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Tox > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

What type of toxic dose: The highest or largest dose which does not result in undesirable or toxic alterations

A

Highest nontoxic dose (HNTD)

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1
Q

What is the prognosis of Naphthalene?

A

Reasonable if treated promptly

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2
Q

Do organophosphates get distributed to the CNS?

A

Yes

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2
Q

What are the natural pyrethrins?

A

Pyrethrin 1 & 2

Cinerin 1 & 2

Jasmolin 1 & 2

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2
Q

Toxicity level of D-Limonene in cats at 5x recommended dose?

A

Mild toxicity

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2
Q

What factors can decrease the toxicity of AR?

A

Pregnancy

Enzyme inducers (phenytoin)

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2
Q

MOA of Bromethalin?

A

Uncoupling of oxidative phosphorylation

Lack of ATP

Insufficient energy for Na+/K+ pumps

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3
Q

What can be done as symptomatic treatment for chlorinated hydrocarbon toxicity?

A

Diazepam or barbiturates for seizures

Oxygen, ventilation, fluids

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3
Q

T/F: Younger animals are more sensitive to Cholecalciferol

A

True

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4
Q

MOa of Ivermectin?

A

GABA agonist

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5
Q

How does the soil half-life of chlorinated hydrocarbons compare to OPs?

A

LONGER

2-15 years (few weeks with OPs)

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6
Q

What type of toxicity: The effect produced by daily exposure from one day to 30 days

A

Subacute toxicity

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6
Q

What precipitate should be used to treat alkaloid poisoning?

A

Tannic acid

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6
Q

What are the common routes by which organophosphates get into the body?

A

Oral (contaminated feed)

Dermal

Inhalation

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7
Q

What does a nicotinic blockade from OP poisoning cause?

A

Paralysis

CNS depression

Coma

Dyspnea

Death (resp. failure)

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8
Q

What are the most characteristic signs of Cholecalciferol?

A

Hematemesis and melena (GI)

PU/PD (renal)

Depression (neurologic)

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9
Q

What is the antidote for apomorphine?

A

Naloxone

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10
Q

What lesions are associated with Bromethalin?

A

Cerebral edema

Diffuse white matter vacuolization through CNS

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11
Q

Which species has less plasma pseudocholinesterase?

A

Ruminants

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11
Q

Dose for a harmless substance?

A

>15g/kg

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11
Q

What is the cause of death in high exposure of OPs?

A

Respiratory failure (paralysis)

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11
Q

In mammals, Rotenone is converted to what kind of metabolite?

A

Non-toxic metabolites

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11
Q

What clinical signs are associated with Naphthalene?

A

Mothball breath

Hemolysis, heinz bodies, methemoglobinemia, seizures

Cataracts in neonates

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11
Q

When i say Bromethalin, you say…

A

Neurotoxicant

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12
Q

What organ metabolizes calcidiol to calcitriol?

A

Kidney

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13
Q

What species is deficient in acetylating enzymes?

A

Dogs

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13
Q

Affect of charcoal broiled foods on enzymes?

A

Induction

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14
Q

What is the adsorbant of choice for toxins?

A

Activated charcoal

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14
Q

How is Ivermectin excreted?

A

Feces

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15
Q

What is the significance of the ABCB1 gene in dogs that receive Ivermectin?

A

Results in ~50x concentration of drug in the CNS

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16
Q

For feed, 100 g/ton = Xppm

A

110ppm

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18
Q

What type of toxicity: The effect produced by daily exposure for a period of 3 months or more

A

Chronic

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19
Q

This toxin can cause acute paralysis in dogs from topical exposure

A

Pyrethrins and Pyrethroids

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19
Q

Low doses of Nicotine can resemble what other toxicity?

A

OP/CM

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20
Q

Describe the atropine response test

A

Administer 0.02 mg/kg of atropine

If strong response, then less likely OP toxicity

Atropine treatment for OP toxicity is 0.1-0.5 mg/kg

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20
Q

High doses of Nicotine can resemble what type of drugs?

A

CNs depressants

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20
Q

What is the prognosis of Cholecalciferol?

A

Variable - the earlier treatment is started, the better

Severe hypercalcemia = more guarded

Hematemesis or mineralization = poorer prognosis

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21
Q

T/F: When treating for AR, you would test the Vitamin K even after it is discontinued

A

True

Check PT 24-48 hours after last dose of Vitamin K

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22
Q

The use of ipecac is contraindicated in what species?

