Term
__________________ is the total knowledge of poisons, including chemical properties, identification, biological effects, and treatment of disease caused by the poison.
a. Toxicity
b. Toxicology
c. Toxic
d. Poison
e. Toxicant |
|
Definition
|
|
Term
____________ is any solid, liquid, or gas that when introduced into a biologic system can interfere with the life processes of the cells of that organism by its own inherent qualities. It has effects at the molecular level, the organism, or the population.
a. Toxicity
b. Toxicology
c. Toxic
d. Poison
e. Toxicant |
|
Definition
|
|
Term
| T/F: a toxicant is essentially the same as a poison, but is considered to be less harsh and is found in feed additives and drugs. |
|
Definition
|
|
Term
A poison that originates from biological processes is a ________________.
a. Toxin
b. Toxicology
c. Toxic
d. Poison
e. Toxicant |
|
Definition
|
|
Term
_______________ is the disease state of being poisoned.
a. Toxicity
b. Toxicology
c. Toxic
d. Poison
e. Toxicosis |
|
Definition
|
|
Term
__________________ is the quantity or amount of toxicant that under a certain set of conditions will cause adverse effects.
a. Toxicity
b. Toxicology
c. Toxic
d. Poison
e. Toxicant |
|
Definition
|
|
Term
Which of the following is not a source of a toxin?
a. Snake bite
b. Nutrient overload
c. Disinfection products
d. Pesticide exposure
e. Chemotherapy treatment
f. All of the above are sources of toxins. |
|
Definition
|
|
Term
For each toxin, list the species most commonly affected:
Lead
Copper
Antifreeze |
|
Definition
Lead--cattle
Copper--sheep
Antifreeze--dog, cat |
|
|
Term
The most frequently poisoned animal is the _________.
a. Dog
b. Cat
c. Sheep
d. Cow
e. Horse |
|
Definition
d. Cow
Cow > dogs > sheep > swine > cats > birds/poultry > horses > others |
|
|
Term
| T/F: toxin diagnosis is related to heavily managed facilities, so most toxicoses come from casual management, with few problems coming from well-managed facilities. |
|
Definition
|
|
Term
The most important factory in determining how to treat an animal with a toxicosis is:
a. History
b. Physical Exam
c. Clinical Signs
d. A and B
e. A, B, and C |
|
Definition
| a. History--history is critical and often physical exam/clinical signs are vague |
|
|
Term
| T/F: the dosage of the toxin determines whether the toxin or the affected animal's biological system will be able to prevail. |
|
Definition
| True--often toxicity is measured in mg/kg and LD50 or lethal doses are known for major toxicants. |
|
|
Term
| What five questions need to be asked when evaluating a toxicosis? |
|
Definition
What?--clinical, performance, lesions, residues
Where?--organ system(s), local, systemic
When?--acute, recent, delayed, chronic
Why?--sources, animal/chemical factors
How?--access, route, mechanism |
|
|
Term
| T/F: "post hoc, ergo propter hoc" (since that event followed this one, that event must have been caused by this one) is the common method for working through cases of toxicity. |
|
Definition
| False. Don't assume that a response is entirely due to the chemical administered or exposed. In addition, don't assume that the magnitude of the response is related to dose or that there is a quantifiable method of measuring the toxic endpoint. Often, factors related to the animal or the environment may alter these ideas. |
|
|
Term
| T/F: the lethal dose 50 (LD50) provides a comparison among different chemicals under the same conditions for exposure. |
|
Definition
|
|
Term
| T/F: the LD50 takes into consideration severity and clinical characteristics. |
|
Definition
| False. It does not address severity or clinical characteristics. It also has no relationship to chronic toxicity or other effects. |
|
|
Term
| The therapeutic index is measured as: |
|
Definition
|
|
Term
| The Margin of Safety, or Standard of Safety Margin is measured as: |
|
Definition
|
|
Term
A "Chronicity factor" is:
a. The likelihood of poisoning occurring under the conditions of usage
b. The comparison among different chemicals under the same conditions of exposure that is lethal to 50% of animals
c. A measure of cumulative toxicity or continued organ damage
d. The level at which there is no observable adverse effect
e. A "quantal" response of a group |
|
Definition
c. a measure of the cumulative toxicity or continued organ damage
Acute LD50/90-day LD50 |
|
|
Term
The "Risk/Hazard Ratio: is:
a. The likelihood of poisoning occurring under the conditions of usage
b. The comparison among different chemicals under the same conditions of exposure that is lethal to 50% of animals
c. A measure of cumulative toxicity or continued organ damage
d. The level at which there is no observable adverse effect
e. A "quantal" response of a group |
|
Definition
a. The likelihood of poisoning occurring under the conditions of usage
Measured as toxicity (mg/kg) : use level (mg/kg) |
|
|
Term
| T/F: "poisoning" is not a diagnosis |
|
Definition
True.
Know the territory--poisons, seasonal effects, environmental sources, management exposures, susceptible animals, resources you can use
Get history of patient, reported clinical findings, environmental history, product/product label, exposure history, and management history.
Observe Clinical signs
Assess pathologic changes
Pursue chemical analysis--get correct specimen, adequate quantity, proper handling
Consider experimental dosing and monitoring response to therapy. |
|
|
Term
| T/F: a diagnosis of toxicosis can be made on the history alone. |
|
Definition
| False: the history is the most important part, but all factors need to be considered. |
|
|
Term
1 ppm =
a. 1 mg/kg
b. 1 ug/g
c. 0.0001%
d. 1 g/ton
e. 1 mg/L
f. all of the above |
|
Definition
|
|
Term
| Redo Homework Calculations! |
|
Definition
|
|
Term
| T/F: it is a clinical emergency if exposure to a poison is confirmed or unknown. |
|
Definition
True
Reported exposures can also occur, but these often have no clinical signs??? (Notes say it is a clinical emergency if there is a confirmed exposure or unknown exposure) |
|
|
Term
List the following steps in the correct order:
Decontaminate to prevent absorption
Monitor patient progress
Administer antidote
Life support: stabilize vital signs
Enhance elimination of adsorbed toxicant
Provide symptomatic/supportive care
Deal with sequelae
Obtain history and clinical evaluation |
|
Definition
1. Life support--ABCs, treat seizures, treat shock/acid-base/ hyper- or hypothermia
2. Obtain history and clinical evaluation--question persons involved, collect samples for lab work, save samples for toxicology if needed, rads or endoscopy in select cases
3. Decontaminate--protect staff, reduce further absorption, empty stomach. gastric lavage, use adsorbents, use cathartics
4. Administer antidote if appropriate--pharmacologic (Vit K, CaNaEDTA), physiologic (atropine)
5. Enhance elimination of adsorbed toxicant--prevent metabolism to toxic forms, support phase II conjugation, increase excretion, ion trapping, endoscopy/sx for physical removal
6. Provide symptomatic/supportive care
7. Monitor patient progress
8. Deal with sequelae |
|
|
Term
| T/F: emetics are most effective if used less than 4 hours from toxin exposure. |
|
Definition
| False: most effective if used < 1 hour from toxin exposure |
|
|
Term
Emetics are indicated in which of the following scenarios?
