Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

RUSVM Toxicology > Toxicology Exam I Material (Insecticides & Rodenticides) > Flashcards

Toxicology Exam I Material (Insecticides & Rodenticides) Flashcards

1
Q

Is Rotenone more toxic via ingestion, inhalation, or cutaneous exposure?

A

inhalation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

With regard to pyrethrins, what type of exposure is most common?

A

Dermal

Ingestion and Inhlation are possible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the mechanism of action (MOA) of Chlorinated Hydrocarbons?

A

Interferes with Na+ channels, causing CNS stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Why is 2-PAM contraindicated with Carbaryl?

A

It can potentially increase the carbamylation process, further potentiating toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

T/F: Tachycardia is a clinical sign associated with muscarinic stimulation

A

False

It’s not.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

T/F: Organophosphates that require desulfuration will be less toxic to young patients

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does DUMBELS stand for?

A
  • Diarrhea
  • Urination
  • Miosis
  • Bronchospasm/Bronchoconstriction/Bradycardia
  • Emesis
  • Lacrimation
  • Salivation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

T/F: Organophosphates and Carbamates undergo storage activation

A

False

Carbamates do not undergo storage activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

A toxicant that is metabolized by oxidative enzymes has a faster rate of metabolism in:

A

Cattle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the specific treatment for organophosphate toxicity?

A

2-PAM

“Cholinesterase reactivating oxime”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

T/F: Some carbamates undergo “lethal synthesis”

A

False

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which of the following toxins acts mainly as an alpha-2 agonist?

  • Amitraz
  • DEET
  • Couphos
  • Pyrethrins
A

Amitraz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which tissues are best for postmortem diagnosis of pyrethrin toxicity?

A

liver and brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What chemical property of Chlorinated Hydrocarbons is responsible for bioaccumulation in the food chain?

A

Chlorinated Hydrocarbons are highly lipophilic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

T/F: Pyrethrins are generally not very toxic to mammals, but very toxic to birds and fish

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Would you expect to see CNS stimulation or CNS depression with D-Limonene toxicity?

A

CNS depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

T/F: Some organophosphates undergo “lethal synthesis”

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

T/F: Chlorinated Hydrocarbons generally degrade relatively quickly in the environment

A

False

Soil half-life reportedly between 2-15 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

T/F: 2-PAM is not reliably effective for treatment of carbamates

A

True

Reversible binding reduces benefit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Why is piperonyl butoxide or MGK-264 added to pyrethrins?

A

Inhibits pyrethrin metabolism in insects

(but potentially increases toxicity in mammals)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

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

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the best tissue to sample post-mortem for diagnosis of Rotenone toxicity?

A

liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Which of the following toxins are dogs more sensitive to than cats?

  • Bromethalin
  • Rotenone
  • Strychnine
  • Amitraz
A

Strychnine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the specific lesions associated with organophosphates?

A

No specific lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Which of the following has direct acetylcholinesterase activity?

  • Dichlorvos
  • Diazinon
  • Fenthion
  • Parathion
A

Dichlorvos

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the mechanism of action (MOA) of D-Limonene?

A

Unknown

However, it is suspected that it may act through central and peripheral vasodilation due to an undetermined neuronal mechanism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the two most common signs of Rotenone toxicity?

A

Respiratory depression and convulsions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the main clinical sign of Chlorinated Hydrocarbon toxicity?

A

CNS Stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the mechanism of action (MOA) of carbamates?

A

Reversible inhibition of cholinesterases

Acetylcholinesterase can hydrolyze carbamates, but at a slower rate than Ach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Why do you want to avoid hypothermia when treating small patients who have had topical pyrethrin exposure?

A

Hypothermia may further alter Na+ channel kinetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

The dose that will produce alterations (hematologic, biochemical, pathologic, or clinical), and administering twice this dose will result in lethality is called:

A

Toxic Dose High (TDH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the mechanism of action for organophosphates?

