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Musculoskeletal > MSK week 2 > Flashcards

MSK week 2 Flashcards

1
Q

Describe rheumatoid arthritis

A

A symmetrical inflammatory arthritis caused by inflammation of the synovial membrane.,

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2
Q

Where does RA usually affect?

A

Commonly affects the small joints of the hands and feet (MCP and PIPs)

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3
Q

Who does RA usually affect?

A

Women more commonly than men.

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4
Q

Which antibodies are you likely to see in association with RA?

A

Rheumatoid Factor

Anti CCP

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5
Q

Which antibody is most specific and relates to disease activity in RA?

A

Anti-CCP.

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6
Q

Pathogenesis of RA

A

An immune response is triggered against the synovium which lines some joints and tendons. An inflammatory panes forms which then attacks and denudes articular cartilage leading to joint destruction.
Tendon ruptures and soft tissue damage can occur leading to joint instability and subluxation.

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7
Q

How do you diagnose RA?

A

Based on clinical presentation, radiographic findings and serological analysis.

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8
Q

Early clinical presentation of RA

A

Symmetrical synovitis (doughy swelling)
Pain
Morning stiffness
Involvement of MCP and PIP but not DIP

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9
Q

Late clinical presentation of RA

A

Larger joints may become involved e.g. cervical spine. Atlanto-axial involvement may cause compression of the spinal cord.

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10
Q

Extra-articular features of RA

A

Rheumatoid nodules- most commonly found on the extensor surfaces or sites of frequent mechanical irritation.
Pleural effusion, interstitial fibrosis and pulmonary nodules
Increased risk of cardiovascular co-morbidities

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11
Q

Investigations into RA

A 
Antibody testing (15-20% of patients don't have antibodies)
CRP, plasma viscosity and ESR are also raised. 
In early disease X-rays will show no joint abnormality (due to early features being soft tissue swelling and bone thinning).
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12
Q

Treatment of RA

A 
Goal- commence DMARD therapy within 3 months of onset of symptoms. 
Try DMARD one- methotrexate. 
If this fails add sulfasalazine 
If this fails add hydroxychloroquine 
Alongside these NSAIDs and aspirin.

If DMARD therapy fails- biologics may work. Anti-TNF alpha drugs given by injection.
To qualify for these must have high level of disease activity.

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13
Q

Disease activity monitoring in RA

A 
DAS 28
Remission<2.6
Low disease activity 2.7-3.2
Moderate disease activity 3.3-5.1
High disease activity >5.1
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14
Q

Describe ankylosing spondylitis

A

Chronic inflammatory disease of the spine and sacroiliac joints which can lead to eventual fusion of the joints.

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15
Q

Who gets ankylosing spondylitis?

A

Young men (late adolescents- early adulthood)

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16
Q

Clinical presentation of ankylosing spondylitis

A

Spinal pain and stiffness
Spinal morning stiffness which improves with exercise
Over time- loss of spinal movement and a question mark spine.

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17
Q

What is a question mark spine?

A

Loss of lumbar lordosis-

Increased thoracic kyphosis.

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18
Q

How can you measure the affect of ankylosing spondylitis

A

Schobers test
Measure 5cm above the superior iliac crests and 10cm below.
Ask the patient to bend over and the space should exceed 20cm between the two marks (unless they have AS)

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19
Q

What will an Xray show of ankylosing spondylitis?

A 
May show sclerosis and fusion of the sacroiliac joints
Syndesmophytes (bony spurs from the vertebral bodies)
Bamboo spine (intervertebral joints fuse together)
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20
Q

Treatment of ankylosing spondylitis?

A

Physiotherapy, NSAIDs, exercise

For more aggressive disease- anti-TNF alpha

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21
Q

What is reactive arthritis?

A

Arthritis that follows infection somewhere else in the body.

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22
Q

What organisms usually cause reactive arthritis?

A

GU- chlamydia, Neissena

GI- campylobacter, salmonella.

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23
Q

Presentation of reactive arthritis

A

Large, swollen red and hot joint 1-3 weeks after infection

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24
Q

What is Reiters syndrome?

A

Triad- urethritis, uveitis or conjunctivitis and arthritis.

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25
Q

Treatment of reactive arthritis?

A

Aimed at underlying cause or symptomatic relief.

Steroid IM or IA

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26
Q

What is psoriatic arthritis?

A

Occurs in up to 30% of patients with psoriasis. Asymmetrical oligoarthritis. May involve hands in a similar pattern to RA.

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27
Q

Triad of symptoms that can occur in psoriatic arthritis

A

Enthesitis
Spondylitis (inflammation of the vertebra)
Dactylitis (inflammation of the digits)

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28
Q

Treatment of psoriatic arthritis

A

Similar to RA- DMARDs 1st line- methotrexate

Anti-TNF therapy for those who do not respond.