a. A horse with ionophore toxicity
b. A Pug with copper toxicosis
c. A lab with rodenticide ingestion
d. A chinchilla that ate paint chips
e. A cat with chronic seizures |
|
Definition
c. A lab with rodenticide ingestion
Contraindicated in: ruminants, horses, rats, small rodents, chinchillas, rabbits
Don't recommend in cats or brachycephalic dogs
Not with seizures, petroleum distillates, caustics, volatiles, or animals in a severe depression or coma |
|
|
Term
All of the following are acceptable emetics except:
a. Hydrogen peroxide
b. Apomorphine
c. Xylazine
d. Salt
e. Syrup of ipecac |
|
Definition
d. Salt
Also shouldn't use dish detergents |
|
|
Term
| T/F: when gastric lavage is used to decontaminate a toxicosis, the second lavage should be retained for diagnostic purposes. |
|
Definition
| False: the first lavage should be retained. |
|
|
Term
| _________________ is the adsorbent of choice. |
|
Definition
|
|
Term
| ___________________ are the traditional cathartics used for decontamination but ________________ (electrolyte abnormality) should be looked for, especially in _____________ (species). |
|
Definition
Saline (Na, Mg) cathartics
Hypermagnesemia
Cats |
|
|
Term
___________________ blocks the recycling of vitamin K1 from epoxide to its reduced form, thus blocking the formation of vitamin K dependent clotting factors.
a. Cholecalciferol
b. Bromethalin
c. Anticoagulants
d. Zinc Phosphide
e. Starlicide |
|
Definition
|
|
Term
This antigoagulant-like compound is often found in sweet-clover and is often a cause of toxicity in ruminants and horses:
a. Dicoumarol
b. Brodifacoum
c. Diphethialone
d. Bromadiolone
e. Warfarin |
|
Definition
|
|
Term
| T/F: anticoagulants such as warfarin and brodifacoum work by blocking vitamin K recycling, thus inhibiting the formation of factor VII early on in the toxicosis, and affecting the formation of factor IX late in the toxicosis. |
|
Definition
True
Factor VII = PT
Factor IX = PTT |
|
|
Term
Anticoagulants are metabolized in the liver and excreted in the _____________________.
a. Bile
b. Urine
c. Milk
d. A and B
e. A, B, and C |
|
Definition
|
|
Term
When are clinical signs of warfarin toxicosis *usually* seen?
a. 12-36 hours post-ingestion
b. 3-6 days post-ingestion
c. 15 minutes post-ingestion
d. 7 hours post-ingestion
e. 2-4 hours post-ingestion |
|
Definition
b. 3-6 days post-ingestion
Note that sometimes clinical signs can manifest by 36 hours though, but this is not the usual case |
|
|
Term
| T/F: platelet function is depressed in animals with anticoagulant toxicosis. |
|
Definition
| False. Platelet function is normal |
|
|
Term
Which of the following is not a clinical sign of an animal with warfarin toxicosis?
a. Anemia
b. Depressed platelet function
c. Ataxia
d. Hemarthrosis
e. Abortion |
|
Definition
b. Depressed platelet function
Clinical signs consistent with hemorrhage but platelet function remains normal: anemia, dyspnea, ataxia (subdural hematoma), melena, hemarthrosis (lameness), hemothorax, abortion (placental hemorrhage) |
|
|
Term
All of the following are differentials for brodifacoum toxicosis except:
a. Liver disease
b. Autoimmune thrombocytopenia
c. Dicoumarol poisoning
d. DIC
e. Primary hyperparathyroidism |
|
Definition
e. Primary hyperparathyroidism--ddx for cholecalciferol
DDx: Liver disease, dicoumarol, idiopathic coagulopathy, autoimmune thrombocytopenia, DIC, hereditary (VonWillebrand's disease) |
|
|
Term
| T/F: clotting times of 2x normal are a diagnostic indicator of anticoagulant toxicosis. |
|
Definition
True--often elevated more than this
PT elevated at 2-3 days post exposure
PTT elevated at 3-5 days post exposure |
|
|
Term
The PIVKA test is a test used to diagnose:
a. Warfarin toxicosis
b. Lead poisoning
c. Cholecalciferol toxicosis
d. Copper toxicity
e. Strychnine toxicosis |
|
Definition
a. Warfarin (or other anticoagulant) toxicosis
PIVKA = Proteins Induced by Vitamin K Antagonists (Thrombotest) |
|
|
Term
| The _______________ is the sample of choice for diagnosing anticoagulant toxicosis in dead animals, while the ____________ is the sample of choice for diagnosing anticoagulant toxicosis in live animals. |
|
Definition
|
|
Term
| T/F: therapy for anticoagulant toxicity should be initiated once the dosage estimate reaches 0.5 of the LD10. |
|
Definition
| False: therapy should be initiated if the dosage estimate reaches 0.25 of the LD10 |
|
|
Term
| T/F: oral vitamin K1 is the treatment of choice for anticoagulant toxicity. |
|
Definition
| True--however, it has a 3-6 hour time lag, so need to give blood or FFP for immediate clotting factors |
|
|
Term
| Vitamin K3 may be preventative for anticoagulant toxicosis, however it should not be used in ______________ due to the risk of nephrotoxicity. |
|
Definition
|
|
Term
Which of the following is true concerning the treatment of anticoagulant toxicity?
a. Oral vitamin K1 is the treatment of choice and should be administered with fatty food.
b. Blood/plasma tranfusions are indicated to confer immediate clotting factors while the oral vitamin K1 begins to work.
c. Vitamin K3 may be helpful in preventing anticoagulant toxicity.
d. PT should be monitored for one month following therapy for anticoagulant toxicosis
e. All of the above are true. |
|
Definition
| e. All of the above are true |
|
|
Term
| 1st generation anticoagulants contain _____% active ingredient, while 2nd generation anticoagulants contain ______% active ingredient. |
|
Definition
0.05%--1st Gen.
