Insecticides Flashcards
1
Q
When was the first organophosphate synthesized?
A
1854
2
Q
What was one of the earliest OP insecticides?
A
Parathion
3
Q
More toxic versions of parathion were developed when?
A
During WWII
4
Q
Thousands of organophosphates have been synthesized in an attempt to do what?
A
Find species-selective compounds to reduce mammalian toxicity.
5
Q
T/F: There are several types of organophosphates.
A
True
6
Q
Name 3 organophosphates that have direct Acetylcholinesterase activity?
A
- Dichlorvos
- Monocrotophos
- Trichlorfon
7
Q
Name 4 organophosphates that must be desulfurated before they become active.
A
- Bromophos
- Diazinon
- Fenthion
- Parathion
8
Q
What is the average amount of time organophosphates persist in the environment?
A
2-4 weeks
9
Q
Name 4 organophosphates that are subject to “storage activation”.
A
- Parathion
- Malathion
- Diazinon
- Coumaphos
10
Q
What is storage activation?
A
If sealed & stored 1-2 years, becomes more toxic.
11
Q
What “grade” of organophosphate is more toxic?
What are 2 reasons why?
A
- Technical grade.
- Heat isomeration, impurities
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
13
Q
What is the most common type of exposure for organophosphates?
A
Oral exposure (contaminated feeds)
14
Q
What are 3 possible routes of exposure for organophosphates?
A
- Oral (contaminated feed)
- Dermal (dip/spray)
- Inhaled (recent aerial spray)
15
Q
Are organophosphates well distributed throughout the body?
A
Yes
16
Q
Can organophosphates affect the CNS?
A
Yes
17
Q
Is there significant tissue accumulation with organophosphates?
A
No
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
19
Q
Where are organophosphates metabolized?
A
Liver
20
Q
Toxins that require desulfuration are activated by liver metabolism in a process known as what?
A
“Lethal synthesis”
21
Q
Is “lethal synthesis” less toxic in young or old patients?
Why?
A
- Young
- Liver metabolism is not completely developed in the young.
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
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
24
Q
Adaptation of ACh receptors to excessive amounts of ACh is known as what?
A
Receptor down-regulation
25
What is the mechanism of action for organophosphates?
Irreversible inhibition of cholinesterases
26
Do organophosphates increase or decrease ACh at all cholinergic sties?
Increase
27
Which receptors do organophosphates stimulate first?
Muscarinic receptors
28
Which receptors do organophosphates stimulate second?
Nicotinic receptors
29
What is the last receptor effect that organophosphates have?
Nicotinic blockade
30
What happens in a nicotinic blockade?
Eventually depolarizes to the point it can't repolarize.
31
What is the cause of death with high exposure to organophosphates?
Respiratory failure/paralysis
32
What is another name for the delayed neurotoxicity possible with organophosphates?
OP induced delayed polyneuropathy
33
How quick is the onset of clinical signs seen with acute organophosphate toxicity?
15 mins - 1 hr
34
What is the initial clinical sign seen with organophosphate toxicity?
Muscarinic stimulation
35
Muscarinic stimulation can cause DUMBBELLS, which stands for what?
```
D - diarrhea
U - urination
M - myosis
B - bronchoconstriction
B - bradycardia
E - emesis
L - lacrimation
S - salivation
```
36
Muscle fasciculation, tremors, twitching, spasm, hypertonicity and stiff gait can be seen with the stimulation of what kind of receptors by organophosphates?
Nicotinic receptors
37
Anxiety, restlessness, hyperactivity, may proceed to tonic-clonic seizures when what is stimulated?
CNS
38
Paralysis, CNS depression, coma, dyspnea and death due to respiratory failure can be cause by what type of blockade?
Nicotinic blockade
39
What can be seen with massive (malicious) doses of organophosphates?
OP induced intermediate syndrome
40
T/F: No muscarinic signs or muscle fasciculations are seen with OP induced intermediate syndrome.
True
41
What type of exposure can lead to OP induced intermediate syndrome?
Chronic exposure
42
What can occur if acute poisoning with an organophosphate happens?
OP induced delayed polyneuropathy
43
What are 3 signs of OP induced delayed polyneuropathy?
