Toxicology Exam I Material (Insecticides & Rodenticides) Flashcards
(125 cards)
1
Q
Is Rotenone more toxic via ingestion, inhalation, or cutaneous exposure?
A
inhalation
2
Q
With regard to pyrethrins, what type of exposure is most common?
A
Dermal
Ingestion and Inhlation are possible
3
Q
What is the mechanism of action (MOA) of Chlorinated Hydrocarbons?
A
Interferes with Na+ channels, causing CNS stimulation
4
Q
Why is 2-PAM contraindicated with Carbaryl?
A
It can potentially increase the carbamylation process, further potentiating toxicity
5
Q
T/F: Tachycardia is a clinical sign associated with muscarinic stimulation
A
False
It’s not.
6
Q
T/F: Organophosphates that require desulfuration will be less toxic to young patients
A
True
6
Q
What does DUMBELS stand for?
A
- Diarrhea
- Urination
- Miosis
- Bronchospasm/Bronchoconstriction/Bradycardia
- Emesis
- Lacrimation
- Salivation
6
Q
T/F: Organophosphates and Carbamates undergo storage activation
A
False
Carbamates do not undergo storage activation
7
Q
A toxicant that is metabolized by oxidative enzymes has a faster rate of metabolism in:
A
Cattle
8
Q
What is the specific treatment for organophosphate toxicity?
A
2-PAM
“Cholinesterase reactivating oxime”
8
Q
T/F: Some carbamates undergo “lethal synthesis”
A
False
8
Q
Which of the following toxins acts mainly as an alpha-2 agonist?
- Amitraz
- DEET
- Couphos
- Pyrethrins
A
Amitraz
8
Q
What is the difference between 1st and 2nd generation pyrethrins?
A
Addition of α-cyano moeity
- 1st gen (Type I) do not contain α-cyano moeity
- 2nd gen (Type II) do contain α-cyano moeity, which increases their insecticidal potency
8
Q
Which tissues are best for postmortem diagnosis of pyrethrin toxicity?
A
liver and brain
9
Q
What chemical property of Chlorinated Hydrocarbons is responsible for bioaccumulation in the food chain?
A
Chlorinated Hydrocarbons are highly lipophilic
10
Q
Which of the following insecticide toxicants would you expect to have the longest half-life?
- Organophosphates
- Carbamates
- Chlorinated Hydrocarbons
- Pyrethrins
A
Chlorinated Hydrocarbons
12
Q
T/F: If there is a strong response to low dose atropine (0.02mg/kg) during an atropine response test, it is less likely that the patient has organophosphate toxicity
A
True
The atropine dose for treatment of organophosphates is about 10x the dose given during the atropine response test. So if the patient responds to such a low dose, it’s probably not OP toxicity
13
Q
T/F: Pyrethrins are generally not very toxic to mammals, but very toxic to birds and fish
A
True
14
Q
Which of the following is consistent with Cholecalciferol Toxicity?
- Increased Ca, Decreased Phosphate, and Increased PTH
- Decreased Ca, Decreased Phosphate, and Increased PTH
- Increased Ca, Decreased Phosphate, and decreased PTH
- Increased Ca, Increased Phosphate, and decreased PTH
A
Increased Ca, Increased Phosphate, and decreased PTH
14
Q
T/F: Pyrethrins are extracted from the tears of migrating antarctic buffalo that left their family to find a better life for their children
A
False
- Close though!*
- Pyrethrins are extracts of pyrethrum flowers (Crysanthemums)*
14
Q
Would you expect to see CNS stimulation or CNS depression with D-Limonene toxicity?
A
CNS depression
16
Q
T/F: Some organophosphates undergo “lethal synthesis”
A
True
17
Q
T/F: For laboratory diagnosis of organophosphate toxicity, <50% acetylcholinesterase activity is considered diagnostic
A
False
<50% activity is considered suspicious.
<25% activity is considered diagnostic
19
Q
T/F: Chlorinated Hydrocarbons generally degrade relatively quickly in the environment
A
False
Soil half-life reportedly between 2-15 years
20
T/F: 2-PAM is not reliably effective for treatment of carbamates
**True**
*Reversible binding reduces benefit*
21
Why is **piperonyl butoxide** or **MGK-264** added to pyrethrins?
