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VETT 1110 Veterinary Diseases and Pathology > Toxicology and Poisonous Plants Lecture Review > Flashcards

Toxicology and Poisonous Plants Lecture Review Flashcards

1
Q

Any substance that when introduced into or applied onto the body can interfere with the life processes of cells of the organism

A

toxicant

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2
Q

The process of removing or neutralizing injurious agents

A

Decontamination

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3
Q

describes a particular way thations and molecules bind metal ions.
Typically used with heavy metal toxicities

A

chelation

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4
Q

represents the individual dose required to kill50percent of a population of test animals

A

LD50

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5
Q

TREAT THE PATIENT NOT THE ____________

A

Poison. Always remember to stabilize your patient first and foremost

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6
Q

methods of decontamination for ocular/topical exposure

A

ocular irrigation
bathing

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7
Q

methods of decontamination for Oral Ingestion

A

dilution
emesis
activated charcoal
cathartics
enemas
gastric lavage
enterogastric lavage

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8
Q

Dilution is the solution for ______________

A

pollution

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9
Q

what is the recommended method of decontamination for corrosive or caustic agents?

A

dilution

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10
Q

When is it appropriate to induce emesis for decontamination?

A

best within 1-3 hours of ingestion, in an asymptomatic patient

never with caustic/corrosive substances
never with petroleum distillates
never in symptomatic patients

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11
Q

What are some agents used to induce emesis?

A

3% hydrogen peroxide (fresh)
syrup of ipecac
apomorphine
xylazine (rarely)

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12
Q

True/False. Salt is an excellent choice to induce emesis

A

FALSE. risk for gastric ulceration

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13
Q

this acts a magnet to adsorb toxicants from the GI tract

A

activated charcoal

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14
Q

used to enhance elimination of the activated charcoal

A

cathartics (Ex: sorbitol, bulk cathartics)

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15
Q

method of decontamination of caustic/corrosive substances and/or petroleum distillates

A

gastric lavage

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16
Q

method of decontamination when potentially lethal oral exposures have occurred; only used under the direct supervision of a DVM

A

enterogastric lavage

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17
Q

Decontamination Dos

A

Treat the patient not the poison.
Stabilize the animal before attempting decontamination procedures.
Get complete history of the animal and the exposure data.
Keep the ASPCA APCC phone number handy in your clinic.1-888-4ANI-HELP

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18
Q

Decontamination Donts

A

Bathe a seizing animal. (Always stabilize the animal first.)

Use salt as an emetic agent.Induce emesis in a seizing, extremely stimulated, or hyperactive animal.

Induce emesis in a vomiting animal.

Induce emesis in a severely lethargic, comatose, or debilitated patient.

Induce emesis in an animal that has had recent abdominal surgery.

Induce emesis with a corrosive ingestion.

Induce emesis with hydrocarbon/ petroleum distillate ingestion.

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19
Q

Most Common side effects when topical/spot-on products are used appropriately

A

taste reaction and/or local application site reaction

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20
Q

Cats: Severe reaction if ______________ products are applied topically, resulting in seizures and/or tremors.

A

permethrin

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21
Q

The general rule of thumb for chocolate is:

A

the more bitter the chocolate, the more toxic it is

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22
Q

clinical signs chocolate toxcity

A

Depending on the dose of methylxanthine, the resulting signs are hyperactivity, tachycardia, tachypnea, trembling and potentially death

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23
Q

clinical signs of onion/garlic toxicity

A

may cause hemolytic anemia

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24
Q

clinical signs rising bread dough ingestion

A

Clinical Signs are associated w/ ethanol toxicosis and foreign body obstruction: severe abdominal pain, bloat, vomiting, incoordination, depression

25
Q

true/false. grapes eaten in any quantity may cause kidney failure

A

TRUE

26
Q

clinical signs tobacco ingestion

A

Clinical signs develop quickly: excitement, tachycardia, tachypnea, salivation, vomiting, diarrhea
Clinical signs after the initial excitability may progress to shallow breathing, muscle weakness, tremors, depression, collapse, coma, death.
Death is due to respiratory paralysis

27
Q

clinical signs xylitol toxicity

A

HYPOGLYCEMIA (LOW Blood Glucose) within 30 minutes of ingestion…. which manifests as weakness, lethargy, collapse, ataxia, vomiting

elevated liver enzymes within 18-72 hours of ingestion

28
Q

treatment of an acidic or alkaline cleaning agent

A

stabilize, DILUTION, check for mucosal ulcerations

29
Q

t/f. drinking toilet bowl water that contains a tank drop-in tablet is not likely to cause signs of toxicity

A

TRUE.

the concentration in the toilet water is very low, so clinical signs unlikely, other than mild gastric irritation

Corrosive effects may be seen if tablet is chewed

30
Q

major source of zinc toxicity; may be found in your wallet

A

pennies minted after 1983

31
Q

heavy metal toxicity causes vague clinical signs but is often associated with damage to