0.005%--2nd Gen. |
|
|
Term
The use of protein-displacing drugs such as phenylbutazone, sulfonamides, steroids, aspirin, or compounds that lower/impair platelets can predispose animals to toxicity with what compound?
a. Cholecalciferol
b. Bromethalin
c. Avicides
d. Anticoagulants
e. Organophosphates |
|
Definition
|
|
Term
| List one major 1st generation anticoagulant and one major 2nd generation anticoagulant: |
|
Definition
1st generation: warfarin
2nd generation: brodifacoum |
|
|
Term
| T/F: vitamin D2 is 10x more potent than vitamin D3 for calcium uptake. |
|
Definition
| False: D3 is 10x more potent than D2 |
|
|
Term
| The active metabolite of vitamin D is ________________________. |
|
Definition
| 1,25 dihydroxy vitamin d (calcitriol) |
|
|
Term
| The enzyme inhibited during anticoagulant toxicosis that halts the recycling of vitamin K1 is _______________. |
|
Definition
| Vitamin K epoxide reductase |
|
|
Term
| Essay time: describe the mechanism of action for cholecalciferol. |
|
Definition
| Cholecalciferol is converted into calcitriol by the kidneys. It then increases serum calcium by (1) increasing Ca/P absorption from the gut, (2) by PTH stimulating osteoclastic bone resorption, and (3) renal retention of calcium via distal tubule resorption. These factors lead to a persistent hypercalcemia and hyperphosphatemia, which causes renal tubular damage and necrosis, abnormal soft tissue mineralization (renal tubules, arterioles), conduction dysfunction (bradycardia w/ increased heart sounds), vasoconstriction, hypertension, low ADH (due to reduction of cAMP), diuresis, and eventual polyuria, hyposthenuria, and azotemia. |
|
|
Term
All of the following are effects of cholecalciferol toxicity except:
a. Hypertension and vasoconstriction
b. Tachycardia and increased heart sounds
c. Diuresis and polyuria
d. Soft tissue mineralization
e. All of the above are effects of cholecalciferol toxicity. |
|
Definition
b. tachycardia and increased heart sounds
BRADYCARDIA occurs, along with increased heart sounds
Will see shortened QT and increased PR intervals |
|
|
Term
| Cholecalciferol is metabolized in the _____________ to 25 hydroxy D3, and is _______________ (pathway) dependent, and is converted to 1,25 dihydroxy D3 in the ___________________. |
|
Definition
|
|
Term
| What is the rate limiting step of cholecalciferol toxicity/ mechanism? |
|
Definition
| Conversion of 25 hydroxy D3 to the toxic 1,25 dihydroxy D3 in the kidney. |
|
|
Term
Metabolites of cholecalciferol are excreted in the:
a. Urine
b. Bile
c. Feces
d. Milk
e. A and C |
|
Definition
|
|
Term
| Clinical signs of cholecalciferol toxicity are apparent _____________ (time frame) after ingestion. |
|
Definition
12-36 hours
Note that toxicosis in rodents is delayed 2-3 days after a single ingestion. |
|
|
Term
All of the following are differentials for cholecalciferol toxicosis except:
a. Lymphoma
b. Anal sac adenocarcinoma
c. Chronic renal failure
d. Hypothyroidism
e. Feline idiopathic hypercalcemia |
|
Definition
d. Hypothyroidism
DDx: hypercalcemia of malignancy (lymphoma, anal sac adenocarcinoma), CRF, primary hyperparathyroidism, feline idiopathic hypercalcemia |
|
|
Term
| Serum calcium levels > ______ mg/dL can indicate a cholecalciferol toxicosis. |
|
Definition
|
|
Term
Which of the following is not *routinely* measured to diagnose cholecalciferol toxicity?
a. Serum calcium
b. Serum phosphorous
c. BUN/creatinine
d. Vitamin D metabolites
e. Serum iPTH |
|
Definition
|
|
Term
| List some therapies for cholecalciferol toxicosis: |
|
Definition
Saline diuresis
Furosemide
Prednisone (blocks osteoclast activation, renal/GI uptake)
Calcitonin
Bisphosphonates
Emetics/cathartics/activated charcoal if early |
|
|
Term
| Cholecalciferol rodenticides usually contain _________% active ingredient. |
|
Definition
|
|
Term
| 1 mg of cholecalciferol = __________ IU |
|
Definition
|
|
Term
| ______________ is a compound that is hydrolyzed in the stomach and forms into phosphine gas, which blocks cytochrome oxidase and membrane ion transport. |
|
Definition
|
|
Term
What species are most often poisoned by zinc phosphide?
a. Dogs
b. Cats
c. Cattle
d. Horses
e. Birds |
|
Definition
a. Dogs
Gallinaceous birds and wild rodents also get poisoned, but dogs are the most poisoned |
|
|
Term
| T/F: toxicity to zinc phosphide is due to the zinc moiety and its power as a strong emetic, rather than the phosphene gas. |
|
Definition
False--phosphene gas is the reason for the toxicity
Forms a pungent acetylene/garlic odor |
|
|
Term
| T/F: zinc phosphide is more toxic in animals that have recently eaten. |
|
Definition
| True--hydrolysation in the stomach is enhanced by a meal |
|
|
Term
The onset of clinical signs for zinc phosphide occurs within:
a. 15 minutes to 7 hours
b. 3-6 days
c. 86 hours
d. 2-7 days
e. None of the above |
|
Definition
|
|
Term
Which of the following is not a clinical sign of zinc phosphide toxicity?