A

Cats

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23
Q

What is the prognosis of Bromethalin?

A

Mild case - resolve over several weeks

Severe case - grave prognosis

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24
Q

How are dogs commonly poisoned with Ivermectin?

A

Overdose due to use of large animal products on small animals

Coming in contact with horse feces after treatment

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26
Q

Which biotransformation reaction is deficient in the neonate?

A

Conjugation

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27
Q

What drugs are examples of extensive first pass effect?

A

Lidocaine

Propranolol

Morphine

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29
Q

What drug has a strong affinity to kidney tissue?

A

Aminoglycosides

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29
Q

What nonspecific pathological lesions are associated with OP poisoning?

A

Pulmonary edema and congestion

Edema of various organs (including brain)

Necrosis in skeletal muscle

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29
Q

What levels of AChE activity are used to determine OP?

A

<50% activity is suspicious

<25% activity is diagnostic

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29
Q

Is Amitraz distributed to the CNS?

A

Yes

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30
Q

What is the acute oral LD50 of Amitraz for dogs?

A

~250mg/kg

Mild signs (sedation) seen in some dogs at 20mg/kg

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32
Q

What type of toxic dose: The lowest dose which produces toxic alterations and administering twice this dose will not cause death

A

Toxic dose low (TDL)

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33
Q

What is the most toxic of the Carbamates?

A

Aldicarb

Mimics the structure of ACh

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34
Q

What are xenobiotics?

A

Foreign chemicals that the body does not produce

Drugs and poisons are xenobiotics

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35
Q

Which reaction phase of biotransformation is the synthetic phase?

A

Phase 2

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36
Q

What is used to treat cerebral edema due to Bromethalin?

A

Mannitol +/- dexamethasone

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37
Q

What is the dose with no toxic signs called?

A

Maximum Tolerated Dose or Minimal Toxic Dose (MTD)

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38
Q

What is the most common biotransformation reaction?

A

Oxidation

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39
Q

What species is deficient in glucuronyl transferase?

A

Cats

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39
Q

What specific treatment is used for Naphthalene?

A

Ascorbic acid - converts MetHgb to Hgb

Methylene blue 1% - faster than ascorbic acid but is an oxidizer

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40
Q

What clinical signs are assocated with CNS stimulation following OP poisoning?

A

Anxiety

Restlessness

Hyperactivity

Tonic-colonic seizures (CNS depression in ruminants)

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41
Q

What species is most sensitive to OP induced delayed polyneuropathy?

A

Chickens

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41
Q

T/F: Chlorinated hydrocarbons are highly lipophilic

A

True

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41
Q

At what dose of nicotine do you see clinical signs in the dog?

A

1 mg/kg

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42
Q

Convert 1ppm to %

A

0.0001%

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42
Q

T/F: OPs are extensively metabolized in the liver

A

True

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42
Q

Clicker question:

If chelation therapy is recommended for a toxicant when levels reach 5mg%, will a blood level of 900mcg/dL require therapy?

A

No

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42
Q

What is used to treat ARs?

A

PO Vitamin K1 (phytonadione)

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43
Q

How long should you treat a patient with Warfarin poisoning?

A

1 week

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44
Q

What pathology is associated with delayed neurotoxicity following OP poisoning?

A

Degeneration and demyelination of peripheral and spinal motor neurons

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44
Q

Clicker question:

Which of the following factors has the shortest half-life?

A. II

B. VII

C. IX

D. X

A

B. VII

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44
Q

What is the half-life of Bromethalin in the rat?

A

5-6 days

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46
Q

What are the poorly perfused tissues?

A

Bone

Adipose tissue

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47
Q

How do the chemical properties of the metabolite differ from the drug?

A

Metabolite is more water soluble, polar, and ionized

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48
Q

Which organophosphates have direct acetylcholinesterase activity?

A

Dichlorvos

Monocrotophos

Trichlorfon

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49
Q

What toxin can cause abortion in cattle?

A

Anticoagulant Rodenticides from placental hemorrhage

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50
Q

What should you use in cats to induce emesis?

A

Xylazine

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51
Q

T/F: ARs are largely protein bound

A

True

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51
Q

What drugs should be avoided when treating Bromethalin?

A

Magnesium cathartics (CNS depressive)

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52
Q

What is the toxic component of Cholecalficerol?