A

Irreversible inhibition of cholinesterases

This will increase acetylcholine at all cholinergic sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What species is most sensitive to Chlorinated Hydrocarbons?

A

Cats

All animals are susceptible (nonspecific) but cats are the most sensitive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the main storage tissue for Chlorinated Hydrocarbons?

A

FAT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What condition in canine patients is commonly treated with o,p-DDD?

A

Pituitary dependent hyperadrenocorticism (Cushing’s Syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the mechanism of action (MOA) of pyrethrins?

A

Delay closure of Na+ channels in the axonal membrane of the insect

This leads to knockdown effect, which is rapid paralysis caused by inhibition of neurons (the insect is immobile, but not dead yet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

T/F: Chlorinated Hydrocarbons (DDT, for instance) are highly lipophilic and excreted in the bile. This suggests that they likely undergo enterohepatic recirculation

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

T/F: Organophosphates become more toxic after being stored for a long period of time

A

True

If sealed and stored for 1-2 years, will become more toxic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Which drug would you use in pyrethrin toxicity to control severe muscle tremors?

A

Methocarbamol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

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?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

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

A

Respiratory failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is the mechanism of action (MOA) of Rotenone?

A

Blocks oxidative phosphorylation, preventing NADH from being oxidized to NAD, thus interfering with production of ATP

Affects cell respiration (crosses cell membranes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

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
A

FFP

Fresh Frozen Plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

How are animals most commonly exposed to organophosphates?

A

Orally (contaminated feed)

Exposure may also occur dermally (when used as a dip or spray) or via inhalation (aerosol spray)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

T/F: Atropine is used to treat muscarinic and neuromuscular signs associated with organophosphate toxicity

A

False

Atropine does not treat the neuromuscular problems; just the muscarinic signs

52
Q

T/F: Alkalinization of the stomach increases absorption of Nicotine

A

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
Q

What is the mechanism of action (MOA) of Nicotine?

A
  • 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
Q

What drug is useful for controlling the parasympathetic effects of Nicotine toxicity?

A

Atropine

55
Q

What is the mechanism of action (MOA) of Amitraz?

A

alpha-2 agonist in the CNS

  • Weak alpha-1 agonist activity
  • Weak monoamine oxidase (MAO) inhibitor
56
Q

What is the most common clinical sign associated with Amitraz toxicity?

A

Transient Sedation

May last 24-72 hours

57
Q

Why is hyperglycemia often seen associated with Amitraz toxicity?

A

alpha-2 inhibition of insulin

58
Q

Name two antidotes for Amitraz toxicity. Which one is considered the better option?

A

Yohimbine and Atipamezole

Atipamezole is considered the better option because it has fewer cardiorespiratory effects than yohimbine

59
Q

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

A

No

5mg% = 5000 mcg/dL

Therefore, 900 mcg/dL is not high enough to require therapy

60
Q

Which three insecticides that we covered in class are CNS depressants?

A

Amitraz, Ivermectin, D-limonene

*Financial AID can be depressing*

61
Q

DEET concentration of ____ppm is considered diagnostic for DEET toxicity

A

20 ppm

62
Q

What is the most common source of Naphthalene toxicity?

A

Ingestion of mothballs

63
Q

What is the mechanism of action (MOA) for Naphthalene?

A

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
Q

T/F: The amount of poison that under a specific set of conditions will result in detrimental biologic changes is known as LD50

A

False

The amount of poison that under a specific set of conditions will result in detrimental biologic changes is called _toxicity_

65
Q

Which of the following toxins works though its inhibition of oxidative phosphorylation in the TCA cycle?

  • Rotenone
  • Methoxychlor
  • Naphthalene
  • Cholecalciferol
A

Rotenone

66
Q

A compound that has a LD50 of 100mg/kg is considered:

  • Practically nontoxic
  • Slightly toxic
  • Highly toxic
  • Moderately toxic
  • Extremely toxic
A

Moderately toxic

67
Q

T/F: Atropine is effective in treating muscle fasciculations as a result of organophosphate toxicity

A

False

68
Q

The effect of a toxicant produced by daily exposure for 30 days or less is decscribed as:

A

subacute toxicosis

69
Q

A compound that has LD50 of 200 mcg/kg is considered:

A

extremely toxic!

