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Toxicology > Insecticides > Flashcards

Insecticides Flashcards

1
Q

When was the first organophosphate synthesized?

A

1854

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2
Q

What was one of the earliest OP insecticides?

A

Parathion

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3
Q

More toxic versions of parathion were developed when?

A

During WWII

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4
Q

Thousands of organophosphates have been synthesized in an attempt to do what?

A

Find species-selective compounds to reduce mammalian toxicity.

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5
Q

T/F: There are several types of organophosphates.

A

True

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6
Q

Name 3 organophosphates that have direct Acetylcholinesterase activity?

A
  • Dichlorvos
  • Monocrotophos
  • Trichlorfon
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7
Q

Name 4 organophosphates that must be desulfurated before they become active.

A
  • Bromophos
  • Diazinon
  • Fenthion
  • Parathion
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8
Q

What is the average amount of time organophosphates persist in the environment?

A

2-4 weeks

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9
Q

Name 4 organophosphates that are subject to “storage activation”.

A
  • Parathion
  • Malathion
  • Diazinon
  • Coumaphos
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10
Q

What is storage activation?

A

If sealed & stored 1-2 years, becomes more toxic.

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11
Q

What “grade” of organophosphate is more toxic?

What are 2 reasons why?

A
  • Technical grade.

- Heat isomeration, impurities

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12
Q

Which is more likely to be readily absorbed from the GIT, skin and mucous membranes or by inhalation: a toxin that is lipophilic or hydrophilic?

A

Lipophilic

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13
Q

What is the most common type of exposure for organophosphates?

A

Oral exposure (contaminated feeds)

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14
Q

What are 3 possible routes of exposure for organophosphates?

A
  • Oral (contaminated feed)
  • Dermal (dip/spray)
  • Inhaled (recent aerial spray)
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15
Q

Are organophosphates well distributed throughout the body?

A

Yes

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16
Q

Can organophosphates affect the CNS?

A

Yes

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17
Q

Is there significant tissue accumulation with organophosphates?

A

No

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18
Q

What is an example of an organophosphate that is more lipophilic than average, meaning it can sequester more in fat and stay in the body longer?

A

Dichlorvos

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19
Q

Where are organophosphates metabolized?

A

Liver

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20
Q

Toxins that require desulfuration are activated by liver metabolism in a process known as what?

A

“Lethal synthesis”

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21
Q

Is “lethal synthesis” less toxic in young or old patients?

Why?

A
  • Young

- Liver metabolism is not completely developed in the young.

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22
Q

Organophosphates that require desulfuration by the liver to be activated are made more toxic if what are present?
What is an example of one?

A
  • Enzyme inducers

- Phenobarbital

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23
Q

Continued exposure to organophosphates can lead to what?

What are 3 reasons for this?

A
  • Tolerance
  • Enzyme induction, functional adaptation to decreased esterases, adaptation of ACh receptors to excessive amounts of ACh
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24
Q

Adaptation of ACh receptors to excessive amounts of ACh is known as what?

A

Receptor down-regulation

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25
Q

What is the mechanism of action for organophosphates?

A

Irreversible inhibition of cholinesterases

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26
Q

Do organophosphates increase or decrease ACh at all cholinergic sties?

A

Increase

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27
Q

Which receptors do organophosphates stimulate first?

A

Muscarinic receptors

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28
Q

Which receptors do organophosphates stimulate second?

A

Nicotinic receptors

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29
Q

What is the last receptor effect that organophosphates have?

A

Nicotinic blockade

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30
Q

What happens in a nicotinic blockade?

A

Eventually depolarizes to the point it can’t repolarize.

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31
Q

What is the cause of death with high exposure to organophosphates?

A

Respiratory failure/paralysis

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32
Q

What is another name for the delayed neurotoxicity possible with organophosphates?

A

OP induced delayed polyneuropathy

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33
Q

How quick is the onset of clinical signs seen with acute organophosphate toxicity?

A

15 mins - 1 hr

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34
Q

What is the initial clinical sign seen with organophosphate toxicity?

A

Muscarinic stimulation

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35
Q

Muscarinic stimulation can cause DUMBBELLS, which stands for what?