A

Vitamin D3

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54
Q

What type of toxicity: The effect of a single dose of multiple doses during a 24 hour period

A

Acute toxicity

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55
Q

T/F: Pancreatitis has been reportedly found in some dogs with the more lipophilic compounds

A

True

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56
Q

How long does it take for clinical signs of AR to set in?

A

1-5 days

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57
Q

T/F: Compared to cholinesterases, chlorinated hydrocarbon toxicity will have less parasympathomimetic signs, and less severe CNS stimulation

A

False

Less parasympathomimetic signs, MORE severe CNS stimulation

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57
Q

What should you monitor when treating D-Limonene toxicity?

A

Temperature

Want to avoid hypothermia just as with Pyrethrins

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59
Q

Which species have high levels of oxidative enzymes?

A

Ruminants

Horses

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59
Q

MOA of DEET?

A

Unknown

Can cause surface irritation

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60
Q

Clicker question:

Which of the following insecticide toxicants would you expect to have the longest half-life?

A. OPs

B. CMs

C. Chlorinated hydrocarbons

D. Pyrethrins

A

C. Chlorinated hydrocarbons

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61
Q

Dose for a slightly toxic substance?

A

0.5g/kg

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63
Q

How do you calculate the standard safety margin?

A

Ratio between LD1 and ED99

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64
Q

What is the main clinical sign associated with chlorinated hydrocarbons?

A

CNS stimulation

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65
Q

What is the lowest canine lethal dose of Naphthalene?

A

~400mg/kg

One mothball can weigh 2.7-4g

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67
Q

How is toxicity expressed in mammals? Birds? Fish?

A

Mammals - LD50 in mg/kg body weight

Birds - LC50 in mg/kg feed

Fish - LC50 in mg/liter water

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68
Q

What type of toxic dose: Smaller to the highest nontoxic dose

A

Maximum tolerated dose or minimal toxic dose (MTD)

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69
Q

What is the prognosis of D-Limonene toxicity?

A

Exelent in sublethal toxicosis

Usually resolves within 6-12 hours

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70
Q

Are dogs or cats more sensitive to DEET?

A

Cats

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71
Q

What is the prognosis of Rotenone?

A

Generally good for mammals

Poor for fish and reptiles

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72
Q

What are our Chlorinated Hydrocarbons (Organochlorines)?

A

Diphenyl aliphatics (DDT, methoxychlor)

Aryl hydrocarbons (Lindane)

Cyclodienes (Aldrin, Toxaphene)

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72
Q

What are some lab findings of AR?

A

+/- anemia

Mild thrombocytopenia

Hypoproteinemia

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73
Q

Does Ivermectin cross the BBB?

A

Not typically

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75
Q

Dose for a moderately toxic substance?

A

> 50-500mg/kg

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77
Q

What is the ratio between acute LD50 and chronic LD50?

A

Chronicity factor

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78
Q

T/F: Cats are more sensitive to D-Limonene than dogs

A

True

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78
Q

How long does it take for acute clinical signs or Bromethalin to set in (less common)?

A

2-24 hours

CNS excitatory signs

Usually with a supralethal dose

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79
Q

Clicker Question:

Which of the following aspects of toxicity are the same between OP and CM insecticides?

A. both toxicants undergo storage activation

B. both toxicants undergo lethal synthesis

C. cholinesterase activity can be tested for either

D. Pralidoxime is an effective treatment for either

A

C. cholinesterase activity can be tested for either

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80
Q

What drugs can cause the ABCB1 mutation?

A

Cyclosporine

Ketoconazole

Verapamil

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81
Q

Which species lacks oxidative enzymes?

A

Birds

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81
Q

MOA of OPs?

A

Irreversible inhibition of cholinesterases

Increase ACh at all cholinergic sites

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82
Q

What are our enzyme inducers?

A

Phenobarbital

Phenylbutazone

Griseofulvin

Rifampin

Chlorinated hydrocarbon insecticides

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82
Q

MOA of Naphthalene?

A

Oxidation products cause methemoglobinemia and hemolysis

Leads to tissue hypoxia

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83
Q

Clicker Question:

All of the following are general contraindications to inducing emesis after toxin ingestion EXCEPT:

A. patient is depressed/unconscious

B. patient is seizuring/high risk of seizures

C. known enterohepatic recirculation

D. known corrosive toxin

A

C. known enterohepatic recirculation

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83
Q

Clicker question:

Which of the following toxicants is primarily a CNS depressant?

