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Myasthenia GravisMyasthenia Gravis
“Grave muscle weakness”“Grave muscle weakness”
YASHWANT KUMAR DILLI BABU-GROUP:8YASHWANT KUMAR DILLI BABU-GROUP:8
Myasthenia Gravis
• Autoimmunediseaseaffecting theneuromuscular
junction
• Not abrain disorder – brain functionsnormally
• Characterized by fluctuating muscleweaknessand
fatigability
• Diseasemay begeneralized or ocular specific
NeuroMuscularJunction(NMJ)
Pathophysiology
• Antibodiesattack Acetylcholine(ACH) receptorsat the
motor end plate
• Decreased number of (ACH) receptor sitesat
neuromuscular junction
• Preventsneurotransmitter (ACH) from attaching and
stimulating musclecontraction
• Resulting in lossof musclestrength
Causes
• No singlecausehasbeen identified
• Abnormal thymustissuefound in most
patientswith MG
• Thymic tumorsfound in 15% of
patients
• Virusinfectionshavebeen found in
somecasesand areasuspected cause
Genetic Factors
• MyastheniaGravisisnot agenetically inherited disease
• Somefamiliesappear to carry agenethat increasesthe
risk for developing thedisease
• No specific genehasbeen identified and thereareno tests
for genetic screening
Signs and Symptoms
• Affectsany of themusclesthat can be controlled
voluntarily, certain musclegroupsaremorecommonly
affected than others
• Eye, face, throat, neck, limb muscles
• Difficulty speaking (dysarthria)
• Difficulty swallowing (dysphagia),
• Drooping eyelids(ptosis)
Signs and Symptoms
• Doublevision (diplopia)
• Nasal-sounding speech and weak neck musclesthat give
thehead atendency to fall forward or backward. 
• Symptomstend to progressover time, usually reaching
their worst within afew yearsafter theonset of the
disease
• Worsening muscleweaknesswith repeat activity
Complications
 Myasthenic crisis: A life-threatening condition, which occurs
when the muscles that control breathing become too weak
to do their jobs. Emergency treatment is needed to provide
mechanical assistance with breathing. Medications and
blood-filtering therapies help people recover from
myasthenic crisis, so they can again breatheon their own.
 Thymus tumors: About 15 percent of the people who have
myasthenia gravis have a tumor in their thymus, a gland
under the breastbone that is involved with the immune
system. Most of thesetumorsarenoncancerous.
Underactive or overactive thyroid: The thyroid gland,
located in the neck, secretes hormones that regulate
metabolism. If thyroid is underactive, body uses energy more
slowly. An overactive thyroid makes body use energy too
quickly.
Lupus: Disease of immune system. Common symptoms
include painful or swollen joints, hair loss, extreme fatigue
and ared rash on theface.
Rheumatoid arthritis: Caused by problems with immune
system. It is most conspicuous in the wrists and fingers, and
can result in joint deformities that make it difficult to use
hands.
Complications
Prognosis
• Chronic diseasewith periodsof exacerbation and
sometimesremissions
• Diseasecourseishighly variable
• Symptomsrespond well to treatment and in most cases
thepatient can liveanormal or nearly normal life
• Ocular Myastheniahasthebest prognosis
Diagnosis
•Edrophonium test (Tensilon)
•Blood analysis
•Repetitivenervestimulation
•Single-fiber electromyography
(EMG)
•Imaging scans
Edrophonium test: Injection of the chemical
edrophonium (Tensilon) may result in a sudden,
although temporary, improvement in muscle
strength — an indication that you may have
myasthenia gravis. Edrophonium acts to block an
enzyme that breaks down acetylcholine, the
chemical that transmits signals from nerve
endingsto musclereceptor sites.
Blood analysis: A blood test may reveal the
presenceof abnormal antibodies that disrupt
the receptor sites where nerve impulses
signal musclesto move.
Repetitive nerve stimulation: Is a type of
nerve conduction study, in which electrodes are
attached to skin over the muscles to be tested. Small
pulses of electricity are sent through the electrodes to
measure the nerve's ability to send a signal to muscle.
To diagnose MG, the nerve will be tested many times
to see if its ability to send signals worsens with
fatigue.
Single-fiber electromyography (EMG):
EMG measures the electrical activity traveling
between brain and muscle. It involves inserting a very
fine wire electrode through skin and into a muscle. In
single-fiber EMGs, asinglemusclefiber istested.
Imaging scans: CT scan or an MRI to confirm a
tumor or other abnormality in thymus.
CT-SCAN SINGLE FIBER EMG
Exacerbation Trigger Factors
• Infection
• Stress
• Fatigue
• Cathartics(laxatives)
• Heat (sauna, hot tubs, sunbathing)
Medications/Treatment
•Plasmapheresis
•Immunoglobulin Therapy
•Thymectomy
•Corticosteroids
•Yogaexercises(Pranayama)
Medications/Treatment
• ImmunosuppressiveTherapy
• Prednisone
• Azathioprine
• AcetylcholinesteraseInhibitors
• First lineof therapy
• Neostigminebromide(Pyridostigmine)
• Edrophonium chloride(Tensilon)
Thymectomy - surgical removal of the
thymusgland. Theroleof thethymusgland in
MG isnot fully understood, and thethymectomy
may or may not improveapatient'ssymptoms.
Plasmapheresis- aprocedurethat removes
abnormal antibodiesfrom theblood and replaces
thepatient'sblood with normal antibodies
through donated blood.