A

the red blood cell

32
Q

t/f
Veterinary treatment of mothball ingestion is always required

A

true

33
Q

organophosphates and/or carbamates found in fly baits and insecticides commonly cause symptoms of

A

“SLUDGE”: Salivation, Lacrimation, Urination, Defecation, GI cramping, Emesis

34
Q

the antidote for organophosphates and/or carbamates,

A

atropine

35
Q

Three main types Rat or Mouse Bait

A

Anticoagulants
Bromethalin
Cholechalciferol

36
Q

clinical signs of anticoagulant rat bait

A

72 hours after ingestion– blood clotting abnormalities and can result in spontaneous hemorrhage

37
Q

antidote anticoagulant rat bait

A

Vitamin K1

38
Q

clinical signs of bromethalin rat bait

A

occur within 24 hr to 2 weeks and include muscle tremors, seizures, hyperexcitability, forelimb extensor rigidity, ataxia, CNS depression, loss of vocalization, paresis, paralysis and death.

39
Q

clinical signs of cholecalciferol rat bait

A

kidney failure

delayed onset of 18-38 hr; vomiting, depression, diarrhea, anorexia, PU/PD, cardiac arrhythmias

kidney failure results from Ca deposition in the kidneys (elevated BUN/CREA)

40
Q

types of antifreeze products

A

Methanol
Propylene Glycol
Ethylene Glycol

41
Q

active ingredient in “safer” forms of antifreeze

A

Propylene Glycol

42
Q

Most dangerous form of antifreeze; most commercial forms of antifreeze contain

A

Ethylene Glycol (EG)

43
Q

clinical signs Ethylene Glycol toxicity

A

Stage 1: This occurs within 30 minutes to 12 hours, and looks similar to alcohol poisoning. Signs of walking drunk, drooling, vomiting, seizing, and excessive thirst and urination may be seen.

Stage 2: This occurs within 12-24 hours post-exposure, and clinical signs seem to “resolve” when in fact more severe internal injury is still occurring.

Stage 3: In cats, this stage occurs 12-24 hours after ethylene glycol exposure. In dogs, this stage occurs 36-72 hours post-ingestion. During this stage, severe acute kidney failure is occurring. Signs of inappetance, lethargy, drooling, halitosis (secondary to kidney failure), coma, depression, vomiting, and seizures may be seen.

44
Q

antidote Ethylene Glycol toxicity

A

Fomepizole is the preferred treatment in dogs but is not effective in cats. It inhibits alcohol dehydrogenase.

Ethanol can be used in dogs and cats. It competes with EG as a substrate for alcohol dehydrogenase.

45
Q

clinical signs of acetaminophen toxicity

A

methemoglobinemia, liver failure

46
Q

what species is particularly susceptible to acetaminophen toxicity

A

cats

47
Q

what makes cats so susceptible to acetaminophen toxicity

A

The parent compound of this drug is relatively safe, but the metabolites are highly toxic. Cats cannot scavenge these byproducts because they are relatively deficient in glutathione stores.

48
Q

clinical signs associated with human NSAID toxicity

A

gastric ulceration–which may cause vomiting of digested blood (coffee ground appearance)

49
Q

Marijuana Clinical Signs:

A

Prolonged depression, vomiting, incoordination, sleepiness or excitation, hypersalivaton, dilated pupils, low blood pressure, low body temperature, seizure, coma, death (rare)

50
Q

Azalea/Rhododendronclinical signs

A

cardiovascular dysfunction

51
Q

Cardiac Glycosides (Oleander, Foxglove)

A

cardiovascular dysfunction

52
Q

clinical signs castor bean

A

contain RICIN (highly toxic)

abdominal pain, drooling, vomiting, diarrhea, excessive thirst, weakness and loss of appetite. Severe cases of poisoning can result in dehydration, muscle twitching, tremors, seizures, coma and death.

53
Q

clinical signs lily ingestion in cats

A

associated with kidney failure

54
Q

sago palm toxicity is associated with

A

Liver failure

55
Q

Calcium-Oxalate-Containing Plants
clinical signs

A

oral irritation, burning of lips, mouth, tongue, drooling, vomiting, difficulty swallowing

56
Q

clinical signs red maple toxicity in horses

A

Horses often die within 18-24 hr of ingestion of wilted leaves

Horses that remain alive for 18-24 hr after ingestion of wilted leaves will be severely depressed and cyanotic and produce dark red or brown urine. (methemoglobinemia)

57
Q

Bracken Fern toxicity cattle

A

Enzootic hematuria; Calves often have difficulty breathing, with pale mucous membranes. Hemorrhages vary from minor mucosal petechia to effusive bleeding, and at times large blood clots form that may be passed in the feces.

Mortality rate in cattle >90%

58
Q

Bracken Fern toxicity horses

A

Bracken Staggers: anorexia, weight loss, incoordination, and a crouching stance while arching the back and neck with the feet placed wide apart. When the horse is forced to move, trembling muscles are noted.

VETT 1110 Veterinary Diseases and Pathology (11 decks)

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