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RUSVM Toxicology > Organochlorines and Organophosphates > Flashcards

Organochlorines and Organophosphates Flashcards

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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
How are organochlorines excreted?
Milk Feces Urine
26
What is the main clinical sign on organochlorine toxicity?
CNS hyper stimulation
27
What are the clinical signs caused by organochlorine pesticides ?
Salivation, vomiting, apprehension, weakness, incoordination, and disorientation Tremors, muscle fasciculation, spastic gait, hyperthermia, abnormal posturing, chewing Tonic-clonic seizure, opisthotonos, coma, death
28
How can you diagnose an organochlorine toxicity?
No specific lesions Chemical analysis -liver brain or blood levels high enough History of exposure, clinical signs, lack of specific lesions, chemical analysis
29
PIG Salivation, vomiting, apprehension, weakness, incoordination, and disorientation Tremors, muscle fasciculation, spastic gait, hyperthermia, abnormal posturing, chewing Tonic-clonic seizure, opisthotonos, coma, death DDx??
Organochlorine toxicity Dehydration/Na imbalance pseudorabies
30
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?
``` Organochlorine Strychnine Fluoroacetate Lead OP Metaldehyde Rabies ```
31
Cattle Salivation, vomiting, apprehension, weakness, incoordination, and disorientation Tremors, muscle fasciculation, spastic gait, hyperthermia, abnormal posturing, chewing Tonic-clonic seizure, opisthotonos, coma, death DDX?
``` Organochlorine OP Lead Urea Polioencephalomalacia Infectious thromboembolic meningoencephalitis Ketosis Nervous forms of coccidiosis ```
32
What is the treatment of organochlorine toxicity?
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
What is the MOA of organophosphates?
Irreversible inactivate acetylcholinesterase —> persistent ACh activity
34
How are animals usually exposed to organophosphates?
Contaminated feed or drinking water Sheep dip or other applications, flea treatment, or medications Overdose Intentional poisoning
35
T/F: thiophosphate OPs are more lipid soluble than phosphate OPs
True
36
Are organophosphates easily degradable??
Yes Generally persist for 2-4wks Residues on fruit, veg, and crops may last longer
37
What is storage activation?
When stored a chemical becomes more toxic Eg Parathion, malathion, diazinon, coumaphos
38
How are organophosphates absorbed?
Skin and mucous membranes, GIT, and inhalation (lipophilic)
39
What are the usual exposures for organophosphates?
Dip or spray -dermal absorption Contaminated feed or water - oral Aerial/indoor spray- inhaled
40
Where are organophosphates metabolized?
Liver- excretion/bioactivation
41
____________ occurs when liver enzymes metabolize thiophosaphate OPs
Lethal synthesis
42
Continued low dose exposure to organophosphates can have what affect on nervous system??
Adaption do decreased acetylcholinesterase (homeostatic response) —> Enzyme induction or increased acetylcholinesterase production —> receptor down regulation or decrease ACh receptor
43
T/F: phospahate OPs require hepatic bioactivation “lethal synthesis”
False Phosphate OPs are biologically active Thiophosphate OPs require lethal synthesis by de-sulfuration
44
T/F: thiophosphate OPs undergo enteroheptic recycling
True Highly lipid soluble
45
Where are thiophosphate OPs stored?
Adipose tissue | Slow release from fat may lead to delayed and/or prolonged cholinesterase inhibiton
46
What is a major route of elimination of thiophosphate OPs?
Paroxonase (serum bound enzyme)
47
What are the three MOAs of organophosphates ?
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
Organophosphate toxicity leads to over stimulation of the muscarinic receptors by ACH, what are the symptoms caused by this?
DUMBELLS ``` Diarrhea Urination Miosis Bronchospasm Emesis Lacrimation Salivation ```
49
Organophosphates have a secondary effect of activation of nicotinic receptors, what signs may you see due to this?
Accumulation of ACh at neuromuscular junction —> paralysis (nicotinic block) Sweating, hypertension, and tachycardia
50
Organophosphates can cross the BBB, what effects will it have int he CNS?
Increased sensory and behavioral disturbances Incoordination Depressed motor and respiratory function
51
What is usually the cause of death in animals with organophosphate toxicity?
Increased pulmonary sections with respiratory failure
52
What pathology can be associated with organophosphates?
Acute death, no specific lesions ``` Pulmonary edema Congestion Cyanosis Hemorrhage Edema Necrosis of skeletal muscle ```
53
How is organophosphate toxicity diagnosed?
Analysis or stomach/rumen contest/ hair/ skin Plasma acetylcholinesterase activity level <50% activity is suspicious <25% activity is diagnostic
54
What test can be done in clinic if you suspect organophosphate toxicity?
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
What is the treatment for OP toxicity?
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
What is the main concern with OP toxicity?
Respiratory failure (asphyxia and death) from excessive airway secretions
57
T/F: carbamates require hepatic bioactivation
False —> this makes them more toxic than some OPs in very young patients
58
Where doe carbamates mostly have an effect?
Respiratory -do not penetrate CNS
59
What is the MOA of carbamates?
Binds acetylcholinesterase but is REVERSIBLE —> shorter duration and less important consequences than OPs
60
What are the clinical signs seen with carbmate poisoning?
Similar to OP toxicity ``` SLUD Salivation Lacrimation Urination Diarrhea ```
61
What tests can be used to diagnose carbamate toxicity
Cholinesterase levels ->because of reversible binding, can dissociate and give a false negative result Response to atropine therapy
62
What is the treatment for carbamate toxicity
Decontamination Supportive therapy Atropine Oxides/PAM-2 no as effective because of reversible binding (in some cases can increase binding)
63
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
D

RUSVM Toxicology (23 decks)

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