Extent of theproblemsisdependent on the
severity of thecondition and thepresenceof other
problemsthat could affect thepatient.
Surgery
THANKS FOR YOUR
ATTENTION 

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Myasthenia gravis yashwant kumar

  • 1. Myasthenia GravisMyasthenia Gravis “Grave muscle weakness”“Grave muscle weakness” YASHWANT KUMAR DILLI BABU-GROUP:8YASHWANT KUMAR DILLI BABU-GROUP:8
  • 2. Myasthenia Gravis • Autoimmunediseaseaffecting theneuromuscular junction • Not abrain disorder – brain functionsnormally • Characterized by fluctuating muscleweaknessand fatigability • Diseasemay begeneralized or ocular specific
  • 4. Pathophysiology • Antibodiesattack Acetylcholine(ACH) receptorsat the motor end plate • Decreased number of (ACH) receptor sitesat neuromuscular junction • Preventsneurotransmitter (ACH) from attaching and stimulating musclecontraction • Resulting in lossof musclestrength
  • 5.
  • 6. Causes • No singlecausehasbeen identified • Abnormal thymustissuefound in most patientswith MG • Thymic tumorsfound in 15% of patients • Virusinfectionshavebeen found in somecasesand areasuspected cause
  • 7. Genetic Factors • MyastheniaGravisisnot agenetically inherited disease • Somefamiliesappear to carry agenethat increasesthe risk for developing thedisease • No specific genehasbeen identified and thereareno tests for genetic screening
  • 8. Signs and Symptoms • Affectsany of themusclesthat can be controlled voluntarily, certain musclegroupsaremorecommonly affected than others • Eye, face, throat, neck, limb muscles • Difficulty speaking (dysarthria) • Difficulty swallowing (dysphagia), • Drooping eyelids(ptosis)
  • 9. Signs and Symptoms • Doublevision (diplopia) • Nasal-sounding speech and weak neck musclesthat give thehead atendency to fall forward or backward.  • Symptomstend to progressover time, usually reaching their worst within afew yearsafter theonset of the disease • Worsening muscleweaknesswith repeat activity
  • 10. Complications  Myasthenic crisis: A life-threatening condition, which occurs when the muscles that control breathing become too weak to do their jobs. Emergency treatment is needed to provide mechanical assistance with breathing. Medications and blood-filtering therapies help people recover from myasthenic crisis, so they can again breatheon their own.  Thymus tumors: About 15 percent of the people who have myasthenia gravis have a tumor in their thymus, a gland under the breastbone that is involved with the immune system. Most of thesetumorsarenoncancerous.
  • 11. Underactive or overactive thyroid: The thyroid gland, located in the neck, secretes hormones that regulate metabolism. If thyroid is underactive, body uses energy more slowly. An overactive thyroid makes body use energy too quickly. Lupus: Disease of immune system. Common symptoms include painful or swollen joints, hair loss, extreme fatigue and ared rash on theface. Rheumatoid arthritis: Caused by problems with immune system. It is most conspicuous in the wrists and fingers, and can result in joint deformities that make it difficult to use hands. Complications
  • 12. Prognosis • Chronic diseasewith periodsof exacerbation and sometimesremissions • Diseasecourseishighly variable • Symptomsrespond well to treatment and in most cases thepatient can liveanormal or nearly normal life • Ocular Myastheniahasthebest prognosis
  • 13. Diagnosis •Edrophonium test (Tensilon) •Blood analysis •Repetitivenervestimulation •Single-fiber electromyography (EMG) •Imaging scans
  • 14. Edrophonium test: Injection of the chemical edrophonium (Tensilon) may result in a sudden, although temporary, improvement in muscle strength — an indication that you may have myasthenia gravis. Edrophonium acts to block an enzyme that breaks down acetylcholine, the chemical that transmits signals from nerve endingsto musclereceptor sites. Blood analysis: A blood test may reveal the presenceof abnormal antibodies that disrupt the receptor sites where nerve impulses signal musclesto move.
  • 15. Repetitive nerve stimulation: Is a type of nerve conduction study, in which electrodes are attached to skin over the muscles to be tested. Small pulses of electricity are sent through the electrodes to measure the nerve's ability to send a signal to muscle. To diagnose MG, the nerve will be tested many times to see if its ability to send signals worsens with fatigue. Single-fiber electromyography (EMG): EMG measures the electrical activity traveling between brain and muscle. It involves inserting a very fine wire electrode through skin and into a muscle. In single-fiber EMGs, asinglemusclefiber istested. Imaging scans: CT scan or an MRI to confirm a tumor or other abnormality in thymus.
  • 17. Exacerbation Trigger Factors • Infection • Stress • Fatigue • Cathartics(laxatives) • Heat (sauna, hot tubs, sunbathing)
  • 19.
  • 20. Medications/Treatment • ImmunosuppressiveTherapy • Prednisone • Azathioprine • AcetylcholinesteraseInhibitors • First lineof therapy • Neostigminebromide(Pyridostigmine) • Edrophonium chloride(Tensilon)
  • 21. Thymectomy - surgical removal of the thymusgland. Theroleof thethymusgland in MG isnot fully understood, and thethymectomy may or may not improveapatient'ssymptoms. Plasmapheresis- aprocedurethat removes abnormal antibodiesfrom theblood and replaces thepatient'sblood with normal antibodies through donated blood. Extent of theproblemsisdependent on the severity of thecondition and thepresenceof other problemsthat could affect thepatient. Surgery
  • 22.