drpkaur
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A 32-year-old farm worker goes to the emergency department with wheezing, increased salivation, vomiting, diarrhea, and blurred vision. Vital signs are significant for hypertension and tachycardia. He is confused but manages to report that he was using an insecticide that morning. His father, who brought him to the emergency department, said that the patient is in good health, does not smoke, does not use drugs, and never had a similar episode before. Which of the following would be the most appropriate treatment for this patient?
A. Diazepam
B. Physostigmine
C. Pilocarpine
D. Pralidoxime
E. Succinylcholine
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| Leopard
Forum Guru
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Pralidoxime
Best of luck
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| docarchana
Forum Guru
Topics: 70
Posts: 515
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+ atropine
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| MRMAVERICK
Forum Guru
Topics: 48
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YUP PRALIDOXIME PLUS ATROPINE
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| fox
Forum Guru
Topics: 70
Posts: 727
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op poisoning
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| drpkaur
Forum Guru
Topics: 196
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correct guys..pralidoxime +atropine.
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| tompat
Forum Elite
Topics: 46
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was not aware that op poisoning cud lead to TACHYCARDIA, HYPERTENTION!!
HERE is the complete physicals
Note that clinical presentation may vary, depending on the specific agent, exposure route, and amount. Symptoms are due to both muscarinic and nicotinic effects.
* Vital signs: Depressed respirations, bradycardia, and hypotension are possible symptoms. Alternatively, tachypnea, hypertension, and tachycardia are possible. Hypoxia should be monitored for with continuous pulse oximetry.
* Paralysis
o Type I: This condition is described as acute paralysis secondary to continued depolarization at the neuromuscular junction.
o Type II (intermediate syndrome): Intermediate syndrome was described in 1974 and is reported to develop 24-96 hours after resolution of acute organophosphate poisoning symptoms and manifests commonly as paralysis and respiratory distress. This syndrome involves weakness of proximal muscle groups, neck, and trunk, with relative sparing of distal muscle groups. Cranial nerve palsies can also be observed. Intermediate syndrome persists for 4-18 days, may require mechanical ventilation, and may be complicated by infections or cardiac arrhythmias. Although neuromuscular transmission defect and toxin-induced muscular instability were once thought to play a role, this syndrome may be due to suboptimal treatment.
o Type III: Organophosphate-induced delayed polyneuropathy (OPIDP) occurs 2-3 weeks after exposure to large doses of certain OPs and is due to inhibition of neuropathy target esterase. Distal muscle weakness with relative sparing of the neck muscles, cranial nerves, and proximal muscle groups characterizes OPIDP. Recovery can take up to 12 months.
* Neuropsychiatric effects: Impaired memory, confusion, irritability, lethargy, psychosis, and chronic organophosphate-induced neuropsychiatric disorders have been reported. The mechanism is not proven.
* Extrapyramidal effects: These are characterized by dystonia, cogwheel rigidity, and parkinsonian features (basal ganglia impairment after recovery from acute toxicity).
* Other neurological and/or psychological effects: Guillain-Barré–like syndrome and isolated bilateral recurrent laryngeal nerve palsy are possible.
* Ophthalmic effects: Optic neuropathy, retinal degeneration, defective vertical smooth pursuit, myopia, and miosis (due to direct ocular exposure to organophosphates) are possible.
* Ears: Ototoxicity is possible.
* Respiratory effects: Muscarinic, nicotinic, and central effects contribute to respiratory distress in acute and delayed organophosphate toxicity.
* Muscarinic effects: Bronchorrhea, bronchospasm, and laryngeal spasm, for instance, can lead to airway compromise.
* Nicotinic effects: These effects lead to weakness and paralysis of respiratory oropharyngeal muscles.
* Central effects: These effects can lead to respiratory paralysis.
* Rhythm abnormalities: Sinus tachycardia, sinus bradycardia, extrasystoles, atrial fibrillation, ventricular tachycardia, and ventricular fibrillation (often a result of, or complicated by, severe hypoxia from respiratory distress) are possible.
* Other cardiovascular effects: Hypotension, hypertension, and noncardiogenic pulmonary edema are possible.
* GI manifestations: Nausea, vomiting, diarrhea, and abdominal pain may be some of the first symptoms to occur after organophosphate exposure.
* Genitourinary and/or endocrine effects: Urinary incontinence, hypoglycemia, or hyperglycemia are possible.
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