A. Chlorinated hydrocarbon

B. CM

C. Amitraz

D. Pyrethrin

A

C. Amitraz

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85
Q

What drug can be effective in treating OP?

A

2-PAM

May not be efective against some OPs

May not be effective if “aging” has occurred (12-24 hours)

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86
Q

What is the point of adding Piperonyl butoxide of MGK-264 to PP?

A

Inhibits pyrethrin metabolism by insects

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88
Q

How long will it take to see clinical signs after OP poisoning?

A

15 minutes - 1 hour

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89
Q

What mammalian species is most effected by Rotenone?

A

Pigs

Highest toxicity in fish and cold-blooded animals

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90
Q

MOA of DDT-type chlorinated hydrocarbons

A

Slow Na+ influx and inhibit K+ efflux leading to partial depolarization

Causes repetitive firing of neuron - axonal hyperactivity

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91
Q

T/F: After treatment of AR, the patient is more sensitive to another exposure shortly after treatment

A

True

Lower toxic dose if repeated exposure within few weeks of treatment

92
Q

What should be tested for direct detection of OP?

A

Stomach or rumen contents

Hair/skin with dermal exposure

93
Q

What species is most sensitive to chlorinated hydrocarbons?

A

Cats

94
Q

Is there a specific antidote for chlorinated hydrocarbon toxicity?

A

No

95
Q

Are 1st or 2nd generation ARs more toxic?

A

Second

95
Q

ARs: What treatment should be done when there are clinical signs, bleeding, PCV <15%

A

Give clotting factors and RBCs

Vitamin K

Supportive care

97
Q

When Cortisone undergoes biotransformation, what happens?

A

Inactive drug -> active metabolite (Hydrocortisone/Cortisol)

97
Q

What drugs can be used to treat seizures caused by PP toxicity?

A

Diazepam

Barbiturates

Propofol CRI

98
Q

Nicotine is better absorbed in what pH environment?

A

Alkaline

100
Q

T/F: Plant charcoal is more effective than animal charcoal?

A

True

102
Q

How do you calculate the therapeutic index?

A

Ration between LD50 and ED50

The larger the value, the wider the safety margin

104
Q

Charcoal is considered a universal antidote except for what two toxins?

A

Ammonia

Cyanide

105
Q

Clicker Question:

Chlorinated hydrocarbons like DDt are highly lipophilic and excreted in the bile. This suggests that they likely undergo which of the following?

A. first-pass metabolism

B. lethal synthesis

C. enterohepatic recirculation

D. poor distribution into fat

A

C. enterohepatic recirculation

106
Q

What are the moderately perfused tissues?

A

Muscle

Skin

107
Q

How long should you treat a patient with AR poisoning but you dont know which one was ingested?

A

3-4 weeks

108
Q

If a patient comes to your clinic and smells like lemons, what do you think could cause this?

A

D-Limonene

108
Q

What clinical signs are associated with early stimulation of Nicotine?

A

Ataxia

Vomiting

Bradycardia

Tremors

Convulsions

108
Q

What factors can predispose an animal to Cholecalciferol toxicity?

A

Renal disease

Hyperparathyroidism

High calcium/phos in diet

109
Q

T/F: Dogs are more sensitive to PP than cats

A

False

Cats are more sensitive than dogs

110
Q

What can be tested for Nicotine?

A

Urine

Stomach contents

Kidney

Liver

Blood

111
Q

MOA of Amitraz?

A

Alpha-2 adrenergic agonist in the CNS

112
Q

What is the most serious clinical sign associated with Amitraz?

A

Cardiovascular colapse and respiratory failure

113
Q

What proetin do acidic drugs tend to bind to?

A

Albumin

115
Q

Define a poison (toxicant)

A

Any substance when applied or introduced into the body may interfere with life processes or biological functions of the cells of the animal

116
Q

What makes up phase 2 metabolic reactions?

A

Conjugation

117
Q

What is the only microsomal conjugation reaction?

A

Glucuronidation

119
Q

Describe the severity of PP

A

Generally acute, mild toxicity

121
Q

What would you do to treat intermediate OP syndrome?

A

Supportive care

2-PAM may have benefit (nicotinic sites)

121
Q

What will increase the toxicity of Amitraz?

A

Meperidine and sympathomimetic amines

Stress, debilitation, age, toy breeds

122
Q

What precipitate should be used to treat lead poisoning?

