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Toxicology > Toxicology Exam 1 > Flashcards

Toxicology Exam 1 Flashcards

1
Q

What is the governing agency that regulates pesticides?

A

EPA - environmental protection agency

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2
Q

What are the two major federal pesticide statuses regulated by the EPA?

A

FIFRA (federael insecticide, fungicide, and rodenticide act) - governs the sale and use of pesticide products in the US.

FFDCA (federal food, drug, and cosmetic act) - governs the limit of pesticide residues on food and feeds

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3
Q

What does the EPA determine?

A

Whether a “safe” level of pesticide residue, called a “tolerance” can be established before registration

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4
Q

The EPA specifies approved uses and conditions of uses, including what?

A

safe methods of handling (personal protection, ventilation, etc), storage, and disposal

must be explained on the product label - material safety data sheet

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5
Q

What are some natural sources of organochlorines?

A

through biological, physical, and chemical processes

  • include bacteria, fungi, plants, marine organisms, insects, and other animals, to forest fires, volcanoes, and other geothermal events
  • major sources include oceans followed by soil
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6
Q

what are some synthetic sources of organochlorines?

A
  • chlorination modifies the physical properties of hydrocarbons in several ways resulting in a wide structural variety and divergent chemical properties that leads to a broad range of names and applications.
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7
Q

what are some chemical properties of organochlorines?

A
  • persistent in the environment –> chlorination of the organic compounds reduces reactivity - results in increased size, decreased volatility, increased boiling point - MORE STABLE
  • persistent in the environment!
  • lipophilic
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8
Q

what are the two main groups of organochlorine pesticides?

A

DDT type compounds

chlorinated alicyclics (open and closed chains)

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9
Q

What was the effect of DDT on many birds?

A
  • biomagnification
  • eggshell thinning - estrogen like activity impairs the shell gland’s ability to excrete calcium carbonate to harden the shell

endocrine disruptor

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10
Q

what was an unintentional consequence of DDT use?

A
  • DDT was used to reduce malaria in Borneo
  • observed that thatched roofs were collapsing because DDT killed the wasps that ate thatch eating caterpilars
  • dead wasps were eaten by lizards and then eaten by cats
  • cats died as a result –> increase in rodents
  • increase in rodent related diseases
  • stop use of DDT
  • CAT DROP to drop an excess of 20 cats in the area
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11
Q

Why were organochlorines developed?

A

to replace DDT (methoxychlor)

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12
Q

what are the uses of Methoxychlor?

A

used to protect crops, ornamentals, livestock, and pets against fleas, mosquitoes, cockroaches, and other insects

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13
Q

what was the problem with organochlorines?

A

Methoxychlor

  • acute toxicity
  • bioaccumulation
  • endocrine disruption

Lindane (lice and scabies)
- banned by the EPA for agricultural use but still used for pharmaceutical use in humans and animals

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14
Q

how are animals exposed to organochlorines?

A
  • label directions not followed
  • concentrations miscalculates for sprays or dips
  • contaminated feed or water
  • packages or containers unsecured or unlabeled
  • lack of appropriate PPE
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15
Q

How are organochlorines absorbed?

A
  • dermal most common - damaged skin facilitates absorption

- inhalation and oral as well

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16
Q

What is the MOA of DDT-type organochlorines?

A
  • neuronal membrane permeability or transport of Na and K is altered
  • axonal Na channels remain open and K channels don’t open completely –> inhibits repolarization
  • continued NT release
  • hyperexcitability
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17
Q

what is the MOA of chlorinated alicyclic type organochlorines?

A
  • binds to but doesn’t activate GABA receptors –> BLOCKS action of GABA (an antagonist)
  • inhibits repolarization
  • hyperexcitability
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18
Q

how are organochlorines metabolized/excreted?

A
  • liver enzymes - most are dechlorinated (CP450), conjugated, and excreted in feces and urine
  • biliary excretion is major route of decontamination (metabolites can enter enterohepatic recycling, be reabsorbed, and result in toxicity!)
  • excreted in milk
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19
Q

what are the main clinical signs with organochlorines?

A
  • CNS HYPERSTIM
  • salivation, vomiting, weakness, incoordination, disorientation
  • tremors, spastic gait, chewing, hyperthermia, muscle spasms
  • tonic-clonic seizures, opisthotonos, coma, and death
  • some mammals may show intermittent or persistent depression instead of CNS excitement
  • birds may show depression, abnormal postures, blindness, death
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20
Q

how do we diagnose organochlorine toxicosis?

A
  • no specific lesions
  • secondary changes - trauma from convulsions, congestion/edema of organs

chemical analysis
- can confirm acute toxicosis if chemical in blood, liver,r or brain at high concentrations

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21
Q

What are the DDx with organochlorine toxicosis with swine?

A
  • dehydration/Na imbalance

- pseudorabies

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22
Q

What are the DDx with organochlorine toxicosis with dogs and cats?

A
  • strychine
  • fluoroacetate
  • lead
  • organophosphate
  • metaldehyde
  • rabies
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23
Q

What are the DDx with organochlorine toxicosis with cattle?

A
  • OP
  • lead
  • polioencephalomalacia
  • infectious thromboembolic meningoencephalitis
  • ketosis
  • coccidiosis
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24
Q

What is the treatment for organochlorine?

A

no specific antidote

decontamination

  • soap and water
  • induce emesis
  • cathartics
  • activated charcoal
  • IV fat emulsion

symptomatic treatments

  • diazepam or barbiturates for seizures
  • oxygen, ventilation, fluids
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25
Q

when is activated charcoal the most effective?

A

1-3 hours (effective up to 6 if toxicant has delayed release)

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26
Q

what is the MOA of organophosphates?

A

irreversibly inactivate acetylcholinesterase = persistent acetylcholine activity

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27
Q

what are the common exposure routes for organophosphates?

