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Neurology (Calum) > Myasthenia Gravis > Flashcards

Myasthenia Gravis Flashcards

1
Q

What signs are seen in LMN conditions?

A

weakness
hypotonia
fasciculations

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2
Q

where do motor cell bodies arise?

A

ventral (anterior) horns of the spinal cord

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3
Q

What is the name of the synapse formed between neurones and muscle?

A

motor end plate

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4
Q

How many motor neurones do each muscle cell respond to?

A

1

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5
Q

what is the process behind muscle contraction?

A

action potential moves along the nerve
depolarisation
calcium channels open allowing Ca2+ influx
ACh released into the synaptic cleft

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6
Q

which enzyme terminates the action of ACh?

A

acetylcholinesterase splits Ach into acetate and choline

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7
Q

What is curare?

A

plant extract used in arrow poisons

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8
Q

What effect does curare have?

A

occupies Ach receptor but doesn’t open ion channels - no contraction - no breathing

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9
Q

Name some presynaptic disorders

A

botulism - clostridium botulinum
botulinum toxin
Lambert Eaton Myasthenic syndrome

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10
Q

What is Lambert Eaton Myasthenic Syndrome?

A

antibodies to presynaptic calcium channels leads to less vesicle release

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11
Q

Which malignancy has a strong association with LEMS?

A

small cell lung carcinoma

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12
Q

name a postsynaptic disorder?

A

myasthenia gravis

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13
Q

What happens in Myasthenia Gravis?

A

antibodies to acetylcholine receptors

reduced number of receptors = muscle weakness and fatiguability

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14
Q

How do postsynaptic membranes become damaged?

A

antibodies trigger an inflammatory cascade that damages them

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15
Q

What is the relation between the thymus and myasthenia gravis?

A

75% of patients have thymus hyperplasia or thymoma

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16
Q

What are the common clinical features of MG?

A

worsening weakness throughout the day
extra ocular weakness
facial and bulbar weakness
limb weakness typically proximal

17
Q

How is MG treated?

A

Ach inhibitors

thymectomy

18
Q

Name an Ach inhibitor used to treat MG?

A

pyridostigmine

19
Q

Which medication should be avoided in the acute illness setting?

A

steroids - cause paradoxical worsening

20
Q

What causes death in MG patients?

A

respiratory failure and aspiration pneumonia

immunosuppressant side-effects

21
Q

Describe some features of smooth muscle

A

not striated
single central nucleus
gap junctions
actin myosin ratio 10:1

22
Q

What are Type 1 muscles?

A

slow oxidative - fatigue resistant

23
Q

What are type 2a muscles?

A

fast oxidative - aerobic metabolism

24
Q

What are Type 2b muscles?

A

easy glycolytic - easily fatigues

25
Q

What are fasciculations?

A

visible, fast twitches of muscle

26
Q

What are fasciculations a sign of in an unhealthy individual?

A

disease of the motor neurone, not the muscle

27
Q

What is myotonia?

A

failure of muscle relaxation after use

28
Q

Name some inflammatory muscle disorders?

A

dermatomyositis

polymyositis

29
Q

Name some inherited muscle disorders

A

muscular dystrophies

30
Q

What is polymyositis?

A

symmetrical, progressive proximal weakness developing over weeks to months

31
Q

What investigation findings are found in polymyositis?

A

raised CK

32
Q

how is polymyositis treated?

A

steroids

33
Q

What is the difference between dermatomyositis and polymyositis?

A

skin involvement - heliotrope rash

underlying malignancy common

34
Q

What is characteristic in inclusion body myositis?

A

thumb sparing

35
Q

What is rhabdomyolysis?

A

dissolution of muscle, damage to muscle causes leakage of large quantities of toxic intracellular contents into plasma

36
Q

What is the common triad of rhabdo symptoms?

A

myalgia
muscle weakness
myoglobinuria

37
Q

Can drugs cause problems in muscle?

A

Yes - HMG co-enzyme A reductase inhibitors
hydroxychloroquine
amiodarone

38
Q

What is the most common muscular dystrophy?

A

myotonic dystrophy

autosomal dominant
weakness, cataracts, ptosis, balding, cardiac defects

Neurology (Calum) (21 decks)

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