70
Q

The first clinical signs in organophosphate poisoning are mainly due to:

A

muscarinic stimulation

71
Q

2-PAM antagonizes the toxic effects of organophosphates by:

A

reactivation of acetylcholinesterase

72
Q

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

A

True

73
Q

The “knockdown” effect is used to describe the action of what insecticide?

A

Pyrethrins

74
Q

The preferred medication for initial control of seizures in a dog with an unknown toxicant would be:

A

Diazepam

75
Q

What animals are most susceptible to Ivermectin toxicity?

A

dogs and small birds

Collie breeds are especially susceptible

76
Q

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?

A

0.03 mL

77
Q

T/F: Ivermectin is well distributed throughout the body and crosses the BBB

A

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
Q

What is the mechanism of action (MOA) of Ivermectin?

A

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
Q

Does D-Limonene cause CNS depression or CNS stimulation?

A

CNS depression

80
Q

What drug is used to treat muscle fasciculations associated with organophosphate toxicity?

A

2-PAM

81
Q

Which of the following should NOT be used in the treatment of organophosphate poisoning in dogs?

  • acepromazine
  • atropine
  • activated charcoal
  • diphenhdramine
  • diazepam
A

acepromazine

82
Q

In a chemical analysis, the result is expressed as 67 µg/g. What is the equivalent to this value in %?

A

0.0067%

1 µg/g = 0.0001%

Fun fact, right? Wrong - That fact isn’t even a little bit fun.

83
Q

The effect of a toxicant produced by daily exposure for 30 days or less is decscribed as:

A

subacute toxicosis

84
Q

The dose which will produce alterations (hematologic, biochemical, pathologic, or clinical) and administering twice this dose will result in lethality is called:

A

toxic dose high (TDH)

85
Q

In a chemical analysis, the result is expressed as 9 µg/g. This is equivalent to what value in %?

A

0.0009%

1 µg/g = 0.0001%

86
Q

The relative toxicity of drug A is 35 mg/kg. How would this drug be classified?

A

Highly toxic

87
Q

T/F: Emesis is recommended for patients with CNS signs as a result of Tea Tree Oil toxicity

A

False

Emesis is not recommended due to risk of aspiration

88
Q

When would you expect onset of clinical signs of tea tree oil (TTO) toxicity?

A

2-12 hours

89
Q

1 kg = ____ lb

A

1 kg = 2.2 lbs

90
Q

100 g/ton = _____ ppm

A

100 g/ton = ~110 ppm

91
Q

1 µg/g = _____%

A

1 µg/g = 0.0001%

92
Q

1 gal = _____ ounces

A

1 gal = 128 ounces

93
Q

1 ppm = _____ mg/L

A

1 ppm = 1 mg/L

94
Q

0.1 mg% = _____ ppm

A

0.1 mg% = 1 ppm

95
Q

If a dog ingests a rat that recently feasted on a pile of warfarin, what is that an example of?

A

Relay Toxicosis (2o toxicosis)

96
Q

What species is most susceptible to anticoagulant rodenticide toxicity?

A

Dogs

Order of sensitivity: Pigs > dogs & cats > ruminants > horses & chickens

97
Q

Which one has a longer half-life: Warfarin or Brodifacoum?

A

Brodifacoum

  • t1/2 of Brodifacoum: 6 days
  • t1/2 of Warfarin: 19 hours
98
Q

What is the general mechanism of action (MOA) of anticoagulant rodenticides?

A

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
Q

When would we expect to see onset of clinical signs with anticoagulant rodenticide toxicity?