A
  • contaminated feed or drinking water
  • use of empty pesticide containers for feeding/watering animals
  • dusting, spraying of animals or animal grounds or housing
  • sheep dip
  • flea treatment, meds
  • overdose
  • intentional poisoning
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28
Q

Why are organophosphates more toxic after 1-2 years in storage?

A

subject to storage activation

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29
Q

are organophosphates lipo or hydrophilic?

A

lipophilic - readily absorbed through the skin and mucus membranes, GIT, and inhalation

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30
Q

how are organophosphates normally metabolized?

A

in liver - excretion/bioactivation

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31
Q

Which organophosphate requires lethal synthesis?

A

thiophosphate

  • liver enzymes (CYP450) metabolize or bioactivate
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32
Q

what can happen with continued low dose/chronic exposure of OPs?

A
  • can lead to adaptation to decreased acetylcholinesterase - homeostatic response
  • enzyme induction or increased acetylcholinesterase production
  • receptor down regulation or decrease in acetylcholine receptor
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33
Q

thiophosphates are biologically inactive until transformed by?

A

the liver to -oxon metabolites

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34
Q

what is the major route of elimination for thiophosphates?

A

paraoxonase - a serum bound enzyme –> hydrolysis of paraoxon

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35
Q

what is the MOA of OPs? (plus primary - tertiary)

A

Irreversible inhibition of cholinesterases! (end result = increase in acetylcholine!)

  • OP binds to cholinesterase
  • aging = conformational change in OP-AChesterase complex that results in increased or irreversible binding of complex over time

primary: muscarinic receptor over stimulation
seconary: nicotinic receptor over stimulation (neuromuscular and CNS stim)
tertiary: nicotinic blockage (neuromuscular blockade, CNS depression)

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36
Q

what is the result of high exposure with OPs?

A

paralysis of diaphragm leading to pulmonary edema, asphyxia, and death due to respiratory failure

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37
Q

delayed neurotoxicity is possible with what OP?

A

thiophosphates

“OP induced delayed polyneuropathy”

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38
Q

what are the muscarinic effects of OP toxicity?

A

DUMBELLS

  • diarrhea
  • urination
  • miosis
  • bronchospasm
  • emesis
  • lacrimation
  • salivation
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39
Q

what are the nicotinic effects of OP toxicity?

A
  • ACh accumulation at the neuromuscular junction ans preganglionic synapses
  • there are initial stimulations and muscle fasciculations followed by paralysis due to nicotinic block
  • stimulation of the SNS may produce sweating, hypertension, and tachycardia
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40
Q

what are the CNS effects of OP toxicity?

A
  • cross the BBB
  • increase sensory and behavioral distrubances, incoordination, depressed motor function, and resp depression
  • resp paralysis
  • increased pulmonary secretions coupled with resp failure = USUAL CAUSE OF DEATH
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41
Q

what is the normal cause of death in a patient with OP toxicity?

A
  • increased pulmonary secretions coupled with respiratory failure
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42
Q

what is OP-induced delayed polyneuropathy?

A
  • develops 10-14 days after exposure
  • distal degeneration of long/large diameter motor and sensory axons of peripheral nerves and spinal cord
  • clinical signs = muscle weakness, ataxia, rear limb paralysis
  • chickens most sensitive
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43
Q

what is OP-induced intermediate syndrome?

A
  • occurs 204 days after acute cholinergic effect and signs of the acute effects are no longer obvious
  • symptoms and signs occur after apparent recovery from acute effects
  • NO muscarinic signs or muscle fasciculations
  • weakness of resp muscles and accessory muscles
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44
Q

what is the pathology of OP toxicity?

A
  • acute death, no specific lesions

non specific lesions

  • pulm edema
  • congestion
  • cyanosis
  • hemorrhages
  • edema of various organs
  • necrosis of skeletal muscle

delayed effects: degeneration and demyelination of peripheral and spinal motor neurons

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45
Q

what lab diagnosis can we use for OPs?

A
  • plasma achetylcholinesterase activity level

- <50% is suspicious, <25% is diagnostic!

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46
Q

what test can we run to see if an animal has been exposed to OPs?

A

atropine response test

  • if the test is POS (dry MM, increased HR, dilated pupils) = LOW LIKELY OP poisoning!
  • if the test is NEG (no signs seen) = LIKELY OP POISONING
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47
Q

how do we generally treat OP poisoning?

A
  1. decontaminate
    - if dermal, wash gently
    - if ingested and RECENT, induce emesis but NOT if resp is depressed of if there are seizures
    - if ingested, give activated charcoal
  2. supportive care
    - rest, nutrition, ventilation, O2 therapy
  3. avoid phenothiazines, aminoglycosides, muscle relaxants, and drugs that depress the respiration (opioids)
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48
Q

what DRUG do we use to treat OP poisoning?

A

Atropine
- specific ACh
antagonist
- repeat with decreasing doses 3-6 hours based on clinical response

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49
Q

what is the main goal for atropine therapy with OP poisoning?

A

to suppress or dry pulmonary secretions

main concern with OP tox is resp failure from excessive airway secretions

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50
Q

How can we treat OP poisoning with 2-PAM?

A
  • it is a cholinesterase reactivator - “oximes”

- binds to OP-inactivated acetylcholinesterase and reverses the binding

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51
Q

Carbamate pesticides are derived from?

A

carbamic acid

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52
Q

What was the first successful carbamate insecticide?

A

Carbaryl

  • broad spectrum of insect control
  • very low mammalian, oral, and dermal toxicity
  • outdoors - used as a lawn and garden insecticide
  • indoors - used in sprays or baits in the control of pests
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53
Q

what is the MOA of Aldicarb?