a. Vomiting, sometimes bloody
b. Anorexia
c. Ataxia, weakness, and seizures
d. Apnea
e. Hyperesthesia |
|
Definition
d. Apnea
Zinc phosphide toxicity causes rapid deep respiration |
|
|
Term
The sample of choice for diagnosing zinc phosphide toxicity is:
a. Liver biopsy
b. Blood sample
c. Stomach contents
d. Brain sample
e. Urine sample |
|
Definition
c. Stomach contents
Run gas chromatography or mass spectrometry
Often difficult to dx--nonspecific signs; dead fish or a garlic odor can be clues |
|
|
Term
| T/F: because zinc phosphide forms a volatile gas, samples should be collected, frozen, and sealed. |
|
Definition
|
|
Term
| Zinc phosphide baits come as _________% active ingredient. |
|
Definition
|
|
Term
____________ antagonizes glycine, which causes loss of inhibitory effects of the reflex arc and leads to uncontrolled excitation of the spinal reflexes, with extensor muscles predominating.
a. Zinc phosphide
b. Strychnine
c. Bromethalin
d. Metaldehyde
e. Avicides |
|
Definition
|
|
Term
| Strychnine is slowly/rapidly absorbed and is excreted through the urine/feces/bile. |
|
Definition
| Rapidly absorbed and excreted through the urine |
|
|
Term
| Which species is most sensitive to strychnine? |
|
Definition
|
|
Term
A "saw horse" stance, much like that of tetanus, is a classic clinical sign associated with poisoning of which agent?
a. Metaldehyde
b. Cholecalciferol
c. Imidacloprid
d. Strychnine
e. Zinc Phosphide |
|
Definition
d. Strychnine
See animals that are nervous, restless, and have muscle tremors early. These animals are sensitive to external stimuli and have an explosive onset of tonic to tetanic seizures. |
|
|
Term
| T/F: death from strychnine poisoning is usually due to anoxia. |
|
Definition
| True--animal can't breath due to constant excitation of muscles |
|
|
Term
Diagnosis of strychnine poisoning can be done by isolating the compound in the:
a. Stomach contents
b. Urine
c. Liver
d. A and B
e. A, B, and C |
|
Definition
e. A, B, and C
However, the urine is usually the sample of choice |
|
|
Term
| T/F: mildly alkaline urine can promote ion trapping, and is done by supplementing ammonium chloride or ascorbic acid. |
|
Definition
| False--mildly ACIDIC urine can promote ion trapping (use ammonium chloride or ascorbic acid); done for strychnine poisoning? |
|
|
Term
Which of the following is the recommended therapy for strychnine poisoning?
a. Gastric lavage and activated charcoal
b. Pentobarbital, diazepam, or methocarbamol
c. Diuresis
d. Ammonium chloride or ascorbic acid supplementation (acidification of urine)
e. All of the above |
|
Definition
|
|
Term
| T/F: strychnine is an indole alkaloid, with 0.5% or less being active ingredient. |
|
Definition
|
|
Term
_____________ uncouples oxidative phosphorylation, causing decreased ATP, inhibition of the sodium pump, fluid accumulation in myelin sheaths, edema of myelin, and paresis.
a. Avicides
b. Starlicide
c. Strychnine
d. Metaldehyde
e. Bromethalin |
|
Definition
|
|
Term
Bromethalin is most toxic to:
a. Dogs
b. Cats
c. Horses
d. Cattle
e. Fish |
|
Definition
|
|
Term
*Low-dose* bromethalin poisoning would cause all of the following signs except:
a. Anisocoria
b. Focal to generalized motor seizures precipitated by light or noise
c. Progressive depression
d. Tremors
e. Hind limb paralysis |
|
Definition
b. Seizures
Low-dose CS: tremors, ataxia, vomiting, anisocoria, progressive depression, hind limb paralysis, lateral recumbency, coma |
|
|
Term
*High-dose* bromethalin poisoning would cause all of the following symptoms except:
a. Tremors
b. Hyperexcitability and running fits
c. Anisocoria
d. Focal to generalized seizures precipitated by light or noise
e. Hyperesthesia |
|
Definition
|
|
Term
Microscopic brain lesions consisting of edema and spongiform change in the myelin of the brain and spinal cord would be most consistent for a diagnosis of:
a. Bromethalin
b. Strychnine
c. Anticoagulants
d. Zinc Phosphide
e. Amitraz |
|
Definition
Bromethalin
Diagnose by characteristic brain lesions, possible hyperglycemia, EEG, and chemical detection of bromethalin in tissues (brain, fat, liver, kidney) |
|
|
Term
| T/F: bromethalin is fat soluble and is therefore found in the highest levels in the brain, fat, liver, and kidney. |
|
Definition
|
|
Term
Which of the following treatments/therapies for bromethalin poisoning helps to prolong survival time but will not reverse the syndrome? (according to notes)
a. Activated charcoal
b. Dexamethasone
c. Mannitol
d. Diazepam
e. Phenobarbital |
|
Definition
|
|
Term
Which of the following agents can be excreted in milk, and therefore presents a food safety risk?
a. Anticoagulants
b. Cholecalciferol
c. Bromethalin
d. A and B
e. A, B, and C |
|
Definition
|
|
Term
_______________ causes reduced brain noradrenaline, serotonin, and 5-HIA, leading to a lower seizure threshold. It also exhibits increased monoamine oxidase activity and GABA inhibition, leading to seizures.
a. Cholecalciferol
b. Organophosphates
c. Metaldehyde
d. Bromethaline
e. Avicides |
|
Definition
c. Metaldehyde
There is also a question of whether hydrolysis to acetylcysteine occurs. |
|
|
Term
| T/F: metaldehyde is absorbed intact from the gastrointestinal tract. |
|
Definition
|
|
Term
| T/F: CYP450 inhibitors help protect against metaldehyde toxicity. |
|
Definition
| False--CYP450 inducers help protect against toxicity |
|
|
Term
Metaldehyde presents the highest hazard to:
a. dogs
b. cats
c. horses
d. cattle
e. fish |
|
Definition
a. dogs
Note that horses also have an extremely low LD50--I'm assuming it is worse in dogs because of access, as dogs can actually handle a higher toxicity than horses |
|
|
Term
Which of the following combinations does not correlate with the clinical signs of metaldehyde toxicity?