**Inhibits pyrethrin metabolism in insects**
(but potentially increases toxicity in mammals)
22
T/F: Cats are more sensitive to D-Limonene than dogs
**True**
23
What is the best tissue to sample post-mortem for diagnosis of **Rotenone** toxicity?
**liver**
25
Which of the following toxins are dogs more sensitive to than cats?
* Bromethalin
* Rotenone
* Strychnine
* Amitraz
**Strychnine**
26
What are the specific lesions associated with **organophosphates**?
**No *specific* lesions**
27
Which of the following has direct acetylcholinesterase activity?
* Dichlorvos
* Diazinon
* Fenthion
* Parathion
**Dichlorvos**
28
What is the mechanism of action (MOA) of D-Limonene?
**Unknown**
*However, it is suspected that it may act through central and peripheral vasodilation due to an undetermined neuronal mechanism*
29
What are the two most common signs of **Rotenone** toxicity?
**Respiratory depression and convulsions**
30
What is the main clinical sign of **Chlorinated Hydrocarbon** toxicity?
**CNS Stimulation**
33
What is the mechanism of action (MOA) of **carbamates**?
**_Reversible_ inhibition of cholinesterases**
*Acetylcholinesterase can hydrolyze carbamates, but at a slower rate than Ach*
34
Why do you want to avoid hypothermia when treating small patients who have had topical pyrethrin exposure?
**Hypothermia may further alter Na+ channel kinetics**
35
The dose that will produce alterations (hematologic, biochemical, pathologic, or clinical), and administering twice this dose will result in lethality is called:
**Toxic Dose High (TDH)**
36
What is the mechanism of action for organophosphates?
****_Ir_**reversible inhibition of cholinesterases**
*This will increase acetylcholine at all cholinergic sites*
37
What species is most sensitive to **Chlorinated Hydrocarbons**?
**Cats**
*All animals are susceptible (nonspecific) but cats are the most sensitive*
39
What is the main storage tissue for **Chlorinated Hydrocarbons**?
**FAT**
39
What condition in canine patients is commonly treated with **o,p-DDD**?
**Pituitary dependent hy**_per_**adrenocorticism (Cushing's Syndrome)**
40
What is the mechanism of action (MOA) of **pyrethrins**?
**Delay closure of Na+ channels** in the axonal membrane of the insect
## Footnote
*This leads to _knockdown effect_, which is rapid paralysis caused by inhibition of neurons (the insect is immobile, but not dead yet*
42
T/F: **Chlorinated Hydrocarbons** (DDT, for instance) are highly lipophilic and excreted in the bile. This suggests that they likely undergo enterohepatic recirculation
**True**
43
T/F: Organophosphates become more toxic after being stored for a long period of time
**True**
*If sealed and stored for 1-2 years, will become more toxic*
44
Which drug would you use in pyrethrin toxicity to control severe muscle tremors?
**Methocarbamol**
45
If you have a patient on phenobarbital and they are exposed to an organophosphate that requires desulfuration, will the organophosphate be more or less toxic?
**More toxic**
*Phenobarbital is an enzyme inducer. Organophosphates that require desulfuration will be activated by liver metabolism (“Lethal Synthesis”), so they will be more toxic if enzyme inducers are present*
47
What is the cause of death in high exposure to organophosphates?
**Respiratory failure**
48
What is the mechanism of action (MOA) of **Rotenone**?
**Blocks oxidative phosphorylation, preventing NADH from being oxidized to NAD, thus interfering with production of ATP**
*Affects cell respiration (crosses cell membranes)*
49
Which of the following is the best treatment for a dog that is hemorrhaging from Brodifacoum toxicosis?
* Vitamin K1 PO
* Vitamin K3 PO
* FFP
* Vitamin K1 SC
**FFP**
*Fresh Frozen Plasma*
50
How are animals most commonly exposed to **organophosphates**?