A
  • mimics the structure of acetylcholine

- MOST TOXIC Carbamate

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54
Q

do carbamates undergo storage activation?

A

NO

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55
Q

what are the toxicokinetics of carbamates?

A
  • do not penetrate the CNS - effects are mostly resp
  • do NOT require hepatic bioactivation (most toxic than some OPs in very young patients)
  • faster onset and shorter duration than OPs
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56
Q

what is the MOA of carbamates?

A
  • REVERSIBLE inhibition of acetylcholinesterase (competitive inhibition)
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57
Q

what are the clinical signs associated with Carbamate poisoning?

A
  • similar to OP toxicity
  • SLUD (salivation, lacrimation, urination, diarrhea)
  • death results from resp failure and hypoxia due to bronchoconstriction leading to tracheobronchial secretion and pulmonary edema
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58
Q

what is the main drug treatment for carbamate poisoning?

A

atropine!

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59
Q

are oximes or 2PAM effective against carbamates?

A

no - reversible binding reduces benefit

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60
Q

Naphthalene is the toxic component of what household item?

A

mothballs

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61
Q

how many mothballs can cause a toxic reaction in dogs/cats?

A

just one can be highly toxic!

  • 400 mg/kg lowest canine lethal dose
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62
Q

how are animals exposed to naphthalene?

A
  • absorbed through inhalation, orally, dermally, vapor (eye irritation)
  • won’t really be absorbed until it hits the intestine if eaten
  • people keep moth balls in closet
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63
Q

how does pH affect the absorption of naphthalene?

A
  • acids delay
  • bases enhance

it is lipid soluble so the oils increase skin and GI tract absorption

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64
Q

where can we find high concentrations of naphthalene in the body?

A
  • fat, kidneys, liver, lungs
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65
Q

why is naphthalene a risk for fetuses and neonates?

A
  • crosses the placenta

- excreted in milk

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66
Q

how is naphthalene metabolized?

A
  1. metabolized in the liver by hepatic enzymes (CYP450)
    - metabolites can for epoxides or quinones - reabsorption may cause cellular damage
    - metabolites can be conjugated with glutathione to non-toxic substances
    - metabolites can be conjugated with sulfate, glucoronic, or mercapturic acid for excretion
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67
Q

how is naphthalene excreted?

A

primarily through urine but also bile

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68
Q

what is the MOA of naphthalene?

A
  • the oxidative metabolites (oxides) in the circulation can cause hemolysis and methemoglobinemia
  • effect is cellular/tissue hypoxia
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69
Q

what are the main clinical signs with naphthalene?

A
  • salivation
  • vomiting
  • mothball scented breath
  • pale or brown gums
  • methemoglobinemia, hemolytic anemia, hemoglobinuria
  • weakness or lethargy
  • labored breathing
  • tremors and seizures
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70
Q

what are some changes we can see in the blood with naphthalene toxicity?

A
  • hemolysis, heinz bodies
  • methemoglobinemia (blood is chocolate brown)
  • hemoglobinuria
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71
Q

what can we use to treat severe cases of naphthalene poisoning?

A

methylene blue 1%

  • reduces methemoglobin to hemoglobin
  • make sure to use correct dose
  • controversial in CATS - can case hemolysis
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72
Q

how is nicotine absorbed?

A
  • readily through MM and resp tract - caustic

- absorption in GIT –> acids delay/bases enhance absorption

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73
Q

what dose of nicotine are clinical signs reported?

A

1mg/kg

*cigars have 45-150mg

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74
Q

how is nicotine metabolized/excreted?

A
  • liver readily extracts nicotine from circulation
  • two principal oxidative metabolites (cotinine and nicotine oxide)
  • metabolites are inactive and extracted by the kidneys and excreted in urine
  • -> renal excretion is decreased in alkaline or high pH - increased reabsorption
  • -> renal excretion increased in acidic or low urine pH
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75
Q

what is the MOA of nicotine?

A
  • potent PSNS stimulation
  • cholinergic receptor agonist
  • at low doses -> mimics acetylcholine and stimulates post synaptic nicotinic receptors
  • at high doses –> stimulation will be followed by blockage
  • stimulates CRTZ –> vomiting
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76
Q

what are the clinical signs associated with nicotine?

A
  1. early stimulation (ganglionic and neuromuscular)
    - ataxia
    - lethargy
    - bradycardia
    - tremors
  2. later (or with high doses) nicotinic blockade
    - CNS depression
    - tachycardia
    - vasodilation
    - paralysis of resp muscles = RESP FAILURE
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77
Q

how do we treat nicotine poisoning?

A
  1. decontamination
    - induce emesis/lavage
    - activated charcoal
    - AVOID antacids, which increase pH and DECREASE excretion/INCREASE GI absorption
  2. enhance excretion
    - diuretics/IV fluids
    - lower pH of urine
  3. atropine for parasympathetic effects
  4. diazepam to control seizures
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78
Q

what are some properties of neonicotinoids?

A
  • water soluble
  • degrades slowly in the environment
  • degraded by direct light
  • charged nitrogen metabolites (toxic to non target species)
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79
Q

what are the toxicokinetics of neonicotinoids?

A
  • poorly absorbed
  • metabolized in liver
  • excreted in bile and urine
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80
Q

what is the MOA of neonicotinoids?

A
  • ACh receptor agonist - binds to nicotinic receptor
  • bind ACh-esterase (binding is irreversible - OPs too)
  • high levels of ACh agonist and neonic-induced inhibition of cholinesterase results in overstimulation, paralysis, DEATH
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81
Q

neonicotinoids cannot cross the BBB in what animals?

A

mammals!

can cross in insects

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82
Q

what is rotenone only approved for as a use?

