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RUSVM Toxicology > Nicotine, Neonicotinids, And Naphthalene > Flashcards

Nicotine, Neonicotinids, And Naphthalene Flashcards

1
Q

How is Naphthalene produced?

A

Combustion

  • cigarette smoke
  • car exhaust
  • forest fire smoke
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2
Q

How do mothballs act as a pesticide?

A

Slow release of naphthalene gas vapor that kills and repels moths/insects

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3
Q

How do the old version of mothballs differ from the new version?

A

Old -naphthalene (highly toxic and flammable)

New- paradichlorobenzes (less toxic)

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4
Q

Are cats or dogs more sensitive to naphthalene?

A

Cats

But dogs are more likely to ingest

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5
Q

What is the lowest canine lethal dose of naphthalene?

A

400mg/kg

One mothball can be 2.7-4g —> single mothball can be highly toxic

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6
Q

Generally, what is the exposure route to naphthalene?

A

Absorbed through inhalation, orally and dermally

Vapor can cause eye irritation

Repeated exposures can cause skin rash/cataracts

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7
Q

How do oils afffect absorption of naphthalene?

A

Lipid soluble —> increase absorption

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8
Q

Acids _________and bases __________ stomach absorption of naphthalene

A

Delay; enhance

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9
Q

Where is naphthalene distributed after is is absorbed?

A

Bloodstream —> rapid distribution to adipose tissue

Found in high concentrations in adipose, kidney, liver, and lungs

Cross placental

Excreted in milk

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10
Q

How is naphthalene metabolized?

A

Hepatic enzyme
-> expoxide or quinones (cause cellular damage)

  • > conjugated with glutathione to non-toxic metabolites
  • > conjugation with sulfate, glucuronic acid, or mercapturic acid to be excreted in urine or bile
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11
Q

What is the MOA of naphthalene?

A

Oxidative metabolites in the circulation can cause hemolysis and methemoglobinemia

  • hemolysis - rupture of RBC
  • methemoglobinemia - decrease ability to bind oxygen —> tissue hypoxia
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12
Q

What are clinical signs associated with naphthalene ?

A

Dissolve slowly when digested in acid stomach but show up days when in basic intestines

Salivation 
Vomiting 
Mothball breath
Pale or brown gums
Methemoglobinemia, hemolytic anemia, or hemoglobinuria 
Weakness or lethargy 
Labored breathing 
Tremors and seizures
Cataracts in neonates
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13
Q

How can you diagnose naphthalene toxicity?

A

Hematologic changes

  • hemolysis and heinz bodies
  • methemoglobinemia (chocolate brown blood)
  • hemoglobinuria
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14
Q

What is the prognosis for naphthalene toxicity?

A

Good for those treated promptly and without pre-existing liver or kidney disease

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15
Q

What is the treatment for naphthalene toxicity?

A

Decontamination

  • emesis and activate charcoal
  • sodium bicarb —> reduced precipitation of hemoglobin in kidney
  • IVfluids

Specific treatment for methemoglobinemia

  • ascorbic acid
  • methylene blue 1%
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16
Q

What role does ascorbic acid play in treatment of naphthalene ?

A

Reduce methemoglobin to hemoglobin (relatively slow conversion)

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17
Q

How does methylene blue help treat naphthalene toxicity?

A

Leucomethylene blue is a reducing agent at low dose to make methemoglobin —> hemoglobin

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18
Q

Do we use a high dose or low does of methylene blue in naphthalene toxicity?

A

Low (reducing quality)

At high doses methylene blue has oxidizing effect and can increase methemoglobin

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19
Q

What does nicotine come from?

A

Water soluble alkaloid from dried eaves of tobacco plant

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20
Q

How are animals exposed to nicotine?

A

Insecticides

  • absorbed through the mucous membranes and respiratory tract (caustic)
  • ingestion of contaminated feces

Ingestion of tobacco products (leaves, cigarettes, cigars)

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21
Q

Do acids delay or enhance grastric absorption of nicotine ?

A

Delay

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22
Q

How toxic is nicotine to dogs?

A

Highly toxic

oral LD50 of 9.2mg/kg

Cigarette has 9-30mg
Cigars 45-150mg

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23
Q

What are the toxicokinetics of nicotine?

A

Enters the body and is distributed rapidly through the bloodstream, including CNS

Half life about 2hrs in human

24
Q

Where is nicotine metabolized and excreted?

A

Liver metabolize to cotinine and nicotine oxide

Metabolites excreted in urine

25
Q

Does renal excretion increase/decrease in an acidic urine?

A

Increase

26
Q

What is the MOA of nicotine toxicity?

A

Potent stimulant of PSNS
-cholinergic receptor agonist

At low dresses, mimics ACh and stimulates CNS, ganglia and neuromuscular junctions

At high dose, stimulation followed by blockage (nicotinic block)

27
Q

What clinical signs are associated with nicotine toxicity?

