Myasthenia Gravis

Question 1

Myasthenia Travis involves

Answer 1

Motor endplate

Question 2

Most common disorder involving neuromuscular transmission

Answer 2

Myasthenia Travis

Question 3

Onset for MG

Answer 3

Women 20-30s

Men 50-60s

Question 4

Myasthenia gravis is

Answer 4

Autoimmune disease affecting neuromuscular junction characterized by fluctuating weakness and fatigability of skeletal muscle

Question 5

MG patho

Answer 5

ACh Receptors at motor end plate decreased and abnormally shapped -> inefficient transmission -> nerve impulses fails to cross neuromuscular junction -> fails to create muscle contraction

Caused by autoimmune reponse mediated by specific anti-ACh receptor antibody

Question 6

MG antibodies

Answer 6

Block the site that normally binds ACh

Damage postsynatpic muscle membrane - endocytosis -> pinching off of regions of cells membrane

Question 7

MG risk factors

Answer 7

Hyperthyroidism
Thymic tumors
Thyrotoxins

75% w/ MG have abnormalities of thymus - have ACh recprots on surface and may serve as antigen to trigger autoimmune reaction

Question 8

MG associated w/

Answer 8

DM and immune disorders such as RA and lupus

Question 9

MG exacerbations may occur

Answer 9

Before menstrual periods or shortly after pregnancy and can be associated w/ any type of infection

Question 10

Cardinal sign of MG

Answer 10

Skeletal muscle weakness and fatiguability
-more noticeable in proximal muscles
85% weakness if generalized and affects limb musculature

Question 11

MG skeletal muscle weakness

Answer 11

Cranial muscles first to show sides
Diplopia and ptosis early signs
May tip head back to see
Weakness neck - head bobbing
Nasal speech 
Difficulty swallowing - aspiration of food
Resp impairment

Question 12

MG fatigue

Answer 12

Chewing
Facial snarl ecause lips do not close
Other neuro signs normal

Question 13

Categories of MG

Answer 13

Ocular
Mild generalized
Acute fulminating
Late severe

Question 14

Other conditions - cranial or muscle weakness to r/o

Answer 14

Drug induced MG
Botulism
Intracranial masses
Progressive ocular disease
Lambert Eaton syndrome

Question 15

MG dx by

Answer 15

Clinical presentation 
History 
Immunological testing
Pharmacological testing
Electrodiagnosic testing

Question 16

Tension

Answer 16

Used to deomstrain improvement by inhibiting AChE (enzyme needed for ACH uptake)-> prolongs presence of ACh in neuromuscular junctions
Rapid improvements in symptoms

Question 17

Myasthenic crisis

Answer 17

Medical emergency

Requires attention to life endangering weakening of respiratory muscles requiring ventilation assistance

Question 18

MG AChE inhibitor medication

Answer 18

Provides improvement regarding weakness but does not tx underlying disease
Timed to achieve most functional benefit
Side effects: vomiting, nausea, abdominal cramping

Question 19

MG sx removal of thymus

Answer 19

Successful of 85% of pts

W/ full remission in 35%

Question 20

MG plasmapharesis

Answer 20

Works to remove substances that affect ACh receptors

Not effective for long term symtpoms control

Question 21

MG immunosuppressant

Answer 21

Effective but have serious side effects

Cushingoid symtpoms and OP

Question 22

MG PT

Answer 22

VC maintained, deep breathing, coughing
Tilt chin when eating to avoid aspiration
Education in pacing activiites
Assessing need for equipment

Question 23

PT mange resp

Answer 23

Evidence that respiratory training is beneficial in improving respiratory function and endurance

Question 24

PT ther ex (mild case)

Answer 24

May benefit form aerobic training and PRE

The

Question 25

MG prognosis

Answer 25

Slow progressive
Clinical manifestation variable
S/s fluctuate during day -> supinimposed on long term spontaneous replaces that last for weeks
Remissions are rarely complete or permanent