A

Sulfate

123
Q

T/F: There are no specific pathological lesions associated with chlorinated hydrocarbons

A

True

123
Q

Clicker question:

If a patient presents with hypercalcemia and significantly elevated PTH, would Cholecalciferol be the top differential on your list?

A

No

124
Q

MOA of Rotenone?

A

Blocks oxidative phosphorylation in the TCA cycle which prevents NADH from being oxadized to NAD and therefore interfering with production of ATP

126
Q

What is the amount of chemical that can be ingested w/o causing deaths, illness or tixic alterations called?

A

No-effect level (Maximum nontoxic level)

127
Q

What is the main clinical sign associated with ARs?

A

Hemorrhage

Signs depend on site of bleeding

129
Q

What would you do to treat OP induced delayed polyneuropathy?

A

Symptomatic therapy only

131
Q

T/F: Carbamates require bioactivation

Therefore more toxic than some OPs in very young patients

A

False

132
Q

When I say Cholecalciferol, you say…

A

Hypercalcemia

133
Q

What is the most common source of Naphthalene poisoning?

A

Mothballs

135
Q

What are our enzyme inhibitors?

A

Chloramphenicol

Cimetidine

Ketoconazole

136
Q

What condition may reduce the effect of Vitamin K1 in treating AR?

A

Liver failure

137
Q

What clinical signs in dogs/cats are associated with DEET?

A

Basically CNS excitement signs:

Hypersalivation

Vomiting

hyperexcitability

Tremors

Ataxia

Seizures

138
Q

MOA of D-Limonene?

A

Unknown (possible vasodilation)

139
Q

The presence of alpha-cyano moiety has what effect on the metabolism?

A

Decreases the rate of hydrolysis

140
Q

What are the primary targets of Bromethalin?

A

Brain and spinal cord

141
Q

How is Bromethalin metabolized in the liver and what is the metabolite?

A

N-demethylation to desmethylbromethalin (more toxic)

143
Q

Describe OP induced intermediate syndrome

A

Seen with massive doses, lipophilic agents, or more chronic exposure

No muscarinic signs or muscle fasciculations

145
Q

What type of toxic dose: The amount of a chemical that can be ingested without causing any deaths, illness or toxic alterations in any of the anumals for the stated period (usually 90 days to two years or more depending on the species)

A

No-effect level (maximum nontoxic level)

146
Q

What are the signs of OP induced delayed polyneuropathy?

A

Muscle weakness

Ataxia

Rear limb paralysis

147
Q

Renal excretion of Nicotine is favored in what pH environment?

A

Acidic

148
Q

MOA of Aryl hydrocarbons and Cyclodienes?

A

Na+ channel effects and also may inhibit GABA

150
Q

Because Chlorinated hydrocarbons are highly lipophilic, what can this lead to?

A

Bioaccumulation in the food chain

151
Q

Where in the body would you look for Rotenone for a diagnosis?

A

Stomach contents

Urine

Feces

Liver (postmortem)

152
Q

The metabolite of what drug causes adrenal necrosis?

A

Midotane

Metabolite = O,P-DDD

153
Q

What is the species order of sensitivity for ARs?

A

Pigs -> dogs/cats -> ruminants -> horses -> chickens

154
Q

What toxin is toxic to fleas at all life stages?

A

D-Limonene

155
Q

What are the plant sources for Rotenone?

A

Derris elliptica

Jicama seeds

155
Q

What lesions are associated with Cholecalciferol?

A

Hemorrhagic gastroenteritis

Mineralization

156
Q

What are the main tissue barriers?

A

Brain

Eye

Testicles

Placenta

Mammary gland

158
Q

Where in the body can you find chlorinated hydrocarbons?

A

If insecticide is in blood, liver, or brain at significant concentrations

159
Q

T/F: Second-generation ARs have short half-lives

A

False

Long half-lives

160
Q

What plant is teratogenic to sows and cattle?

A

Nicotiana tabacum (Nicotine)

162
Q

Clicker question:

What condition in canine patients is commonly treated with

O,P-DDD?

A. Hypoadrenocorticism (Addison’s)

B. Pituitary dependent hyperadrenocorticism(Cushing’s)

C. Overdose of exogenous corticosteroids

D. Primary pituitary hyperplasia

A

B. Cushing’s

163
Q

Clicker question:

If AR intoxication is suspected but you do not know what specific rodenticide was ingested. How long should you treat with vitamin K1?