A

piscicide

  • used by fish managers to kill unwanted fish in rivers and lakes - NOT SPECIES SPECIFIC - repopulation needed!
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83
Q

explain the exposure routes and metabolism of rotenone

A
  • it is readily degraded upon exposure to warm air and light
  • more LIPOphilic than hydrophilic
  • GIT and dermal absorption is LOW and incomplete UNLESS mixed with fats/oils
  • inhalation is more toxic - direct pathway to circulatory system
  • metabolized in liver and excreted in feces/urine within 24 hours
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84
Q

rotenone is highly neurotoxic to what animals?

A
  • fish and arthropods
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85
Q

what is the route of exposure with rotenone?

A

through the gills or trachea

  • resp mechanism of fish directly linked to water
  • rotenone passes directly into the bloodstream through the gills and is converted to highly toxic metabolites in the LIVER
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86
Q

why isn’t rotenone highly toxic to mammals and birds?

A
  • route of exposure is normally through the gut

- rotenone is readily broken down to less toxic metabolites before toxic quantities can enter the blood stream

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87
Q

what is the MOA of rotenone?

A
  • blocks oxidative phosphorylation in the citric acid cycle
  • interferes with the electron transport chain/ATP production in mitochondria
  • cellular oxygen is reduced, resulting in reactive oxygen species (ROS)
  • ROS can result in oxidative stress, damaging DNA and organelles resulting in neuronal death –> NEUROTOXICITY
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88
Q

What are the clinical signs with rotenone toxicity?

A
  1. dermal exposure
    - local irritation such as conjunctivitis, congestion, dermatitis
  2. oral exposure
    - GIT irritation, convulsions, muscle tremors, lethargy, incontinence, and resp stimulation followed by resp depression
  3. resp exposure
    - severe pulmonary irritation and asyphyxia

Generally as a neurotoxin, depression and convulsions are the main CS

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89
Q

what lab results might we see antemortem with rotenone toxicity?

A
  • hypoglycemia
  • liver enzyme changes
  • hypoxemia/hypercapnia
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90
Q

what is the treatment for rotenone toxicity?

A
  • no specific treatment (rapid metabolism - 24hr)
  • detox if appropriate
  • supportive treatment for seizures/hypoglycemia
91
Q

How are pyrethrin/pyrethroids used?

A
  • home and farm insecticide
  • farm animals
  • companion animals (fleas/ticks)

most cannot be used on cats

92
Q

what is the relationship between pyrethrins and pyrethroids?

A

pyrethroids are synthetic analogs of pyrethrins

  • pyrethroids now make up the majority of commercial household insecticides (like BOP)
93
Q

are pyrethrins water or lipid soluble?

A

lipid

94
Q

so synthetic pyrethroids or natural pyrethrins have higher risk for acute toxicity?

A

natural pyrethrins

95
Q

how does an animal get a chronic toxicity to pyrethrins?

A

respiration mainly, less by dermal

96
Q

in what animals do pyrethrins cause high toxicity?

A
  • high toxicity in bees
  • high acute toxicity in fish and aquatic invertebrates
  • high acute toxicity in cats
97
Q

which generation of pyrethroids are more toxic?

A

second generation (type 2) - do not contain alpha-cyano moiety which increases insecticidal potency and decreases metabolism

98
Q

what are the toxicokinetics of pyrethroids?

A
  • more lipophilic
  • dermal exposure isn’t common –> ingestion and inhalation are rare but possible
  • rapid metabolism through hydrolysis and oxidation
  • conjugated metabolites are excreted in urine within 24hrs after exposure
  • cats are MORE sensitive than dogs (reduced rate of metabolism becauuse of their shitty liver)
  • presence of the alpha-moiety in pyrethroid type 2 decrease metabolism by decreasing hydrolysis
  • doesn’t accumulate in tissues
99
Q

what are pyrethroids commonly formulated with for a synergistic effect?

A

piperonyl butoxide or MGK-264

- both increase toxicity in insects and non-targeted species by delayed metabolism

100
Q

what is the MOA of pyrethrins/pyrethroids?

A
  1. are axonic excitotoxins
  2. similar to organochlorine DDT-type MOA
    - neuronal membrane permeability of Na is altered
    - continued NT release
    - hyperexcitability of the nerve –> depolarization –> paralysis
  3. type 2 pyrethroids have a greater effect on Na channels
    - similar to organochlorine alicyclic MOA at high concentrations - GABA antagonist
    - inhibit neuronal Ca, Mg ATPase activity –> hyperexcitability
101
Q

what endocrine organ might pyrethrins/pyrethroids stimulate?

A

adrenal glands

- increased cortisol resulting in hyperglycemia

102
Q

True/False:

insect metabolism of pyrethrins is much faster than that of mammals

A

FALSE

it’s SLOWER - especially with piperonyl butoxide

103
Q

what are the main clinical signs with acute pyrethrin toxicity?

A
  • generalized muscle tremors, depression, blindness (reversible), ataxia, lethargy
  • salivation, vomiting, diarrhea, hyperexcitability, drooling
  • may progress to seizures, death

many cats DIE or need to be euthanized because of the severity

104
Q

how do we diagnose pyrethrin toxicity?

A
  • no specific lesions
  • generally low tissue levels
  • brain and liver in post mortem are best
  • tissue levels don’t correlate well

diagnosis is generally made with history and appropriate clinical signs

105
Q

how do we treat pyrethrin toxicity?

A
  • no specific antidote
  • decontaminate –> wash with soap/water
  • activated charcoal is NOT used (rapid metabolism)
  • avoid exacerbating the toxicity (monitor and control temp, treat hyperthermia and prevent hypothermia)
  • symptomatic treatment ( methocarbamol for more severe tremors or diazepam/barbs/propofol)
106
Q

what is the prognosis for pyrethrin tox?

A

good except for cats

107
Q

what is the chemistry of DEET?