A

1-5 days

100
Q

T/F: Animals with anticoagulant rodenticide toxicity may die without external evidence of bleeding

A

True

101
Q

Name the lesions associated with anticoagulant rodenticide toxicity:

A

Intrapulmonary, intrathoracic/abdominal hemorrhage, petechiation, ecchymosis

102
Q

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)
A

PIVKA

Proteins induced by vitamin K antagonists (PIVKA)

103
Q

What Vitamin K-dependent clotting factor has the shortest half-life?

A

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
Q

T/F: Vitamin K3 is the treatment of choice for anticoagulant rodenticide toxicity

A

False

Vitamin K3 is not effective and has stupid side effects. Use Vitamin K1

105
Q

T/F: Phytonadione is the treatment of choice for anticoagulant rodenticide toxicity

A

True

Phytonadione is Vitamin K1 (oral route is recommended)

106
Q

T/F: Vitamin K1 should always be given IV

A

False

Vitamin K1 should pretty much always be given orally. If given IV there is a high risk of anaphylaxis

107
Q

T/F: Response to Vitamin K1 may be reduced in liver failure

A

True

108
Q

What would your duration of Vitamin K treatment be for Warfarin?

A

~1 week

109
Q

What would your duration of Vitamin K treatment be for Brodifacoum?

A

~4 weeks

110
Q

If anticoagulant rodenticide intoxication is suspected but you do not know what specific rodenticide was ingested, how long should you treat with Vitamin K1?

A

4 weeks (28 days)

111
Q

T/F: Nursing animals can be exposed to cholecalciferol rodenticides through the milk

A

True

112
Q

What is the general mechanism of action (MOA) of cholecalciferol rodenticides?

A

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
Q

When do you expect onset of clinical signs associated with cholecalciferol rodenticides?

A

24-36 hours

114
Q

If a patient presents with hypercalcemia and significantly elevated parathyroid hormone (PTH) level, would cholecalciferol rodenticide be on the top of your differential list?

A

No

  • The top differential would be hyperparathyroidism*
  • Cholecalciferol rodenticide toxicity results in hypercalcemia, hyperphosphatemia, and decreased PTH*
115
Q

T/F: Bromethalin is effective against warfarin resistant rodents

A

True

116
Q

T/F: Guinea pigs are resistant to Bromethalin

A

True

Guinea pigs lack the correct metabolic enzymes for Bromethalin

117
Q

T/F: Bromethalin undergoes “lethal synthesis”

A

True

Metabolized by N-demethylation in the liver to the metabolite desmethylbromethalin (more toxic)

118
Q

T/F: Bromethalin does not undergo hepatic recirculation

A

False

It does.

119
Q

What is the mechanism of action (MOA) for Bromethalin?

A

Uncoupling of oxidative phosphorylation

Basically this will alter ATP production, resulting in a lack of cellular energy, resulting in cell death

120
Q

What are the ‘primary targets’ for Bromethalin?

A

brain and spinal cord

121
Q

Are acute or delayed clinical signs typically associated with Bromethalin toxicity?

A

Delayed (subacute)

Acute signs are more rare and usually only occur with supralethal doses

122
Q

A dog showing signs of anorexia, vomiting blood, cardiac arrhythmias, polyuria and polydipsia is MOST likely intoxicated with what rodenticide?

A

Cholecalciferol

123
Q

Which of the following is an indicator of much poorer prognosis in cases of cholecalciferol rodenticide poisoning?

  • GI bleeding
  • PU/PD
  • Anorexia
  • Lethargy
A

GI Bleeding

124
Q

T/F: Anticoagulant rodenticides inhibit production of precursor proteins of clotting factors II, VII, IX, and X

A

False

Anticoagulant rodenticides inhibit _activation_ of precursor proteins of clotting factors II, VII, IX, and X

125
Q

List the species sensitivity to anticoagulant rodenticides in decreasing order:

A

pigs > dogs & cats > ruminants > horses > chickens

RUSVM Toxicology (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions