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Year 3 Clinical > Muscle and NM Junction > Flashcards

Muscle and NM Junction Flashcards

1
Q

3 main symptoms of Lower Motor Neurone (LMN) disorders?

A

Weakness

Low tone

Fasciculations

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2
Q

3 levels around the level of muscle contraction?

A
  1. Motor neurone
  2. NM junction
  3. Muscle
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3
Q

What are motor end plates?

A

Skeletal muscle fibres are innervated by motor neurones whose cell bodies arise in the anterior (ventral) horn of the spinal cord

Synapses formed between motor neurones and striated muscle are called motor end plate

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4
Q

What is a motor unit?

A

Collection of muscle fibres innervated by a single motor neurone

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5
Q

Function of acetylcholinesterase?

A

Enzyme that degrades ACh into:
• Acetate
• Choline

Sequestred into pre-synaptic vesicles

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6
Q

What is curare?

A

Occupies the ACh receptor but does not open it; thus, there is no muscle contraction and respiration stops

Time of onset varies from 1 minute, for IV administration, to 15 minutes, for IM administration

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7
Q

What is botulinum toxin?

A

Clostridium botulinum is found in soild; food and wounds can become affected

IV drug users may encounter this in black tar heroin

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8
Q

Effects of botulinum toxin?

A

Cleaves presynaptic proteins inv. in vesicle formation and block vesicle docking, with the presynaptic membrane

There is rapid onset of weakness without sensory loss

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9
Q

Uses of botulinum toxin?

A

There are medical and cosmetic uses

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10
Q

What is Lambert Eaton Myasthenic Syndrome?

A

Abs to presynaptic Ca2+ channels; there is reduced vesicle release

Strong assoc. with underlying Small Cell Lung Carcinoma (SCLC)

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11
Q

What type of disorder is myasthenia gravis?

A

Post-synaptic disorder

It is the most common disorder of the NM junction

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12
Q

Pathogenesis of myasthenia gravis?

A

Autoimmune; Abs are produced to the ACh receptors (AChR)

Thus, there are a reduced no. of functioning ACh receptor and flattening of end-plate folds; even with normal amounts of ACh, transmission becomes inefficient

Additionally, the Abs trigger inflammatory cascades that damage folds of the post-synaptic membrane

Symptoms begin when ACh receptors have decreased by 30%; these are muscle weakness and fatiguability

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13
Q

Thymus in myasthenia gravis?

A

75% of patient have hyperplasia of the thymus OR thymoma

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14
Q

Occurrence of myasthenia gravis?

A

May occur at any age but there are 2 peaks:
• Females - 3rd decade
• Males - 6th/7th decade

Female to male ratio 3:2

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15
Q

Clinical features of myasthenia gravis?

A

Most commonly presents with:
• Extraocular weakness
• Facial weakness
• Bulbar weakness

Weakness typically fluctuating (worse throughout the day)

Proximal limb weakness

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16
Q

Treatment of myasthenia gravis?

A

Acetylcholinesterase inhibitor, e.g: Pyridostigmine, allow persistence of ACh in synaptic cleft

Thymectomy

Steroids / azathioprine

Emergency treatment - plasma exchange or Ig

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17
Q

Prognosis of myasthenia gravis?

A

Morbidity due to:
• Respiratory failure
• Aspiration pneumonia
• Side effects of immunosuppression in the elderly
• Comorbidities can cause issues with tolerating immunosuppression

80-90% of patients enter remission within 3 months

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18
Q

Structure of skeletal muscle?

A

Smallest contractile unit is the muscle fibre; each is surrounded by a thin layer of endomysium

20-80 group together to form a fascicle encapsulated by perimysium; a large no. of these are sheathed in epimysium to form an individual muscle

19
Q

Structure of smooth muscle?

A

Non-striated muscle with a single central nucleus

Gap junctions exist between the cells

Smooth muscle has significant connective tissue around it

There are no sarcomeres

20
Q

Actin to myosin ratio of smooth muscle?

A

10 : 1

21
Q

Types of muscle fibres?

A

Type I - slow oxidative; have a dense capillary network and myoglobin so they resist fatigue

Type IIa - fast oxidative; carry out aerobic metabolism

Type IIb - fast glycolytic; easily fatigued

Most muscles have a mixture, depending on their function

22
Q

What are fasciculations?

A

Visible, fast, fine spontaneous twitches

23
Q

When do fasciculations occur?

A

May occur in healthy muscle (precipitated by stress, caffeine and fatigue)

Occur in denervated muscle, which becomes hyperexcitable

Typically a sign of disease in the motor neurone, not the muscle

24
Q

What is myotonia?

A

Failure of muscle relaxation after use

Ass

25
Q

Symptoms/signs of muscle disease?

A

Myalgia

Muscle weakness (often specific patterns of weakness depending on cause, e.g: proximal muscle weakness in polymyositis)

Wasting

Hyporeflexia

26
Q

Inflammatory muscle disorders?

A

Dermatomyositis

Polymyositis

27
Q

Inherited muscle disorders?

A

Muscular dystrophies

Dystrophinopathies, limb girdle muscular dystrophies

Myotonic dystrophy

28
Q

Congenital muscle disorders?

A

Congenital myasthenic syndromes

Congenital myopathies

29
Q

Symptoms of polymyositis?

A

Symmetrical, progressive proximal weakness developing over weeks-months

30
Q

Ix for polymyositis?

A

Raised CK

31
Q

Treatment of polymyositis?

A

Responds to steroids

32
Q

Symptoms of dermatomyositis?

A

Presents similar to polymyositis but is assoc. with skin lesions

Heliotrope rash is present on the face

33
Q

Causes of dermatomyositis?

A

Up to 50% have an underlying MALIGNANCY

34
Q

What is inclusion body myositis?

A

A degenerative muscle disorder; it was thought to be inflammatory but there is little response to steroids

35
Q

Symptoms of inclusion body myositis?

A

Typically slowly progressive weakness in 6th decade of life with characteristic THUMB-SPARING

36
Q

What is myotonic dystrophy?

A

Autosomal dominant and the most common muscular dystrophy; it is a trinucleotide repeat disorder with anticipation

There is multi-systemic involvement, resulting in:
• Myotonia
• Weakness
• Cataracts
• Ptosis
• Frontal balding
• Cardiac defects
37
Q

Pathogenesis of myotonic dystrophies?

A

Inherited conditions that are progressive but non-inflammatory

There is no central or peripheral nerve abnormality

38
Q

Infective causes of muscle disorders?

A

Viral (Coxsackie)

Trypanosomiasis

Cistercercosis (uncooked pork)

Borrellia

39
Q

Toxic causes of muscles disorders?

A

Drugs

Venomes

40
Q

Drugs causing myopathies?

A

Necrotising myopathies:
• HMG CoA-reductase inhibitors (statins)
• Fibrates

Lysosomal storage myopathy:
• Hydroxychloroquine
• Amiodarone

Hypokalaemic myopathy:
• Diuretics
• Oral contraceptives

41
Q

What is rhabdomyolysis?

A

Dissolution of muscle, i.e: damage to skeletal muscle causes leakage of large quantities of toxic intracellular contents into the plasma

42
Q

Potential causes of rhabdomyolysis?

A

Crush injuries
Toxins
Post-convulsions

43
Q

Triad of rhabdomyolysis?

A

Myalgia

Muscle weakness

Myoglobinuria

44
Q

Complications of rhabdomyolysis?

A

Acute renal failure

DIC (disseminated intravascular coagulation)

Year 3 Clinical (100 decks)

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