A
  • nearly colorless liquid with faint odor
  • lipophilic
  • relatively stable but sensitive to light
108
Q

what is the MOA of DEET?

A
  • mosquito attraction to a host is thought to involve long-range (visual) and short range (olfactory) stimuli
  • lactic acid on the skin may be an essential olfactory stimulant to attract mosquito to land
  • effectiveness may be due to its ability to mask sensory perception
109
Q

what is the general toxicity of DEET?

A
  • slightly toxic to some fresh water fish
  • dogs are more susceptible, care more sensitive
  • young animals more sensitive
  • caustic
110
Q

what are the toxicokinetics of DEET?

A
  • dermal absorption (can accumulate and persist in fat)
  • guinea pigs - 19-48% of a topical dose absorbed
  • can increase dermal absorption of other products
  • GI absorption
  • metabolized in the liver and excreted in urine
111
Q

what is the MOA of DEET?

A
  • undetermined!
  • known to affect the olfactory and nervous system in insects
  • when DEET is combined with carbamates the effects are potentiated
112
Q

what are the CS with DEET toxicity?

A
  • rabbits/rats: depression, excitation, ataxia, tremors, seizures, and coma
  • dogs/cats: hypersalivation, vomiting, hyperexcitability, tremors, ataxia, seizures, skin and MM irritation
113
Q

how do we diagnose DEET toxicity?

A
  • history, presentation +/- chem analysis
  • no specific lesions
  • chem analysis can be performed (blood, urine, skin, stomach contents, bile, kidney)
  • 20ppm is diagnostic
  • must differentiate between other CNS excitatory toxins (strychnine, metaldehyde, organochlorine, OP/carbamate)
114
Q

how do we treat DEET toxicity?

A
  • no specific antidote
  • decontaminate
  • if dermal: wash with soap and water
  • emesis if not contraindicated
  • activated charcoal may be given (avoid magnesium cathartics as this may cause CNS depression)
115
Q

the active ingredient of which pesticide might be used to treat the effects of myasthenia gravis?

A

carbamates and OPs

116
Q

which is correctly matched with its MOA?

pyrethrin: monoamine oxidase inhibitor
ivermectin: octapomine receptor antagonist
amitraz: alpha adrenergic receptor agonist

DEET: uncoupling of oxidative phosphoylation

A

amitraz - alpha adrenergic receptor agonist

117
Q

what is the MOA of pyrethrin?

A

Na channel agonist

118
Q

what is the MOA of ivermectin?

A

GABA agonist

119
Q

what is the MOA of rotenone?

A

uncoupling of oxidative phosphorylation

120
Q

what is the MOA of OPs and carbamates?

A

ACh-esterase inhibitors

121
Q

what is the MOA of nicotine and neonics?

A

nicotinic adrenergic receptor agonists

122
Q

what is the MOA of naphthalene?

A

toxic oxides –> hemolysis, methemoglobinemia

123
Q

what drug can increase dermal absorption of DEET?

A

pyrethroids

124
Q

what are the main reasons we use amitraz?

A
  • rapid action against ectoparasites such as ticks and mites
  • can control all life stages
  • used in beekeeping to control Varroa mite
125
Q

what is the MOA of amitraz?

A
  • kills by interfering with nervous system
  • octopamine receptor antagonist
  • works as repellent (detachment effect)
126
Q

what are the main CS with amitraz toxicity?

A
  • hyperexcitability, paralysis, death
127
Q

in what species is amitraz contraindicated in?

A

cats and horse

128
Q

what are some uses of amitraz?

A
  • used in flea and tick collars
  • topical liquid
  • generalized demodicosis in dogs
  • ascaricide/tickicide for swine and cattle
129
Q

does amitraz bioaccululate in the fat?

A

no

130
Q

what are the toxicokinetics of amitraz?

A
  • dermal absorption is low (less than 10% in dogs and pigs)
  • not readily absorbed into tissues, but quickly distributed throughout the body including the brain
  • GIT absorption is moderate - most is quickly excreted unchanged
  • rapidly metabolized in liver and excreted in urine
131
Q

what are the 3 MOAs for amitraz in mammals/vertebrates?

A
  1. alpha adrenergic receptor agonist
    - alpha 2 agonist in CNS
    - alpha 1 and alpha 2 agonist in PNS
    - increase in epinephrine, NE, and dopamine
    - neurotoxic and preconvulsant effects
  2. inhibition of monoamine oxidases
    - can lead to suppression of insulin in dogs
    - also increases NTs
  3. inhibits synthesis of PGs
    - inhibits synthesis from arachidonic acid
132
Q

what is the MOA of amitraz with arthropods?

A

interaction with octopamine receptors

  • toxic effects on arthropods, less so on vertebrates
  • this receptor is less sensitive in vertebrates
  • kills by interfering with nervous system
  • tick’s sharp barbed mouth becomes paralyzed and cannot pierce skins so it falls off
133
Q

what are the main CS seen with amitraz toxicity?

A
  • hyperglycemia
  • hypothermia
  • PU
  • anorexia
  • vomiting
  • diarrhea
  • depression
  • tremors
  • bradycardia

ultimately can lead to CV collapse and rep failure

134
Q

how do we treat amitraz toxicity?

A
  • decontaminate
  • if collar ingested: induce emesis and/or remove, activated charcoal, cathartics, gastric lavage
  • supportive care
  • ANTIDOTE: alpha2 antagonists = yohimbine or atipamezole
135
Q

what is the MOA of ivermectin?

A

gaba agonist
- induces neurological damage by binding to glutamate gates chloride ion channels in nerve and muscle cells of invertebrates that results in paralysi and death

136
Q

what is the main use of ivermectin?