A. 96 hours

B. 1 week

C. 10 days

D. 4 weeks

A

D. 4 weeks

165
Q

What is the highest dose that does not result in undesirable/toxic effects called

A

Highest Nontoxic Dose (HNTD)

166
Q

What is the elimination half-life of Amitraz and how long does it take to reach peak plasma concentrations?

A

~24 hours

Peak concentration after 5 hours

167
Q

What clinical signs in rabbits/rats are associated with DEET?

A

Depression

Excitation

Ataxia

Tremors

Seizures

Coma

167
Q

What is the main clinical sign associated with Ivermectin?

A

CNS depression

169
Q

What is the most common conjugation reaction?

A

Glucuronic acid

171
Q

What protein do basic drugs tend to bing to?

A

Acid alpha1-glycoproteins

Lipoproteins

172
Q

MOA of PP?

A

Delay closure of sodium ion channels in the axonal membrane of the insect

May inhibit ATPase

Type 2 pyrethroids have a greater effect on sodium channels and interfere with GABA at high concentrations

173
Q

What is the best way to enhance excretion of Nicotine?

A

IV fluids

Acidification of the urine

174
Q

What are the highly perfused tissues?

A

Brain

Liver

Kidney

Endocrine glands

176
Q

What is the prognosis of chlorinated hydrocarbon toxicity?

A

Guarded to good depending on dose and early detoxification

177
Q

When diagnosing DEET, what level is considered diagnostic?

A

20ppm

178
Q

How do you treat CM toxicity?

A

Atropine just like for OPs

179
Q

What lab changes will you see with Cholecalciferol?

A

Hypercalcemia, hyperphosphatemia

Elevated calcidiol and calcitriol

Decreased PTH

180
Q

What is the prognosis of DEET?

A

If sublethal exposure, usually respond in 24-72 hours

181
Q

Which organophosphate has more significant tissue accumulation?

A

Dichlorvos because it is more lipophilic

181
Q

What are the synthetic pyrethrins?

A

First generation (type 1) do not contain an alpha-cyano moiety

Second generation (type 2) do contain the alpha-cyano moeity which increases their insecticidal potency

182
Q

What type of exposure is most common with PP?

A

Dermal

Ingestion and inhalation are possible too

183
Q

What clinical signs will you see later on after Nicotine exposure?

A

CNS depression

Tachycardia

Paralysis of respiratory muscles causing death

184
Q

ARs: What treatment should be done for very recent exposure and normal coag panel?

A

Decontamination (emesis, activated charcoal)

Start Vitamin K to be safe

185
Q

What drug is used to treat muscle tremors caused by PP toxicity?

A

Methocarbamol

187
Q

What drug is contraindicated with Carbaryl poisoning (CM)?

A

2-PAM

Can potentially increase the carbamylation process

188
Q

Which species is deficient in sulfate conjugating enzymes?

A

Pigs

190
Q

What effect does grapefruit have on enzymes?

A

Inhibitor

192
Q

What is the lowest dose which produces toic alterations and administering 2x this dose will NOT cause death called?

A

Toxic Dose LOW (TDL)

193
Q

Clicker question:

Which of the following is not one of the vitamin K dependent factors?

A. II

B. VI

C. IX

D. X

A

B. VI

194
Q

How long will ARs persist in the environment?

A

Weeks to months

196
Q

Which species has low levels of drug metabolizing enzymes?

A

Fish

197
Q

What is used to treat seizures/tremors due to Bromethalin?

A

Diazepam, phenobarbital

198
Q

What electrolytes are lost because of Cholecalciferol?

A

Sodium and potassium

199
Q

What happens when Rotenone comes into contact with nerve axons?

A

Anesthetic effect

201
Q

What is the most common clinical sign associated with Amitraz?

A

Sedation lasting 24-72 hours

202
Q

With ARs, what species can be poisoned by relay toxicosis?

A

Swine, dogs, and cats

203
Q

Which has a faster onset and shorter duration of action? OPs or Carmabates

A

Carbamates

204
Q

What % hydrogen peroxide should be used to induce emesis?

A

3%

206
Q

T/F: Pyrethrins bind more strongly at lower temperatures

A

True

207
Q

Dose for an extremely toxic substance?

A

≤ 1mg/kg

208
Q

Chemical composition of metabolite conjugates?

A

Inactive

Water soluble

209
Q

What is the prognosis of Ivermectin?

