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Musculoskeletal > Soft Tissue Pathology > Flashcards

Soft Tissue Pathology Flashcards

1
Q

What is the function of the perimysium?

A

Surrounds bundles of muscle fibres

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2
Q

Function of the endomysium?

A

Surrounds individual fibres

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3
Q

Function of the epimysium?

A

Surrounds the entire muscle

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4
Q

Ragged red fibres are seen in muscle when?

A

Mitochondrial disease, metabolic disease, normal features in small numbers at the extremes of age

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5
Q

Tubular aggregates are seen in muscle when?

A

Tubular aggregate myopathy, periodic paralysis, alcoholic myopathy, incidental finding

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6
Q

Types of skeletal muscle fibre? (3)

A

Red (Type 1, slow twitch, lots of mitochondria & myoglobin, good for marathon runners, able to regenerate ATP v quickly)
White (Fast twitch, Type 2A; fast oxidative glycolytic, type 2b; fast glycolytic)
Intermediate

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7
Q

Muscle Biopsy Indications

A

Evidence of muscle disease
-Weakness
-Muscle symptoms (atrophy, fasciculation)
-Elevate creatine kinase (CK)
Presence of neuropathy (+ nerve biopsy)
Presence of vascular disorder (vasculitis)

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8
Q

Creatine Kinase High, Intermediate and Low levels

A

High: (e.g. Dystrophies) 200-300 times of normal.
Intermediate: (e.g. Inflammatory myopathy) 20-30 times of normal.
Low: (e.g. Neurogenic disorder) 2-5 times of normal

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9
Q

What is electron microscopy used for?

A

To examine the ultra-structure of the muscle

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10
Q

Duchenne (DMD) method of inheritance and where found?

A

X-linked recessive, pelvic girdle

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11
Q

Becker (BMD) method of inheritance and where found?

A

X-linked recessive, pelvic girdle

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12
Q

Limb girdle (LGMD) method of inheritance and where found?

A

Autosomal recessive, pelvic girdle

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13
Q

Fascioscapulohumeral method of inheritance and where found?

A

Dominant, face, shoulder girdle and arm

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14
Q

Scapulohumeral method of inheritance and where found?

A

Autosomal recessive, shoulder girdle and arm

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15
Q

Oculopharyngeal method of inheritance and where found?

A

Dominant, external ocular and pharynx

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16
Q

Myotonic dystrophy method of inheritance and where found?

A

Dominant, face, respiratory and arms

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17
Q

Signs of Duchennes?

A

Proximal weakness, pseudohypertrophy of calves

RAISED CK

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18
Q

DMD pathogenesis

A
  • Mutations in dystrophin gene on long arm chromosome X
  • Alterations in anchorage of actin cytoskeleton to basement membrane
  • Fibres liable to tearing
  • Uncontrolled Ca2+ entry into cells
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19
Q

Variant of DMD?

A

BMD (Becker)

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20
Q

Are muscular dystrophies inherited?

A

Yes

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21
Q

Which inflammatory marker will be raised in Duchennes?

A

CK!!!

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22
Q

Most common types of Myotonic dystrophy?

A

DM1 and DM2

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23
Q

Non-muscle features of myotonic dystrophy?

A

Frontal baldness (in men), low intelligence, cataracts (clouding of the lens), cariomyopathies

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24
Q

Atrophy of which type of fibres in myotonic dystrophy?

A

Atrophy of type 1 fibres in myotonic dystrophy

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25
Q

Myotonic dystrophy histological features?

A 
Atrophy of type 1 fibres
Ring fibres
Central nuclei
Fibrofatty replacement
Fibre necrosis
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26
Q

In which condition might you see ring fibres?

A

Myotonic dystrophy

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27
Q

Primary inflammation of muscle inflammatory myopathies

A

Infective agents
Polymyositis
Dermatopolymyositis

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28
Q

Most common form of muscular dystrophy?

A

Myotonic dystrophy

-Characterised by progressive muscle wasting and weakness

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29
Q

At what age do the features of myotonic dystrophy tend to develop? (bearing in mind they can actually develop at any age)

A

20’s-30’s

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30
Q

Where does DM1 affect?

A

Distal

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31
Q

Where does DM2 affect?

A

Proximal

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32
Q

Features of Polymyositis?

A

Progressive muscular weakness, PAIN and TENDERNESS :(

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33
Q

Genes involved in myotonic dystroophy?

A

Ch19 and Ch3

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34
Q

Polymyositis histological findings?

A

Endomysial lymphocytic infiltrate, invasion of muscle by CD8+ T lymphocytes
Segmental fibre necrosis

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35
Q

What is dermatositis?