A

broad spectrum antiparasitic agent

  • kills a wide range of internal and external parasites in commercial livestock and companion animals
  • GI roundworms, lungworms, heartworms, mites, lice, and horn flies
137
Q

how are animals exposed to ivermectin?

A
  • extra label use for parasites in dogs/cats
  • formulation errors are most common
  • excessive licking after a pour on
138
Q

what is the gene mutation resulting in multi-drug resistance?

A
  • ABCB1/MDR1 gene codes for P-glycoprotein
  • dogs will have a dysfunctional BBB
  • don’t treat
139
Q

true/false: cats have a higher bioavailability to ivermectin

A

false - lower

give them a higher dose

140
Q

what is the MOA of selamectin?

A
  • binds to glutamate gated Cl channels in parasite NS –> blocks berve transmission
  • no effect in mammal NS

selamectin is revolution

141
Q

what are the main CS with ivermectin toxicity?

A
  • CNS DEPRESSION!!

- mydriasis, blindness, vomiting, drooling, weakness, ataxia, coma

142
Q

how do we diagnose ivermectin toxicity?

A
  • history, clinical presentation
  • no specific lesions
  • chemical analysis possible but not usually necessary
143
Q

how do we treat ivermectin toxicity?

A
  • no specific antidote
  • decontaminate
  • activated charcoal is more useful than emesis
  • supportive care
144
Q

what are the CS associated with EO overexposure?

A
  • unsteadiness
  • depression
  • low body temp (in severe cases)
  • vomiting
  • diarrhea
145
Q

what are the characteristics of D-Limonene?

A
  • cyclic monoterpene hydrocarbon
  • clear, colorless
  • volatile
  • lipophilic
146
Q

what are the sources of exposure for D-Limonene?

A
  1. botanical insecticide
    - 5% d-limonene - controls lice, fleas, ticks
  2. botanical herbicide
    - 70% d-limonene - broad spectrum weed killer
  3. biodegradeable cleaning agents and solvents
    - up to 100% d-limonene defatting and degreasing
147
Q

what percentage of D-limonene is considered safe in a product?

A

1-5%

148
Q

what are the toxicokinetics of D-limonene?

A
  • lipid soluble
  • readily absorbed through skin and GIT
  • maximal blood concentrations 10 mins after dermal exposure
  • metabolized by liver and excreted in urine
149
Q

what is the MOA of D-limonene?

A
  • unknown
150
Q

what CS do we see with d-limonene toxicity?

A
  • ataxia
  • weakness
  • recumbency
  • paralysis
  • CNS depression
  • hypothermia
  • hypotension
  • skin reaction
  • smells like lemons
151
Q

how do we treat D-limonene toxicity?

A
  • decontaminate with shampoo and mild dish soap
  • monitor temp
  • other supportive care
152
Q

what is the most common type of molluscicide used?

A

metaldehyde

  • other types are ACh-esterase inhibitors (OPs), metal salts, and methiocarb (banned in 2014)
153
Q

when using a molluscicide what is mollusk death due to?

A
  • excessive mucus, dehydration, cell damage
154
Q

what are the main properties of metaldehyde?

A
  • restricted use
  • polymer of acetylaldehyde
  • highly flammable
  • hydrophobic
  • short soil half life
155
Q

how are animals exposed to metaldehyde?

A
  • ingestion of bait most common
  • brightly colored and flavored –> dogs want to eat it
  • sometimes malicious poisoning
  • snail baits often mixed with tasty items that would attract other species by accident
156
Q

what are the common routes of exposure for metaldehyde?

A
  • inhalation = most toxic
  • dermal = least toxic
  • ingestion = most common and intermediate toxic
157
Q

what are the toxicokinetics of metaldehyde?

A
  • once ingested, undergoes GIT acid hydrolysis to acetaldehyde
  • readily absorbed as wither metaldehyde or acetaldehyde
  • both cross BBB (neurotox)
  • rapidly metabolozed by liver by P450
  • undergo enterohepatic recirculation (prolongs tox)
  • enzyme inducers may decrease tox
  • excreted in urine
158
Q

what is the MOA of metaldehyde?

A
  • decreased brain GABA -> neuro stimulation
  • increased monoamine oxidase - decreased brain serotonin and NE –> reduced seizure threshold
  • increased neuromuscular activity and production of metaldehyde metabolites –> metabolic acidosis, hyperthermia
  • death from resp failure (acute) or liver failure (chronic)
159
Q

what are the main CS with metaldehyde toxicity?

A
  • acute neuro manifestations within 1-3hr after ingestion
  • initial onset: severe muscle tremors, salivation, ataxia, tachycardia, hyperthermia
  • progression into acidosis: V, D, depression, tonic convulsions that are unresponsive to ext stimuli
  • seizures eventually lead to CNS depression, resp failure, and death within 4-24hrs
160
Q

what are the lesions associated with metaldehyde poisoning?

A
  • acute: nothing specific
  • stomach contents will have a specific apple cider odor
  • petechiae/ecchymoses in GIT
  • congestion, edema, hemorrhage in lungs, liver, kidneys
  • longer survival may result in degenerative changes in liver and brain (ganglion cells)
161
Q

how do we treat metaldehyde poisoning?

A
  • no specific antidote
  • decontaminate
  • emetics
  • gastric lavage
  • activated charcoal
  • enemas
  • fluids to address metabolic acidosis
  • treat seizures
  • muscle relaxants
162
Q

what is the problem with some barbiturates when treating metaldehyde?

A
  • some barbs (pento) can interfere with metabolism of acealdehyde and cause displacement from protein binding sites
  • BUT phenobarb can help accelerate elimination of the toxin!
163
Q

what is the LEAST accurate answer following acute exposure to metaldehyde?

  • increase GABA
  • increased monoamine oxidase
  • decreased serotonin
  • decreased NE
A

increased GABA

164
Q

what happens when ammonia comes in contact with MM?

