COMPREHESIVE WEEK #3 CASE STUDY FOR A 45
YEAR OLD PATIENT WITH REASON FOR
ENCOUNTER OF ARM WEAKNESS ACTUAL CASE
STUDY
What is Myasthenis gravis?
an autoimmune disorder causing improper functioning of the neuromuscular
junction. The immune system produces antibodies that damage the
acetylcholine receptors on the sarcolemma.
Why is this young woman experiencing difficulty chewing and double vision?
The muscles of her face and eyes are weakening due to the lack of impulse
transmission.
How are the anti-acetylcholine receptor antibodies interfering with her normal
skeletal muscle activity?
By damaging the acetylcholine receptors on the sarcolemma, these antibodies
are causing interference with normal contraction impulse transmission
between the motor neurons and muscle fibers. Acetylcholine can't bind to the
muscle cell, so an action potential can't develop and contraction won't occur.
How do the anticholinesterase drugs act to improve Jill's skeletal muscle
function?
They prevent the release of acetylcholinesterace so the acetylcholine in the
synaptic cleft will not be broken down. Having the acetylcholine linger in the
gap will increase the chance of contraction impulse being transmitted in the
presence of fewer functioning acetylcholine receptors on the muscle fiber.
YEAR OLD PATIENT WITH REASON FOR
ENCOUNTER OF ARM WEAKNESS ACTUAL CASE
STUDY
What is Myasthenis gravis?
an autoimmune disorder causing improper functioning of the neuromuscular
junction. The immune system produces antibodies that damage the
acetylcholine receptors on the sarcolemma.
Why is this young woman experiencing difficulty chewing and double vision?
The muscles of her face and eyes are weakening due to the lack of impulse
transmission.
How are the anti-acetylcholine receptor antibodies interfering with her normal
skeletal muscle activity?
By damaging the acetylcholine receptors on the sarcolemma, these antibodies
are causing interference with normal contraction impulse transmission
between the motor neurons and muscle fibers. Acetylcholine can't bind to the
muscle cell, so an action potential can't develop and contraction won't occur.
How do the anticholinesterase drugs act to improve Jill's skeletal muscle
function?
They prevent the release of acetylcholinesterace so the acetylcholine in the
synaptic cleft will not be broken down. Having the acetylcholine linger in the
gap will increase the chance of contraction impulse being transmitted in the
presence of fewer functioning acetylcholine receptors on the muscle fiber.
