Nicotine/Neonicotinoids/Napthalene/Rotenone

Question 1

What chemical is in moth balls?

Answer 1

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

Paradichlorobenzene - less toxic - will sink in salt solution

Question 2

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

Answer 2

Cigarette smoke
Car exhaust
forest fire smoke

Question 3

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

Answer 3

Cats are more sensitive but dogs are more likely to ingest

Question 4

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

Answer 4

Acids delay

Bases enhance

Question 5

Where does napthalene distribute upon entering the blood stream?

Answer 5

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

Crosses the placenta - excreted in milk

Question 6

How is napthalene excreted?

Answer 6

Through the urine primarily and bile.

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

Question 7

What is the MOA of napthalene?

Answer 7

Oxidative metabolites in the circulation can cause hemolysis and methmoglobinemia

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

Question 8

How is napthalene poisoning diagnosed?

Answer 8

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

Question 9

What can be used to treat methemoglobinemia?

Answer 9

Methylene blue

Question 10

What is the prognosis for patients that have eaten mothballs?

Answer 10

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

Question 11

How is nicotine absorbed?

Answer 11

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

Question 12

What is the LD50 of nicotine in dogs?

Answer 12

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)

Question 13

What is the metabolism/excretion of nicotine in animals?

Answer 13

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

Question 14

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

Answer 14

decreased excretion - increased re-absorption

Question 15

Renal excretion of nicotine in acidic urine is ______

Answer 15

Increased

Question 16

What is the MOA of nicotine?

Answer 16

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

Question 17

What is the prognosis of nicotine toxicosis?

Answer 17

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

Question 18

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

Answer 18

Neonicotinoids aka neonics

Question 19

What is the most widely used insecticide in the world?

Answer 19

Imidacloprid (neonicotinoid)

Question 20

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

Answer 20

LESS

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

Question 21

Neonics degrade fast or slow in the environment?

Answer 21

SLOWLY

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

Question 22

What part of neonics are toxic to non targeted species?

Answer 22

The charged nitrogen metabolites - occurs during environmental degradation

Question 23

What is the mechanism of action of neonics?

Answer 23

Neonics bind to ACh-esterase irreversibly

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

Question 24

How do animals typically get rotenone poisoning?

Answer 24

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)

Question 25

What is the metabolism/excretion process of rotenone?

Answer 25

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

Question 26

Who is most affected by rotenone toxicity?

Answer 26

Highly neurotoxic to fish and cold blooded animals

Route of exposure through the gills or trachea

Question 27

What is the MOA of rotenone?

Answer 27

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

Question 28

What are the predominating clinical signs seen with rotenone toxicosis?

Answer 28

Depression and convulsions

Question 29

what is the prognosis for rotenone poisoning?

Answer 29

Good for mammals and birds

poor for fish and cold blooded animals

Question 30

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

Answer 30

all of the above