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29
Q

What is enteropathic arthritis?

A

Inflammatory arthritis involving peripheral joints and sometimes the spine inpatients with IBD

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30
Q

Which joints tend to be affected by enteropathic arthritis?

A

Tends to be the large joints.

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31
Q

Treatment of enteropathic IBD

A

Treat underlying disease.

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32
Q

What is gout?

A

Uric acid depositation in the joints. Uric acid is made from the breakdown of purine bases (adenine and guanine) in DNA replication.

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33
Q

What is hyperuricaemia due to?

A

Renal under excretion (thiazide diuretics do this, so does renal failure)
Excessive alcohol, red meat and fish intake.

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34
Q

What triggers the crystals to precipitate in joints?

A

Dehydration
Trauma
Surgery

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35
Q

Which joints are affected by gout

A

The first MTP joint
The ankle and the knee
(however can be any)

36
Q

How does gout present?

A

Intensely hot, painful, swollen joint. Symptoms last for 7-10 days if untreated.

37
Q

What are gout tophi?

A

Painless white accumulations of uric acid in the soft tissues- they may erupt through the skin.

38
Q

How to diagnose gout

A

Analyse a sample of synovial fluid with polarised microscopy

Needle shaped, negatively birefringent.

39
Q

Treatment of an acute attack of gout

A

NSAIDs, corticosteroids and opioid analgesics

40
Q

Treatment of chronic gout

A

After the acute attack has subsided- allopurinol is a uric acid decreaser.

41
Q

What is calcium pyrophosphatase?

A

Psuedogout

42
Q

Appearence of psuedogout

A

Rhomboid shaped, weakly positive birefringent.

43
Q

What is chondrocalcinosis?

A

calcium pyrophosphatase deposits in cartilage and other soft tissues in the absence of acute inflammation.

44
Q

What are seronegative inflammatory arthropathies?

A

No antibodies in serum.

45
Q

What are connective tissue diseases?

A

Diseases which present with symptoms similar to lupus, scleroderma or polymyositis.

46
Q

What is systemic lupus erythematous?

A

Chronic autoimmune condition which presentation is highly variable.

47
Q

Pathogenesis of SLE

A

Defect in apoptosis meaning excessive cell death occurs and there is a change in immune tolerance.
The defective clearance of apoptotic cell debris leads to immune complex depostitation in some tissues (the basement membrane of the skin and kidneys) and increased circulating immune complexes.
Some of these immune complexes lodge in blood vessels which activates complement and therefore an inflammatory reaction occurs.

48
Q

Who gets SLE?

A

Women of child bearing age are the ones most affected.

90% of overall is women.

49
Q

Prognosis of SLE

A

10 year survival exceeds 90%

50
Q

How would you diagnose SLE?

A 
Based on 4 or more of the following (need at least one clinical and one lab finding)
LAB
Anti nuclear antibody
Anti-sm antibody
Anti double stranded DNA antibody
Antiphospholipid antibody
Low complement
Clinical
-Acute cutaneous lupus
Chronic cutaneous lupus
Oral or nasal ulcers
Non-scarring alopecia
Arthritis
Serositis
Renal
Neurologic
Haemolytic anaemia 
Leukopenia 
Thrombocytopenia
51
Q

Skin presentation of SLE

A 
Malar/butterfly rash
Discoid lupus
Alopecia
Oral/nasal ulceration
Raynauds
Photosensitivity
52
Q

MSK presentation of SLE

A

Arthralgia, arthritis and myalgia. Arthritis isn’t erosive or deforming.

53
Q

Renal presentation of SLE

A

Lupus nephritis

54
Q

Respiratory presentation of SLE

A 
Pleurisy
Pulmonary hypertension
Pulmonary emboli
Pleural effusion
Pneumonitis
55
Q

Haematological presentation of SLE

A

Leukopenia, lymphopenia, thrombocytopenia, anaemia

56
Q

Cardiac presentation of SLE

A

Pericarditis
Pericardial effusion
Endocarditis

57
Q

Antibodies involved in SLE

A

Anti double stranded DNA antibody- most specific. Also correlates to disease activity
Anti- nuclear antibody- not very specific however positive in 95% of patients
Anti-Sm antibody- specific however low sensitivity
Anti Ro/Anti-la and anti-RNP- may be seen in SLE but can be seen in other autoimmune conditions.

58
Q

What happens to complement in SLE

A

Complement goes down when disease activity is high.

59
Q

What other investigations would you do into SLE?

A

Full blood count
Urinalysis- to look for glomerular nephritis
Imaging- look for organ involvement.