A

Polymyositis and skin changes

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36
Q

What does dermatomysitis share a 10% link with?

A

Malignancy

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37
Q

Skin features of dermatmyositis?

A

Upper body erythema

Eyelid swelling with purple discolouration

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38
Q

Which condition would you find immune complex and complement deposition within & around capillaries within muscle?

A

Polymyositis
You would also find perifasicular muscle fibre injury
and B-lymphocytes and CD4 + T cells > cf polymyositis

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39
Q

Neurogenic disorders of muscle (histological findings)

A
  • Small, angulated muscle fibres (adults)
  • Small, round muscle fibres (infants)
  • Target fibres
  • Fibre type grouping
  • Grouped atrophy
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40
Q

Motor Neurone Disease

A

Progressive degeneration of anterior horn cells

Denervation atrophy, fasciculation and weakness

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41
Q

Which cells progressively degenerate in motor neurone disease?

A

Anterior horn cells

42
Q

Method of Spinal Muscular Atrophy Inheritance?

A

Autosomal recessive

43
Q

What gene is affected in spinal muscular atrophy?

A

Ch5

44
Q

How many types of muscular atrophy are there?

A

4

45
Q

Age and gender usually affected by myasthenia gravis?

A

Women aged 20-40

46
Q

Which thymus conditions are linked with myasthenia gravis?

A

25% have thymoma

Others have thymic hyperplasia

47
Q

Myasthenia gravis symptoms?

A

Fatigue, muscle weakness, proptosis and DYSPHAGIA

48
Q

Rhabdomyolysis histological findings

A

Breakdown of skeletal muscle:

  • Myoglobinuria
  • Hyperkalaemia
  • Necrosis & shock
49
Q

What might you test the urine for in rhabdomyolysis?

A

Myoglobin

myoglobulinuria

50
Q

Outcome of rhabdomyolysis?

A

Acute Renal Failure
Hypovolaemia & hyperkalaemia
Metabolic acidosis
Disseminated intravascular coagulation

51
Q

Which condition might present with acute kidney failure and disseminated intravascular co-agulation?

A

Rhabdomyolysis (acute renal failure so u would probs see hypovolaemia and hyperkalaemia aswell)

52
Q

What kind of drugs do connective tissue disorders usually respond to?

A

Anti-inflammatory

53
Q

What anti-bodies do you see in SLE?

A

Anti-nuclear! omgeeee

54
Q

What drugs can induce SLE?

A

Hydralazine and pracainamide

55
Q

Lol, every single SLE symptom

A

Skin –“butterfly” rash (sun exposed areas), discoid lupus erythematosus (DLE)
Joints – arthralgia
Kidneys – glomerulonephritis
CNS – psychiatric symptoms, focal neurological symptoms
CVS – pericarditis, myocarditis, necrotising vasculitis
Lymphoreticular – lymphadenopathy & splenomegaly
Lungs – pleuritis, pleural effusions
Haematological – anaemia, leucopenia, thrombophilia

56
Q

Hypersensitivity in SLE

A

Visceral lesions – mediated by Type III hypersensitivity

Haematological effects – mediated by Type II hypersensitivity

57
Q

What does PAN stand for?

A

Polyarteritis nodosa

58
Q

What is PAN?

A

Inflammation and fibrinoid necrosis of small/medium arteries

59
Q

Target organs for PAN?

A

Major - kidneys, heart, liver, GI tract

Minor – skin, joints, muscles, nerves, lungs

60
Q

Which infection is PAN often associated with?

A

Streptococcal infection

61
Q

Diagnosis of PAN

A

Biopsy- FIBRINOID NECROSIS OF VESSELS

62
Q

Which condition is characterised by fibrinoid necrosis of vessels (found from bioopsy?)

A

PAN! Polyarteritis nodosa

63
Q

Which antibody would you find in PAN?

A

pANCA (perinuclear antineutrophil cytoplasmic autoantibody)

64
Q

Clinical Features of PAN?

A

Non-specific +/- organ specific features such as hypertension, haematuria, abdominal pain, melaena, diarrhoea, mononeuritis multiplex, rash, cough, dyspnoea

65
Q

Clinical features of polymyalgia rheumatica?

A

Pain, stiffness in shoulder & pelvic girdles
No muscle weakness
Responds to corticosteroids

66
Q

Where is the pain in polymyalgia rheumatica?

A

Shoulders and pelvic girdle

67
Q

Who is affected by polymyalgia rheumatica?

A

The elderly!

68
Q

What kind of medication does polymyalgia rheumatica respond to?