a. Hyperthermia and seizures
b. Hyperesthesia and opisthotonus
c. Hyperpnea and acidosis
d. Nystagmus and mydriasis
e. Hypothermia and alkalosis |
|
Definition
| e. Hypothermia and alkalosis |
|
|
Term
A dog presents with acute neurologic signs and a temperature of 108F. You suspect a toxicity. What toxicant do you suspect and what sample do you want?
a. Metaldehyde. Sample the stomach content and freeze the samples.
b. Bromethalin. Sample the brain.
c. Strychnine. Sample the urine
d. Zinc phosphide. Sample the stomach contents and keep samples frozen.
e. Warfarin. Sample the liver. |
|
Definition
a. Metaldehyde. Sample the stomach content and keep samples frozen.
Could also sample bait, serum, or urine. Stomach contents may have the odor of acetylcysteine. Note that histopath of the liver and brain may also reveal hepatocellular swelling and neuronal degeneration, respectively. |
|
|
Term
| T/F: metaldehyde often comes in 3-5% baits and may contain organophosphates and carbamates. |
|
Definition
True
If the bait contains OPs or carbamates, muscarinic clinical signs may present. |
|
|
Term
| T/F: more than 50% of metaldehyde toxicosis cases die within 4-24 hours post-ingestion due to respiratory failure if early, aggressive therapy is not implemented. |
|
Definition
|
|
Term
| __________________ is the avicide discussed in class. |
|
Definition
|
|
Term
_________________ enhances acetylcholine release at synapses (especially neuromuscular junctions), causing hyperexcitability, tremors, salivation, incoordination, convulsions, and cardiac/respiratory arrest in animals with toxicosis.
a. Strychnine
b. 4-aminopyridine
c. Metaldehyde
d. Nitenpyram
e. Starlicide |
|
Definition
|
|
Term
Which species is most susceptible to avicide toxicosis?
a. dog
b. cat
c. horse
d. cattle
e. fish |
|
Definition
|
|
Term
| The Differential Convulsant Panel at ISU tests for which four toxicants? |
|
Definition
4-aminopyridine
Strychnine
Nicotine
Caffeine |
|
|
Term
Which avicide has an unknown mechanism and is highly nephrotoxic?
a. 4-aminopyridine
b. metaldehyde
c. brodifacoum
d. dicoumarol
e. 3-chloro-4-methylalanine |
|
Definition
e. 3-chloro-4-methylalanine
This is a starlicide; also called 3-chloro-p-toluidine
On histopath, will see tubular necrosis of epithelial cells |
|
|
Term
The most toxic group of insecticides are the _________________.
a. Carbamates
b. Pyrethroids
c. Organophosphates
d. Chlorinated hydrocarbons
e. Insect Growth Regulators |
|
Definition
|
|
Term
___________________ are diphenyl aliphatics that interfere with sodium flow in nerve endings, slowing sodium influx and preventing potassium outflow. This partially polarizes the cell and lowers the threshold for another action potential, enhancing the initiation of action potentials.
a. Organophosphates
b. Chlorinated hydrocarbons
c. Pyrethroids
d. Imidacloprid
e. Amitraz |
|
Definition
| b. Chlorinated hydrocarbons |
|
|
Term
______________ are cyclodienes that inhibit the post-synaptic binding of GABA, causing stimulation of neurons.
a. Chlorinated hydrocarbons
b. Organophosphates
c. Carbamates
d. Bromethalin
e. Strychnine |
|
Definition
| a. Chlorinated hydrocarbons |
|
|
Term
The classification as a diphenyl aliphatic or a cyclodiene refers to compounds in the category of:
a. Organophosphates
b. Carbamates
c. Metaldehyde
d. Pyrethroids
e. Chlorinated hydrocarbons |
|
Definition
| e. Chlorinated hydrocarbons |
|
|
Term
| T/F: chlorinated hydrocarbons are very persistent, as they are fat soluble and distribute to the brain, fat, liver, and kidney. |
|
Definition
|
|
Term
Which of the following is not excreted in the milk?
a. Anticoagulants
b. Cholecalciferol
c. Chlorinated hydrocarbons
d. Phenoxy fatty acids
e. Bromethalin |
|
Definition
|
|
Term
_________ are the most sensitive to chlorinated hydrocarbon toxicity.
a. Dogs
b. Cats
c. Horses
d. Cattle
e. Fish |
|
Definition
b. Cats
Have a very low LD50 |
|
|
Term
| T/F: Lindane, an agent used as an ectoparasiticide in dogs, is a potential source of iatrogenic or accidental toxicosis with chlorinated hydrocarbons. |
|
Definition
|
|
Term
You make a farm call because a producer has a cow that is acting strangely. When you pull up, you see a random cow walking backwards and making chewing movements. The producer tells you that the cow has been apprehensive and beligerent and has been having muscle tremors. As you get a history and look at the enviroment, you notice large cans of DEET lying around. Your primary differential is ____________.
a. Chlorinated hydrocarbons
b. Organophosphates
c. Amitraz
d. Fipronil
e. Pyrethroids |
|
Definition
| a. Chlorinated hydrocarbons |
|
|
Term
| T/F: Chlorinated hydrocarbon toxicity is reportable in food animals. |
|
Definition
|
|
Term
Which insecticide can produce environmental effects such as eggshell thinning?
a. Carbamates
b. Pyrethroids
c. Amitraz
d. Rotenone
e. Chlorinated hydrocarbons |
|
Definition
| e. Chlorinated hydrocarbons |
|
|
Term
______________ produce slow opening and closing of neural sodium and potassium (and perhaps chloride) channels, decreasing the threshold for firing of nerves and extending action potentials, leading to stimulation, muscle tremors, and excitement.