A 
D - diarrhea 
U - urination 
M - myosis 
B - bronchoconstriction 
B - bradycardia 
E - emesis 
L - lacrimation 
S - salivation
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36
Q

Muscle fasciculation, tremors, twitching, spasm, hypertonicity and stiff gait can be seen with the stimulation of what kind of receptors by organophosphates?

A

Nicotinic receptors

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37
Q

Anxiety, restlessness, hyperactivity, may proceed to tonic-clonic seizures when what is stimulated?

A

CNS

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38
Q

Paralysis, CNS depression, coma, dyspnea and death due to respiratory failure can be cause by what type of blockade?

A

Nicotinic blockade

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39
Q

What can be seen with massive (malicious) doses of organophosphates?

A

OP induced intermediate syndrome

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40
Q

T/F: No muscarinic signs or muscle fasciculations are seen with OP induced intermediate syndrome.

A

True

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41
Q

What type of exposure can lead to OP induced intermediate syndrome?

A

Chronic exposure

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42
Q

What can occur if acute poisoning with an organophosphate happens?

A

OP induced delayed polyneuropathy

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43
Q

What are 3 signs of OP induced delayed polyneuropathy?

A
  • Muscle weakness
  • Ataxia
  • Rear limb paralysis
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44
Q

How long does it take after exposure for OP induced delayed polyneuropathy to develop?

A

10-14 days

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45
Q

Distal degeneration of long/large diameter motor and sensory axons of peripheral nerves and spinal cord can occur with what?

A

OP induced delayed polyneuropathy

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46
Q

What species is most sensitive to OP induced delayed polyneuropathy?

A

Chickens

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47
Q

Are there any specific lesions with acute death associated with organophosphates?

A

No

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48
Q

Dogs exposed to more lipophilic organophosphates can have what condition develop?

A

Pancreatitis

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49
Q

How are organophosphates diagnosed?

A

Direct detection

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50
Q

Residues of which organophosphate may be seen in samples from fat or liver tissue?

A

Chlorpyrifos

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51
Q

What is something that can be tested antemortem to detect organophosphate toxicity?

A

Acetylcholinesterase activity level

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52
Q

How soon does a sample for organophosphate toxicity need to be assessed?

A

ASAP to preserve activity.

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53
Q

Less than what percentage of acetylcholinesterase activity is considered suspicious in suspected OP toxicity?
What percentage is considered diagnostic?

A

-

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54
Q

What are 3 things to be considered for clinical diagnosis of OPs?

A
  • History of exposure
  • Clinical signs
  • Lab testing
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55
Q

If a strong response to a low dose (0.02mg/kg) of this drug is seen, then it is less likely to be OP toxicity.

A

Atropine

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56
Q

Should emesis be induced with OP toxicity?

A

Only if recent. Not if depressed or seizures.

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57
Q

What can be done with dermal exposure to OPs?

A

Wash gently with tepid, soapy water.

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58
Q

Can activated charcoal be used for OPs?

A

Yes

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59
Q

What are 4 things that should be avoided with OP toxicity?

A
  • Phenothiazines
  • Aminoglycosides
  • Muscle relaxants
  • Drugs that depress respiration (opioids)
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60
Q

What drug can be used to treat OP toxicity?
What is the MOA?
Doses?

A
  • Atropine
  • Specific physiologic antagonist
  • SA/horses: 0.2 mg/kg
    Food/LA: 0.5mg/kg
    Give 1/4 dose IV then rest IM or SC, repeat 3-6 hr based on clinical response.
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61
Q

What is the most effective treatment of OP toxicity in acute cases?
Dose?

A
  • 2-PAM (Pralidoxime, Protopam)

- 25-50 mg/kg 10% solution slow IV

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62
Q

Is 2-PAM effective against all OPs?

A

No

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63
Q

2-PAM may not be effective if what has occurred?

A

Aging

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64
Q

What is “aging”?

A

OP bound for a long time, changes chemically so that 2-PAM can no longer pull it off.

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65
Q

What is the main form of treatment with OP intermediate syndrome?

A

Supportive care

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66
Q

Is atropine more or less effective with OP intermediate syndrome compared to acute toxicity?

A

Less effective

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67
Q

With OP intermediate syndrome, 2-PAM should be reserved for what type of cases?

A

Severe cases

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68
Q

What is the treatment for OP induced delayed polyneuropathy?

