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Y3R2 - Toxicology ☠️ > L2: Pesticides > Flashcards

L2: Pesticides Flashcards

1
Q

Def of Pesticides

A
  • Any substance used for preventing, destroying or repelling any pest.
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2
Q

Classification of Pesticides

A
  • Insecticides
  • Rodenticides
  • Herbicides
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3
Q

Examples of Insecticides

A
  • Cholinesterase inhibitors (Organophosphates and Carbamates)
  • Chlorinated Hydrocarbons (DDT, Toxaphene)
  • Pyrothroids
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4
Q

Examples of Rodenticides

A
  • Warfarine
  • zinc phosphide
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5
Q

Examples of Herbicides

A

Paraquat.

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6
Q

Types of Insecticides

(Cholinesterase inhibitors)

A

Organophosphates:
- Diazinon
- Malathion
- Parathion.

Carbamates:
- Carbaryl
- Sevin
- Temik.

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7
Q

Toxic action of OPC & Carbamates

A

Inhibition of AChE

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8
Q

How do OPC & Carbamates inhibit AChE?

A
  • Inhibition of AChE and plasma or butayrl cholinesterase (pseudocholinesterase or BuChE)
  • This inhibition blocks conversion of acetylcholine to its degradation products → acetic acid and choline.
  • Once AChE has been inactivated, acetylcholine accumulates in autonomic nervous system, somatic nervous system and brain,
  • resulting in overstimulation of muscarinic and nicotinic receptors.
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9
Q

OPCs inactivate AChE (Permenantly/temporarily) giving rise to ………

A
  • inactivate AChE permanently giving rise to cholinergic toxic syndrome and the syndrome persists until new enzyme is synthesized.
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10
Q

Cholinergic Transmission, OCP & Atropine

A
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11
Q

Carbamates inhibit AChE (Permenantly/Temporarily) leading to …..

A

Temporarily

  • Leading to less severe intoxication with much shorter duration (‡ 24 hours).
  • Carbamates also penetrate the blood-brain barrier poorly, producing fowor CNS offocts.
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12
Q

Routes of exposure to OPC

A

All Routes

  • Most organophosphates are highly lipid soluble compounds and are well absorbed from intact skin, oral mucous membranes, conjunctiva, gastrointestinal & respiratory tracts.
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13
Q

CP of OPC Exposure

A
  • Acute organophosphates poisoning
  • Chronic organophosphates poisoning
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14
Q

Onset of Acute OPC Toxicity

A
  • Immediate
  • Delayed
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15
Q

Immediate onset of Acute OPC Toxicity

A
  • Toxic manifestations appear within 30 minutes - 3 hours of exposure.
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15
Q

Delayed onset of Acute OPC Toxicity

A
  • Symptoms may be delayed up to 8-12 hours especially after extensive skin exposure or indirect agent

e.g: malathion that require reactivation to active form

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16
Q

Examples of pesticides causing delayed onset of Acute OPC Toxicity

A

Malathion

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17
Q

Fatalities due to Pesticides Exposure

A
  • Most fatalities occur within 24 hours.
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18
Q

Cause of Death in Acute OPC Toxicity

A

Respiratory failure

  • It is a major cause of mortality in patients with acute cholinesterase inhibitor toxicity.
  • All of acute clinical manifestations as muscarinic, nicotinic, and CNS effects can contribute to respiratory failure.
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19
Q

Acute lung injury, pulmonary edema, and chemical pneumonitis due to aspiration of hydrocarbon solvents may complicate multiple respiratory disturbances thaf characterize cholinesterase inhibitor poisoning.

A

..

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20
Q

Manifestations of Acute OPC Toxicity

A
  • Muscarinic Manifestations
  • Nicotinic Manifestations
  • General Neurological Manifestations
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21
Q

Cause of muscarinic manifestations of Acute OPC Toxicity

A

Due to inhibition of cholinesterase at muscarinic receptors

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22
Q

Muscarinic manifestations of Acute OPC Toxicity

A
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23
Q

Cause of Nicotinic manifestations of Acute OPC Toxicity

A
  • Due to inhibition of cholinesterase at nicotinic receptors
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24
Q

Nicotinic Manifestations of Acute OPC Toxicity

A
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25
Q

Cause of Neurologic Manifestations of Acute OPC Toxicity

A
  • Due to inhibition of cholinesterase at central receptors in CNS
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26
Q

Neurologic Manifestations of Acute OPC Toxicity

A
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27
Q

what is DUMBBLLES a mnemonic for?

A
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28
Q

What is the most important sequale of OPC poisoning?

A

Specific Neurological Manifestations (Paralysis)

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29
Q

Types of Specific Neurological Manifestations due to Acute OPC Toxicity

A
  • Type I paralysis (Acute paralysis)
  • Type Il paralysis (Intermediate syndrome)
  • Type Ill paralysis (OPIDN)
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30
Q

Onset of Type I Paralysis (Acute Paralysis) of Acute OPC Toxicity

A
  • Within 24-48 h
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31
Q

Mechanism of Type I Paralysis (Acute Paralysis) of Acute OPC Toxicity

A

Persistent depolarization:
- At neuromuscular junction resulting from blockade of AChE.

