatment combines atropine with the cholinesterase-reactivating oxime pralidoxime chloride, or 2-pyridine aldoxime methochloride (2-PAM).

Question 29

Upon ingestion of extremely acidic or alkaline household cleaners, what should the first step be?
a. Emesis using 3% hydrogen peroxide
b.Immediate gastric lavage
c. Administer milk or water
d.Administer activated charcoal

Answer 29

Administer milk or water

Because of the rapid action of corrosive agents, much of the damage from exposure occurs before treatment can be started. For oral exposures, emesis, gastric lavage and activated charcoal are contraindicated because of the risk of further mucosal exposure to corrosive material and perforation of weakened esophageal/gastric walls; instead, dilution with milk or water is recommended.

Question 30

Prepubertal gilts were observed to have enlarged mammary glands, enlarged vulvas, and some with uterine prolapse after eating some feeds stored in the barn for quite a while. What is the possible toxin responsible for these signs?
a.Ergotoxin
b.Zearalenone
c.Aflatoxin
d.Mycotoxin

Answer 30

Zearalenone

Caused by Fusarium graminearum, zearalenone binds to receptors for 17-beta-estradiol, and this complex binds to estradiol sites on DNA, causing estrogenism. Physical and behavioral signs of estrus are induced in young gilts by dietary zearalenone at a concentration as little as 1 ppm. In weaned and prepubertal gilts, it causes hyperemia and enlargement of the vulva (known as vulvovaginitis). There is hypertrophy of the mammary glands and uterus, and abdominal straining results in prolapse of the uterus and rectum in severe cases. It also causes estrogenism in cattle and sheep, and reduced egg production in poultry.

Question 31

Ibuprofen, 2-(4-isobutylphenyl) propionic acid is used for its anti-inflammatory, antipyretic and analgesic properties. It is recommended at a dose of 5mg/kg in dogs. Why is prolonged use of ibuprofen in dogs not recommended?
a.Platelet aggregation
b.Coma
c.Gastric ulceration and perforation
d.Melena

Answer 31

Gastric ulceration and perforation

Due to its narrow margin of safety, prolonged use at this dosage may cause gastric ulcers and perforations. NSAIDs inhibit the enzyme cyclooxygenase (COX; also referred to as prostaglandin synthetase), blocking the production of prostaglandins. Inhibition of PGE2 promotes production of gastric acid and pepsin, and decreases the ability of the mucosa to secrete mucus glycoproteins and bicarbonate and respond to injury.

Question 32

What is the treatment for lead poisoning in livestock?
a. D-penicillamine
b.DMSA
c. Calcium disodium edetate
d.Cyproheptadine

Answer 32

Calcium disodium edetate

In food-producing animals, calcium disodium edetate (Ca-EDTA) is administered IV or SC (110 mg/kg per day) divided twice a day for 3 days; this treatment should be repeated 2 days later. This serves as a chelating agent, and mobilizes the lead from bone, excreting it via the kidneys. D-penicillamine (a) and DMSA (b) are both used as lead chelator in dogs, with the latter also used in birds. Cyproheptadine (d) is used for selective serotonin reuptake inhibitors/tricyclic antidepressants such as 5-hydroxytryptophan

Question 33

A 6-month old Labrador Retriever puppy licked his coat after swimming in a lake with a bluish slimy layer on the surface. Soon, he started showing signs of bloody diarrhea, vomiting, difficulty in breathing, cyanosis and convulsions.

What is the possible source of the toxin?
a. Clostridium botulinum
b.Clostridium tetani
c. Enterohemolytic E. coli
d.Blue Green Algae

Answer 33

Blue Green Algae

Cyanobacteria, formerly known as blue-green algae, are ancient photosynthetic freshwater, brackish water, marine and soil-dwelling prokaryotes with a worldwide
distribution. Proliferation of toxigenic cyanobacteria have been termed freshwater harmful algal blooms (FHABs)
when they affect local ecosystems and animal health via oxygen depletion and/or toxin production.

