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RUSVM Toxicology Summer 2019 > Organochlorines and Organophosphates > Flashcards

Organochlorines and Organophosphates Flashcards

1
Q

What is a pesticide?

A

Chemical (natural or synthetic) and other products used to kill, repel, or control pests

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2
Q

What is the major federal agency regulating pesticides?

A

U.S environmental protection agency (EPA)

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3
Q

The federal insecticide, fungicide, and rodenticide act governs??

A

Sale and use of pesticide products within the US

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4
Q

The federal food, drug, and cosmetic act governs ???

A

The limit of pesticide residues on food or feeds

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5
Q

Who approves uses and conditions of use (safe methods, personal protection, ventilation, storage, and disposal ) of pesticides?

A

EPA

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6
Q

EPA determines a “safe” level of pesticide residue called a ____________

A

Tolerance

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7
Q

What are sources of organochlorines?

A

Natural through biological, physical, and chemical processes

-> bacteria, fungi, plants, marine organisms, insects ect

Synthetic -> chlorination process modifying hydrocarbon

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8
Q

Are organochlorines hydrophilic or lipophilic?

A

Lipophilic

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9
Q

What makes organochorines so persistent in the environment?

A

Chlorination of organic compounds reduces reactivity,

Increased size, decreased volatility, increased boiling point

==> stability = environmental persistence

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10
Q

What are the two main groups of organochlorine pesticides??

A

Dichlorodiphenyltrichloroethane (DDT)

Chlorinated alicyclics

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11
Q

What environmental impacts does DDT have?

A

Bioaccumulation-> long half life and accumulation infatty tissue -> toxic levels and death

Biomagnification -> organisms higher in food chain eat lower food chain with concentrations of DDT that is magnified

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12
Q

What type activity does DTT have that can lean to egg-shell thinning?

A

Estrogen like activity

-impairs the shell gland’s ability to excrete calcium carbon to harden the egg shell

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13
Q

______________ was developed to replace DDT, caused acute toxicty, bioaccumulation, and endocrine disruption activity

A

Methoxychlor

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14
Q

_______________ has been banned by EPA for agricultural use but is still approved by FDA for pharmaceutical treatment of lice and scabies

A

Lindane

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15
Q

Exposure to organochlorines usually results from??

A

Not following label directions
Miscalculation of concentrations for sprays to dipping
Unsecured/unlabeled packages/containers
Lack of PPE

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16
Q

How are organochlorines pesticides absorbed?

A

Dermal -> damaged skin facilitates absorption

Lindane and Endosulfan -well absorbed
DDT, Mirex, dicofol, toxophene -less

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17
Q

T/F: when you suspect organochlorine toxicity, you should give fats or organic solvents to decrease absorption across the GI wall

A

False

Organochlorines are lipophilic -> fats and organic solvents will increase their absorption

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18
Q

Where are organochlorines distributed and stored in the body?

A

Stored in fat/lipid fraction of blood and other tissues

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19
Q

T/F: organochlorines are biologically inactive when partitioned and stored in adipose tissue ?

A

True

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20
Q

What can cause mobilization of organochlorines resulting in toxic levels in the circulation?

A

Disease, aging, fasting, lactation

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21
Q

What is the MOA of DDT type pesticides ?

A

Prevents neuronal repolarization by maintaining Na channels open —> continued neurotransmitter release and hyperexcitabilty of the nervous system

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22
Q

What is the MOA of organochlorine pesticides?

A

Binds but does not activate GABA receptors (antagonist)

GABA is inhibitory in CNS -> reduces neuronal excitability/enhance repolariztion

—> inhibit repolariztion

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23
Q

How are organochlorines metabolized?

A

Liver enzymes —> most dechlorinated, conjugated, and excreted

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24
Q

Metabolites of organochlorines which means they can be re-absorbed through what route?

A

Enterohaptic recycling

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25
Q

How are organochlorines excreted?