A
  • forms ammonium hydroxide which is irritating and caustic
165
Q

how does an animal become exposed to ammonia?

A
  • inhalation***
  • environmental conditions
  • decomposing manure in confined animal houses
  • burning plastics
  • used in agricultural fertilizer
166
Q

at what level of NH3 will eyes burn?

A

25-35ppm

167
Q

what exposure of NH3 can cause acute death?

A

5000ppm

168
Q

what are the toxicokinetics of NH3?

A
  • converted to a strong base irritant (ammonium hydroxide) on MM
  • primarily absorbed by inhalation and is distributed to tissue cells
169
Q

what is the MOA of NH3?

A
  1. direct irritation of MM
  2. causes pulmonary edema and lung congestion
    3 alkalosis and compensatory acidosis
  3. inhibit TCA cycle
  4. increased susceptibility can lead to resp infections due to continuous exposure - irritation - inflammation - secondary infections
    - 50-75ppm: decreased ability to clear bacteria from the lungs –> resp dysfunction
  5. decreased growth of young animals
    - 100ppm: decreased growth rate by 32% in swine
170
Q

what are the CS with acute NH3 toxicity?

A

red MM, lacrimation, coughing, sneezing, nasal discharge, keep eyes shut

171
Q

what are the CS with chronic NH3 toxicity?

A
  • decreased growth rate and production

- dyspnea - fluid in the lungs caused by pulmonary edema/congestion

172
Q

what are the CS with terminal NH3 toxicity?

A

CNS stimulation, clonic convulsions, cyanosis

173
Q

how do we diagnose NH3 toxicity?

A
  • history
  • odor of ammonia
  • CS
  • lesions (blisters on MM)
174
Q

how do we treat NH3 toxicity?

A
  • remove source
  • fresh air
  • soothing ointments for eyes
  • antibiotics may prevent secondary infections
  • diuretics for pulm edema
  • treat any secondary infections
175
Q

what are the main properties of hydrogen sulfide gas (H2S?)

A
  • colorless
  • odor of rotten eggs
  • heavier than air
  • flammable
  • water soluble
  • irritant because converted to sulfuric acid
  • forms black or dark colored compounds in GIT and tissues
176
Q

what are the main routes of exposure for H2S?

A
  • INHALATION
  • by product or waste material from industry **
  • may be liberated in coal pits, gas wells, or sulfur springs
  • also associated with natural gas and crude oil production
177
Q

humans can detect H2S at what level?

A

0.025ppm

178
Q

at what level does H2S cause eye irritation?

A

20ppm

179
Q

at what level is H2S possibly fatal?

A

400ppm

180
Q

what does 1000ppm H2S cause?

A

rapid unconsciousness and death in about 1 hour

181
Q

> 2000ppm H2S cause what?

A

resp paralysis after 1-2 breaths

182
Q

what are the toxicokinetics of H2S?

A
  • readily absorbed through the lungs and GIT
  • converted to alkali sulfides in the blood
  • hydrosulfide radical is normally oxidized to sulfate and is excreted in urine
  • some sulfide is excreted in feces
183
Q

what is the MOA of H2S?

A
  • direct irritation of MM
  • inhibition of cellular respiration
  • decreased cytochrome oxidase
  • stimulation of the chemoreceptorsof the carotid body - depressed resp drive
  • DIE FROM ASPHYXIATION
184
Q

what are the CS from acute H2S exposure?

A
  • sudden collapse
  • cyanosis
  • dyspnea
  • convulsions
  • rapid death
185
Q

what are the CS from chronic H2S exposure?

A
  • eye, resp, and lung irritation
186
Q

what are the lesions associated with H2S poisoning?

A
  • blood is dark and may not clot
  • tissues may be dark or greenish purple
  • carcass may have sewage odor
  • if ingested, the GI contents may be black or dark gray and smel of sewage
187
Q

how do we treat H2S toxicity?

A
  • removal of source
  • sodiun nitrite IV may be partly effective by forming methemoglobin - binds sulfide radicals and reactivates cytochrome oxidase
  • oxygen therapy, ventilation
  • educate about prevention (get H2S monitors!)
188
Q

what are the properties of carbon monoxide (CO)?

A

odorless, colorless, not water soluble

189
Q

what are common exposure routes for CO?

A
  • accidental exposure with fires (incomplete combustion of carbon containing products - wood, paper, petroleum products)
  • propane powered equipment, space heaters, portable cookers, de-icers
  • automobile exhaust in confined spaces
190
Q

what is the MOA of CO?

A
  • CO combines with hemoglobin to form carboxyhemoglobin and reduced the level of O2 (hemoglobin has a 240x higher affinity for CO)
  • carboxyhemoglobin interferes with release and availability of O2 carried by hemoglobin
  • some intereference with cellular resp
  • also competes with O2 for binding sites on myoglobin
191
Q

what is death due to from CO poisoning?

A

hypoxia

192
Q

what are the main CS with CO poisoning?

A
  • sudden death at 60-70% COHb

- in low exposure (30-60% COHb) signs = hypoxia, drowsiness, incoordination, dyspnea, lethargy, coma

193
Q

what are the lesions associated with CO toxicity?

A
  • blood is bright red and the MM are pink
  • no significant lesions in acute cases
  • in chronic cases there may be brain edema, hemorrhage, and ecrosis which may cause deafness in dogs/cats
194
Q

what lab diagnostics can we run to confirm CO toxicity?

A
  • measuring CO in air

- percentage of COHb in the blood (correlation to CS is poor)

195
Q

how do we treat CO toxicity?

A
  • oxygen or 5% CO2 in oxygen administered with positive pressure
  • blood transfusion
  • fluid for acidosis but bicarb use is controversial
196
Q

what are the common sources of Nitrogen Oxide gases?