Question 34

A 6-month old Labrador Retriever puppy licked his coat after swimming in a lake with a bluish slimy layer on the surface. Soon, he started showing signs of bloody diarrhea, vomiting, difficulty in breathing, cyanosis and convulsions.

What possible toxin did the puppy ingest in the lake?
a. Botulinum toxin
b.Tetanus toxin
c. Enterotoxin
d.Microcystin

Answer 34

Microcystin

Microcystins are the most common cause of poisoning associated with FHABs. They often cause hepatocellular necrosis, which can present as acute liver failure. Microcystin exposure can lead to onset of clinical signs within minutes to days of ingestion. Affected animals can present peracutely with signs of shock including pale mucous membranes, or show signs of acute hepatotoxicosis such as diarrhea, vomiting, and weakness.

Question 35

A 6-month old Labrador Retriever puppy licked his coat after swimming in a lake with a bluish slimy layer on the surface. Soon, he started showing signs of bloody diarrhea, vomiting, difficulty in breathing, cyanosis and convulsions.

Which of the following is NOT a factor in contributing to the growth of the microorganism?
a. Warm temperatures
b.Runoff from farms containing animal waste and fertilizer
c. Frequent rainfall
d.Light wind conditions

Answer 35

Frequent rainfall

FHABs have been increasing worldwide and appear to be increasingly toxigenic due to anthropogenic changes to ecosystems. Contributing factors to the increased incidence of FHABs include climate change, water temperatures > 20°C (a), and pollution, particularly eutrophication (nutrient loading) of bodies of water from inputs of phosphorus and nitrogen (b).
Blooms are sometimes visible on surfaces of
lakes or ponds, where they can accumulate
downwind (d).

Question 36

A 6-month old Labrador Retriever puppy licked his coat after swimming in a lake with a bluish slimy layer on the surface. Soon, he started showing signs of bloody diarrhea, vomiting, difficulty in breathing, cyanosis and convulsions.

What is NOT part of the treatment for this condition?
a. Botulinum antitoxin
b.Copious lavage of the coat with uncontaminated fresh water
c. Atropine
d.Activated charcoal

Answer 36

Botulinum antitoxin

Although ingestion is considered the major type of exposure for domestic animals, immediate dermal decontamination of animals with exposure to water contaminated with cyanobacteria is critical to prevent ingestion through grooming behaviors. Early decontamination is the best defense for all types of FHAB exposures:
• Removal of the animal from the source of the FHAB
• Removal of FHAB material from the haircoat via copious lavage with uncontaminated fresh water
• GI decontamination for ingested material

Question 37

A farmer has been letting his horses graze on a field with young Sudan grass for quite some time. Eventually, the horses developed incoordination of the hind limbs along with urinary incontinence.

What is the toxin in Sudan grass that causes these clinical signs?
a. Dicumarol
b.Prussic acid
c.Nitric acid
d.Hydrochloric acid

Answer 37

Prussic acid

Hydrocyanic acid/prussic acid is commonly formed in the seeds and leaves of sorghum plants and also from Cassava. Cyanide is a rapidly acting poison that inhibits the action of cytochrome oxidase that links oxygen with erythrocytes. Plants can kill livestock by asphyxia at a lethal dose of 2mg/kg (or CG doses of >200ppm).

Question 38

What is NOT included in the other clinical signs caused by Sudan grass poisoning?
a.Hemorrhages
b.Axonal degeneration
c.Alopecia of the hindlimbs
d.Cystitis

Answer 38

Hemorrhages

Sorghum poisoning is characterized by caudal ataxia or incoordination, cystitis, urinary incontinence (which predisposes both male and female horses to cystitis), and alopecia on the hind legs due to urine scalding. The loss of urinary bladder function is related to axonal degeneration of spinal cord neurons. Incoordination may progress to irreversible flaccid paralysis (“Sorghum Cystitis Ataxia Syndrome”). Deformities of the fetal
musculoskeletal system and abortion may occur during late pregnancy.