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32
Q

Manifestations of Type I Paralysis (Acute Paralysis) of Acute OPC Toxicity

A
  • Muscle Fasciculations
  • Muscle Cramps
  • Muscle Twitching
  • Muscle Weakness—> It may involve respiratory muscles —->respiratory failure.
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33
Q

TTT of Type I Paralysis (Acute Paralysis) of Acute OPC Toxicity

A

Oxime therapy

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34
Q

Onset of Type II Paralysis (Intermediate Syndrome) of Acute OPC Toxicity

A
  • 96 h: Alter resolution of acule cholinergic poisoning symptoms
35
Q

Mechanism of Type II Paralysis (Intermediate Syndrome) of Acute OPC Toxicity

A

Unknown

The exact mechanism is not known but many theories exist as

  • Release of lipophilis pesticide from fat stores
  • Inadequate oxime therapy
  • Complication of cholinergic myopathy
36
Q

Manifestations of Type II Paralysis (Intermediate Syndrome) of Acute OPC Toxicity

A

Muscle Weakness

  • Weakness of neck flexors (Patient complains from inability to lift his head from pillow)
  • Weakness in proximal groups of muscle with relative sparing of distal groups.

Cranial Nerve Palsies

37
Q

TTT of Type II Paralysis (Intermediate Syndrome) of Acute OPC Toxicity

A

Supportive measures:
- It does not respond to oximes or atropine

38
Q

Onset of Type III Paralysis (OPIDN) of Acute OPC Toxicity

A
  • 1-3 weeks: After exposure to large doses of certain OPCs
39
Q

Mechanism of Type III Paralysis (OPIDN) of Acute OPC Toxicity

A

Esterose lnhibition:

  • Inhibition of neuropathy larget esterase (NTE) via phosphorylation
40
Q

Manifestations of Type III Paralysis (OPIDN) of Acute OPC Toxicity

A

Muscle Weakness:

  • Initially complains of symmetric lower extremity weakness.
  • Glove & stocking paresthesia
  • Leg cramping & calf pain.

Muscle Atrophy:

  • Atrophy and paralysis of peroneal muscles → foot drop and eventually ataxia.
  • Steppage gait develops with loss of reflexes
41
Q

progression of Type III Paralysis (OPIDN) of Acute OPC Toxicity

A
  • This progresses to upper extremities.
42
Q

Recovery of Type III Paralysis (OPIDN) of Acute OPC Toxicity

A
  • Sensory symptoms resolve over
    1-2 months, but paralysis remains
43
Q

TTT of Type III Paralysis (OPIDN) of Acute OPC Toxicity

A

Supportive measure: It does not respond to oximes or atropine

44
Q

What is OPIDN?

A

Organophosphate-induced delayed polyneuropathy

45
Q

Criteria of Chronic Organophosphate Posioning

A
  • It refers to the effects of long-term or repeated low-level exposures to a toxic substance and may take years to produce signs and symptoms.
46
Q

Effects of Chronic Organophosphate Posioning

A
  • Carcinogenicity, Mutagenicity, Teratogenicity & Oncogenicity,
  • Hepatic damage: Jaundice, Fibrosis & Cirrhosis.
  • Reproductive disorders: Sperm Count, Sterility & Miscarriage.
47
Q

Investigations to diagnose of Acute OPC Toxicity

A

Cholinestrase Level

  • Decrease in Levels up. to 30-50% ofnormal value indicates exposure
48
Q

Where is RBC (True) Cholinestrase found? and its characters

A

lt is found in
- CNS gray matter
- RBCs
- Motor end plate

It is considered more accurate
“indicator of neurological toxicity”

49
Q

Where is Plasma (Pseudo) Cholinestrase found? and its characters

A

It is found in
- CNS white matter
- Plasma
- Liver
- Pancreas
- Heart.

Easier to assay and generally more readily available.

50
Q

TTT Aspects of Acute OPC Toxicity

A
  • Observation
  • Emergency & supportive measures
  • Decontamination
  • Antidotes
51
Q

observation in cases of Acute OPC Toxicity

A
  • Observe asymptomatic patients for at least 8-12 hours to rule out delayed onset symptoms.
52
Q

Emergency & Supportive measures for Acute OPC Toxicity

A
53
Q

Skin & Eye Decontamination after Acute OPC Toxicity

A
  • Remove contaminated clothes and give shower to patient with water and soap.
  • Flush eyes with copious water for 10-15 minutes.
  • Clean skin folds and under fingernails.
  • Avoid contact with contaminated clothing and body fluids by wearing rubber gloves.
54
Q

Gastric Decontamination after Acute OPC Toxicity

A

Gastric Lavage:
- Not useful due to early onset of symptoms including vomiting.

Activated charcoal:
- One dose if mixed ingestions reported

55
Q

What are antidotes for Acute OPC Toxicity?

A
  • Atropine sulphate (Anti-cholinergic)
  • Oxime therapy (Cholinesterase reactivators)
55
Q

MOA of Atropine Sulphate

A

It antagonizes muscarinic effects only of organophosphates on CNS, CVS and gastrointestinal tract.