**Orally (contaminated feed)**
*Exposure may also occur dermally (when used as a dip or spray) or via inhalation (aerosol spray)*
51
T/F: Atropine is used to treat muscarinic and neuromuscular signs associated with organophosphate toxicity
**False**
*Atropine does not treat the neuromuscular problems; just the muscarinic signs*
52
T/F: Alkalinization of the stomach increases absorption of **Nicotine**
**True**
*In the case of toxicity, this would be a _bad_ thing. So for instance, you would not want to give your patient with Nicotine toxicity an antacid because it will enhance the absorption*
53
What is the mechanism of action (MOA) of **Nicotine**?
* At low doses mimics Ach and stimulates post-synaptic nicotinic receptors (CNS, ganglia, NM junctions)
* Stimulates CRTZ (chemoreceptor trigger zone - may see vomiting)
* At high doses stimulation will be followed by blockage (persistent depolarization)
54
What drug is useful for controlling the parasympathetic effects of **Nicotine** toxicity?
**Atropine**
55
What is the mechanism of action (MOA) of **Amitraz**?
**alpha-2 agonist in the CNS**
* Weak alpha-1 agonist activity
* Weak monoamine oxidase (MAO) inhibitor
56
What is the most common clinical sign associated with **Amitraz** toxicity?
**Transient Sedation**
*May last 24-72 hours*
57
Why is **hyperglycemia** often seen associated with **Amitraz** toxicity?
**alpha-2 inhibition of insulin**
58
Name two antidotes for Amitraz toxicity. Which one is considered the better option?
**Yohimbine and Atipamezole**
## Footnote
*Atipamezole is considered the better option because it has fewer cardiorespiratory effects than yohimbine*
59
If chelation therapy is recommended for a toxicant when levels reach 5mg%, will a blood level of 900mcg/dL require therapy?
**No**
5mg% = 5000 mcg/dL
Therefore, 900 mcg/dL is not high enough to require therapy
60
Which three insecticides that we covered in class are **CNS depressants**?
****_A_**mitraz, **_I_**vermectin, _D_-limonene**
*\*Financial _AID_* *can be depressing\**
61
DEET concentration of \_\_\_\_ppm is considered diagnostic for DEET toxicity
**20 ppm**
62
What is the most common source of **Naphthalene** toxicity?
**Ingestion of mothballs**
63
What is the mechanism of action (MOA) for **Naphthalene**?
**Causes oxidative damage to RBCs --\> _methemoglobinemia_**
*Will not be able to bind O2, and will also alter O2 binding at other heme sites, leading to tissue hypoxia*
64
T/F: The amount of poison that under a specific set of conditions will result in detrimental biologic changes is known as LD50
**False**
*The amount of poison that under a specific set of conditions will result in detrimental biologic changes is called **_toxicity_***
65
Which of the following toxins works though its inhibition of oxidative phosphorylation in the TCA cycle?
* Rotenone
* Methoxychlor
* Naphthalene
* Cholecalciferol
**Rotenone**
66
A compound that has a LD50 of 100mg/kg is considered:
* Practically nontoxic
* Slightly toxic
* Highly toxic
* Moderately toxic
* Extremely toxic
**Moderately toxic**
67
T/F: Atropine is effective in treating muscle fasciculations as a result of organophosphate toxicity
**False**
68
The effect of a toxicant produced by daily exposure for 30 days or less is decscribed as:
**subacute toxicosis**
69
A compound that has LD50 of 200 mcg/kg is considered:
**extremely toxic!**
70
The first clinical signs in organophosphate poisoning are *mainly* due to:
**muscarinic stimulation**
71
2-PAM antagonizes the toxic effects of organophosphates by:
**reactivation of acetylcholinesterase**
72
T/F: As a rule of thumb, 100g/ton of a toxicant in a feed is pretty much equivalent to 110ppm of the toxicant in the feed
**True**
73
The "knockdown" effect is used to describe the action of what insecticide?
**Pyrethrins**
74
The preferred medication for initial control of seizures in a dog with an unknown toxicant would be:
**Diazepam**
75
What animals are most susceptible to Ivermectin toxicity?
**dogs and small birds**
*Collie breeds are especially susceptible*
76
If you wanted to use Ivomec® extra-label and you know that toxicity can be seen at doses as low as 300mcg for a 1 kg kitten, how many milliliters of undiluted (1%) Ivomec® would that be?