- Muscle weakness
- Ataxia
- Rear limb paralysis
44
How long does it take after exposure for OP induced delayed polyneuropathy to develop?
10-14 days
45
Distal degeneration of long/large diameter motor and sensory axons of peripheral nerves and spinal cord can occur with what?
OP induced delayed polyneuropathy
46
What species is most sensitive to OP induced delayed polyneuropathy?
Chickens
47
Are there any specific lesions with acute death associated with organophosphates?
No
48
Dogs exposed to more lipophilic organophosphates can have what condition develop?
Pancreatitis
49
How are organophosphates diagnosed?
Direct detection
50
Residues of which organophosphate may be seen in samples from fat or liver tissue?
Chlorpyrifos
51
What is something that can be tested antemortem to detect organophosphate toxicity?
Acetylcholinesterase activity level
52
How soon does a sample for organophosphate toxicity need to be assessed?
ASAP to preserve activity.
53
Less than what percentage of acetylcholinesterase activity is considered suspicious in suspected OP toxicity?
What percentage is considered diagnostic?
-
54
What are 3 things to be considered for clinical diagnosis of OPs?
- History of exposure
- Clinical signs
- Lab testing
55
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.
Atropine
56
Should emesis be induced with OP toxicity?
Only if recent. Not if depressed or seizures.
57
What can be done with dermal exposure to OPs?
Wash gently with tepid, soapy water.
58
Can activated charcoal be used for OPs?
Yes
59
What are 4 things that should be avoided with OP toxicity?
- Phenothiazines
- Aminoglycosides
- Muscle relaxants
- Drugs that depress respiration (opioids)
60
What drug can be used to treat OP toxicity?
What is the MOA?
Doses?
- 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.
61
What is the most effective treatment of OP toxicity in acute cases?
Dose?
- 2-PAM (Pralidoxime, Protopam)
| - 25-50 mg/kg 10% solution slow IV
62
Is 2-PAM effective against all OPs?
No
63
2-PAM may not be effective if what has occurred?
Aging
64
What is "aging"?
OP bound for a long time, changes chemically so that 2-PAM can no longer pull it off.
65
What is the main form of treatment with OP intermediate syndrome?
Supportive care
66
Is atropine more or less effective with OP intermediate syndrome compared to acute toxicity?
Less effective
67
With OP intermediate syndrome, 2-PAM should be reserved for what type of cases?
Severe cases
68
What is the treatment for OP induced delayed polyneuropathy?
Symptomatic therapy
69
Prognosis for OP toxicity is better if patient is what?
Alive
70
What are 2 determiners of prognosis for OP toxicity?
- Dose
| - How long since exposure
71
Mild to moderate signs with OP toxicity are generally what?
Treatable
72
Acute cases of OP toxicity that respond to treatment can recover within what time frame?
24 hours
73
What is an example of a carbamate?
Carbaryl (Sevin)
74
What is something that carbamates do not undergo that OPs do?
Storage activation
75
Do carbamates require hepatic bioactivation?
No
76
Which has a faster onset: OPs or carbamates?
| Shorter duration of action?
- Carbamates
| - Carbamates
77
T/F: A low exposure to carbamates may recover without treatment.
True
78
Are carbamates metabolized slowly or rapidly?
Very rapidly
79
What is the MOA of carbamates?
Reversible inhibition of acetylcholinesterase
80
What can be tested in the lab when looking for carbamate toxicity?
Cholinesterase levels
81
What can happen if a sample for carbamate testing is not tested fast enough?
False negative due to reversible binding.
82
What drug is used to treat carbamates?
Atropine
83
Is 2-PAM a good choice for carbamates?
| Why?
- No
| - Reversible binding reduces benefit.
84
Which carbamate is 2-PAM contraindicated with?
| Why?
- Carbaryl (Sevin)
| - Can potentially increase carbamylation process.
85
What happens with a high dose exposure of carbamates?
Animal dies too quickly for treatment.
86
What happens with a low dose exposure of carbamates?
Animal may survive without treatment if signs are not severe.
87
What type of insecticide are Diphenyl aliphatics (DDT, methoxychlor?
