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Toxicology > Exam I -Organochlorine, OP,Carb, Nicotine, Napthalene, Rotenone > Flashcards

Exam I -Organochlorine, OP,Carb, Nicotine, Napthalene, Rotenone Flashcards

1
Q

What irreversibly inactivates acytylcholinesterase?

A

Organophosphates (OP)

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2
Q

What is the major cause of animal poisoning?

A

Organophosphates

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3
Q

What is the most common organophosphate?

A

Malathion

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4
Q

T/F organophosphates have a various degree of water and lipid solubility

A

True

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5
Q

T/F Organophosphates produce a major issue with tissue and environmental residue

A

False - produce little tissue and environmental residue

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6
Q

What is responsible for 70% of pesticidal use in the US?

A

Organophosphates

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7
Q

Why was Parathion synthesized?

A

To replace DDT as an insecticide

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8
Q

Some organophosphates are micro encapsulated, what does this do?

A

Active ingredient is released slowly, increases the duration of activity and reduces toxicity

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9
Q

Which one is more lipid soluble, Thiophosphate OP or phosphate OP?

A

Thiophosphate

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10
Q

OP degrade relative quickly when exposed to the environment, how long do they generally persist?

A

2-4 weeks

Residues on fruit, vegetables and crops may last longer

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11
Q

What will happen if OPs are sealed and stored for 1-2 years?

A

they become more toxic

‘Storage activation’

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12
Q

What are examples of OPs that have this ‘storage activation’ ability?

A

Parathion
Malathion
Diazinon
Coumaphos

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13
Q

T/F Technical grade chemicals are less pure than reagent grade chemicals

A

True

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14
Q

T/F impurities are less toxic

A

False - more toxic

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15
Q

How are Organophosphates absorbed?

A 
Readily absorbed through: 
skin 
mucous membranes, 
GIT 
inhalation
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16
Q

T/F. OP are extensively metabolized in the liver making them into a “lethal synthesis”

A

True

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17
Q

What could continued exposure to OPs lead to?

A

Adaptation to decreased acetylcholinesterase

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18
Q

What are they types of OPs?

A

Phosphates and Thiophosphates

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19
Q

T/F Thiophsphates are biologically active and phosphates require bioactivation

A

False - phosphates are biologically active and thiophosphates require bioactivation

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20
Q

What OPs has direct effect on acetylcholinesterase (AChE) activity?

A

Phosphates

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21
Q

Thiophosphates are biologically inactive until transformed by liver to ______

A

-oxon metabolites

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22
Q

Thiophosphates are highly ____ soluble and rapidly absorbed in _____ tissue

A

Lipid

Adipose

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23
Q

What may slow release of thiophosphates from fat lead to?

A

delayed and/or prolonged cholinesterase inhibition

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24
Q

What is the major route by which thiophosphate is eliminated?

A

Paraoxonase - a serum bound enzyme

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25
Q

What is the MOA for OPs?

A

Irreversible inhibition of cholinesterase (ACh accumulates throughout CNS)
1st - muscarinic receptor over stimulation
2nd - nicotinic receptor over stimulation
3rd - nicotinic blockade

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26
Q

What could high exposure to OPs lead to?

A

Respiratory failure, paralysis and death

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27
Q

What are the muscarinic effects of OPs overstimulating the PSN?

A 
DUMBELLS
Diarrhea
Urination
Miosis
Bronchospasm
Emesis
Lachrymation
Salivation
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28
Q

What are the nicotinic effects of OPs overstimulation?

A

Acetylcholine accumulation at the neuromuscular junction causes initial stimulation or fasciculations in muscle groups

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29
Q

What would stimulation of the SNS lead to?

A

sweating, hypertension and tachycardia

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30
Q

what does the recovery of OPs ultimately depend on?

A

On the generation of new enzyme or Ach-esterase in critical tissue

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31
Q

What will be the delayed effect of OPs after 10-14 day exposure?

A

Organophosphate-induced delayed polyneuropathy

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32
Q

What occurs in organophosphate induced delayed polyneuropathy?

A

Distal degeneration of long/large diameter motor and sensory axons of peripheral nerves and spinal cord

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33
Q

What clinical signs will you see with organophosphate induced delayed polyneuropathy?

A

Muscle weakness, ataxia, rear limb paralysis

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34
Q

When does organophosphate induced intermediate syndrome occur?

A

2-4 days after acute cholinergic effect and signs of the acute effects are no longer obvious

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35
Q

what sings will you see with organophosphate induced intermediate syndrome?

A

weakness of respiratory muscles (diaphragm, intercostal) and accessory muscles, including neck muscles and of proximal limb muscles

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36
Q

MOA for OPs?

A

Irreversible inhibition of cholinesterase

Non competitive inhibition

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37
Q

How fast is the onset of OP toxicity?

A

15min - 1 hr

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38
Q

How would you be able to detect OP toxicosis?

A

Analysis of stomach/rumen contents
Analysis of hair/skin
may find residues in fat/liver with OPs that are more lipophilic

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39
Q

Why would you normally not use the liver/kidney to assess a patient for OP toxicity?

