Nicotine/Neonicotinoids/Napthalene/Rotenone Flashcards Preview

Toxicology Fall17 > Nicotine/Neonicotinoids/Napthalene/Rotenone > Flashcards

Flashcards in Nicotine/Neonicotinoids/Napthalene/Rotenone Deck (30)
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1
Q

What chemical is in moth balls?

A

Napthalene - highly toxic and flammable - will float in salt solution

Paradichlorobenzene - less toxic - will sink in salt solution

2
Q

Napthalene is produced when things burn.. what are some examples that animals may be exposed to?

A

Cigarette smoke
Car exhaust
forest fire smoke

3
Q

What species is more sensitive to napthalene (mothballs)? What species are more prone to ingestion?

A

Cats are more sensitive but dogs are more likely to ingest

4
Q

What will delay napthalene absorption in the stomach and what will enhance?

A

Acids delay

Bases enhance

5
Q

Where does napthalene distribute upon entering the blood stream?

A

Rapid distribution - found in high concentrations in adipose tissue, kidneys, liver, lungs

Crosses the placenta - excreted in milk

6
Q

How is napthalene excreted?

A

Through the urine primarily and bile.

It is first metabolized in the liver - metabolites can form expoxides or quinones that may cause cellular damage

7
Q

What is the MOA of napthalene?

A

Oxidative metabolites in the circulation can cause hemolysis and methmoglobinemia

*Hemoglobin in the ferric state = no oxygen binding = tissue hypoxia

8
Q

How is napthalene poisoning diagnosed?

A

History, hematological changes - hemolysis, heinz bodies, methemoglobinemia, hemoglobinuria

9
Q

What can be used to treat methemoglobinemia?

A

Methylene blue

10
Q

What is the prognosis for patients that have eaten mothballs?

A

Good for pets who are treated promptly and those who have NO pre-existing liver or kidney disease

11
Q

How is nicotine absorbed?

A

Readily absorbed through the mm and respiratory tract

Absorption in the GIT is less in the stomach bc of the low pH - but will be absorbed more in the intestines as the pH increases

12
Q

What is the LD50 of nicotine in dogs?

A

HIGHLY toxic - LD50 = 9.2 mg/kg

Clinical signs are reported at 1mg/kg

A cigar contains 45-150 mg (which is about 5 times what is found in a cigarette)

13
Q

What is the metabolism/excretion of nicotine in animals?

A

Liver readily extracts nicotine from circulation - the metabolites are inactive and extracted by the kidneys and excreted in the urine

14
Q

Renal excretion of nicotine is increased or decrease in alkaline urine?

A

decreased excretion - increased re-absorption

15
Q

Renal excretion of nicotine in acidic urine is ______

A

Increased

16
Q

What is the MOA of nicotine?

A

Potent stimulant of the parasympathetic nervous system

cholinergic receptor agonist

low doses - mimics acetylecholine and stimulates post synaptic nicotinic receptors

High doses - stimulation will be followed by nicotinic blockage

Stimulated chemo-receptor trigger zone to initiate vomiting

17
Q

What is the prognosis of nicotine toxicosis?

A

If an animal survives the first 4 hours, prognosis is good

In dogs, survival is grave to poor when large amounts of nicotine have been ingested

18
Q

_____ are a class of neuro-active insecticides chemically similar to nicotine

A

Neonicotinoids aka neonics

19
Q

What is the most widely used insecticide in the world?

A

Imidacloprid (neonicotinoid)

20
Q

Neonics cause more or less toxicity in non-targeted species when compared to OPs and carbamate insecticides?

A

LESS

But these are linked to honey bee colony declines and have a negative impact on monarch butterfly population

21
Q

Neonics degrade fast or slow in the environment?

A

SLOWLY

they are degraded by direct light (half life is 34 days)

22
Q

What part of neonics are toxic to non targeted species?

A

The charged nitrogen metabolites - occurs during environmental degradation

23
Q

What is the mechanism of action of neonics?

A

Neonics bind to ACh-esterase irreversibly

longer it is bound = harder it is to reverse or treat

24
Q

How do animals typically get rotenone poisoning?

A

Inhalation = most toxic - respiratory exposure in fish

GI tract and dermal absorption is low and incomplete unless mixed with fats and oils (not highly toxic to mammals)

25
Q

What is the metabolism/excretion process of rotenone?

A

Metabolized in the liver and excreted in the urine/feces within 24 hrs

26
Q

Who is most affected by rotenone toxicity?

A

Highly neurotoxic to fish and cold blooded animals

Route of exposure through the gills or trachea

27
Q

What is the MOA of rotenone?

A

Blocks oxidative phosphorylation in the TCA cycle

Interferes with the electron transport chain and NADH during ATP production

Reactive oxygen species will cause neuronal death

28
Q

What are the predominating clinical signs seen with rotenone toxicosis?

A

Depression and convulsions

29
Q

what is the prognosis for rotenone poisoning?

A

Good for mammals and birds

poor for fish and cold blooded animals

30
Q

Regarding the toxicity of various pesticides, indicate the answer that is true:

  1. Napthalene induced oxides in circulation can cause methemoglobinema
  2. Nicotine is a potent stimulant of the parasympathetic NS
  3. Rotenone blocks oxidative phosphorylation
  4. 1 & 3
    All of the above
    None of the above
A

all of the above