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Flashcards in MSK week 2 Deck (85):
1

Describe rheumatoid arthritis

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

2

Where does RA usually affect?

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

3

Who does RA usually affect?

Women more commonly than men.

4

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

Rheumatoid Factor
Anti CCP

5

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

Anti-CCP.

6

Pathogenesis of RA

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.

7

How do you diagnose RA?

Based on clinical presentation, radiographic findings and serological analysis.

8

Early clinical presentation of RA

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

9

Late clinical presentation of RA

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

10

Extra-articular features of RA

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

11

Investigations into RA

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).

12

Treatment of RA

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.

13

Disease activity monitoring in RA

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

14

Describe ankylosing spondylitis

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

15

Who gets ankylosing spondylitis?

Young men (late adolescents- early adulthood)

16

Clinical presentation of ankylosing spondylitis

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

17

What is a question mark spine?

Loss of lumbar lordosis-
Increased thoracic kyphosis.

18

How can you measure the affect of ankylosing spondylitis

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)

19

What will an Xray show of ankylosing spondylitis?

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

20

Treatment of ankylosing spondylitis?

Physiotherapy, NSAIDs, exercise
For more aggressive disease- anti-TNF alpha

21

What is reactive arthritis?

Arthritis that follows infection somewhere else in the body.

22

What organisms usually cause reactive arthritis?

GU- chlamydia, Neissena
GI- campylobacter, salmonella.

23

Presentation of reactive arthritis

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

24

What is Reiters syndrome?

Triad- urethritis, uveitis or conjunctivitis and arthritis.

25

Treatment of reactive arthritis?

Aimed at underlying cause or symptomatic relief.
Steroid IM or IA

26

What is psoriatic arthritis?

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

27

Triad of symptoms that can occur in psoriatic arthritis

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

28

Treatment of psoriatic arthritis

Similar to RA- DMARDs 1st line- methotrexate
Anti-TNF therapy for those who do not respond.

29

What is enteropathic arthritis?

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

30

Which joints tend to be affected by enteropathic arthritis?

Tends to be the large joints.

31

Treatment of enteropathic IBD

Treat underlying disease.

32

What is gout?

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

33

What is hyperuricaemia due to?

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

34

What triggers the crystals to precipitate in joints?

Dehydration
Trauma
Surgery

35

Which joints are affected by gout

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

36

How does gout present?

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

37

What are gout tophi?

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

38

How to diagnose gout

Analyse a sample of synovial fluid with polarised microscopy
Needle shaped, negatively birefringent.

39

Treatment of an acute attack of gout

NSAIDs, corticosteroids and opioid analgesics

40

Treatment of chronic gout

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

41

What is calcium pyrophosphatase?

Psuedogout

42

Appearence of psuedogout

Rhomboid shaped, weakly positive birefringent.

43

What is chondrocalcinosis?

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

44

What are seronegative inflammatory arthropathies?

No antibodies in serum.

45

What are connective tissue diseases?

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

46

What is systemic lupus erythematous?

Chronic autoimmune condition which presentation is highly variable.

47

Pathogenesis of SLE

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

Who gets SLE?

Women of child bearing age are the ones most affected.
90% of overall is women.

49

Prognosis of SLE

10 year survival exceeds 90%

50

How would you diagnose SLE?

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

Skin presentation of SLE

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

52

MSK presentation of SLE

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

53

Renal presentation of SLE

Lupus nephritis

54

Respiratory presentation of SLE

Pleurisy
Pulmonary hypertension
Pulmonary emboli
Pleural effusion
Pneumonitis

55

Haematological presentation of SLE

Leukopenia, lymphopenia, thrombocytopenia, anaemia

56

Cardiac presentation of SLE

Pericarditis
Pericardial effusion
Endocarditis

57

Antibodies involved in SLE

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

What happens to complement in SLE

Complement goes down when disease activity is high.

59

What other investigations would you do into SLE?

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

60

Management of SLE (generally)

Depends on manifestation of the disease.

61

Skin disease and arthralgia in SLE management

Hyroxychloroquine (DMARD), topical steroids and NSAIDS

62

Inflammatory arthritis and organ involvement in SLE management

Immunosupression e.g. azathioprine
Corticosteroids at moderate doses.

63

Severe organ disease in SLE management

IV steroids and cyclophosphamide

64

Unresponsive cases of SLE management

IV immunoglobulin
Rituximab

65

How is SLE monitored?

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

66

What is sjogrens syndrome?

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

67

Presentation of sjogrens syndrome?

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

68

How would you diagnose sjogrens

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

Management of sjogrens syndrome?

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

70

What is systemic sclerosis?

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

71

What causes skin and organ changes in systemic sclerosis

Collagen depositation in the skin and organs.

72

Minor features of systemic sclerosis

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

73

Major features of systemic sclerosis

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

74

Three phases of cutaneous involvement in systemic sclerosis

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

75

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

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

76

What organ involvement can you get with systemic sclerosis?

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

77

What are the classifications of systemic sclerosis

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

Management of systemic sclerosis

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

79

What is mixed connective tissue disease?

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

80

What symptoms could you see in mixed connective tissue disease?

Raynauds
Arthralgia/arthritis
Myositis
Sclerodactyly
Pulmonary hypertension
ILD

81

Treatment of mixed connective tissue disease?

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

82

What is anti-phospholipid syndrome?

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

83

Presentation of antiphospholipid syndrome

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

Investigations into antiphospholipid syndrome?

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

85

Management of anti-phospholipid syndrome

anticoagulation
Low molecular weight heparin if pregnant.