60
Q

Management of SLE (generally)

A

Depends on manifestation of the disease.

61
Q

Skin disease and arthralgia in SLE management

A

Hyroxychloroquine (DMARD), topical steroids and NSAIDS

62
Q

Inflammatory arthritis and organ involvement in SLE management

A

Immunosupression e.g. azathioprine

Corticosteroids at moderate doses.

63
Q

Severe organ disease in SLE management

A

IV steroids and cyclophosphamide

64
Q

Unresponsive cases of SLE management

A

IV immunoglobulin

Rituximab

65
Q

How is SLE monitored?

A

Frequent FBC and urinalysis
Check anti-ds-dna antibody
BP and cholesterol (to stop cardiovascular morbidities)
Complement levels

66
Q

What is sjogrens syndrome?

A

Autoimmune connective tissue disease that causes lymphatic infiltrates into exocrine glands.

67
Q

Presentation of sjogrens syndrome?

A

Ocular dryness, oral dryness, vaginal dryness. Parotid gland swelling
Arthralgia and fatigue

68
Q

How would you diagnose sjogrens

A

Need 4 or more of the following
Ocular symptoms- dry eyes (greater than 3months)
Oral symptoms- dry mouth, recurrent swollen salivary glands, need water to digest food
Ocular signs- Schirmers performed without anesthesia
Oral signs- abnormal salivary scintigraphy
Anti-Ro or anti-La antibodies

69
Q

Management of sjogrens syndrome?

A

Mainly symptomatic- eye drops
Regular dental care
Pilocarpine can help saliva production (side effects are flushing)
Hydroxychloroquine can help with arthralgia and fatigue.

70
Q

What is systemic sclerosis?

A

Systemic connective tissue disease characteristically including vasomotor disturbances (Raynauds), fibrosis, atrophy of the skin and subcutaneous tissues.

71
Q

What causes skin and organ changes in systemic sclerosis

A

Collagen depositation in the skin and organs.

72
Q

Minor features of systemic sclerosis

A

Sclerodactyly (thickening and tightness of the skin)
Atrophy of the fingertips
Bilateral lung fibrosis

73
Q

Major features of systemic sclerosis

A

Centrally located skin sclerosis (hardening)- affects arms, face and neck.

74
Q

Three phases of cutaneous involvement in systemic sclerosis

A

Oedematous, indurative and atrophic
Skin becomes thickened and hard
Calcinosis- deposits of calcium- may be seen in digits.

75
Q

What can happen to the skin on the face in systemic sclerosis?

A

Pinching of the nose can cause a beak like appearance. Skin becomes tighter around the mouth.

76
Q

What organ involvement can you get with systemic sclerosis?

A

Pulmonary hypertension and pulmonary fibrosis
GI- dysphagia, malabsorption and bacterial overgrowth.
Inflammatory arthritis and myositis may be seen.

77
Q

What are the classifications of systemic sclerosis

A

Limited- skin involved is confined to the face, hands, forearms and feet. Organ involvement is later. Anti-centromere antibody.
Diffuse- skin changes develop more rapidly and on the trunk. Early significant organ involvement. Anti Scl 70 antibody.

78
Q

Management of systemic sclerosis

A

No specific management- mostly symptomatic.
For Raynauds- calcium channel blockers
Renal involvement- ACE inhibitors
GI- PPI for reflux
ILD-immunosuppression- usually cyclophosphamide

79
Q

What is mixed connective tissue disease?

A

Condition which features symptoms also seen in other connective tissue diseases.

80
Q

What symptoms could you see in mixed connective tissue disease?

A 
Raynauds
Arthralgia/arthritis
Myositis
Sclerodactyly
Pulmonary hypertension
ILD
81
Q

Treatment of mixed connective tissue disease?

A

Varies according to presentation
Calcium blockers for Raynauds
Significant muscle or lung disease-immunosuppression.

82
Q

What is anti-phospholipid syndrome?

A

Manifests as recurrent arterial or venous thrombosis and/or fatal loss. May occur in relation to other autoimmune disorders

83
Q

Presentation of antiphospholipid syndrome

A

Increased frequency of stroke or MI (especially in the young)
Recurrent pulmonary emboli or thrombosis
Pulmonary hypertension
Late spontaneous fetal loss (common- but can occur at any point during pregnancy)
Cutaneous feature- livedo reticularis.

84
Q

Investigations into antiphospholipid syndrome?

A

Lupus anticoagulant
Anti-cardiolipid antibodies
Anti-beta 2 glycoprotein.

85
Q

Management of anti-phospholipid syndrome

A

anticoagulation

Low molecular weight heparin if pregnant.

Musculoskeletal (36 decks)

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