my seminar

1. A SEMINAR PRESENTATION BY
G. HARISH,
091D1R0014,
UNDER THE SUPERVISION OF
Dr. BIGALA RAJKAMAL.
M.Pharm, PhD, FAGE.
PRINCIPAL
GANGA PHARMACY COLLEGE,
DASNAGAR,
NIZAMABAD.
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2. 1. INTRODUCTION
2. ETIOLOGY
3. PATHOPHYSIOLOGY
4. SIGNS& SYMPTOMS
5. DIAGNOSIS
6. TREATMENT
7. CONCLUSION
8. REFERENCES
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3. 1. INTRODUCTION:
Myasthenia gravis (MG) is an autoimmune syndrome caused by the failure
of neuromuscular transmission, which results from the binding of auto antibodies to
proteins involved in signaling at the neuromuscular junction (NMJ)
MG is caused by a decrease in the numbers of postsynaptic acetylcholine
receptors at the neuromuscular junction, which decreases the capacity of the
neuromuscular end-plate to transmit the nerve signal.
Normally, in response to a stimulus resulting in depolarization, acetylcholine
is released presynaptically and acts on the motor end plate to initiate a muscle action
potential. In MG, the number of activated postsynaptic receptors may be insufficient
to trigger an action potential.
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4. 2. ETIOLOGY:
(1) Acquired autoimmune.
(2) Transient neonatal caused by the passive transfer of maternal anti-AChR
antibodies
(3) Drug induced: D-penicillamine is the prototype of drug induced myasthenia
gravis. Clinical presentation may be identical to typical acquired autoimmune
myasthenia gravis and the antibody to AChR may be found.
(4) Congenital myasthenic syndromes (AChR deficiency, slow channel syndrome, and
fast channel syndrome) are distinct heritable disorders of postsynaptic neuromuscular
transmission with characteristic age of onset, pathology, electrophysiology, and
treatment.
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5. 3. PATHOPHYSIOLOGY:
A. Normal Neuromuscular Transmission
Acetylcholine (ACh) is synthesized in the
nerve terminal by action of the enzyme
choline acetyltransferase. ACh is then
stored in vesicles
ACh then binds to the post-synaptic ACh
receptor, resulting in a transient increase in
membrane permeability to Na, K, Ca, and
Mg, leading to an Endplate potential
(EPP).
Acetycholinesterase and diffusion deactivates the Ach and terminates neuromuscular
transmission.
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6. B. Acetylcholine Receptor Antibody:
The antibody blocks neuromuscular transmission by several mechanisms -
blockade of receptor sites by steric hindrance, destruction of AChR
(complement mediated), and cross linking of AChR which causes increased
turnover by endocytosis
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7. C. Structural Changes
The chronic inflammation of Myasthenia gravis
causes several changes in the structure of the
Neuromuscular Junction which also inhibit
transmission and contribute to weakness
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8. D. Genetic factors:
Certain HLA types associated with MG (HLA-DR3 and DQ2)
E. Role of Thymus:
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9. 4. SIGNS& SYMPTOMS:
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10. A.Eye Muscles:
 Diplopia.
 Photophobia.
 Ptosis.
B.Facial Muscles weakness:
C.Orbicularis Oculi Weakness.
D. Orbicularis Oris Weakness
E.Oropharyngeal Muscles.
 Tongue Weakness.
 Weakness in Chewing.
 Dysphagia.
F.Respiratory Muscle Weakness
G.Pelvic Floor Muscle Weakness 10

11. 5. DIAGNOSIS:
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12. 6. TREATMENT:
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13. 1. Anticholinesterases:
Neostigimine
pyridostigmine
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14. 2. EPHEDRINE
Ephedrine may be useful as an ancillary medication,
added to anticholinesterases, for those Myasthenia
gravis patients who need a little extra strength and are
not bothered by its possible side effects of
nervousness, heart palpitations, or insomnia. For adult
Myasthenia gravis it is taken as a 25-mg capsules two
to three times a day.
3. PLASMAPHERESIS.
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15. 4. INTRAVENOUS IMMUNOGLOBULIN’S
5. IMMUNOSUPPRESSIVE DRUG THERAPY
A. CORTICOSTEROIDS
B. AZATHIOPRINE:
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16. C.CYCLOSPORINE
SURGICAL THYMECTOMY:
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17. 7. CONCLUSION
In the management of myasthenia gravis, no standard measure of disease severity
and no medical treatment approach has been proven efficacious by rigorous,
prospective, controlled studies. The preponderance of evidence certainly links a
“connection” between the immune system and the central nervous system beyond a
reasonable doubt.
However the latest techniques like intra venous immunoglobulins, plasma
pheresis and surgical thymectomy were found to be effective. But research is going
on to findout the effective medical treatment for myasthenia gravis. May be in
future we can treat the myasthenia gravis without any adverse effects.
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18. 8. BIBLIOGRAPHY:
1. A text book of pharmacology by rang and dales, sixth edition, published by
churchill livingstone, page numbers 52,166,745.
2. A text book of pharmacology by tripati, sixth edition, jaypee publications, page
number 102-104
3. A text book of pharmacology by goodman&gillman, chapter 52
4. Journal of neurosurg psychiatry 2012 july, masuda.j, motmura.m et.al..
5. International journal of padiatric ortorhniolarynglogy19(1990)273-276, elsevier.
6. The journal of clinical investigation volume 116, number 11, nov 2006
7. The journal of clinical evaluation and management of myasthenia gravis by john c.,
keesey.md et. al..
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