a. Organophosphates
b. Amitraz
c. Type I pyrethroids
d. Type II pyrethroids
e. Carbamates |
|
Definition
|
|
Term
_______________ initiate membrane depolarization through GABA channels, resulting in weakness and paralysis.
a. Organophosphates
b. Amitraz
c. Type I pyrethroids
d. Type II pyrethroids
e. Carbamates |
|
Definition
|
|
Term
| Pyrethrins/pyrethroids are derived from Chrysanthemum and are not very stable, while pyrethrins/pyrethroids are sunthetic and are more stable compounds. |
|
Definition
Pyrethrins--Chrysanthemum
Pyrethroids--synthetic |
|
|
Term
Pyrethrin presents the highest risk to _________.
a. Dogs
b. Cats
c. Horse
d. Cattle
e. Fish |
|
Definition
b. Cats
Most are quite safe and not very toxic, but cats are especially sensitive |
|
|
Term
| T/F: oral toxicity of pyrethrins is high, as absorption is rapid. |
|
Definition
False--oral toxicity low, destroyed in gut
Usually get exposure through skin or inhalation. |
|
|
Term
| Toxicosis due to chlorinated hydrocarbons is acute/chronic. |
|
Definition
|
|
Term
| Toxicosis due to pyrethrins is acute/chronic. |
|
Definition
|
|
Term
Which of the following is not a clinical signs of pyrethroid toxicosis?
a. Marked hyperthermia (108F)
b. Tremors, seizures, and ataxia
c. Salivation, weakness, and abnormal posture
d. Topical allergic pruritus, hyperemia, and urticaria
e. Paw shaking, ear twitching, and flicking of the tail |
|
Definition
a. Marked hyperthermia--seen with metaldehyde toxicosis
Salivation, weakness, and abnormal posture can be seen with toxicity due to type II pyrethroids |
|
|
Term
| T/F: finding high concentrations of pyrethroids through chemical analysis is the best way to diagnose pyrethroid toxicosis. |
|
Definition
| False--high concentrations of pyrethroids are suggestive of toxicosis, but are NOT definitive |
|
|
Term
| Alpha-cyano is found in type 1/type II pyrethroids. |
|
Definition
|
|
Term
_________________ irreversibly inhibit acetylcholinesterase at cholinergic synapses, causing continuous parasympathetic stimulation by accumulated acetylcholine and resulting in the clinical manifestations of "SLUDD."
a. Chlorinated hydrocarbons
b. Pyrethroids
c. Organophosphates
d. Carbamates
e. Rotenone |
|
Definition
|
|
Term
_________________ reversibly inhibit acetylcholinesterase at cholinergic synapses, causing continuous parasympathetic stimulation by accumulated acetylcholine and resulting in the clinical manifestations of "SLUDD."
a. Chlorinated hydrocarbons
b. Pyrethroids
c. Organophosphates
d. Carbamates
e. Rotenone |
|
Definition
|
|
Term
| Organophosphates and carbamates are absorbed slowly/rapidly, distribute in the plasma to the __________ and ______________, and are metabolized by the __________________ system and are deactivated by _________________________. Their metabolites are excreted in the _______________. |
|
Definition
Rapid absorption
Plasma-->liver-->CNS
Mixed function oxidase system
Deactivated by hydrolysis
Excreted in the urine |
|
|
Term
| Cats/dogs and bulls/females are more susceptible to organophosphate or carbamate toxicity. |
|
Definition
Cats
Bulls (or males in general)--testosterone associated |
|
|
Term
| T/F: phenothiazines help reduce toxicity associated with organophosphates and carbamates. |
|
Definition
| False--phenothiazines increase toxicity |
|
|
Term
| Which of the species are most sensitive to organophosphate toxicity (3 of them)? |
|
Definition
|
|
Term
| Organophosphate or carbamate toxicity is acute/chronic. |
|
Definition
|
|
Term
Which of the following clinical signs is consistent with organophosphate toxicity?
a. SLUDD
b. Muscle tremors, stiffness, paralysis
c. Apprehension, nervousness
d. Anorexia and weight loss in exotic cattle
e. All of the above |
|
Definition
e. All of the above
Parasympathetic = SLUDD
Nicotinic receptors--tremors, stiffness, paralysis (RARELY see seizures)
Death from respiratory failure
Cats have delayed signs (1-5 days) that can last for 2-4 weeks
Exotic cattle have delayed signs (10-14 days) and bulls are more susceptible--testosterone associated |
|
|
Term
_________________ is the treatment of choice for organophosphate/carbamate toxicity.
a. Phenothiazines
b. Diazepam
c. Atropine
d. Methocarbamol
e. All of the above |
|
Definition
| c. Atropine--note that atropine loses its efficacy after 2-3 doses, so don't over atropinize |
|
|
Term
| T/F: oral activated charcoal is valuable for ruminants suffering from organophosphate/carbamate toxicosis. |
|
Definition
|
|
Term
2-PAM can be useful as an acute treatment for toxicosis with what agent?
a. Carbamates
b. Organophosphates
c. Chlorinated hydrocarbons
d. Amitraz
e. Pyrethroids |
|
Definition
b. Organophosphates
MUST be given early--NOT for chronic toxicity. 2-PAM is an oxime reactivator, and therefore does not need to be used with carbamate toxicity (carbamates form reversible bonds) |
|
|
Term
_______________ acts as an alpha-2 adrenergic agonist, causing GI stasis, bradycardia, depression, hyperglycemia, and sedation.
a. Organophosphates
b. Pyrethroids
c. Amitraz
d. Chlorinated hydrocarbons
e. Paraquat |
|
Definition
|
|
Term
Amitraz should never be used on:
a. Dogs
b. Cats
c. Fish
d. Cattle
e. Sheep |
|
Definition
|
|
Term
Horses can die from colic due to GI stasis when they come into contact with:
a. Starlicide
b. Cholecalciferol
c. Carbamates
d. Amitraz
e. Imidacloprid |
|
Definition
|
|
Term
| T/F: chemical detection of amitraz in the stomach, urine, feces, tissues, blood, and skin confirms exposure, but does not correlate with the severity of clinical signs. |
|
Definition
True
The blood and skin are the best samples to take |
|
|
Term
The clinical signs of amitraz can be reversed with:
a. Atropine
b. Yohimbine
c. Atipamezole
d. A and B
e. B and C |
|
Definition
|
|
Term
________________ mimics the action of acetylcholine at cholinergic synapses.
a. Amitraz
b. Nicotine
c. Rotenone
d. Fipronil
e. Pyrethroids |
|
Definition
|
|
Term
Which of the following signs would be most consistent with a small dose of nicotine in a dog?