A

Corticosteroids

69
Q

Another name for Giant Cell Arteritis?

A

Temporal arteritis

70
Q

Diagnosis of temporal arteritis?

A

raised ESR

Temporal artery biopsy; inflammation,+/- giant cells, fragmentation of internal elastic lamina

71
Q

What is scleroderma?

A

Excessive fibrosis of organs and tissues (excessive collagen production)

72
Q

CREST syndrome

A
  • Calcinosis
  • Raynaud’s
  • Oesophageal dysfunction
  • Sclerodactyly
  • Telangectasia
73
Q

Death due to Scleroderma

A
  • Renal failure secondary to malignant hypertension
  • Severe respiratory compromise
  • Cor pulmonale
  • Cardiac failure or arrhythmias secondary to myocardial fibrosis
74
Q

Which condition is associated with CREST?

A

Scleroderma

75
Q

Epstein-Barr virus could predispose to which connective tissue disease?

A

SLE

76
Q

Silica dust (found in cleaning powders, cigarette smoke and cement) may increase risk of developing what?

A

Silica dust (found in cleaning powders, cigarette smoke and cement) may increase risk of developing SLE

77
Q

Aetiology of SLE

A

Environmental factors:
Viruses eg Epstein-Barr Virus
UV light may stimulate skin cells to secrete cytokines stimulating B-cells
Silica dust (found in cleaning powders, cigarette smoke and cement) may increase risk of developing SLE

78
Q

In SLE, what is the significance of nuclear material release from necrotic cells?

A

The nuclear material released from necrotic cells may act autoantigens
Autoimmunity possibly results by the extended exposure to nuclear and intracellular autoantigens

79
Q

Possible source of autoantigens in SLE?

A

Nuclear material released from necrotic cells may act as autoantigens
Autoimmunity possibly results by the extended exposure to nuclear and intracellular autoantigens

80
Q

Coombes test

A

Coombes test involves taking a blood sample and checking it for the presence of antibodies which may destroy red blood cells
-Do not count in the presence of haemolytic anemia

81
Q

When would you not count coombes test?

A

In the presence of haemolytic anemia

82
Q

Requirements for classification of lupus?

A

At least 4 clinical and 1 laboratory finding

Or biopsy proven lupus nephritis with positive ANA or anti-DNA

83
Q

Serositis in SLE?

A

Pericarditis, pleuritis, peritonitis

84
Q

Levels of C3, C4 and CH50 in active SLE?

A

Levels of C3, C4 and CH50 will decrease because SLE is highly active and body will use them up

85
Q

What is lupus nephritis?

A

Kidney inflammation caused by lupus

86
Q

Levels of IgG and anti-dsDNA in active SLE?

A

Levels of IgG and anti-dsDNA will increase

87
Q

Jaccoud arthropathy

A 
Jaccoud arthropahy (JA) is a deforming non erosive arthropathy characterised by ulnar deviation of the second to 5th fingers with MCP subluxation.
-Can be seen in SLE
88
Q

Pulmonary features of SLE?

A
  • Pleurisy
  • Infections
  • Pulmonary hypertension
  • Pulmonary infarct
  • Diffuse lung infiltration and fibrosis
89
Q

Which type of endocarditis might be seen in SLE?

A

Libman-sach endocarditis

90
Q

SLE cardiac features

A

Cardiomyopathy
Libman-sach endocarditis
Pulmonary hypertension
Pericarditis

91
Q

Screening tests for suspected SLE

A 
Full blood count
Renal function incl. urine
ANA
ENA
Anti-DNA
Complement levels
92
Q

Which immunological thingy is specific for SLE?

A

Anti-DNA
-Correlates with disease activity
-may be associated with lupus nephritis
Anti-Sm also very specific

93
Q

Anti-DNA is highly specific for what?

A

SLEEEEEE
-Correlates with activity
-may be associated with lupus nephritis
Anti-Sm is also very specific

94
Q

Anti-Ro is associated with which manifestations

A

Cutaneous

95
Q

Anti-RNP overlap features

A

Overlap features – sclerodermatous skin lesions, Raynaud’s phenomenon, low grade myositis

96
Q

If you have SLE should you go to the desert?

A

No, you want to avoid excessive sun exposure

97
Q

Anti-CD20

A

Rituximab (one of the biologics used in SLE)

98
Q

Anti-Blys

A

Belimumab

99
Q

Ciclosporin A and tacrolimus are what kind of drug?

A

Calcineurin inhibitors

100
Q

Name 2 calcineurin inhibitor

A

Ciclosporin A and tacrolimus

Musculoskeletal (44 decks)

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