Chlorinated hydrocarbon (Organochlorine)
88
What type of insecticide are aryl hydrocarbons (Lindane)?
Chlorinated hydrocarbon (Organochlorine)
89
What type of insecticide are cyclodienes (Aldrin, Toxaphene)?
Chlorinated hydrocarbon (Organochlorine)
90
What insecticide was banned in the USA in 2003?
Methoxychlor
91
Are chlorinated hydrocarbons lipophilic or hydrophilic?
Highly lipophilic
92
Are chlorinated hydrocarbons soluble in water?
No
93
The lipophilic nature of chlorinated hydrocarbons leads to what?
Bio-accumulation in the food chain.
94
What is the soil half-life of chlorinated hydrocarbons?
2-15 years
95
Which can survive longer in the environment: organophosphates or chlorinated hydrocarbons?
Chlorinated hydrocarbons
96
Which species is more sensitive to chlorinated hydrocarbons: dogs or cats?
Cats
97
Do chlorinated hydrocarbons generally have a low or high toxicity to mammals?
Low
98
Which animals are susceptible to chlorinated hydrocarbons?
All animals
99
Are chlorinated hydrocarbons readily absorbed?
Yes - highly lipophilic
100
Do chlorinated hydrocarbons cross into the CNS?
Yes
101
T/F: Chlorinated hydrocarbons undergo metabolism by liver microsomal enzymes.
True
102
Do the metabolites of chlorinated hydrocarbons undergo enterohepatic recycling?
Yes
103
What are 4 ways the metabolites of chlorinated hydrocarbons can be excreted from the body?
- Milk
- Feces
- Urine
- Bile
104
What is the half-life of chlorinated hydrocarbons?
Weeks to months
105
What can disrupt equilibrium and allow a large amount of chlorinated hydrocarbon metabolites to be released into the blood stream?
Weight loss
106
What is the main clinical sign for chlorinated hydrocarbon toxicity?
CNS stimulation
107
Some mammals can show what instead of typical CNS excitability with chlorinated hydrocarbon toxicity?
Intermittent or persistent depression
108
Which species may show depression, abnormal postures, apparent blindness and death with chlorinated hydrocarbon toxicity?
Birds
109
Which species can have seizures as a result of chlorinated hydrocarbon toxicity?
Cattle
110
Are there any specific pathological lesions for chlorinated hydrocarbons?
No
111
Acute chlorinated hydrocarbon toxicity can be confirmed if insecticide is in what 3 types of samples at significant concentrations?
- Blood
- Liver
- Brain
112
A diagnosis of chlorinated hydrocarbon toxicity is made with what 4 factors?
- History of exposure
- Clinical signs
- Lack of specific lesions
- Chemical analysis of tissues
113
Compared to cholinesterases, chlorinated hydrocarbon toxicity has less or more parasympathetic signs?
CNS stimulation?
- Less parasympathetic signs
| - More severe CNS stimulation (convulsive seizures)
114
Is there any specific antidote for chlorinated hydrocarbon toxicity?
No
115
What are 3 forms of decontamination that can be used with chlorinated hydrocarbons?
- Induce emesis (if indicated)
- Wash soap/water if dermal exposure
- Activated charcoal (better) or mineral oil
116
What 2 drugs can be given to help control seizures caused by chlorinated hydrocarbon toxicity?
Diazepam or barbiturates
117
What are 3 types of symptomatic treatment that can be given with chlorinated hydrocarbon toxicity?
- Oxygen
- Ventilation
- Fluids
118
What is the prognosis for chlorinated hydrocarbon toxicity?
| What are 2 factors this depends on?
- Guarded to good
| - Dose, early detoxification
119
What toxin can lead to embryo toxicity and eggshell thinning in raptors?
Chlorinated hydrocarbons
120
What toxin can by toxic to aquatic wildlife and some amphibians?
Chlorinated hydrocarbons
121
What is an example of a pyrethrum flower from which pyrethrins can be extracted?
Crysanthemum cinerariaefolium
122
What are synthetic analogs of pyrethrins known as?
Pyrethroids
123
Which type of toxin is unstable in air and light which both cause it to break down quickly?
Pyrethrins/Pyrethroids
124
What are 6 examples of natural pyrethrins?