**0.03 mL**
77
T/F: **Ivermectin** is well distributed throughout the body and crosses the BBB
**False**
*Ivermectin _is_ well distributed throughout the body, but does _not_ cross the BBB. It is kept out of the CNS by p-glycoprotein efflux pump*
78
What is the mechanism of action (MOA) of **Ivermectin**?
**GABAA agonist**
*Binding to glycine and voltage-gated chloride channels also occurs in overdose situations. At low concentrations, it may _reduce_ GABA and cause excitatory signs (reversed as concentrations increase)*
79
Does **D-Limonene** cause CNS depression or CNS stimulation?
**CNS depression**
80
What drug is used to treat muscle fasciculations associated with organophosphate toxicity?
**2-PAM**
81
Which of the following should NOT be used in the treatment of organophosphate poisoning in dogs?
* acepromazine
* atropine
* activated charcoal
* diphenhdramine
* diazepam
**acepromazine**
82
In a chemical analysis, the result is expressed as 67 µg/g. What is the equivalent to this value in %?
**0.0067%**
1 µg/g = 0.0001%
Fun fact, right? Wrong - That fact isn't even a little bit fun.
83
The effect of a toxicant produced by daily exposure for 30 days or less is decscribed as:
**subacute toxicosis**
84
The dose which will produce alterations (hematologic, biochemical, pathologic, or clinical) and administering twice this dose will result in lethality is called:
**toxic dose high (TDH)**
85
In a chemical analysis, the result is expressed as 9 µg/g. This is equivalent to what value in %?
**0.0009%**
1 µg/g = 0.0001%
86
The relative toxicity of drug A is 35 mg/kg. How would this drug be classified?
**Highly toxic**
87
T/F: Emesis is recommended for patients with CNS signs as a result of **Tea Tree Oil toxicity**
**False**
*Emesis is **not** recommended due to risk of aspiration*
88
When would you expect onset of clinical signs of **tea tree oil** (TTO) toxicity?
**2-12 hours**
89
1 kg = ____ lb
**1 kg = 2.2 lbs**
90
100 g/ton = _____ ppm
**100 g/ton = ~110 ppm**
91
1 µg/g = \_\_\_\_\_%
**1 µg/g = 0.0001%**
92
1 gal = _____ ounces
**1 gal = 128 ounces**
93
1 ppm = _____ mg/L
**1 ppm = 1 mg/L**
94
0.1 mg% = _____ ppm
**0.1 mg% = 1 ppm**
95
If a dog ingests a rat that recently feasted on a pile of warfarin, what is that an example of?
**Relay Toxicosis (2o toxicosis)**
96
What species is most susceptible to anticoagulant rodenticide toxicity?
**Dogs**
Order of _sensitivity_: Pigs \> dogs & cats \> ruminants \> horses & chickens
97
Which one has a longer half-life: **Warfarin** or **Brodifacoum**?
**Brodifacoum**
* *t1/2 of Brodifacoum: 6 days*
* *t1/2 of Warfarin: 19 hours*
98
What is the general mechanism of action (MOA) of **anticoagulant rodenticides**?
**Inhibit Vitamin K epoxide reductase**
*(Vitamin K epoxide reductase is the enzyme that converts Vit K epoxide to reduced form). This inhibition leads to depletion of reduced Vit K and reduced activation of clotting factors II, VII, IX, and X.*
99
When would we expect to see onset of clinical signs with **anticoagulant rodenticide** toxicity?
**1-5 days**
100
T/F: Animals with anticoagulant rodenticide toxicity may die without external evidence of bleeding
**True**
101
Name the lesions associated with anticoagulant rodenticide toxicity:
**Intrapulmonary, intrathoracic/abdominal hemorrhage, petechiation, ecchymosis**
102
Of the following coagulation parameters, which will become abnormal *first* with anticoagulant rodenticide toxicity?
* Activated clotting time (ACT)
* Prothrombin time (PT)
* Activated partial thromboplastin time (aPTT)
* Proteins induced by vitamin K antagonists (PIVKA)
**PIVKA**
*Proteins induced by vitamin K antagonists (PIVKA)*
103
What Vitamin K-dependent clotting factor has the shortest half-life?