a. Muscle weakness/paralysis
b. Depression
c. Rapid respiration
d. Coma
e. Collapse |
|
Definition
c. Rapid respiration
Small doses stimulate: salivation, emesis, diarrhea, rapid respiration, marked muscle tremors/twitching
Large doses paralyze: muscle weakness, paralysis, depression, shallow rapid respiration, collapse, coma
Death occurs from respiratory paralysis |
|
|
Term
Which of the following is NOT a valid treatment strategy for nicotine toxicosis?
a. Atropine and activated charcoal
b. Artificial respiration with oxygen
c. IV fluids
d. Acidification of urine
e. Antacids |
|
Definition
| e. Antacids--promote nicotine absorption (from gut?) |
|
|
Term
_______________ complexes with NADH to inhibit electron transport.
a. Amitraz
b. Fipronil
c. Rotenone
d. Nicotine
e. Fenvalerate |
|
Definition
|
|
Term
| Rotenone is activated to its toxic form in the _____________ and needs to be ________________ (process) to detoxify. |
|
Definition
Liver
Demethylate to detoxify |
|
|
Term
| T/F: the toxicity of rotenone is enhanced with combination with pyrethrins. |
|
Definition
|
|
Term
| ______________ is a natural organic insecticide from Derris root, that is unstable in light and air. |
|
Definition
|
|
Term
____________ blocks post-synaptic nicotinic acetylcholine receptors in insects.
a. Imidacloprid
b. Rotenone
c. Pyrethroids
d. Cholecalciferol
e. Metaldehyde |
|
Definition
|
|
Term
| T/F: 95% of imidacloprid is excreted within 48 hours, making it a fairly safe (nontoxic) compound, with the only adverse reactions being hair loss at the site of application at high doses. |
|
Definition
|
|
Term
| ____________ is a GABA inhibitor in insects, which causes excitation. |
|
Definition
|
|
Term
______________ is a cockroach pesticide that has a low toxicity for mammals, with the only adverse effects coming from the plastic trays (mouth lacerations, foreign bodies).
a. Hydramethylnon
b. Fipronil
c. Imidacloprid
d. Rotenone
e. Organophosphates |
|
Definition
|
|
Term
| Methoprene/Lufenuron prevents larval development into adult fleas, while methoprene/lufenuron inhibits chitin formation in the eggs and exoskeleton of fleas. |
|
Definition
Methoprene--prevents larval development
Lufenuron--inhibits chitin formation |
|
|
Term
| T/F: herbicides generally have low mammalian toxicity. |
|
Definition
|
|
Term
A pre-emergent herbicide:
a. Targets plants prior to seed germination
b. Kills growing plants
c. Only harms certain plants
d. Kills all plants
e. None of the above |
|
Definition
| a. targets plants prior to seed germination |
|
|
Term
Post-emergent herbicides:
a. Targets plants prior to seed germination
b. Kills growing plants
c. Only harms certain plants
d. Kills all plants
e. None of the above |
|
Definition
|
|
Term
Selective herbicides:
a. Targets plants prior to seed germination
b. Kills growing plants
c. Only harms certain plants
d. Kills all plants
e. None of the above |
|
Definition
| c. only harms certain plants |
|
|
Term
Non-selective herbicides:
a. Targets plants prior to seed germination
b. Kills growing plants
c. Only harms certain plants
d. Kills all plants
e. None of the above |
|
Definition
|
|
Term
____________ has selective uptake by alveolar cells via the diamine-polyamine transport molecule, resulting in single electron reduction to a free radical.
a. Rotenone
b. Cholecalciferol
c. Hydramethylnon
d. Paraquat
e. Bromethalin |
|
Definition
|
|
Term
__________________ concentrates 10x more in pulmonary tissue than any other tissue.
a. Paraquat
b. Metaldehyde
c. Strychnine
d. Lufenuron
e. Amitraz |
|
Definition
|
|
Term
Which of the following would not be expected as a classic clinical sign for paraquat toxicosis?
a. Moist rales
b. Vomiting
c. saw-horse stance
d. Pneumomediastinum
e. Decreased respiratory compliance |
|
Definition
c. Saw-horse stance
CS: vomiting, ataxia, seizures, tachypnea, dyspnea, moist rales, hypoxia, cyanosis, pneumomediastinum, decreased respiratory compliance, and death by day 8 |
|
|
Term
| An assay of the ______________ is diagnostic for paraquat toxicosis, as levels persist for 2-3 days post-exposure. |
|
Definition
|
|
Term
Necrosis of Type I alveolar cells, atelectasis, emphysema, and pulmonary congestion and hemorrhage would be most consistent with which toxic substance?
a. Phenoxy fatty acids
b. Dinitrocompounds
c. Paraquat
d. Amitraz
e. Carbamates |
|
Definition
|
|
Term
| _________________ is the preferred adsorbant for paraquat toxicosis. |
|
Definition
|
|
Term
| T/F: oxygen supplementation should be provided for animals with paraquat toxicosis. |
|
Definition
| False: provide ventilation/respiratory support, but no oxygen |
|
|
Term
All of the following are biochemical antagonists to paraquat except:
a. Acetylcysteine
b. Superoxide dismutases
c. Ascorbic acid
d. All of the above
e. None of the above |
|
Definition
|
|
Term
________________ function by decreasing chloride conductance, inhibiting ribonucleotide synthesis, and uncoupling oxidative phosphorylation.