A

Milk
Feces
Urine

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26
Q

What is the main clinical sign on organochlorine toxicity?

A

CNS hyper stimulation

27
Q

What are the clinical signs caused by organochlorine pesticides ?

A

Salivation, vomiting, apprehension, weakness, incoordination, and disorientation

Tremors, muscle fasciculation, spastic gait, hyperthermia, abnormal posturing, chewing

Tonic-clonic seizure, opisthotonos, coma, death

28
Q

How can you diagnose an organochlorine toxicity?

A

No specific lesions

Chemical analysis -liver brain or blood levels high enough

History of exposure, clinical signs, lack of specific lesions, chemical analysis

29
Q

PIG

Salivation, vomiting, apprehension, weakness, incoordination, and disorientation

Tremors, muscle fasciculation, spastic gait, hyperthermia, abnormal posturing, chewing

Tonic-clonic seizure, opisthotonos, coma, death

DDx??

A

Organochlorine toxicity
Dehydration/Na imbalance
pseudorabies

30
Q

DOG or CAT
Salivation, vomiting, apprehension, weakness, incoordination, and disorientation

Tremors, muscle fasciculation, spastic gait, hyperthermia, abnormal posturing, chewing

Tonic-clonic seizure, opisthotonos, coma, death

DDX?

A 
Organochlorine 
Strychnine 
Fluoroacetate 
Lead 
OP
Metaldehyde 
Rabies
31
Q

Cattle

Salivation, vomiting, apprehension, weakness, incoordination, and disorientation

Tremors, muscle fasciculation, spastic gait, hyperthermia, abnormal posturing, chewing

Tonic-clonic seizure, opisthotonos, coma, death

DDX?

A 
Organochlorine 
OP 
Lead 
Urea 
Polioencephalomalacia 
Infectious thromboembolic meningoencephalitis 
Ketosis 
Nervous forms of coccidiosis
32
Q

What is the treatment of organochlorine toxicity?

A

No specific antidote

Decontaminate

  • wash soap/water if dermal exposure
  • Induce emesis
  • mineral oil or activated charcoal
  • IV lipid or fat emulsion (last resort)

Symptomatic

  • diazepam or barbiturates to control seizures
  • oxygen, ventilation, fluids
33
Q

What is the MOA of organophosphates?

A

Irreversible inactivate acetylcholinesterase —> persistent ACh activity

34
Q

How are animals usually exposed to organophosphates?

A

Contaminated feed or drinking water

Sheep dip or other applications, flea treatment, or medications

Overdose

Intentional poisoning

35
Q

T/F: thiophosphate OPs are more lipid soluble than phosphate OPs

A

True

36
Q

Are organophosphates easily degradable??

A

Yes
Generally persist for 2-4wks
Residues on fruit, veg, and crops may last longer

37
Q

What is storage activation?

A

When stored a chemical becomes more toxic

Eg Parathion, malathion, diazinon, coumaphos

38
Q

How are organophosphates absorbed?

A

Skin and mucous membranes, GIT, and inhalation (lipophilic)

39
Q

What are the usual exposures for organophosphates?

A

Dip or spray -dermal absorption
Contaminated feed or water - oral
Aerial/indoor spray- inhaled

40
Q

Where are organophosphates metabolized?

A

Liver- excretion/bioactivation

41
Q

____________ occurs when liver enzymes metabolize thiophosaphate OPs

A

Lethal synthesis

42
Q

Continued low dose exposure to organophosphates can have what affect on nervous system??

A

Adaption do decreased acetylcholinesterase (homeostatic response)

—> Enzyme induction or increased acetylcholinesterase production
—> receptor down regulation or decrease ACh receptor

43
Q

T/F: phospahate OPs require hepatic bioactivation “lethal synthesis”

A

False

Phosphate OPs are biologically active

Thiophosphate OPs require lethal synthesis by de-sulfuration

44
Q

T/F: thiophosphate OPs undergo enteroheptic recycling

A

True

Highly lipid soluble

45
Q

Where are thiophosphate OPs stored?