- Pyrethrin I & II
- Cinerin I & II
- Jasmolin I & II
125
What are 2 types of synthetic pyrethrins?
- First generation/Type 1
| - Second generation/Type 2
126
What do second generation/Type 2 synthetic pyrethrins contain that first generation/Type 1 do not?
What does this do?
- Alpha-cyano moiety
| - Increases their insecticidal potency
127
Is the overall toxicity low or high in mammals?
Low
128
What two forms of toxicity are not found with pyrethrins/pyrethroids?
Which one is?
- Subacute or chronic
| - Acute
129
What two species are pyrethrins/pyrethroids very toxic in?
- Fish
| - Some birds
130
Are cats more or less sensitive than dogs to pyrethrins/pyrethroids?
More
131
Are pyrethrins/pyrethroids lipid soluble?
Yes
132
What is the most common type of exposure seen with pyrethrins/pyrethroids?
What are 2 other possible forms of exposure?
- Dermal
| - Ingestion & inhalation
133
Where are 3 locations pyrethrins/pyrethroids can be rapidly metabolized?
- GIT
- Plasma
- Liver
134
How are conjugated metabolites of pyrethrins/pyrethroids excreted?
Urine
135
The presence of alpha-cyano moiety (Type 2) decreases the rate of what?
Hydrolysis
136
Do pyrethrins/pyrethroids accumulate in tissues?
No
137
What can be added to pyrethrins/pyrethroids that acts as a synergist?
What does it do?
- Piperonyl butoxide or MGK-264
| - Inhibits pyrethrin metabolism by insects
138
Generalized muscle tremors, depression, blindness (reversible) and ataxia are clinical signs that can be seen with which category of toxin?
Pyrethrins/pyrethroids
139
With pyrethrin/pyrethroid toxicity, some dogs can show what which may occur as a topical hypersensitivity reaction or firing of sensory peripheral nerves?
"Acute paralysis" which is actually paresthesia (abnormal sensation of prickling, itching)
140
Are there any specific pathological lesions seen with pyrethrins/pyrethroids?
No
141
Are pyrethrins/pyrethroids easy or difficult to detect in tissue samples?
Difficult
142
T/F: Tissue levels of pyrethrins/pyrethroids correlate well with severity of clinical signs.
False - Tissue levels do not correlate well with severity of clinical signs.
143
What 3 factors are used to make a diagnosis of pyrethrin/pyrethroid toxicity?
- History of exposure
- Appropriate clinical signs
- Ruling out other causes
144
Is there any specific antidote for pyrethrin/pyrethroid toxicity?
No
145
For which category of toxin is activated charcoal generally not used?
Pyrethrins/pyrethroids
146
It is important to monitor and control what with pyrethrin/pyrethroid toxicity?
Temperature (hypothermia)
147
With pyrethrin/pyrethroid toxicity that has very mild signs, what is the treatment?
Decontamination
148
If there are severe muscle tremors seen with pyrethroid/pyrethrin toxicity, what can be given for treatment?
Methocarbamol
149
What are 3 drugs that can be given for seizures seen with pyrethrin/pyrethroid toxicity?
- Diazepam
- Barbiturates
- Propofol CRI
150
What is the prognosis for pyrethrin/pyrethroid toxicity?
Generally very good
151
What is one of the oldest botanical insecticides?
Rotenone
152
What is a common use of rotenone in pets?
Treatment of lice, ticks, mites
153
Rotenone is very toxic to what 2 species?
- Fish
| - Cold-blooded animals
154
Which mammal species is more sensitive to rotenone?
Pigs
155
Which is more toxic with rotenone: inhalation or ingestion?
Inhalation
156
Low and incomplete absorption of rotenone is seen where in the body?
GIT
157
Do fats/oils increase or decrease the absorption of rotenone?
Increase
158
Which formulation of rotenone is highly toxic relative to other formulations?
Emulsified concentrate
159
What is rotenone converted to in fish/insects?
| In mammals?
- Toxic metabolites
| - Non-toxic metabolites
160
How long does it take for rotenone to be eliminated?
| In what form?
- 24 hours
| - Feces
161
Which toxin is an irritant that can cause local irritation such as conjunctivitis, congestion, dermatitis, GI upset if ingested?
