Neuromuscular Junction Disorders Flashcards Preview

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Flashcards in Neuromuscular Junction Disorders Deck (9)
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1
Q

For information:

Acetylcholinesterase hydrolysed ACh into acetyl and choline. The choline is then taken up into vesicles.

Therefore…

A

Acetylcholinesterase inhibitors increase the concentration of acetylcholine. Because acetylcholine does not get broken down.

2
Q

What is lambert Eaton myasthenia syndrome ?

Strong association with what?

A

Antibodies to PRE-synaptic calcium channels leads to less vesicle release.

With small cell lung cancer.

3
Q

How do you differentiate lambert Eaton and myasthenia gravis?

A

Lambert Eaton = pre-synaptic

Myasthenia gravis = post-synaptic

Differentiating features = lambert Eaton improves with exercise, hyporeflexia.

4
Q

What are the 2 peaks of incidence for mysathenia gravis?

A

Females in 3rd decade.

Males in 6th or 7th decade.

Autoantibodies to nicotinic/acetylcholine receptors on post synaptic membrane

5
Q

Clinical features of mysathenia gravis?

A

Weakness that typically fluctuates throughout the day.

Extraocular weakness is the most common, facial weakness, bulbar weakness.

Limb weakness typically proximal.

6
Q

Treatment of mysathenia gravis?

A

Acetylcholinesterase inhibitors

Or

Thymectomy

Can also give steroids / azathioprine.

In an emergency, give a plasma exchange or immunoglobulin.

7
Q

Mysathenia Crisis?

A

Severe relapse resulting in weakness of respiratory muscles and difficulty breathing.

Management = ventilatory support or IV Ig.

8
Q

Muscle groups in myasthenia gravis tend to be affected in the following order:

A

1) Extraocular = double vision, ptosis.
2) Bulbar = dysphasia, difficulty chewing, dysarthria.
3) Face: drooping of facial muscles and snarled expression.

Normal sensation and reflexes
Normal muscle appearance and tone.

9
Q

Management of lambert Eaton syndrome?

A

3,4 diphenhydramine

IV Immunoglobulins.