A

Depends on exposure and ability to pay for care

Generally no long-term sequelae if they survive

210
Q

What are the most commonly used diuretics?

A

mannitol

Furosemide

211
Q

What type of toxic dose: The dose which produces toxic alterations and administering twice this dose will result in death

A

Toxic high dose (THD)

212
Q

Clicker question:

What is the MOA of the organochlorine toxicants?

A. Alteration of neuronal sodium channels

B. Increased release of GABA

C. Reversible inhibition of AChE

D. Acute cerebral edema

A

A. Alteration of neuronal sodium channels

213
Q

What is it called when OPs that require desulfuration are activated by liver metabolism?

A

Lethal synthesis

Less toxic to youn patients

More toxic if enzyme inducers are present

214
Q

What organ metabolizes Cholecalciferol to calcidiol?

A

Liver

215
Q

How is Bromethalin excreted?

A

Mainly in bile

Small amount in urine

216
Q

What is the prognosis of AR?

A

Generally treatable depending on where hemorrhage has occurred

218
Q

What is the prognosis of Amitraz?

A

Pretty good

219
Q

The RBCs of what species are more susceptible to oxidative injury?

A

Cats

220
Q

T/F: Bromethalin is effective against warfarin-resistant rodents

A

True

221
Q

What trype of enzymes can enzyme inducers induce?

A

Microsomal

222
Q

What is the dose which produces toxic alterations and administering 2x this dose WILL cause death called?

A

Toxic Dose HIGH (TDH)

223
Q

What drugs should be avoided in the treatment of OP?

A

Phenothiazines

Aminoglycosides

muscle relaxants

Drugs that depress respiration (opioids)

225
Q

What are the predominant clinical signs of Rotenone?

A

Depression and convulsions

227
Q

What type of toxicity: The effect of exposure drom 30 days to 90 days

A

Subchronic toxicity

228
Q

What precipitate should be used to treat oxalate poisoning?

A

Calcium

228
Q

Which of the following blood products would you use for a hemorrhaging AR patient?

A. Fresh frozen plasma

B. Frozen plasma

C. Fresh whole blood

D. Stored whole blood

E. Cryoprecipitate

F. Platelet-rich plasma

A

A,C,E

229
Q

What is “storage activation” and which organophosphates are subject to it?

A

If sealed and stored 1-2 years, it is more toxic

Parathion

Malathion

Diazinon

Coumaphos

230
Q

MOA of Caholecalciferol?

A

Causes hypercalcemia and hyperphosphatemia

Increased GI absorption and decreased renal excretion of Ca2+

231
Q

How long after exposure to OP does OP induced delayed polyneuropathy occur?

A

10-14 days

232
Q

What should be avoided when treating DEET?

A

Magnesium cathartics (may cause CNS depression)

233
Q

MOA of CMs?

A

Reversible inhibition of AChE

AChE can hydrolyze CMs but at a slower rate than ACh (~15-30 minutes compared to ~150 microseconds

234
Q

When Parathion undergoes biotransformation, what happens?

A

Nontoxic drug -> toxic metabolite (Paroxon)

235
Q

Toxicity level of D-Limonene in cats at 15x recommended dose?

A

Severe toxicity lasting for 5 hours

237
Q

Clicker question:

If you wanted to use Ivomec® extra-label and you know that toxicity can be seen at doses as low as 300mcg for a 1kg kitten, how many milliliters of undiluted (1%) Ivomec® would that be?

A. 0.003mL

B. 0.03mL

C. 0.3mL

D. 3mL

A

B. 0.03mL

238
Q

In fish and insects, Rotenone is converted to what type of metabolite?

A

Highly toxic metabolites

239
Q

Which organophosphates have no acetylcholinesterase activity and must be desulfurated before they become active?

A

Bromophos

Diazinon

Fenthion

Parathion

240
Q

What is the only fluid that you do not freeze for sample collection?

A

Whole blood - refrigerate it!!!

241
Q

When Aspirin undergoes biotransformation, what happens?

A

Active drug -> active metabolite (Salicylic acid)

243
Q

What drugs should be avoided when treating Nicotine toxicity?

A

Antacids (which would increase absorption and reduce excretion)

244
Q

T/F: As a result of bioinactivation, most drugs are bioinactivated or detoxified

A

True

245
Q

What species is deficient in hydroxylation and dealkylation?

A

Cats

245
Q

What tissue acts as a “sink” for chlorinated hydrocarbons?