**Factor VII**
*For clotting factor tests associated with anticoagulant rodenticide toxicity, PIVKA will be prolonged 1st. However, because PIVKA blows, we'll look at PT. Because PT tests Factor VII, it should be the next one to go down.*
104
T/F: Vitamin K3 is the treatment of choice for anticoagulant rodenticide toxicity
**False**
Vitamin K3 is not effective and has stupid side effects. Use Vitamin K1
105
T/F: Phytonadione is the treatment of choice for anticoagulant rodenticide toxicity
**True**
Phytonadione is Vitamin K1 (oral route is recommended)
106
T/F: Vitamin K1 should always be given IV
**False**
## Footnote
*Vitamin K1 should pretty much always be given orally. If given IV there is a high risk of anaphylaxis*
107
T/F: Response to Vitamin K1 may be reduced in liver failure
**True**
108
What would your duration of Vitamin K treatment be for **Warfarin**?
**~1 week**
109
What would your duration of Vitamin K treatment be for **Brodifacoum**?
**~4 weeks**
110
If anticoagulant rodenticide intoxication is suspected but you do not know what specific rodenticide was ingested, how long should you treat with Vitamin K1?
**4 weeks (28 days)**
111
T/F: Nursing animals can be exposed to cholecalciferol rodenticides through the milk
**True**
112
What is the general mechanism of action (MOA) of **cholecalciferol rodenticides**?
**Causes hypercalcemia and hyperphosphatemia**
* *Increased serum calcium due to increased GI absorption and decreased renal excretion of Ca++*
* *Deposition of calcium in soft tissues such as kidney tubules, cardiac and lung tissues, vascular walls, and stomach*
* *Leads to tissue damage, increased capillary permeability and hemorrhage, renal ischemia*
* *Increased renal loss of sodium and potassium (competition with calcium for reabsorption)*
113
When do you expect onset of clinical signs associated with **cholecalciferol rodenticides**?
**24-36 hours**
114
If a patient presents with hypercalcemia and significantly elevated parathyroid hormone (PTH) level, would **cholecalciferol rodenticide** be on the top of your differential list?
**No**
* The top differential would be hyperparathyroidism*
* Cholecalciferol rodenticide toxicity results in hypercalcemia, hyperphosphatemia, and **decreased** PTH*
115
T/F: Bromethalin is effective against warfarin resistant rodents
**True**
116
T/F: Guinea pigs are resistant to **Bromethalin**
**True**
*Guinea pigs lack the correct metabolic enzymes for Bromethalin*
117
T/F: Bromethalin undergoes "lethal synthesis"
**True**
*Metabolized by N-demethylation in the liver to the metabolite desmethylbromethalin (more toxic)*
118
T/F: **Bromethalin** does not undergo hepatic recirculation
**False**
It does.
119
What is the mechanism of action (MOA) for **Bromethalin**?
**Uncoupling of oxidative phosphorylation**
*Basically this will alter ATP production, resulting in a lack of cellular energy, resulting in cell death*
120
What are the 'primary targets' for **Bromethalin**?
**brain and spinal cord**
121
Are **acute** or **delayed** clinical signs typically associated with Bromethalin toxicity?
**Delayed (subacute)**
*Acute signs are more rare and usually only occur with supralethal doses*
122
A dog showing signs of anorexia, vomiting blood, cardiac arrhythmias, polyuria and polydipsia is MOST likely intoxicated with *what rodenticide*?
**Cholecalciferol**
123
Which of the following is an indicator of much poorer prognosis in cases of cholecalciferol rodenticide poisoning?
* GI bleeding
* PU/PD
* Anorexia
* Lethargy
**GI Bleeding**
124
T/F: Anticoagulant rodenticides inhibit production of precursor proteins of clotting factors II, VII, IX, and X
**False**
*Anticoagulant rodenticides inhibit **_activation_** of precursor proteins of clotting factors II, VII, IX, and X*
125
List the species sensitivity to anticoagulant rodenticides in decreasing order:
**pigs \> dogs & cats \> ruminants \> horses \> chickens**
