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Data pasien Intoksikasi Baygon by juwita1valen1ramadha. Copyright: © All Rights Reserved. Download as DOCX, PDF, TXT or read online from Scribd. intoksikasi baygon pdf editor. Quote. Postby Just» Tue Apr 16, am. Looking for intoksikasi baygon pdf editor. Will be grateful for any help! Top. Karya Ilmiah Bukan Hasil Penelitian yang dipublikasikan sebagai Penulis Utama. •. Satoto D. Peran Spesialis Anestesiologi pada tatalaksana nyeri kanker.
There appear to be both presynaptic and postsynaptic effects. Interference with propagation of the nerve action potential at the nerve terminal and reduced ACh release may account for the presynaptic effects.
Neuromuscular blocking drugs may be modified by the degree of neuromuscular block, the associated disease state, acid base status of the patient, and associated electrolyte imbalance. In patients with MG and Lambert Eaton syndrome relatively small amounts of nondepolarizing agents can produce profound and prolonged NMJ blockade. Prolonged paralysis from neuromuscular blockers may occur on occasion in patients without NMJ disease. Factors which may influence the duration of neuromuscular blockade include dosage and duration of therapy, concurrent drug use including muscle relaxants, magnesium, and cimetidine , severity of underlying disease, electrolyte abnormalities, and renal insufficiency which may lead to high drug concentrations.
In many patients there are multiple concomitant factors leading to the paralytic picture. The inhibition of hydrolysis by cholinesterase inhibitors will result in prolonged duration of action. Patients with MG are less sensitive to this drug than the nondepolarizing agents. Occasionally, patients with MG have their disease unmasked by the use of these drugs. Pharmacological effects of neuromuscular blockers are influenced by antibiotics, general anesthetics, local anesthetics, and antiarrhythmics which may complicate clinical weakness.
Newer neuromuscular blocking agents having shorter duration of action may still aggravate MG and Lambert-Eaton syndrome weakness. Occasional reports of reduced plasma cholinesterase levels by plasma exchange or by genetic abnormalities have been associated with reports of prolonged apnea and muscle weakness in patients receiving depolarizing neuromuscular blocking drugs. Subsequently, numerous case reports of neuromuscular weakness from antibiotic administration thought to be a result of impaired neuromuscular transmission have been reported in normal patients, those concurrently receiving neuromuscular blocking drugs, those with MG, those with other disorders that might alter pharmacokinetics, and patients with exposure to other drugs having an adverse effect on neuromuscular transmission.
Cholinesterase inhibitors, infusion of calcium, and aminopyridines can partially reverse the weakness produced by aminoglycosides.
Tobramycin appears to have predominantly presynaptic effects similar to hypermagnesemia with impairment of ACh release. Fluoroquinolones have also been associated with anecdotal reports of increased weakness in myasthenic patients, development of muscle weakness in subclinical MG patients and, from in vitro studies, to adversely affect neuromuscular transmission. Acute worsening of MG has been reported following administration of ciprofloxacin, a fluroroquinolone.
These drugs have pre- and postsynaptic affects by microelectrode studies with reduced MEPP frequency, reduced evoked transmitter release, and reduced sensitivity of the postjunctional AChR. Clindamycin may also directly block muscle contractility.
The mechanism for this effect is not known. Some studies show no deleterious effect of tetracycline. The patient required mechanical ventilation for six days.
The same patient had previously had a similar exacerbation after taking another macrolid, erythromycin. Therefore, these antibiotics should also be used with caution in patients with MG. It belongs to the family of ketolides, closely related to macrolide antibiotics. Telithromycinss primary indication has been for the treatment of serious respiratory infections such as bacterial pneumonia. Telithromycin has been implicated in the exacerbation or unmasking of myasthenia gravis.
Based on these observations telithromycin is not generally recommended for use in patients with myasthenia gravis and if physicians determine that 13 there are no other therapeutic alternatives in a critically ill patient then such patients must be closely monitored for increasing myasthenic weakness.
Clearly the issue of antibiotic effects on neuromuscular transmission is complex and poses a vexing dilemma for the clinician. Nearly every antibiotic ever studied has demonstrated some deleterious effect or has been the subject of a clinical report suggesting exacerbation of MG. If a patient requires antibiotic treatment for an infection then the appropriate drugs should be utilized. When managing patients with junctional disease it simply behooves the clinician to remain alert to the potential for clinically significant adverse effects, especially if the patient becomes weaker in the setting of antibiotic use.
Cardiovascular Drugs Class Ia Antiarrhythmics Class Ia drugs affect heart rhythm by inhibiting sodium channels and increasing action potential duration. The drugs have also been found to block Ach receptors, either by blocking nicotinic or muscarinic Ach receptor- mediated signaling or in the NMJ.
It has been shown that quinidine and its stereoisomer quinine can aggravate weakness in MG. In large doses it may also have a postsynaptic effect with a curare-like action. A number of references in the literature suggest that quinine can also aggravate myasthenic weakness. Quinidine has been observed to potentiate weakness induced by nondepolarizing and depolarizing neuromuscular blocking drugs. Harvey and Whitehill in reported the differential affects of quinine and prostigmine in the diagnostic evaluation of MG.
At progressively larger concentrations the MEPP becomes undetectable. The effect on MEPP is not reversed by neostigmine. Single-channel patch-clamp analysis of quinine effects reveal a 14 long-lived open-channel and a closed-channel block of AChR.