A

Adipose tissue

Slow release from fat may lead to delayed and/or prolonged cholinesterase inhibiton

46
Q

What is a major route of elimination of thiophosphate OPs?

A

Paroxonase (serum bound enzyme)

47
Q

What are the three MOAs of organophosphates ?

A

Inhibit cholinesterase

Primary: muscarinic over stimulation —>PSNS

Secondary: nicotinic receptor over stimulation —> CNS and neuromuscular stimulation

Tertiary: nicotinic blockade —> neuromuscular blockade and CNS depression

48
Q

Organophosphate toxicity leads to over stimulation of the muscarinic receptors by ACH, what are the symptoms caused by this?

A

DUMBELLS

Diarrhea 
Urination 
Miosis 
Bronchospasm 
Emesis 
Lacrimation 
Salivation
49
Q

Organophosphates have a secondary effect of activation of nicotinic receptors, what signs may you see due to this?

A

Accumulation of ACh at neuromuscular junction —> paralysis (nicotinic block)

Sweating, hypertension, and tachycardia

50
Q

Organophosphates can cross the BBB, what effects will it have int he CNS?

A

Increased sensory and behavioral disturbances
Incoordination
Depressed motor and respiratory function

51
Q

What is usually the cause of death in animals with organophosphate toxicity?

A

Increased pulmonary sections with respiratory failure

52
Q

What pathology can be associated with organophosphates?

A

Acute death, no specific lesions

Pulmonary edema 
Congestion 
Cyanosis 
Hemorrhage 
Edema 
Necrosis of skeletal muscle
53
Q

How is organophosphate toxicity diagnosed?

A

Analysis or stomach/rumen contest/ hair/ skin

Plasma acetylcholinesterase activity level
<50% activity is suspicious
<25% activity is diagnostic

54
Q

What test can be done in clinic if you suspect organophosphate toxicity?

A

Atropine response test
-has antimuscarinic effect —> ininbit the PSNS

Has no effect on the nicotinic induce paralysis

If atropine positive—> dry skin and mucous membranes, increased heart rate, dilate pupls (low likelyhood of OP poisoning)
If atropine neg-> see none of the above signs due to excessive ACh stimulation —> OP toxicity

55
Q

What is the treatment for OP toxicity?

A

Decontamination
Supportive care

Atropine —> block muscarinic receptor interaction

Cholinesterase reactivators—> reverses OP binding to acetylcholinesterase (pralidoximine or 2-PAM)

Avoid phenothiazines, aminoglycosides, muscle relaxants, and drugs that depress respiration

56
Q

What is the main concern with OP toxicity?

A

Respiratory failure (asphyxia and death) from excessive airway secretions

57
Q

T/F: carbamates require hepatic bioactivation

A

False

—> this makes them more toxic than some OPs in very young patients

58
Q

Where doe carbamates mostly have an effect?

A

Respiratory

-do not penetrate CNS

59
Q

What is the MOA of carbamates?

A

Binds acetylcholinesterase but is REVERSIBLE

—> shorter duration and less important consequences than OPs

60
Q

What are the clinical signs seen with carbmate poisoning?

A

Similar to OP toxicity

SLUD
Salivation 
Lacrimation 
Urination 
Diarrhea
61
Q

What tests can be used to diagnose carbamate toxicity

A

Cholinesterase levels
->because of reversible binding, can dissociate and give a false negative result

Response to atropine therapy

62
Q

What is the treatment for carbamate toxicity

A

Decontamination
Supportive therapy

Atropine

Oxides/PAM-2 no as effective because of reversible binding (in some cases can increase binding)

63
Q

With regards to toxicity, which option is false

A. Phosphate OPs require hepatic bioactivation
B. Thiophosphate OPs do not require hepatic bioactivation
C. Carbamate required hepatic bioactivation
D. All of the above

A

D

RUSVM Toxicology Summer 2019 (10 decks)

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