56
Q

Doses of Atropine Sulphate

A

Starting, Reassessment & Loading

57
Q

Starting dose of Atropine Sulphate

A

0.5-2 mg IV (0.05-0.2 mg/kg in children) With repeating dose every 5-10 min.

58
Q

Reassessment in dosing of Atropine Sulphate

A
  • Initially, reassess patient’s secretions, oxygen saturation, and respiratory rate every 5-10 minutes.
  • The most important indication for redosing atropine is → Persistent wheezing or bronchorrhea.
  • Tachycardia is not necessarily a contraindication to additional atropine in the context of severe respiratory secretions.
59
Q

what is the most important indication for redosing of Atropine Sulphate?

A

Persistent wheezing or bronchorrhea.

59
Q

Is tachycardia a contraindication for Atropine Sulphate?

A
  • Tachycardia is not necessarily a contraindication to additional atropine in the context of severe respiratory secretions.
60
Q

Mantainence dose of Atropine Sulphate

A
  • Once respiratory secretions have boon initially controlled,
  • Continuous infusions of atropine may be useful in selected cases (0.02-0.05 mg/kg/hr.),
  • Clinical cautious is required lo provent over-atropinization.
61
Q

End point of therapy by Atropine Sulphate

A
  • Clearing up of the secretions from tracheobronchial tree and drying up of most secretions.
  • On the opposite side: Mydriasis is not a therapeutic end point.
62
Q

Indication for Oxime Therapy (Cholinestrase reactivation

A
  • Oxime therapy should be started as early as possible in cases of acute OP poisoning,
  • To prevent permanent binding of organophosphate to acetyl-cholinesterase and allow receptor regeneration.
63
Q

MOA of Oxime Therapy (Cholinestrase reactivation

A
  • A direct conversion of organophosphate to a harmless compound
  • Transient protection of enzyme from further inhibition.
  • Reactivation of the inhibited enzyme.
64
Q

Examples of Oxime Therapy (Cholinestrase reactivation

A
  • Pralidoxime
  • Obidoxime
65
Q

Doses of Pralidoxime

A
  • Loading dose
  • Maintenance dose
66
Q

Maintenance dose of Pralidoxieme

A

continuous infusion of 8-20 mg/kg/h (up to 650 mg/h).

66
Q

Loading dose of pralidoxieme

A

(30-50 mg/kg, total of 1-2 g in adults) over 30 minutes

67
Q

Maintenance dose of Obidoxime

A

intravenous infusion of 750 mg over 24 h

68
Q

End point of therapy of Oxime Therapy (Cholinestrase reactivation

A

24 hours after patient becomes asymptomatic (stoppage of atropine).

68
Q

Loading dose of Obidoxime

A

250 mg (4 mg/kg) by slow intravenous injection.

69
Q

AE of Oxime Therapy (Cholinestrase reactivation

A

Drowsiness, visual disturbances, nausea, tachycardia and muscle weakness.

70
Q

CI of Oxime Therapy (Cholinestrase reactivation

A

In some carbamates poisoning due to formation of toxic compounds.

71
Q

Toxic action of Pyrethroids Toxicity

A
  • Allergenic.
  • Neurotoxic
72
Q

CP of Pyrethroids Toxicity

A
  • Allergic reaction.
  • Bronchospasm.
  • Anaphylaxis.
  • Tremors
  • Convulsions
73
Q

Dx of Pyrethroids Toxicity

A

No specific test

74
Q

TTT of Pyrethroids Toxicity

A
  • Adrenaline.
  • Antihistamines
  • Activated charcoal.
  • Diazepam
74
Q

Toxic action of Warfarin Toxicity

A
  • It is an anticoagulant.
  • It inhibits hepatic synthesis of vitamin K-dependent
    coagulation factors II, VIl, IX and X.
75
Q

CP of Warfarin Toxicity

A
  • Onset 48 hours after exposure
  • Bleeding, Massive occhymoses, Brain, hemorrhage & Shock.
76
Q

Dx of Warfarin Toxicity

A
  • Elevated INR
  • Blood in urine and feces
77
Q

TTT of Warfarin Toxicity

A
  • Vitamin K. Fresh
  • Frozen plasma.
  • Iron.
  • Activated Charcoal.
78
Q

Toxic Action of Zinc Phosphide Toxicity

A
  • Toxicity is mediated by release of phosphine gas.
79
Q

CP of Zinc Phosphide Toxicity

A
  • Tachypnea.
  • Hypotension.
  • Pulmonary edema.
  • Convulsion, coma
80
Q

Dx of Zinc Phosphide Toxicity

A

History of exposure.

81
Q

TTT of Zinc Phosphide Toxicity

A

Cardio-respiratory support

Decontamination:

  • Gastric aspiration and use of 3-5% sodium bicarbonate in lavage fluid has been proposed
  • To reduce stomach acid and resulting production of phosphine → but is not of proven benefit.

Y3R2 - Toxicology ☠️ (15 decks)

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