A

Symptomatic therapy

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69
Q

Prognosis for OP toxicity is better if patient is what?

A

Alive

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70
Q

What are 2 determiners of prognosis for OP toxicity?

A
  • Dose

- How long since exposure

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71
Q

Mild to moderate signs with OP toxicity are generally what?

A

Treatable

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72
Q

Acute cases of OP toxicity that respond to treatment can recover within what time frame?

A

24 hours

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73
Q

What is an example of a carbamate?

A

Carbaryl (Sevin)

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74
Q

What is something that carbamates do not undergo that OPs do?

A

Storage activation

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75
Q

Do carbamates require hepatic bioactivation?

A

No

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76
Q

Which has a faster onset: OPs or carbamates?

Shorter duration of action?

A
  • Carbamates

- Carbamates

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77
Q

T/F: A low exposure to carbamates may recover without treatment.

A

True

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78
Q

Are carbamates metabolized slowly or rapidly?

A

Very rapidly

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79
Q

What is the MOA of carbamates?

A

Reversible inhibition of acetylcholinesterase

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80
Q

What can be tested in the lab when looking for carbamate toxicity?

A

Cholinesterase levels

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81
Q

What can happen if a sample for carbamate testing is not tested fast enough?

A

False negative due to reversible binding.

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82
Q

What drug is used to treat carbamates?

A

Atropine

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83
Q

Is 2-PAM a good choice for carbamates?

Why?

A
  • No

- Reversible binding reduces benefit.

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84
Q

Which carbamate is 2-PAM contraindicated with?

Why?

A
  • Carbaryl (Sevin)

- Can potentially increase carbamylation process.

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85
Q

What happens with a high dose exposure of carbamates?

A

Animal dies too quickly for treatment.

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86
Q

What happens with a low dose exposure of carbamates?

A

Animal may survive without treatment if signs are not severe.

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87
Q

What type of insecticide are Diphenyl aliphatics (DDT, methoxychlor?

A

Chlorinated hydrocarbon (Organochlorine)

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88
Q

What type of insecticide are aryl hydrocarbons (Lindane)?

A

Chlorinated hydrocarbon (Organochlorine)

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89
Q

What type of insecticide are cyclodienes (Aldrin, Toxaphene)?

A

Chlorinated hydrocarbon (Organochlorine)

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90
Q

What insecticide was banned in the USA in 2003?

A

Methoxychlor

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91
Q

Are chlorinated hydrocarbons lipophilic or hydrophilic?

A

Highly lipophilic

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92
Q

Are chlorinated hydrocarbons soluble in water?

A

No

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93
Q

The lipophilic nature of chlorinated hydrocarbons leads to what?

A

Bio-accumulation in the food chain.

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94
Q

What is the soil half-life of chlorinated hydrocarbons?

A

2-15 years

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95
Q

Which can survive longer in the environment: organophosphates or chlorinated hydrocarbons?

A

Chlorinated hydrocarbons

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96
Q

Which species is more sensitive to chlorinated hydrocarbons: dogs or cats?

A

Cats

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97
Q

Do chlorinated hydrocarbons generally have a low or high toxicity to mammals?

A

Low

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98
Q

Which animals are susceptible to chlorinated hydrocarbons?

A

All animals

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99
Q

Are chlorinated hydrocarbons readily absorbed?

A

Yes - highly lipophilic

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100
Q

Do chlorinated hydrocarbons cross into the CNS?

A

Yes

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101
Q

T/F: Chlorinated hydrocarbons undergo metabolism by liver microsomal enzymes.

A

True

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102
Q

Do the metabolites of chlorinated hydrocarbons undergo enterohepatic recycling?

A

Yes

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103
Q

What are 4 ways the metabolites of chlorinated hydrocarbons can be excreted from the body?

A
  • Milk
  • Feces
  • Urine
  • Bile
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104
Q

What is the half-life of chlorinated hydrocarbons?

A

Weeks to months

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105
Q

What can disrupt equilibrium and allow a large amount of chlorinated hydrocarbon metabolites to be released into the blood stream?

A

Weight loss

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106
Q

What is the main clinical sign for chlorinated hydrocarbon toxicity?

A

CNS stimulation

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107
Q

Some mammals can show what instead of typical CNS excitability with chlorinated hydrocarbon toxicity?