Rotenone
162
What are the 2 predominate clinical signs seen with rotenone?
- Depression
| - Convulsions
163
What are 3 things that can be seen antemortem with lab testing for rotenone toxicity?
- Hypoglycemia
- Liver changes
- Hypoxemia/hypercapnea
164
Diagnosis of rotenone toxicity is based on what?
History and documentation of compound
165
Are there any specific treatments for rotenone toxicity?
No
166
What are 2 things that can be done for rotenone toxicity?
- Detoxification
| - Supportive care
167
What is the prognosis for rotenone toxicity in mammals?
| In fish/reptiles?
- Generally good
| - Poor
168
What is the main source of D-Limonene?
OTC products for control of lice, fleas ticks (usually shampoos)
169
What are 3 things D-Limonene can be combined with?
- Other essential oils
- Piperonyl butoxide
- Enzyme inhibitors
170
D-Limonene is toxic to the flea at which life stages?
All life stages
171
Which species is more sensitive to D-Limonene: dogs or cats?
Cats
172
What is seen in cats with D-Limonene toxicity at:
5x recommended dose?
15x recommended dose?
- Mild toxicity
| - Severe signs lasting 5 hours
173
Is D-Limonene lipid soluble?
Yes
174
D-Limonene can reach maximal blood concentration how long after dermal exposure?
10 mins
175
Does D-Limonene have wide distribution in the body?
Yes
176
Where is D-Limonene metabolized?
| Excreted?
- Liver
| - Urine
177
What is a patient with D-Limonene toxicity said to smell like?
Lemons
178
Are there any specific pathological lesions for D-Limonene toxicity?
No
179
Is there any specific lab testing available for D-Limonene toxicity?
No
180
What 2 things are D-Limonene toxicity based on?
- Exposure history
| - Scent of patient
181
What are 3 forms of treatment for D-Limonene toxicity?
- Decontamination
- Monitor temperature (iatrogenic hypothermia)
- Supportive care (fluids, etc.)
182
What is the prognosis for sub-lethal D-Limonene toxicity?
Excellent
183
Sub-lethal D-Limonene toxicity usually resolves in what time frame?
6-12 hrs
184
Prognosis for D-Limonene toxicity is worse if there is what?
Skin reactions
185
What is one of the most common essential oils encountered?
| What is it used for?
- Melaleuca oil (tea tree oil)
| - Topically for flea control
186
Parts of the plant from which nicotine is derived are teratogenic to what 2 species?
- Sows
| - Cattle
187
T/F: Nicotine is highly toxic to dogs.
True
188
What is the oral LD50 of nicotine in dogs?
| At what dose can clinical signs be seen?
- 9.2 mg/kg
| - 1 mg/kg
189
What other ingredient might nicotine gum contain that is also toxic to dogs (but not humans or cats)?
Xylitol
190
Nicotine is absorbed well through what 2 routes of administration?
- Inhalation
| - Intact skin
191
Through what route of administration is nicotine poorly absorbed?
Ingestion
192
What would increase absorption of nicotine in the stomach?
| What do you not give a dog with GI signs?
- Alkalinization of the stomach.
| - Antacids
193
Where is nicotine metabolized?
| Excreted?
- Liver
| - Bile & urine
194
Which route of excretion is decreased with an alkaline pH?
| Why?
- Renal excretion
| - Increases reabsorption
195
What clinical sign is seen in 25% of nicotine toxicity cases?
Ataxia
196
What clinical sign can be seen within 1 hour or exposure to nicotine?
Tremors
197
What are 3 clinical signs that can be seen with higher doses?
- CNS depression
- Tachycardia
- Vasodilation
198
Is the clinical course of nicotine toxicity slow or rapid?
Rapid (mins to hours)
199
A patient that smells like an old cigar might have what type of toxicity?
Nicotine
200
What are 5 areas that can be tested for nicotine?
- Urine
- Stomach contents
- Kidney
- Liver
- Blood
201
Nicotine at low doses may resemble what?
| Higher doses/later stages?
- Cholinesterase inhibitors ( OP/Carbamate
| - CNS depressants
202
What are 2 forms of decontamination that can be used with nicotine toxicity?
