Pyridostigmine is a medication used to treat myasthenia gravis.
Usually administered by mouth, but can also be used by intravenous injection.
Its effects generally begin within 45 minutes and last up to 6 hours.
It can be used with atropine to end the effects of neuromuscular blocking medications of the non-depolarizing type.
Trade name Mestinon.
Pregnancy category AU: C
Bioavailability 7.5-10%.
Elimination half-life 1.75-2 hours
Excretion kidney
Common side effects: nausea, diarrhea, frequent urination, and abdominal pain.
More severe side effects include: hypotension, weakness, and allergic reactions.
It is unclear of its safety in pregnancy to the fetus.
It is an acetylcholinesterase inhibitor.
It blocks the action of acetylcholinesterase and therefore increases the levels of acetylcholine.
It is used to treat muscle weakness in people with myasthenia gravis and to combat the effects of curariform drug toxicity.
Approved for military use during combat situations as an agent to be given prior to exposure to nerve agents.
Its use has been implicated as a causal factor in Gulf War syndrome.
It has use in the postural tachycardia syndrome.
Contraindications to its use include:
mechanical intestinal or urinary obstruction and should be used with caution in patients with bronchial asthma.
Common side effects include:
Sweating, diarrhea, nausea, vomiting,
abdominal cramps, increased salivation,
tearing, increased bronchial secretions,
constricted pupils, facial flushing due to vasodilation, and erectile dysfunction.
Additional side effects include:
Muscle twitching
Muscle cramps and weakness
Pyridostigmine inhibits acetylcholinesterase in the synaptic cleft.
It slows down the hydrolysis of acetylcholine.
It is an inhibitor of cholinesterase that does not cross the blood–brain barrier which carbamylates about 30% of peripheral cholinesterase enzyme.
The carbamylated enzyme eventually regenerates by natural hydrolysis and excess ACh levels revert to normal.
The acetylcholine diffuses across the synaptic cleft and binds to receptors on the post synaptic membrane, causing an influx of Na+, resulting in depolarization,
resulting in an action potential.
To prevent constant stimulation once the acetylcholine is released, an enzyme called acetylcholinesterase is present in the endplate membrane close to the receptors on the post synaptic membrane, and quickly hydrolyses acetylcholine.