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Questions and Answers
What is the primary role of atropine in organophosphate intoxication?
What is the primary role of atropine in organophosphate intoxication?
- To cause respiratory distress
- To act as a muscarinic antagonist (correct)
- To inhibit cholinesterase activity
- To increase salivation
Which of the following is NOT a symptom of organophosphate intoxication?
Which of the following is NOT a symptom of organophosphate intoxication?
- Blurred vision
- Increased lacrimation
- Muscle rigidity (correct)
- Diarrhea
What effect does PAM (pralidoxime methiodide) have in the detoxication process?
What effect does PAM (pralidoxime methiodide) have in the detoxication process?
- It induces seizures
- It acts as a muscle relaxant
- It blocks nicotinic receptors
- It reactivates cholinesterase (correct)
What is one of the muscarinic effects of organophosphate intoxication?
What is one of the muscarinic effects of organophosphate intoxication?
Which of the following is a CNS effect of organophosphate intoxication?
Which of the following is a CNS effect of organophosphate intoxication?
During the experimental procedure, what should be observed after administering DDV to the rabbit?
During the experimental procedure, what should be observed after administering DDV to the rabbit?
What is an expected symptom of the gastrointestinal effects of organophosphate intoxication?
What is an expected symptom of the gastrointestinal effects of organophosphate intoxication?
How does the administration of atropine affect the muscarinic symptoms of organophosphate intoxication?
How does the administration of atropine affect the muscarinic symptoms of organophosphate intoxication?
Flashcards
Mechanism of Organophosphate Intoxication
Mechanism of Organophosphate Intoxication
Organophosphates are a class of chemicals that inhibit the enzyme acetylcholinesterase. This inhibition leads to the accumulation of acetylcholine, a neurotransmitter, at the synapses.
Muscarinic Effects of Organophosphate Intoxication
Muscarinic Effects of Organophosphate Intoxication
Muscarinic effects are caused by the accumulation of acetylcholine at muscarinic receptors. This leads to various symptoms such as blurred vision, increased salivation, and bradycardia.
Nicotinic Effects of Organophosphate Intoxication
Nicotinic Effects of Organophosphate Intoxication
Nicotinic effects are caused by the accumulation of acetylcholine at nicotinic receptors. These effects include hypertension and muscle twitching.
Atropine as an Antidote
Atropine as an Antidote
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PAM as an Antidote
PAM as an Antidote
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Clinical Presentation of Organophosphate Poisoning
Clinical Presentation of Organophosphate Poisoning
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Exposure Routes for Organophosphates
Exposure Routes for Organophosphates
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Symptoms Across Body Systems in Organophosphate Intoxication
Symptoms Across Body Systems in Organophosphate Intoxication
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Study Notes
Organophosphates Intoxication and Detoxification
- Organophosphates induce intoxication by inhibiting acetylcholinesterase (AChE)
- AChE breaks down acetylcholine (ACh)
- Inhibition leads to an accumulation of ACh
- Accumulation over-stimulates muscarinic and nicotinic receptors
- This results in a range of symptoms
Experimental Purposes
- To understand the symptoms of organophosphate intoxication.
- To determine the effectiveness of atropine and pralidoxime methiodide (PAM) in detoxifying organophosphates.
- To compare the effectiveness of atropine and PAM.
Experimental Principle
- Understanding the mechanism and symptoms of organophosphate-induced intoxication
- Understanding the mechanism of action of antidotes.
Mechanism of Organophosphate Intoxication
- Acetylcholine (ACh) is broken down by acetylcholinesterase (AChE)
- Organophosphates inhibit AChE
- Acetylcholine accumulates in the body
- Receptors are overstimulated leading to symptoms
- Symptoms fall into two categories: muscarinic and nicotinic
Muscarinic Effects
- Blurred vision (miosis)
- Increased lacrimation (tears)
- Bradycardia (slow heart rate)
- Hypotension (low blood pressure)
- Severe respiratory distress
- Nausea, vomiting, abdominal pain
- Diarrhea, fecal incontinence
- Urine incontinence
Nicotinic Symptoms
- Hypertension (high blood pressure)
- Decreased muscle tension, muscular twitching
CNS effects
- Anxiety
- Seizures
- Coma
Antidotes and their Mechanisms
- Atropine: Muscarinic antagonist.
- Reverses muscarinic symptoms (miosis, hypersalivation, incontinence, cardiovascular inhibition)
- PAM: Cholinesterase reactivator.
- Restores cholinesterase activity, breaking down excess acetylcholine
Experimental Materials
- Animal: Rabbit (2-3kg)
- Instruments: Rabbit cage, syringes
- Drugs:
- 0.08% dichlorovinyl dimethyl phosphate (DDV)
- 0.1% atropine
- 2.5% PAM
Experimental Procedure
- Weigh the rabbit, and monitor normal indices (respiration, pupils, salivation, feces, urine, muscle tension, muscle twitching)
- Administer 0.08% DDV intramuscularly (1ml/kg)
- Observe changes in indices
- If obvious symptoms (seizures) develop, administer atropine intravenously (1mg/kg)
- Observe changes in indices
- If M symptoms resolve, administer PAM intravenously (2mg/kg)
- Record changes of indices
Results and Analysis
- Data collection on rabbit responses after intoxication, treatment with atropine, and treatment with PAM.
- Analysis of data is needed.
Questions
- Mechanisms of organophosphate poisoning
- Detoxification mechanisms of atropine and PAM
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