- Induce emesis
| - Activated charcoal
203
What should be avoided in treatment of nicotine toxicity?
Antacids
204
What are 2 ways to enhance the excretion of nicotine?
- IV fluids
| - Acidification of urine
205
What can be given to treat parasympathetic effects seen with nicotine toxicity?
Atropine
206
This is a foramidine insecticide/acaracide (ticks/mites).
Amitraz
207
How does Amitraz work on ticks/mites?
Paralyzes the mouth parts.
208
Where can amitraz be found?
Flea/tick collars
209
What is amitraz used for in swine and cattle?
Miticide/insecticide
210
Amitraz is not labeled for use in what 2 species?
- Cats
| - Horses
211
This toxin is a mild irritant and concentrates are flammable.
Amitraz
212
What is the acute oral LD50 of amitraz for dogs?
250 mg/kg
213
What type of signs can be seen in dogs with 20 mg/kg of amitraz?
Mild signs/sedation
214
What are 2 drugs that can increase the toxicity of amitraz?
- Meperidine (Demerol)
| - Sympathomimetic amines
215
What are 4 things that can increase the toxicity of amitraz?
- Stress
- Debilitation
- Advanced age
- Toy breeds
216
Amitraz is readily absorbed by what route?
| What are 2 other routes it can be absorbed through?
- Oral
| - Inhalation, Skin
217
Peak plasma concentrations of Amitraz can be seen when?
| Elimination half-life?
- After 5 hours
| - 24 hours
218
Is amitraz well distributed throughout the body?
Yes
219
Where is amitraz rapidly metabolized?
| Excreted?
- Liver
| - Urine
220
What is the most common clinical sign seen with amitraz?
| How long is it seen?
- Transient sedation
| - 24-72 hours
221
What can be seen with amitraz toxicity due to alpha-2 inhibition of insulin?
Hyperglycemia
222
Are there any specific pathological lesions for amitraz?
No
223
Can tissue be analyzed for amitraz?
Yes
224
What are 3 factors for diagnosing amitraz toxicity?
- History
- Clinical signs
- Specific analysis
225
What is the most significant differential diagnosis for amitraz toxicity?
CNS depressants
226
What is the antidote for amitraz toxicity?
| What are 2 examples?
- Alpha-2 antagonists
| - Yohimbine (short acting), Atipamezole ( few cardio-respiratory effects than yohimbine)
227
What is the prognosis for amitraz toxicity?
Pretty good
228
Wht is thechemical nof N,N-diethyl-m-tolumide?
DEET
229
DEET is used for the control of what 3 things?
- Mosquitoes
- Flies
- Ticks
230
What are 2 other insecticides that DEET can be combined with?
- Fenvalerate
| - Pyrethroid
231
The concentration of DEET can range from what to what?
| What is the typical amount in pet products?
- 5-100%
| -
232
Which toxin has a characteristc sweet odor?
DEET
233
Which toxin may damage synthetic fibers or plastics?
DEET
234
Which species is more sensitive to DEET, cats or dogs?
Cats
235
Which are more sensitive to DEET, young or old animals?
Young
236
What might increase the toxicity of DEET?
CNS depressants
237
What pecenage of DEET is absorbed from the skin in dogs?
7.9-12.8%
238
Where in the body can DEET accumulate and persist?
Skin
239
Which insecticide can increase dermal absorption of others?
DEET
240
Where is DEET metabolized?
| Excreted?
- Liver
| - Urine
241
With DEET, depression, excitiation, ataxia, tremors, seizures and coma are clinical signs in what 2 species?
- Rabbits
| - Rats
242
With DEET, hypersalvation, vomiting, hyperexcitibility, tremors, ataxia and seizures are clinical signs that can be seen with what 2 species?
- Dogs
| - Cats
243
Are there any specific patholgical lesions for DEET toxicity?
No
244
What amount of DEET is considered diagnostic?
| Considered supportive?
- 20 ppm
| - Urine > 1ppm, Tissue >10ppm
245
What are 4 other CNS excitatory toxins DEET must be differentiated from?
- Strychnine
- Metaldehyde
- Organochlorine
- OP/carbamate
246
Are there any specific antidotes for DEET toxicity?