A

rapid metabolism

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40
Q

How could you do a laboratory diagnosis of OP toxicity?

A

By Plasma acetylcholinesterase activity level

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41
Q

What activity level of acetylcholinesterase is diagnostic of OP toxicity?

A

less than 50% activity is suspicious and less than 25% activity is diagnostic

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42
Q

How could you clinically diagnose OP toxicity?

A

Do a Atropine response test - administer atropine and wait 15 mins.
If positive - dry skin/mucous membranes, increased HR, dilated pupils, decreased bowel sounds
If negative - few or no signs seen

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43
Q

How could you treat an animal with OPs toxicosis?

A

Emesis if ingested and no respiratory depression or seizures seen.
activated charcoal
Wash gently is on skin
Atropine

44
Q

What should you avoid giving a patient with OPs toxicosis?

A

Phenothiazines, Aminoglycosides, muscle relaxants, drugs that depress respiration (opioids)

45
Q

What drug could you give as a specific physiologic antagonist to OPs?

A

Atropine

46
Q

What drug could you give that will reverse the OP binding on the acetylcholinesterase?

A

Pralidoxime or 2PAM

47
Q

How could you treat OP induced delayed polyneuropahty?

A

symptomatic therapy only

48
Q

How could you treat OP induced intermediate syndrome?

A 
Supportive care (rest, nutrition, ventilation) 
2-PAM in severe cases 
May last for weeks
49
Q

What is the prognosis of OP toxicosis?

A

Overall “Guarded”

Depends on each situation

50
Q

What Carbomate is the most toxic?

A

Aldibarb

51
Q

Do carbamates undergo storage activation?

A

no

52
Q

T/F Carbamates penetrate the CNS, require hepatic bioactivation, have a slower onset and longer duration than OPs

A

FALSE
Do NOT penetrate the CNS
Do NOT require hepatic bioactivation
Faster onset and shorter duration than OPs

53
Q

What are carbamates MOA?

A

REVERSIBLE inhibition of acetylcholinesterase

Competitive inhibition

54
Q

What signs will you see with carbamate poisoning?

A 
SLUD
Salivation 
Lacrimation 
Urination 
Diarrhea
55
Q

How do animals usually die from carbamate toxicity?

A

Respiratory failure and hypoxia due to bronchoconstriction leading to tracheobronchial secretrion and pulmonary edema.

56
Q

Would you be able to detect carbamate drug residues in tissue, blood or secretions?

A

no, because of rapid metabolism

57
Q

How could you treat carbamate toxicity?

A

Atropine - same as for OPs

58
Q

Could you also use oxides or 2-PAM in carbamate toxicity like in OP toxicity?

A

its not reliably effective against carbamates

59
Q

What was naphthalene first registered as in the US?

A

Pesticide - then as an insecticide and pest repellent

60
Q

What are mothballs?

A

Pesticides - slowly release of gas vapor kills and repel moths and their larva and other insects

61
Q

The old version of mothballs contained naphthalene, which were highly toxic and flammable, what do the new version of them contain?

A

Paradichlorobenzene - less toxic

62
Q

How could you tell which type of mothball you have?

A

Do a float test - add the ball in saturated salt water, if it floats, its naphthalene based, if it doesnt float, its paradichlorobenzene

63
Q

Where is naphthalene derived from?

A

Crude oil or coal tar

64
Q

Which animal is more susceptible to naphthalene, cats or dogs?

A

Cats more sensitive, but dogs more likely to ingest.

65
Q

What is the lowest canine lethal dose of naphthalene?

A

~400 mg/kg

One naphthalene mothball can be toxic

66
Q

How could naphthalene be absorbed?

A

Orally or dermally

67
Q

What increased the absorption of naphthalene?

A

oils - its lipid soluble. acid in the stomach delays absorption

68
Q

What could repeated exposure to naphthalene cause in the eyes and skin?

A

Cataracts and skin irritation/rash

69
Q

Naphthalene enters the bloodstream and is rapidly distributed, crosses the placenta and is excreted in milk. Where would you find high concentrations of it?

A

In adipose tissue, kidneys, liver, and lungs

70
Q

Naphthalene is metabolized in the liver by hepatic enzymes (CYP450), the metabolites can then form epoxides or quinone, which may cause

A

cellular damage (hemolysis of RBCs)

71
Q

how are naphthalene metabolites excreted?

A

in urine and bile

72
Q

What is Naphthalene MOA?

A

Oxidation products (oxides) in the circulation can cause methemoglobinemia and hemolysis

  • decreased ability to bind oxygen
  • leads to cellular/tissue hypoxia
73
Q

What major signs of toxicity would you see with naphthalene?

A 
Vomiting
Mothball scented breath
Pale or brown gums
Weakness or lethargy 
Labored breathing
Tremors
Seizures
74
Q

T/F Mothballs dissolve quickly when ingested and toxicity is very short lived

A

False - mothballs dissolve slowly when ingested (acid stomach) and toxicity can be delayed by several days

75
Q

How could you diagnose naphthalene toxicity?