A

Fat

Half-life can be weeks to months

Weight loss can disrupt equilibrium

247
Q

1ppm = what mg/kg?

A

1mg/kg

248
Q

T/F: Inhalation of Rotenone is more toxic than ingestion

A

True

250
Q

How long does it take for ARs to reach peak blood level?

A

6-12 hours

251
Q

What do you do to treat Cholecalciferol?

A

Treat the hypercalcemia

252
Q

Is there a specific antidote for Amitraz?

A

Yes

Atipamezole (better) or Yohimbine

253
Q

How is Cholecalciferol excreted from the body?

A

Mainly in bile/feces

254
Q

MOA of ARs?

A

Inhibit vitamin K epoxide reductase

Reduces vitamin K precursors

Second-generation are more potent than first-generation

255
Q

Clicker question:

Which of the following tests is most appropriate for follow-up monitoring of a patient who has been treated for AR toxicosis?

A. PIVKA

B. PT

C. PTT

D. ACT

A

B. PT

257
Q

What factors can enhance AR toxicity?

A

Vitamin K deficiency

Liver disease

Enzyme inhibitors (cimetidine)

Trauma, surgery

258
Q

T/F: Nicotine stimulates the CRTZ

A

True

259
Q

How long does it take for clinical signs of Cholecalciferol to appear?

A

24-36 hours

261
Q

ARs: What treatment should be done when there are clinical signs, bleeding, but PCV > 15-20% and stable?

A

Vitamin K

Clotting factors (FFP, cryoprecipitate)

Consider giving RBCs (fresh whole blood)

262
Q

How long should you treat a patient with Brodifacoum poisoning?

A

4 weeks

263
Q

Which of the coagulation parameters is the first to be affected by ARs?

A
  1. PIVKA
  2. PT
  3. PTT (when 70% gone)
  4. ACT (when 95% gone)
264
Q

How much more sensitive are insect sodium channels than mammalian ones?

A

1000x

265
Q

Dose for a highly toxic substance?

A

1-50mg/kg

266
Q

Administration of sodium bicarbonate will enhance the excretion of what drugs?

A

Weak acids

Ex: NSAIDs, phenobarbital

267
Q

How long does it take for subacute clinical signs to set in (more common)?

A

2-3 days, progress over 1-2 weeks

CNS depression

268
Q

What is it important to monitor when treating PP toxicity?

A

Temperature

Hypothermia can prolong clinical signs

269
Q

What drug is commonly trapped by the thyroid gland?

A

Iodine

270
Q

What makes up phase 1 of metabolic reactions?

A

Oxidation

Reduction

Hydrolysis

271
Q

T/F: Ipecac increases the effectiveness of activated charcoal?

A

False

Decreases the effectiveness

272
Q

What is the prognosis of PP toxicity?

A

Generally very good

273
Q

Clicker question:

Which of the following findings would make you the least worried about the risk of renal failure?

A. Hematuria

B. Hemoglobinuria

C. Myoglobinuria

A

A. Hematuria

274
Q

What are other possible DDx of Amitraz?

A

CNS depressants

Ethanol

Ivermectin

Ethylene glycol

Marijuana

275
Q

What is the elimination half-life of Ivermectin?

A

~2 days

276
Q

When I say Anticoagulant Rodenticides, you say…

A

Bleeding

277
Q

Dose for a practically nontoxic substance?

A

> 5-15g/kg

278
Q

What species is resistant to Bromethalin and why?

A

Guinea pigs because they lack the correct metabolic enzymes

279
Q

How long after dermal exposure to D-Limonene does it take to reach maximal blood concentration?

A

10 minutes

280
Q

What drug has a strong affinity to calcium in skeletal tissues?

A

Tetracycline

281
Q

Administration of ammonium chloride or methionine enhance the excretion of what drugs?

A

Weak bases

Ex: alkaloids, amphetamines

282
Q

T/F: CNS stimulants may increase the toxicity of DEET

A

False

CNS depressants

283
Q

What clinical signs are associated with nicotinic stimulation from OP poisoning?

A

Muscle fasciculation

Tremors

Twitching

Spasm

Hypertonicity

Stiff gait

284
Q

ARs: What treatment should be done when there are no clinical signs but prolonged coags?

A

Vitamin K

Consider giving clotting factors (FFP, cryoprecipitate)

285
Q

What does Nicotine mimic at low doses?

A

ACh

Tox (5 decks)

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