A

Early

  • ataxia, lethargy
  • hypersalivation, vomiting
  • bradycardia
  • tremors/convulsions

Late

  • CNS depression, tachycardia, vasodilation
  • paralysis of respiratory muscles (resp failure)
28
Q

How can you diagnose nicotine toxicity?

A

Observation
History of exposure and clinical signs

Antemortem- tox analysis of blood, vomitus, gastric contents, and urine

PM- liver analysis, kidney, other tissues

29
Q

Early

  • ataxia, lethargy
  • hypersalivation, vomiting
  • bradycardia
  • tremors/convulsions

Late

  • CNS depression, tachycardia, vasodilation
  • paralysis of respiratory muscles (resp failure)

What is your DDx?

A 
Strychnine 
Methylxanthines 
Tremorgenic mycotoxins 
Organophosphates 
Carbamates 
Depressants
30
Q

How do you treat nicotine/neonicotinoid toxicity?

A

Decontamination

  • emesis or gastric lavage
  • auto decontamination-CRTZ stimulation and vomiting
  • activated charcoal
  • avoid antacids which promote absorption
Enhance excretion (diuretics) 
-iv fluids or lower urine pH

Atropine for parasympathetic effects (in late phase)

Diazepam to control seizure

31
Q

What is the prognosis for nicotine toxicity?

A

If animal survives the first 4 hours, prognosis is good

Grave if large amounts have been ingested

32
Q

What is one of the most widely used insecticide used in the world (about 25% of all insecticide use)

A

Neonicotinoids

-imidacloprid (the most widely used)

33
Q

What is the source of neonicotinioids?

A

Synthetic insecticides that are similar to nicotine

34
Q

Are neonicotinoids lipid/water soluble??

A

Water soluble

35
Q

How are neonicotinoids degraded?

A

By light

In environment -> slowly
34day halflife

36
Q

How are neonicotinoids absorbed, metabolized, and excreted?

A

Absorbed -poorly
Metabolized - liver
Excreted- bile and urine

37
Q

What is the MOA of neonicotinoids ?

A

ACh receptor agonist -> binds to nicotinic receptors

Bind acetylcholinesterase (irreversible)

—> high levels cause overstimulation of cholinesterase -> paralysis and death

38
Q

What is the toxicity of neonicotinoids to mammals and birds?

A

Relatively low toxicity to mammals and birds

Cannot cross BBB in mammals

39
Q

What are the metabolized products of neonicotinoids ?

A

Charged nitrogen metabolites - potential for toxicity in non-targeted or mammalian species

40
Q

Where does rotenone come from?

A

Plant extract - naturally in seeds and stems of several plants (vines and roots of Fabaceae plants)

41
Q

Rotenone is readily degraded when exposed to??

A

Warm air and light

42
Q

Is rotenone lipid/water soluble?

A

More lipophilic than hydrophilic

43
Q

The GI tract and dermal absorption of rotenone is low unless ??

A

Mixed with fats/oils

44
Q

In ingestion or inhalation more toxic for rotenone toxicity?

A

Inhalation

-> direct pathway to circulatory system

45
Q

Where is rotenone metabolized and excreted

A

Metabolized - liver

Excreted - urine/feces

46
Q

Rotenone is highly toxic to what species?

A

Fish and Arthropoda

-exposure through gills or trachea —> bloodstream and converted to highly toxic metabolites in liver

47
Q

T/F: rotenone is not highly toxic to mammals and birds

A

True

  • route of exposure is typically through gut
  • broken down to less toxic metabolites before entering bloodstream
48
Q

What is the MOA of rotenone?

A

Blocks oxidative phosphorylation in Krebs cycle
Interfere with election transport chain and ATP production

—> ROS result in oxidative stress damaging DNS and intracellular organelles —> neuronal cell death (neurotoxicity)

49
Q

Dermal exposure to rotenone results in what clinical signs?

A

Local irritation such as conjunctivitis, congestion, and dermatitis

50
Q

Oral exposure to rotenone results in what clinical sings?

A

GI tract irritant, convulsions, muscle tremors, lethargy, incontinence, and respiratory stimulation followed by depression

51
Q

Respiratory exposure to Rotenone results in what clinical signs?

A

Severe pulmonary irritation and asphyxia

52
Q

What are the predominate signs of rotenone toxicity?

A

Neurotoxin, depression, and convulsions

53
Q

In the labwork, what changes would you see due to rotenone toxicity?

A

Hypoglycemia
Liver enzyme changes
Hypoxemia/hypercapnia

54
Q

How can you diagnose rotenone toxicity?

A

History or documentation of exposure

55
Q

What is the treatment of Rotenone?

A

No specific treatment- rapidly metabolized (24hrs)

Detox if appropriate

Supportive treatment (seizures, hypoglycemia)

56
Q

What is the prognosis of rotenone poisoning?

A

Good for bird and mammals

Poor in fish, reptile, amphibians

RUSVM Toxicology (23 decks)

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