A

Intermittent or persistent depression

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108
Q

Which species may show depression, abnormal postures, apparent blindness and death with chlorinated hydrocarbon toxicity?

A

Birds

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109
Q

Which species can have seizures as a result of chlorinated hydrocarbon toxicity?

A

Cattle

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110
Q

Are there any specific pathological lesions for chlorinated hydrocarbons?

A

No

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111
Q

Acute chlorinated hydrocarbon toxicity can be confirmed if insecticide is in what 3 types of samples at significant concentrations?

A
  • Blood
  • Liver
  • Brain
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112
Q

A diagnosis of chlorinated hydrocarbon toxicity is made with what 4 factors?

A
  • History of exposure
  • Clinical signs
  • Lack of specific lesions
  • Chemical analysis of tissues
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113
Q

Compared to cholinesterases, chlorinated hydrocarbon toxicity has less or more parasympathetic signs?
CNS stimulation?

A
  • Less parasympathetic signs

- More severe CNS stimulation (convulsive seizures)

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114
Q

Is there any specific antidote for chlorinated hydrocarbon toxicity?

A

No

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115
Q

What are 3 forms of decontamination that can be used with chlorinated hydrocarbons?

A
  • Induce emesis (if indicated)
  • Wash soap/water if dermal exposure
  • Activated charcoal (better) or mineral oil
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116
Q

What 2 drugs can be given to help control seizures caused by chlorinated hydrocarbon toxicity?

A

Diazepam or barbiturates

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117
Q

What are 3 types of symptomatic treatment that can be given with chlorinated hydrocarbon toxicity?

A
  • Oxygen
  • Ventilation
  • Fluids
118
Q

What is the prognosis for chlorinated hydrocarbon toxicity?

What are 2 factors this depends on?

A
  • Guarded to good

- Dose, early detoxification

119
Q

What toxin can lead to embryo toxicity and eggshell thinning in raptors?

A

Chlorinated hydrocarbons

120
Q

What toxin can by toxic to aquatic wildlife and some amphibians?

A

Chlorinated hydrocarbons

121
Q

What is an example of a pyrethrum flower from which pyrethrins can be extracted?

A

Crysanthemum cinerariaefolium

122
Q

What are synthetic analogs of pyrethrins known as?

A

Pyrethroids

123
Q

Which type of toxin is unstable in air and light which both cause it to break down quickly?

A

Pyrethrins/Pyrethroids

124
Q

What are 6 examples of natural pyrethrins?

A
  • Pyrethrin I & II
  • Cinerin I & II
  • Jasmolin I & II
125
Q

What are 2 types of synthetic pyrethrins?

A
  • First generation/Type 1

- Second generation/Type 2

126
Q

What do second generation/Type 2 synthetic pyrethrins contain that first generation/Type 1 do not?
What does this do?

A
  • Alpha-cyano moiety

- Increases their insecticidal potency

127
Q

Is the overall toxicity low or high in mammals?

A

Low

128
Q

What two forms of toxicity are not found with pyrethrins/pyrethroids?
Which one is?

A
  • Subacute or chronic

- Acute

129
Q

What two species are pyrethrins/pyrethroids very toxic in?

A
  • Fish

- Some birds

130
Q

Are cats more or less sensitive than dogs to pyrethrins/pyrethroids?

A

More

131
Q

Are pyrethrins/pyrethroids lipid soluble?

A

Yes

132
Q

What is the most common type of exposure seen with pyrethrins/pyrethroids?
What are 2 other possible forms of exposure?

A
  • Dermal

- Ingestion & inhalation

133
Q

Where are 3 locations pyrethrins/pyrethroids can be rapidly metabolized?

A
  • GIT
  • Plasma
  • Liver
134
Q

How are conjugated metabolites of pyrethrins/pyrethroids excreted?

A

Urine

135
Q

The presence of alpha-cyano moiety (Type 2) decreases the rate of what?

A

Hydrolysis

136
Q

Do pyrethrins/pyrethroids accumulate in tissues?

A

No

137
Q

What can be added to pyrethrins/pyrethroids that acts as a synergist?
What does it do?

A
  • Piperonyl butoxide or MGK-264

- Inhibits pyrethrin metabolism by insects

138
Q

Generalized muscle tremors, depression, blindness (reversible) and ataxia are clinical signs that can be seen with which category of toxin?

A

Pyrethrins/pyrethroids

139
Q

With pyrethrin/pyrethroid toxicity, some dogs can show what which may occur as a topical hypersensitivity reaction or firing of sensory peripheral nerves?

A

“Acute paralysis” which is actually paresthesia (abnormal sensation of prickling, itching)

140
Q

Are there any specific pathological lesions seen with pyrethrins/pyrethroids?

A

No

141
Q

Are pyrethrins/pyrethroids easy or difficult to detect in tissue samples?

A

Difficult

142
Q

T/F: Tissue levels of pyrethrins/pyrethroids correlate well with severity of clinical signs.

A

False - Tissue levels do not correlate well with severity of clinical signs.

143
Q

What 3 factors are used to make a diagnosis of pyrethrin/pyrethroid toxicity?

A
  • History of exposure
  • Appropriate clinical signs
  • Ruling out other causes
144
Q

Is there any specific antidote for pyrethrin/pyrethroid toxicity?

A

No

145
Q

For which category of toxin is activated charcoal generally not used?

A

Pyrethrins/pyrethroids

146
Q

It is important to monitor and control what with pyrethrin/pyrethroid toxicity?

A

Temperature (hypothermia)

147
Q

With pyrethrin/pyrethroid toxicity that has very mild signs, what is the treatment?

A

Decontamination

148
Q

If there are severe muscle tremors seen with pyrethroid/pyrethrin toxicity, what can be given for treatment?

A

Methocarbamol

149
Q

What are 3 drugs that can be given for seizures seen with pyrethrin/pyrethroid toxicity?

A
  • Diazepam
  • Barbiturates
  • Propofol CRI
150
Q

What is the prognosis for pyrethrin/pyrethroid toxicity?

A

Generally very good

151
Q

What is one of the oldest botanical insecticides?

A

Rotenone

152
Q

What is a common use of rotenone in pets?

A

Treatment of lice, ticks, mites

153
Q

Rotenone is very toxic to what 2 species?

A
  • Fish

- Cold-blooded animals

154
Q

Which mammal species is more sensitive to rotenone?

A

Pigs

155
Q

Which is more toxic with rotenone: inhalation or ingestion?

A

Inhalation

156
Q

Low and incomplete absorption of rotenone is seen where in the body?

A

GIT

157
Q

Do fats/oils increase or decrease the absorption of rotenone?

A

Increase

158
Q

Which formulation of rotenone is highly toxic relative to other formulations?

A

Emulsified concentrate

159
Q

What is rotenone converted to in fish/insects?

In mammals?

A
  • Toxic metabolites

- Non-toxic metabolites

160
Q

How long does it take for rotenone to be eliminated?

In what form?

A
  • 24 hours

- Feces

161
Q

Which toxin is an irritant that can cause local irritation such as conjunctivitis, congestion, dermatitis, GI upset if ingested?

A

Rotenone

162
Q

What are the 2 predominate clinical signs seen with rotenone?

A
  • Depression

- Convulsions

163
Q

What are 3 things that can be seen antemortem with lab testing for rotenone toxicity?

A
  • Hypoglycemia
  • Liver changes
  • Hypoxemia/hypercapnea
164
Q

Diagnosis of rotenone toxicity is based on what?

A

History and documentation of compound

165
Q

Are there any specific treatments for rotenone toxicity?

A

No

166
Q

What are 2 things that can be done for rotenone toxicity?

A
  • Detoxification

- Supportive care

167
Q

What is the prognosis for rotenone toxicity in mammals?

In fish/reptiles?

A
  • Generally good

- Poor

168
Q

What is the main source of D-Limonene?

A

OTC products for control of lice, fleas ticks (usually shampoos)

169
Q

What are 3 things D-Limonene can be combined with?

A
  • Other essential oils
  • Piperonyl butoxide
  • Enzyme inhibitors
170
Q

D-Limonene is toxic to the flea at which life stages?

A

All life stages

171
Q

Which species is more sensitive to D-Limonene: dogs or cats?

A

Cats

172
Q

What is seen in cats with D-Limonene toxicity at:
5x recommended dose?
15x recommended dose?

A
  • Mild toxicity

- Severe signs lasting 5 hours

173
Q

Is D-Limonene lipid soluble?

A

Yes

174
Q

D-Limonene can reach maximal blood concentration how long after dermal exposure?

A

10 mins

175
Q

Does D-Limonene have wide distribution in the body?

A

Yes

176
Q

Where is D-Limonene metabolized?

Excreted?

A
  • Liver

- Urine

177
Q

What is a patient with D-Limonene toxicity said to smell like?

A

Lemons

178
Q

Are there any specific pathological lesions for D-Limonene toxicity?

A

No

179
Q

Is there any specific lab testing available for D-Limonene toxicity?

A

No

180
Q

What 2 things are D-Limonene toxicity based on?

A
  • Exposure history

- Scent of patient

181
Q

What are 3 forms of treatment for D-Limonene toxicity?

A
  • Decontamination
  • Monitor temperature (iatrogenic hypothermia)
  • Supportive care (fluids, etc.)
182
Q

What is the prognosis for sub-lethal D-Limonene toxicity?

A

Excellent

183
Q

Sub-lethal D-Limonene toxicity usually resolves in what time frame?

A

6-12 hrs

184
Q

Prognosis for D-Limonene toxicity is worse if there is what?

A

Skin reactions

185
Q

What is one of the most common essential oils encountered?

What is it used for?

A
  • Melaleuca oil (tea tree oil)

- Topically for flea control

186
Q

Parts of the plant from which nicotine is derived are teratogenic to what 2 species?

A
  • Sows

- Cattle

187
Q

T/F: Nicotine is highly toxic to dogs.

A

True

188
Q

What is the oral LD50 of nicotine in dogs?

At what dose can clinical signs be seen?

A
  • 9.2 mg/kg

- 1 mg/kg

189
Q

What other ingredient might nicotine gum contain that is also toxic to dogs (but not humans or cats)?

A

Xylitol

190
Q

Nicotine is absorbed well through what 2 routes of administration?

A
  • Inhalation

- Intact skin

191
Q

Through what route of administration is nicotine poorly absorbed?

A

Ingestion

192
Q

What would increase absorption of nicotine in the stomach?

What do you not give a dog with GI signs?

A
  • Alkalinization of the stomach.

- Antacids

193
Q

Where is nicotine metabolized?

Excreted?

A
  • Liver

- Bile & urine

194
Q

Which route of excretion is decreased with an alkaline pH?

Why?

A
  • Renal excretion

- Increases reabsorption

195
Q

What clinical sign is seen in 25% of nicotine toxicity cases?

A

Ataxia

196
Q

What clinical sign can be seen within 1 hour or exposure to nicotine?

A

Tremors

197
Q

What are 3 clinical signs that can be seen with higher doses?

A
  • CNS depression
  • Tachycardia
  • Vasodilation
198
Q

Is the clinical course of nicotine toxicity slow or rapid?

A

Rapid (mins to hours)

199
Q

A patient that smells like an old cigar might have what type of toxicity?

A

Nicotine

200
Q

What are 5 areas that can be tested for nicotine?

A
  • Urine
  • Stomach contents
  • Kidney
  • Liver
  • Blood
201
Q

Nicotine at low doses may resemble what?

Higher doses/later stages?

A
  • Cholinesterase inhibitors ( OP/Carbamate

- CNS depressants

202
Q

What are 2 forms of decontamination that can be used with nicotine toxicity?

A
  • Induce emesis

- Activated charcoal

203
Q

What should be avoided in treatment of nicotine toxicity?

A

Antacids

204
Q

What are 2 ways to enhance the excretion of nicotine?

A
  • IV fluids

- Acidification of urine

205
Q

What can be given to treat parasympathetic effects seen with nicotine toxicity?

A

Atropine

206
Q

This is a foramidine insecticide/acaracide (ticks/mites).

A

Amitraz

207
Q

How does Amitraz work on ticks/mites?

A

Paralyzes the mouth parts.

208
Q

Where can amitraz be found?

A

Flea/tick collars

209
Q

What is amitraz used for in swine and cattle?

A

Miticide/insecticide

210
Q

Amitraz is not labeled for use in what 2 species?

A
  • Cats

- Horses

211
Q

This toxin is a mild irritant and concentrates are flammable.

A

Amitraz

212
Q

What is the acute oral LD50 of amitraz for dogs?