A

Hematologic changes - hemolysis, hemoglobinuria, Heinz bodies
Methemoglobinemia - blood s a chocolate brown color

76
Q

What are your Ddx for naphthalene toxicity?

A

Heinz bodies due to acetaminophen, onions, nitrates

77
Q

How could you treat naphthalene toxicity?

A 
Emesis then activated charcoal +/- cathartics
Sodium bicarbonate (can reduce precipitation of hemoglobin in the kidneys)
78
Q

How could you specifically treat methemoglobinemia?

A

Ascorbic acid

Methylene blue 1%

79
Q

How does ascorbic acid work?

A

Reduces methemoglobin to hemoglobin by a non enzymatic reserve mechanism

80
Q

How does methylene blue 1% work?

A

Acts rapidly and works through its conversion to leucomethylene blue, which acts as a reducing agent converting methemoglobin to hemoglobin

81
Q

Why should you not use methylene blue in cats?

A

because feline RBCs are susceptible to oxidative injury

82
Q

T/F Nicotine is a lipid soluble alkaloid readily absorbed through the skin, mucous membranes and respiratory tract

A

False - its a water soluble alkaloid. rest is true

83
Q

The liver readily extracts nicotine from circulation and makes two principal oxidative metabolites cottoning and nicotine-1-N-oxide, how are they excreted?

A

By the kidneys - renal excretion is increased in acidic or low urine pH. If urine pH is increased, re-absorpiton will occur

84
Q

Nicotine is a potent stimulant of ____ nervous system

A

Parasympathetic

85
Q

What does nicotine mimic at low doses?

A

acetylcholine and stimulates post-synaptic nicotinic receptors (CNS, ganglia, neuromuscular junctions)

86
Q

what would high dosed of nicotine cause?

A

stimulation will be followed by blockage (persistent depolarization)

87
Q

What does nicotine stimulate to cause auto decontamination?

A

Stimulates the Chemo-receptor trigger zone (CRTZ) to initiate vomiting

88
Q

What are the clinical signs of early nicotine toxicity?

A

Ataxia, lethargy, hypersalivation, vomiting (CRTZ reaction), bradycardia (vagal stimulation), tremors, convulsions

89
Q

What are the clinical signs of late or high dose toxicity with nicotine?

A

CNS depression, tachycardia, vasodilation, paralysis or respiratory muscles and death

90
Q

What will your Ddx be for nicotine toxicity?

A 
Strychnine
Methylxanthines
Tremorgenic mycotoxins
Organophosphates
Carbamates
Depressants
91
Q

How could you treat nicotine toxicity?

A 
Emesis, gastric lavage
Activated charcoal
Enhance excretion - IV fluids
Atropine (for PSN effects)
Diazepam (seizures)
92
Q

What should you avoid giving animals with nicotine toxicity?

A

Antacids - they raise pH and increase GI absorption and decrease excretion

93
Q

What is a direct nicotinic antagonist drug used in humans (has no known use in animals)?

A

Mecamylamine

94
Q

What is the prognosis of an animal with nicotine toxicity?

A

if the animal survives first hrs, its good

If animal ingested large amounts - survival is grave to poor

95
Q

Where does rotenone come from?

A

Plant extract - jicama vine plant and roots of several members of fabaceae

96
Q

What is rotenone used for?

A

Pets/horses - lice/tick
Chickens - mites
crops for aphids (plant lice)
Rivers/lakes to kill unwanted fish

97
Q

T/F Rotenone has minor and transient environmental side effects, its readily degraded upon exposure to warm air and light, and more hydrophilic than lipophilic

A

False - its more lipophilic than hydrophilic. all else is true

98
Q

What route of absorption is rotenone more toxic?

A

Inhalation - direct pathway to circulatory system

99
Q

GI tract and dermal absorption is low and incomplete with rotenone, unless if mixed with what?

A

fats/oils

100
Q

Rotenone is metabolized in the liver and excreted in urine/feces within ___ hrs

A

24

101
Q

Rotenone is highly neurotoxic to ___ and cold blooded animals

A

Fish

102
Q

T/F In fish, route of exposure to rotenone is through the gills or trachea, it passes directly into the bloodstream through the gills and converted to highly toxic metabolites in the liver

A

True

103
Q

T/F Rotenone is highly toxic to humans, mammals, and birds. Route of exposure is typically through the gut

A

False - its not highly toxic to these species

104
Q

What is the MOA of rotenone?

A
  • Blocks oxidative phosphorylation in the citric acid cycle (TCA cycle)
  • interferes with the mitochondria electron transport chain and NADH during ATP production
105
Q

What clinical signs will you see with rotenone?

A

Irritant - conjunctivitis, congestion, dermatitis
Depression, convulsions
PO - GI tract irritant, convulsions, muscle tremors, lethargy, incontinente,
Pulmonary irritation, asphyxia

106
Q

How could you treat rotenone toxicity?

A

No specific treatment
Detoxification if appropriate
Supportive treatment (treat seizures, hypoglycemia)

Toxicology (7 decks)

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