A
  1. farm
    - NO2 and N2O4 gases are produced by incomplete reduction of nitrates during fermentation process in silo’s
    - nitrogen oxide poisoning = Silo filler’s disease
  2. industry
    - NO2 is a major pollutant (burning of fossil fuels)
197
Q

what are the major properties of Nitrogen Oxide gases?

A
  • NO2 gas is reddish brown
  • N2O4 is colorless
  • NO2 is heavier than air but the gases are about as dense as air - forms layers on top of silage and settles down on the chute
  • gas mixture has an irritating chlorine-like odor
  • low solubility in water
198
Q

which nitrogen oxide gas exposure is more toxic - acute or chronic?

A

acute

199
Q

what are the toxicokinetics of nitrogen oxide gases?

A
  • animal quarters that develop the irritant odor or yellow haze in the air must not be entered
  • nitrogen dioxide and tetraoxide gases form nitric acid upon contact with mucus membranes
  • cross resp mucosa and cause cellular damage in the lungs - pulmonary edema
200
Q

what is the MOA of nitrogen oxide gases?

A
  • direct irritation of the MM by nitric acid
  • low water solubility - passes from upper to lower resp tract and causes damage in the lungs
  • lung damage - due to caustic reaction with the PFAs at cellular membrane - pulmonary edema, hemorrhage
  • death is from hypoxia -resp failure
201
Q

what are the CS associated with nitrogen oxide gas toxicity?

A
  • resp signs - generally similar to ammonia poisoning (irritation of MM, effects on respiration)
202
Q

what lesions are associated with nitrogen gas toxicity?

A
  • pulmonary edema
  • hemorrhage
  • emphysema
  • cyanosis
  • methemoglobinemia
  • necrosis of skeletal muscle
203
Q

how do we treat nitrogen oxide gas toxicity?

A
  • supportive treatment
  • diuretics if pulmonary edema
  • methylene blue IV for methemoglobinemia
  • antibiotic ointment for MM
204
Q

at what percentage of methemoglobinemia do we normally start seeing toxic signs?

A

15% (normal is 1%)

205
Q

what are the common sources of exposure with sulfure oxide gases?

A
  • sulfur dioxide SO2 and sulfur trroxide (SO3) are industrial pollutants
  • fossil fuel combustion at power plants
206
Q

what are the main properties of sulfur oxide gases?

A
  • highly soluble in water
  • sharply irritant to MM because the form sulfurous and sulfuric acids on contact with water
  • odor causes coughing, choking, and suffocation
207
Q

SO2 at ___ppm is fatal to cats within 30-60mins

A

500

208
Q

SO2 at 500ppm for __ hour(s) is dangerous to grazing animals

A

1

209
Q

SO2 at ___ppm for 8 days causes poisoning in pigs

A

5-40

210
Q

what is the MOA of sulfur oxide gases?

A
  • direct irritation of the MM - primarily upper resp tract
  • reflex bronchoconstriction - lung damage
  • death due to hypoxia
211
Q

what are the CS and lesions associated with sulfur oxide gas toxicity?

A
  • similar to other toxic gases (irritation to MM, effects on respiration)
212
Q

what all does “smoke” include?

A

vapors, gases, fumes, heated air and particulate matter, liquid and solid aerosols

213
Q

why is there no LD50 for smoke?

A

it is a heterogenous mixture of gases - too many variable

214
Q

inhalation of super-heated air and steam can cause?

A

thermal burns to resp tract and enhance absorption of gases

burns in the resp tract enhances toxicity

215
Q

what are the MOAs of smoke inhalation?

A
  1. simple asphyxiants - inert (CO2) gases or vapors displace O2
    - low concentration, generally have little if any physiological effect
  2. chemical asphyxiant - prevent uptake of O2
    - produce toxic local (lungs) and systemic effects
    - carbon monoxide –> COHb
  3. irritants
    - chemically reactive on contact with MM to cause local effects
    - sulfur dioxide –> sulfuric acid
    - particle - ash and soot
216
Q

what are the CS associated with chemical asphyxiants?

A
  1. resp
    - cough, dyspnea, tachypnea
    - wheezing, decreased breath sounds, crackles
  2. CV
    - tachycardia, hypoxemia
    - hypotension, dysrhythmias
  3. signs of irritation
    - conjunctivitis, pharyngitis, rhinitis, drooling, hoarseness
    - edema, mucosal ulcerations
    - corneal abrasions common from ash/soot
  4. CNS
    - agitation, confusion, ataxia, abnormal posture, seizure
  5. surface burns
217
Q

what kind of lesions might we see with smoke inhalation (chemical asphyxiants?)

A
  • burns
  • pulmonary changes
  • cerebral edema
218
Q

how do we treat smoke inhalation (chem asphyxiants)?

A
  • prompt removal from the smoke environment + O2 support
  • B2 adrenergic agonists may benefit for bronchoconstriction
  • NO STEROIDS
  • remove soot from skin
  • avoid cough suppressants and opioids
  • maintain airway patency, ventilation, etc
219
Q

____ of the toxin (gas, chemical) is the most importany determinant of resp injury

A

solubility

220
Q

highly soluble particles (smoke inhalation) end up where in the resp tract?

A

upper airway

- injury to the mucosa, inflammatory mediators, free radicals –> increased permeability –> edema

221
Q

low water soluble particles (smoke inhalation) end up where in the resp tract?

A
  • lung, bronchiole, alveoli

- slower reaction, delayed effect

222
Q

ammonia and sulfur dioxide have high or low water solubility?

A

high - end up in upper airway

- chemically reactive on contact with mucus

223
Q

nitrogen oxides have high or low water solubility?

A
  • low - end up in pulmonary parenchymal injury in the alveoli, alveolar ducts

Toxicology (12 decks)

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