a. Paraquat
b. Phenoxy fatty acids
c. Dinitrocompounds
d. Carbamates
e. Triazenes |
|
Definition
|
|
Term
_____________ causes anorexia, rumen atony, diarrhea, bloat, oral ulceration, and rumen stasis in cattle.
a. Paraquat
b. Phenoxy Fatty acids
c. Dinitrocompounds
d. Carbamates
e. Triazenes |
|
Definition
|
|
Term
| The most commonly used group of herbicides are the ___________________. |
|
Definition
|
|
Term
All of the following act by uncoupling oxidative phosphorylation except:
a. Phenoxy fatty acids
b. Dinitrocompounds
c. Bromethalin
d. Paraquat
e. All of the above work by uncoupling oxidative phosphorylation. |
|
Definition
| d. Paraquat--works by free radical formation |
|
|
Term
| T/F: triazenes are relatively toxic to ruminants. |
|
Definition
|
|
Term
| Roundup is composed of _______________ and is the 2nd most used herbicide in domestic, public, and agriculture environments. |
|
Definition
|
|
Term
|
Definition
|
|
Term
| T/F: a metal is any chemical element whose atoms readily lose electrons to form cations, and form metallic bonds between other metal atoms and ionic bonds with nonmetal atoms, elements, or compounds. |
|
Definition
|
|
Term
| T/F: metals are readily degraded in the environment. |
|
Definition
| False: not degraded or destroyed |
|
|
Term
| T/F: metals with element densities >7 gm/cm2, specific gravity >4, and atomic weight > sodium are considered heavy metals. |
|
Definition
|
|
Term
| T/F: many heavy metals for coodrinate covalent bonds, where the heteroatom of the ligand contributes and unshared pair of electrons to the bond. |
|
Definition
True
Sulfur, Nitrogen, and Oxygen bind to heavy metals through this type of bond, which can be a asis for toxicity. |
|
|
Term
Lead functions by all of the following mechanisms except:
a. Binds to sulfhydryl groups, inhibiting heme synthesis and GABA transmission.
b. Produces free radicals causing oxidative tissue damage.
c.Competes with divalent cations to displace them from binding proteins, leading to altered nerve and muscle transmission.
d. Inhibits membrane associated enzymes such as calmodulin and Na/K pumps.
e. Alters vitamin D metabolism, leading to impaired Calcium absorption and zinc related enzymes. |
|
Definition
b. Free radical damage
This is caused by selenium toxicity |
|
|
Term
| T/F: a cow that is accidentally shot in the semimembranosus muscle with a lead bullet has a high risk of lead toxicosis. |
|
Definition
| False: lead needs to be solubilized, and requires the acidic environment of the gut to do so. A lead bullet in soft tissues won't do this. (I'm sure there is some random mechanism by which it can cause toxicosis, but it's not in the notes) |
|
|
Term
| ____% of lead binds to RBCs, with some going to albumin. |
|
Definition
|
|
Term
| T/F: lead can penetrate the BBB of young animals and cross the placenta into fetuses, causing abortion and brain damage. |
|
Definition
|
|
Term
| Organic/Metallic lead has slow absorption and distribution, while Organic/Metallic lead has rapid absorption and distribution. |
|
Definition
Organic = rapid
Metallic = slow |
|
|
Term
| Lead tends to concentrate in the gut before traveling to the _________, ______________, and _______________, and is stored in the ______________. |
|
Definition
|
|
Term
Lead is excreted in the:
a. Feces
b. Milk
c. Urine
d. A and B
e. A, B, and C |
|
Definition
e. A, B, and C
Note that the primary route of excretion is the feces |
|
|
Term
Which species is resistant to lead poisoning?
a. Cattle
b. Dogs
c. Pigs
d. Horses
e. Cats |
|
Definition
c. Pigs
Cattle most frequently poisoned
Dogs also poisoned more frequently |
|
|
Term
| Onset of clinical signs associated with lead toxicosis is rapid/delayed. |
|
Definition
| Delayed--need time for absorption and binding to active sites |
|
|
Term
Nucleated red blood cells with basophilic stippling in the absence of severe anemia is indicative of lead poisoning in what species?
a. Dog
b. Cat
c. Cattle
d. Horse
e. Pig |
|
Definition
a. Dog
CS in dogs: vomiting, anorexia, tender abdomen, diarrhea/constipation, lethargy, hysteria, convulsions, ataxia, blindness, mydriasis, nRBCs w/ basophilic stippling without severe anemia |
|
|
Term
Blindness, head bobbing, bruxism, and circling are clinical signs associated with lead toxicosis in what species?
a. Dog
b. Cat
c. Cattle
d. Horse
e. Birds |
|
Definition
c. Cattle
CS in cattle: anorexia, rumen stasis, gaunt, salivation, blindness, muscle twitching, head bobbing, depression, bruxism, circling, convulsions, acute convulsive death in calves. |
|
|
Term
Excessive salivation, elevated ALT/AST, and minimal CNS involvement are typical clinical signs for lead toxicosis in what species?
a. Dog
b. Cat
c. Cattle
d. Horse
e. Pig |
|
Definition
b. Cat
CS in cats: lethargy, anorexia, weight loss, excessive salivation, minimal CNS, inconstant nRBCs and basophilic stippling, elevated AST/ALP |
|
|
Term
Weight loss, esophageal paralysis, and regurgitation are all clinical signs associated with lead toxicosis in:
a. Dog
b. Cat
c. Cattle
d. Horse
e. Birds |
|
Definition
e. Birds
CS in birds: depressed, weak, anorectic, weight loss, esophageal paralysis, regurgitation, diarrhea, wing droop |
|
|
Term
Recurrent left laryngeal paralysis, ataxia, incoordination, and metaphyseal sclerosis are clinical signs associated with lead toxicity in:
a. Dog
b. Cat
c. Cattle
d. Horse
e. Pig |
|
Definition
|
|
Term
The sites to check for lead toxicosis include all of the following except:
a. Stomach
b. Kidney
c. Feces
d. Blood
e. Brain
f. Liver
g. Bone
h. All of the above |
|
Definition
|
|
Term
| T/F: charcoal is the adsorbent of choice for heavy metal toxicosis. |
|
Definition
| False: charcoal is not effective for metals |
|
|
Term
| T/F: lead is a highly cumulative substance. |
|
Definition
|
|
Term
All of the following are acceptable therapies for lead toxicosis except:
a. Cathartics/emetics
b. Oral MGSO4 in cattle
c. Activated charcoal
d. Chealators such as CaEDTA or D-penicillamine
e. Supportive care such as fluids, thiamine, and anti-convulsants |
|
Definition
| c. Activated charcoal--not effective |
|
|