A

250 mg/kg

213
Q

What type of signs can be seen in dogs with 20 mg/kg of amitraz?

A

Mild signs/sedation

214
Q

What are 2 drugs that can increase the toxicity of amitraz?

A
  • Meperidine (Demerol)

- Sympathomimetic amines

215
Q

What are 4 things that can increase the toxicity of amitraz?

A
  • Stress
  • Debilitation
  • Advanced age
  • Toy breeds
216
Q

Amitraz is readily absorbed by what route?

What are 2 other routes it can be absorbed through?

A
  • Oral

- Inhalation, Skin

217
Q

Peak plasma concentrations of Amitraz can be seen when?

Elimination half-life?

A
  • After 5 hours

- 24 hours

218
Q

Is amitraz well distributed throughout the body?

A

Yes

219
Q

Where is amitraz rapidly metabolized?

Excreted?

A
  • Liver

- Urine

220
Q

What is the most common clinical sign seen with amitraz?

How long is it seen?

A
  • Transient sedation

- 24-72 hours

221
Q

What can be seen with amitraz toxicity due to alpha-2 inhibition of insulin?

A

Hyperglycemia

222
Q

Are there any specific pathological lesions for amitraz?

A

No

223
Q

Can tissue be analyzed for amitraz?

A

Yes

224
Q

What are 3 factors for diagnosing amitraz toxicity?

A
  • History
  • Clinical signs
  • Specific analysis
225
Q

What is the most significant differential diagnosis for amitraz toxicity?

A

CNS depressants

226
Q

What is the antidote for amitraz toxicity?

What are 2 examples?

A
  • Alpha-2 antagonists

- Yohimbine (short acting), Atipamezole ( few cardio-respiratory effects than yohimbine)

227
Q

What is the prognosis for amitraz toxicity?

A

Pretty good

228
Q

Wht is thechemical nof N,N-diethyl-m-tolumide?

A

DEET

229
Q

DEET is used for the control of what 3 things?

A
  • Mosquitoes
  • Flies
  • Ticks
230
Q

What are 2 other insecticides that DEET can be combined with?

A
  • Fenvalerate

- Pyrethroid

231
Q

The concentration of DEET can range from what to what?

What is the typical amount in pet products?

A
  • 5-100%

-

232
Q

Which toxin has a characteristc sweet odor?

A

DEET

233
Q

Which toxin may damage synthetic fibers or plastics?

A

DEET

234
Q

Which species is more sensitive to DEET, cats or dogs?

A

Cats

235
Q

Which are more sensitive to DEET, young or old animals?

A

Young

236
Q

What might increase the toxicity of DEET?

A

CNS depressants

237
Q

What pecenage of DEET is absorbed from the skin in dogs?

A

7.9-12.8%

238
Q

Where in the body can DEET accumulate and persist?

A

Skin

239
Q

Which insecticide can increase dermal absorption of others?

A

DEET

240
Q

Where is DEET metabolized?

Excreted?

A
  • Liver

- Urine

241
Q

With DEET, depression, excitiation, ataxia, tremors, seizures and coma are clinical signs in what 2 species?

A
  • Rabbits

- Rats

242
Q

With DEET, hypersalvation, vomiting, hyperexcitibility, tremors, ataxia and seizures are clinical signs that can be seen with what 2 species?

A
  • Dogs

- Cats

243
Q

Are there any specific patholgical lesions for DEET toxicity?

A

No

244
Q

What amount of DEET is considered diagnostic?

Considered supportive?

A
  • 20 ppm

- Urine > 1ppm, Tissue >10ppm

245
Q

What are 4 other CNS excitatory toxins DEET must be differentiated from?

A
  • Strychnine
  • Metaldehyde
  • Organochlorine
  • OP/carbamate
246
Q

Are there any specific antidotes for DEET toxicity?

A

No

247
Q

What are 3 forms of decontamination that can be used for DEET toxicity?

A
  • Dermal exposure: wash soap/water
  • Emesis
  • Activated charcoal +/- cathartic (avoid magnesium cathartic)
248
Q

What is the main form of treatment for DEET toxicity?

A

Symptomatic treatment

249
Q

What is the prognosis for sublethal DEET toxicity?

A

Usually respond in 24-72 hrs

250
Q

What is the most common source of naphthalene?