Question 39

Why are ruminants more prone to Sudan grass poisoning as compared to other farm animals?
a. Lower abomasal pH
b.Neutral abomasal pH
c. Higher abomasal pH
d.Slower digestion due to different anatomy

Answer 39

Higher abomasal pH

Ruminant animals are more likely to be poisoned than monogastric animals (horses and pigs) because the lower pH in the stomach of monogastric animals destroys enzymes that change CG to hydrocyanic acid. Beta-glucosidase and hydroxynitrile lyase are also present in the rumen microflora, and a rumen pH of ~6.5–7 favors conversion of cyanogenic glycosides to cyanide.

Question 40

Which among the following is NOT used as treatment for Sudan grass poisoning across different farm animal species?
a.Amyl nitrite via IM
b.Hydroxocobalamin administration via slow IV
c.Sodium nitrite via IV
d.Sodium thiosulfate administration via IV or PO

Answer 40

Amyl nitrite via IM

The contents of one 0.3-mL vial of amyl nitrite should be inhaled by the animal as soon as possible after exposure, followed by an IV infusion of sodium nitrite over 3–4 minutes. Nitrite treatment is then followed by a slow IV injection of sodium thiosulfate. Oral administration of thiosulfate can also be considered in an attempt to convert any cyanide in the stomach/rumen into thiocyanate. Hydroxocobalamin detoxifies cyanide by binding to it and forming cyanocobalamin, which is then
excreted in urine.

Question 41

Aflatoxins are produced by Aspergillus flavus/parasiticus on corn, soybeans, peanuts and other cereals when the conditions are favorable for mold growth.

What is the target organ of this toxin?
a. Liver
b.Kidney
c.Stomach
d.Heart

Answer 41

Liver

Aflatoxins are metabolized in the liver to an epoxide that binds to macromolecules, especially nucleic acids and nucleoproteins. High dosages of aflatoxins result in
hepatocellular necrosis; prolonged low dosages result in reduced growth rate, immunosuppression, and liver enlargement. Liver damage can lead to reduced clotting
factor synthesis

Question 42

Anticaking agents can be used to bind aflatoxins and reduce absorption from the GI tract. Which among the following is the most effective binder?
a.Sodium bentonite
b.Polymeric glucomannan
c. Hydrated sodium calcium aluminosilicates
d.Zeolite

Answer 42

Hydrated sodium calcium aluminosilicates

Hydrated sodium calcium aluminosilicates (HSCAs) are effective in binding aflatoxin in the feed and reducing absorption in the gut at a dose of 5kg/ton of feed. The use of HSCAs can reduce, but not eliminate, contamination of aflatoxin M1 in milk of dairy animals fed aflatoxin contaminated feed. Other binders have shown variable but partial efficacy in reducing low-level aflatoxin residues in poultry and dairy cattle.

Question 43

Which among the following DOES NOT characterize acetaminophen toxicity?
a. Mud-brown mucous membranes
b.Methemoglobinemia
c. Renal and hepatic injury
d.Corneal ulceration

Answer 43

Corneal ulceration

Methemoglobinemia and hepatotoxicity characterize acetaminophen toxicosis. Renal injury is also possible. Acute keratoconjunctivitis sicca has been reported in some dogs after acetaminophen ingestion. Cats primarily develop methemoglobinemia which makes mucous membranes brown or muddy in color. It is usually accompanied by tachycardia, hyperpnea, weakness, and lethargy.

