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Questions and Answers
What happens to the bond formed between organophosphates and acetylcholinesterase if no antidote is administered within a certain time frame?
What happens to the bond formed between organophosphates and acetylcholinesterase if no antidote is administered within a certain time frame?
What causes the bond between organophosphates and acetylcholinesterase to become irreversible?
What causes the bond between organophosphates and acetylcholinesterase to become irreversible?
What is the time frame within which an antidote must be administered to prevent the aging process of the OP-AchE bond?
What is the time frame within which an antidote must be administered to prevent the aging process of the OP-AchE bond?
Which factor contributes to the aging of the OP-AchE bond?
Which factor contributes to the aging of the OP-AchE bond?
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Which functional group detachment is responsible for the permanent bond formation in organophosphate toxicity?
Which functional group detachment is responsible for the permanent bond formation in organophosphate toxicity?
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What does an initial ECG showing sinus tachycardia indicate?
What does an initial ECG showing sinus tachycardia indicate?
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What is suggested by the presence of pulmonary edema on a chest radiograph?
What is suggested by the presence of pulmonary edema on a chest radiograph?
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Bronchospasm indicated on a radiograph is most likely associated with which condition?
Bronchospasm indicated on a radiograph is most likely associated with which condition?
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Which underlying condition could potentially cause both tachycardia and pulmonary edema?
Which underlying condition could potentially cause both tachycardia and pulmonary edema?
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What is a common clinical significance of both tachycardia and bronchospasm?
What is a common clinical significance of both tachycardia and bronchospasm?
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Study Notes
Organophosphate (OP) Toxicity
- AChE bond may become permanent if antidote is not administered within 24-36 hours, a process known as aging.
- Aging occurs when the diethyl group leaves the phosphate, resulting in an irreversible bond.
Clinical Signs and Symptoms
- Initial ECG findings include sinus tachycardia and heart block (HB).
- Chest radiographs may show pulmonary edema and bronchospasm.
- Characteristic garlic-like odor of breath noted in certain toxic exposures.
- Physical examination may reveal anxiety, diaphoresis, tachycardia, vomitus, and diarrhea.
- Specific symptoms include salivation and gastrointestinal distress.
Mechanism of Phosphine Gas Toxicity
- Zinc sulfide phosphine gas acts as a cytochrome C oxidase inhibitor.
- Causes cellular toxicity leading to necrosis of the gastrointestinal tract, and injuries to the liver, kidney, and lungs, particularly upon inhalation.
Symptoms of Zinc Phosphide Toxicity
- Central nervous system effects include headache, ataxia, seizures, and coma.
- Gastrointestinal symptoms may present as nausea and black vomitus with a rotten fish odor.
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Description
This quiz delves into the toxic effects of AChE inhibitors and the irreversible binding of these compounds to acetylcholinesterase. Key concepts such as the aging process and the role of the diethyl group in toxicity are explored. Understand the critical timing for antidote administration to mitigate irreversible effects.
