Download AlterationsofthePeri..

Myasthenia Gravis
Introduction

Definition:
-chronic, immune neurological disease
-defect in transmission of nerve impulses
at the neuromuscular junction
-antibodies attack acetylcholine receptors






Peak onset: 20 – 30 yrs. Old
Females are 3X > Males
About 20 per 100,000 affected*
Not hereditary ( small familial incidence)
Thymus gland often abnormal (hyperplasia)
Strong association between MG and
hyperthyroidism
*http://www.myasthenia.org/amg_whatismg.cfm

Muscle weakness within voluntary muscles
-ptosis
-abnormal vision
-difficulty chewing/swallowing
-weakness of arms and legs
-chronic muscle fatigue
-possibly difficulty breathing

Tensilon test (anticholinesterase) edrophonium
chloride:med will enhance neurotransmission
shows marked muscle tone improvement for
about 4-5 mins.
ANTIDOTE for Tensilon: Atropine Sulfate

EMG (electromyography): muscle response
decreased with repeated stimulation
Thyroid function tests: some MG patients
have increase
 Serum protein electrophoresis: evaluate for
immunologic disorders
 Acetylcholine receptor antibodies testelevated