Question 44

What is the antidote for acetaminophen toxicity?
a. Acetylcysteine
b.Flumazenil
c. Atropine
d.Activated charcoal

Answer 44

Acetylcysteine

Administration of N-acetylcysteine (NAC), a sulfur-containing amino acid, can reduce the extent of liver injury or methemoglobinemia. NAC provides sulfhydryl groups, directly binds with acetaminophen metabolites to enhance their elimination, and serves as a glutathione precursor. The loading dose is 140 mg/kg of a 5% solution IV or PO (diluted in 5% dextrose or sterile water), followed by 70 mg/kg, PO, qid for generally seven or more treatments (some authors recommend up to 17 doses)

Question 45

A herd of cows suddenly became cyanotic, dyspneic and ataxic after feeding on a lush pasture fertilized by surface run-off from a neighboring poultry farm. Some developed brown coloration of the mucous membranes and had convulsions before dying. Upon necropsy, it was observed that their blood was chocolate in color.

What must be administered to the other cows exhibiting the same clinical signs?
a. D5LRS solution
b.5% sulfamethazine injection IV
c.5% DCM solution IV
d.Methylene blue in 1% solution IV

Answer 45

Methylene blue in 1% solution IV

Nitrate poisoning in animals (especially ruminants) results from excess consumption of nitrates from plants or water or via ingestion of nitrate-containing fertilizers. The nitrate ion (NO3–) is reduced to nitrite ion (NO2–), which is rapidly absorbed and leads to the formation of methemoglobin, which inhibits oxygen transport. This results in dyspnea, cyanotic mucous membranes, weakness; and, if severe, death due to anoxia. Methylene blue, administered IV at a dose of 4-22mg/kg, will reverse the methemoglobinemia and may be effective as a treatment with supportive care.

Question 46

What practice is the best to ensure that nitrate content is reduced?
a.Turning forages into dried hay
b.Turning forages into green chop
c.Turning forages into silage
d.Turning forages into fodder

Answer 46

Turning forages into silage

Question 47

Carbamates and organophosphates are similar in their mode of action to produce toxicity. How are they similar?
a. Inhibition of cholinesterase
b.Methemoglobinemia
c. Placid paralysis
d.Inhibition of GABA-gated chloride channels

Answer 47

Inhibition of cholinesterase

The toxicity of OP and carbamate insecticides is due to inhibition of the AChE enzyme within the nervous tissue and at the neuromuscular junction. The OPs inhibit AChE irreversibly by phosphorylation, and carbamate

Question 48

The clinical signs of carbamate poisoning are associated with:
a. Overstimulation of muscarinic receptors
b.Overstimulation of nicotinic receptors
c. Overstimulation of the central nervous system
d.All of the above

Answer 48

All of the above

With OP and Carbamate toxicity, accumulation of acetylcholine (ACh) occurs, which overstimulates muscarinic and nicotinic ACh receptors, causing hypersecretions (salivation, lacrimation, urination, and diarrhea), convulsions, and muscle fasciculations. Seizures and death ensue due to noncholinergic mechanisms in the CNS involving hyperstimulation of N-methyl-D-aspartate (NMDA) receptors, adenosinergic,
gamma-aminobutyric acid (GABA-ergic), monoaminergic systems, and others.

Question 49

Death from carbamate poisoning is caused by:
a. Heart failure
b.Respiratory failure
c. Liver failure
d.Kidney failur

Answer 49

Respiratory failure

The persistence of excitotoxicity for more than an hour can lead to neuroinflammation and neurodegeneration in the cortex, amygdala, and hippocampus, which are areas of the brain primarily involved in initiation and propagation of convulsions and seizures. Finally, death
occurs due to respiratory failure through paralysis, central apnea and pulmonary dysfunction.

Question 50

What is the antidote to carbamate toxicity?
a. Atropine
b.Atropine + 2-Pralidoxime
c. Yohimbine
d.Atipamezole

Answer 50

Atropine

Treatment of carbamate poisoning is similar to that of OP poisoning in that atropine sulfate injections readily reverse the effects. Pralidoxime (b) should not be used to treat carbamate poisoning, and is only for organophosphate poisoning. Yohimbine (c) is the reversal agent for xylazine, while atipamezole (d) is for alpha-2 adrenergic agonists such as dexmedetomidine,
medetomidine, xylazine, and amitraz.