Tests for competitive inhibition or desensitization of the AChR by quinine in these concentrations are negative. Quinolone drugs adversely affect both presynaptic and postsynaptic aspects of neuromuscular transmission at concentrations close to those employed in clinical practice.
Therefore they should not be used, or used only with extreme caution, in disorders having a reduced safety margin of neuromuscular transmission. In both cases the patients developed markedly increased weakness within hours to days of starting the medication.
II. ANAMNESIS (Autoanamnesis)
Anecdotal reports suggest that consumption of tonic water containing small amounts of quinine can result in exacerbation of myasthenic symptoms. Procainamide can also lead to acute worsening of MG. Although the drug can induce autoimmune phenomena, the immediate onset of weakness and neuromuscular blockade would suggest a direct effect on neuromuscular transmission, as opposed to an indirect autoimmune process.
Bretylium may induce muscle weakness as well as potentiate the effect of neuromuscular blockers. It has been associated with acute neuromuscular weakness, including respiratory failure, and there is speculation that it has a curare-like action at the neuromuscular junction.
In addition, the drug can potentiate neuromuscular blockade in patients receiving nondepolarizing and depolarizing neuromuscular blocking drugs. Furthermore, occasional patients describe transient diplopia in the setting of beta blocker usage to raise the question of a NMJ 15 mechanism in such patients.
Reduced MEPP amplitude can be caused by any of the beta blockers, suggesting a postsynaptic site of action. Presynaptic abnormalities include reduced MEPP frequency, and with metoprolol and propranolol there is reduced quantal content.
Propranolol seems to have the most marked effect impairing neuromuscular transmission with atenolol having the least. In 10 patients with mild to moderate MG who received intravenous propranolol 0. A variety of observations indicate that calcium channel blockers may adversely affect neuromuscular transmission. Verapamil doses of 0. Those observations suggest that P-type channels mediate transmitter release at the motor nerve terminals. It is unclear whether these patients represent statin-induced MG or aggravated of mild or sub-clinical disease.
In 5 of the 6 patients the symptoms resolved following discontinuation of statin therapy. Antiepileptic Drugs Phenytoin has demonstrated presynaptic and postsynaptic affects on neuromuscular transmission invitro. In vitro studies of nerve-muscle preparations have shown that phenytoin reduces quantal release of acetylcholine from the motor nerve terminal; also, it produces a simultaneous increase in spontaneous release of neurotransmitter and therefore increases the MEPP frequency.
One explanation for this effect is a reduction in the size of the nerve action potential at the motor nerve terminal, or perhaps a reduction in calcium influx into the motor nerve terminal. Postsynaptic effects have also been observed with phenytoin including reduction in the MEPP amplitude thought to be related to desensitization of the endplate.
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The same authors followed up their clinical experience with an evaluation of gabapentin in rats with experimental autoimmune myasthenia gravis, noting an 17 abnormal decremental response to 3 Hz repetitive stimulation, transiently, following the exposure to gabapentin, while no decrement was observed in normal rats. The authors rightfully conclude that the drug should be used with some caution in myasthenia gravis. The point is of particular importance in myasthenics who have muscle cramps.
Such patients should avoid quinine, and it has been a common practice to prescribe gabapentin for control of muscle cramps. Another recent report emphasized the presence of a defect of neuromuscular transmission as demonstrated by a decremental response at high frequency repetitive stimulation in children who had received an overdose of carbamezapine.
In my judgment the overall risk of using anticonvulsants in MG patients is small.
Analgesics Narcotic analgesics do not directly interfere with neuromuscular transmission in myasthenia. Slaughter in demonstrated that cholinesterase inhibitors neostigmine may potentiate the effects of morphine, codeine, hydromorphone, and opium alkaloids.
Using a lower starting dose of corticosteroids, with a gradual increase over time, may reduce the risk of early exacerbation. Abramsky et al. On occasion estrogen therapy has been associated with increasing weakness in MG, including parenteral use after 3 to 5 days.
Within one week of removal of the implant her symptoms markedly improved. The mechanism is unclear.
Any patient with underlying MG who develops progressive weakness should be screened for abnormal thyroid function unless there is an obvious alternative explanation. Ophthalmologic Medications Timolol, the beta adrenergic blocking eye drop, has been reported to be associated with increased myasthenic weakness.
Phenothiazines Chlorpromazine was reported to produce increased muscle weakness in a schizophrenic patient with MG by McQuillen in Chlorpromazine and promazine can antagonize applied ACh, and may prolong effects of succinylcholine.
Occasional reports note that in patients receiving chlorpromazine or phenelzine, subsequent administration of depolarizing neuromuscular blocking drugs results in prolonged neuromuscular blockade.
Lithium Subjective weakness is a common side effect of lithium carbonate. Exacerbation or unmasking of MG is reported.
The onset of weakness in a patient with MG can occur within days of starting lithium. Amitriptyline, amphetamines, droperidol, haloperidol, imipramine, paraldehyde, and trichloroethanol have been found to impair neuromuscular transmission in experimental settings. It has a variety of potential neurologic complications, including peripheral neuropathy and myopathy, as well as an effect on neuromuscular transmission. The mechanism of the chloroquine effect on neuromuscular transmission is controversial and may be multifactorial.
Chloroquine appears to have a direct effect at the presynaptic level with reduced MEPP amplitude as well as having a postsynaptic effect with competitive postjunctional blockade.
In addition, there is some belief that the drug may induce an autoimmune disorder similar to that triggered by D-penicillamine. These patients had AChR antibodies which eventually disappeared, as did the other abnormalities following discontinuation of the drug.
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