No
247
What are 3 forms of decontamination that can be used for DEET toxicity?
- Dermal exposure: wash soap/water
- Emesis
- Activated charcoal +/- cathartic (avoid magnesium cathartic)
248
What is the main form of treatment for DEET toxicity?
Symptomatic treatment
249
What is the prognosis for sublethal DEET toxicity?
Usually respond in 24-72 hrs
250
What is the most common source of naphthalene?
Mothballs
251
Newer mothballs contain what instead of naphthalene?
Paradichlorobenzene
252
How do you tell if you have old fashioned mothballs with naphthalene?
Put in water, mothballs with naphthalene will float, those with paradichlorobenzene will sink.
253
What naphthalene derived from?
Coal tar/petroleum hydrocarbons
254
What happens to naphthalene at room temp?
Sublimates - go from a solid directly to a gas
255
Which are more sensitive to naphthalene toxicity, cats or dogs?
Cats
256
Which are more susceptible to naphthalene toxicity, cats or dogs?
Dog - more likely to ingest
257
What is the lowest canine lethal dose for naphthalene toxicity?
400 mg/kg
258
How many mothballs can be toxic to a dog?
1 or 2
259
What are 3 ways naphthalene can be absorbed?
- Oral
- Inhalation
- Intact skin
260
What are 2 things that can be caused by the oxidation products of naphthalene?
- Methemoglobinemia
| - Hemolysis
261
What is a common clinical sign of naphthalene ingestion?
Mothball breath
262
Which insecticide can cause heinz bodies?
Naphthalene
263
Hepatic injury and secondary renal injury can occur with which insecticide?
Naphthalene
264
What clinical sign can occur in neonates due to naphthalene toxicity?
Cataracts
265
What do you need to differentiate the characteristic hematologic changes seen with naphthalene from?
What are 3 examples?
- Other causes of RBC oxidative injury
| - Acetaminophen, onions, nitrates
266
Which species RBCs are more susceptible to oxidative injury than other species?
Cats
267
What are 2 specific treatments for naphthalene toxicity?
| Which is faster?
- Ascorbicaci (20 mg/kg)
- Methylene blue 1%
- Methylene blue 1%
268
What can be used to reduce precipitation of Hgb in the kidneys due to naphthalene toxicity?
Sodium bicarbonate
269
What is the prognosis for naphthalene toxicity?
Reasonable if treated promptly
270
What type of insecticide is ivermectin?
Macrocytic lactone
271
What is ivermectin used for in dogs and cats?
Prevention of heartworm
272
Ivermectin toxcity is usually caused by what?
Overdose
273
What is a potential source of ivermectin exposure in dogs?
Horse feces
274
What are 2 species susceptible to ivermectin toxicity?
- dogs
| - small birds
275
Why are Collies more susceptible to ivermectin toxicity?
ABCB1/MDR1 mutation
276
Ivermectin is 95% absorbable via what route?
Orally
277
In what species is oral absorption of ivermectin lower?
Ruminants
278
T/F: Dogs may have lower bioavailability than cats.
False - Cats may have lower bioavailability than dogs.
279
Does ivermectin typically cross the BBB?
No
280
How is ivermectin excreted?
Mainly unchanged in feces.
281
What is the elimination half-life of ivermectin in dogs?
2 days
282
Deletion/mutation of the ABCB1/MDR1 gene can result in how much of an increase in concentration of certain drugs in the CNS?
50x
283
What as been seen with co-administation of off-label (high dose) ivermectin and comfortis (Spinosad)?
Neurotoxicity
284
What is the main type of clinical sign seen with ivermecti toxicity?
CNS depression
285
Are there any specific pathologic lesions seen with ivermectin toxicity?
No
286
Do tissue levels of ivermectin correlate well to brain levels?
No
287
Is there any specific antidote for ivermectin?
No
288
Caution needs to be used with what types of drugs with ivermectin toxicity?
GABA agonists (diazepam, barbiturates, propofol)
289
What does prognosis of ivermectin toxicity depend on?
Exposure & ability to pay for care
290
T/F: Generally there are no long-term sequelae from ivermectin toxicity if the animal survives.
True