A

Mothballs

251
Q

Newer mothballs contain what instead of naphthalene?

A

Paradichlorobenzene

252
Q

How do you tell if you have old fashioned mothballs with naphthalene?

A

Put in water, mothballs with naphthalene will float, those with paradichlorobenzene will sink.

253
Q

What naphthalene derived from?

A

Coal tar/petroleum hydrocarbons

254
Q

What happens to naphthalene at room temp?

A

Sublimates - go from a solid directly to a gas

255
Q

Which are more sensitive to naphthalene toxicity, cats or dogs?

A

Cats

256
Q

Which are more susceptible to naphthalene toxicity, cats or dogs?

A

Dog - more likely to ingest

257
Q

What is the lowest canine lethal dose for naphthalene toxicity?

A

400 mg/kg

258
Q

How many mothballs can be toxic to a dog?

A

1 or 2

259
Q

What are 3 ways naphthalene can be absorbed?

A
  • Oral
  • Inhalation
  • Intact skin
260
Q

What are 2 things that can be caused by the oxidation products of naphthalene?

A
  • Methemoglobinemia

- Hemolysis

261
Q

What is a common clinical sign of naphthalene ingestion?

A

Mothball breath

262
Q

Which insecticide can cause heinz bodies?

A

Naphthalene

263
Q

Hepatic injury and secondary renal injury can occur with which insecticide?

A

Naphthalene

264
Q

What clinical sign can occur in neonates due to naphthalene toxicity?

A

Cataracts

265
Q

What do you need to differentiate the characteristic hematologic changes seen with naphthalene from?
What are 3 examples?

A
  • Other causes of RBC oxidative injury

- Acetaminophen, onions, nitrates

266
Q

Which species RBCs are more susceptible to oxidative injury than other species?

A

Cats

267
Q

What are 2 specific treatments for naphthalene toxicity?

Which is faster?

A
  • Ascorbicaci (20 mg/kg)
  • Methylene blue 1%
  • Methylene blue 1%
268
Q

What can be used to reduce precipitation of Hgb in the kidneys due to naphthalene toxicity?

A

Sodium bicarbonate

269
Q

What is the prognosis for naphthalene toxicity?

A

Reasonable if treated promptly

270
Q

What type of insecticide is ivermectin?

A

Macrocytic lactone

271
Q

What is ivermectin used for in dogs and cats?

A

Prevention of heartworm

272
Q

Ivermectin toxcity is usually caused by what?

A

Overdose

273
Q

What is a potential source of ivermectin exposure in dogs?

A

Horse feces

274
Q

What are 2 species susceptible to ivermectin toxicity?

A
  • dogs

- small birds

275
Q

Why are Collies more susceptible to ivermectin toxicity?

A

ABCB1/MDR1 mutation

276
Q

Ivermectin is 95% absorbable via what route?

A

Orally

277
Q

In what species is oral absorption of ivermectin lower?

A

Ruminants

278
Q

T/F: Dogs may have lower bioavailability than cats.

A

False - Cats may have lower bioavailability than dogs.

279
Q

Does ivermectin typically cross the BBB?

A

No

280
Q

How is ivermectin excreted?

A

Mainly unchanged in feces.

281
Q

What is the elimination half-life of ivermectin in dogs?

A

2 days

282
Q

Deletion/mutation of the ABCB1/MDR1 gene can result in how much of an increase in concentration of certain drugs in the CNS?

A

50x

283
Q

What as been seen with co-administation of off-label (high dose) ivermectin and comfortis (Spinosad)?

A

Neurotoxicity

284
Q

What is the main type of clinical sign seen with ivermecti toxicity?

A

CNS depression

285
Q

Are there any specific pathologic lesions seen with ivermectin toxicity?

A

No

286
Q

Do tissue levels of ivermectin correlate well to brain levels?

A

No

287
Q

Is there any specific antidote for ivermectin?

A

No

288
Q

Caution needs to be used with what types of drugs with ivermectin toxicity?

A

GABA agonists (diazepam, barbiturates, propofol)

289
Q

What does prognosis of ivermectin toxicity depend on?

A

Exposure & ability to pay for care

290
Q

T/F: Generally there are no long-term sequelae from ivermectin toxicity if the animal survives.

A

True

Toxicology (19 decks)

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