Rheumatoid Arthritis Flashcards

1
Q

Describe the Aetiology of Rheumatoid Arthritis

A
  • Gender: women are affected 3 times more often than men
  • Genetic factors: Increase incidence in first degree relative and high concordance in twins.
  • Environment: Smoking and other forms of bronchial stress increase risk of RA
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2
Q

Describe the Pathophysiology of Rheumatoid Arthritis

A
  • Synovial hypertrophy and chronic inflammation leads to joint damage
    • Modification of our own antigens so no longer recognisable as self antigens. APC present these antigens to activate T-Helper cells
    • Leads to Plasma cells prudction and autoantibody production
    • Antibodies enter blood stream and enter joint space
    • T cells recruit macrophages into the joint space (Interferon-y, Interferon-17). Macropahe produce cytokines (IL-1, IL-6, TNF-a)
    • This leads to Pannus formation which overtime damages cartilage, soft tissue and bone. Protesae released by activated synovial cells which can also break down cartilages
    • Exposure of RANKL can leads to osteoclastic activaton by T cells
    • Increased secretion of Rheumatoid Factor and ANTI-CCP into joint space which form immune complexes to activate the complement system leading to further damage
    • Chronic inflammation also causes angiogenisis which increase the number of immune cells that arrive
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3
Q

What are pathological changes seen in Rheumatoid Arthritis?

A
  • Nodules
    • Central fibrinous necrosis with surrounding macrophages and fibroblasts
  • Synovium
    • Inflammatory infiltrate of T lymphocytes, plasma cells, macrophages
    • Inflammation extends to subchondral bone
    • Proliferative synovitis with synovial cell hyperplasia and hypertrophy
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4
Q

What are some symptoms of Rheumatoid Arthritis?

A
  • Pain and stiffness of hands (MCPs, PIPs) and feet (MTPs). DIPs usually spared.
  • Worse in the morning
  • Wrists, Elbows, Shoulders, Knees and Ankles are also affected
  • Fatigue and disturbed sleep
  • Joints are warm and tender with some swelling
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5
Q

What are Articular Complications of Rheumatoid Arthritis?

A
  • Septic Arthritis
  • Amyloidosis
  • Hands and Wrist deformities
  • Subcutaneous nodule which are firm and intradermal occurring at pressure points
  • Tenosynovitis of flexor tendons of hands
  • Muscle wasting around joint
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6
Q

What are some hand and wrist deformities seen as a result of Rheumatic Disease?

A
  • Ulnar deviation and palmar subluxation
  • Fixed flexion of PIP joints – boutonniere deformity
  • Fixed hyperextension of PIP – swan neck deformity
  • Swelling and dorsal subluxation of ulnar styloid which causes wrist pain and may cause rupture of finger extensor tendons leading in turn to sudden onset of finger drop of little and ring fingers predominantly
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7
Q

What are the extra articular presentations of Rheumatoid Arthritis?

A
  • Anaemia
  • Respiratory: pulmonary fibrosis, pleural effusion, pulmonary nodules, bronchiolitis obliterans, methotrexate pneumonitis, pleurisy
  • Ischaemic heart disease: RA carries a similar risk to type 2 diabetes mellitus
  • Increased risk of infections
  • Ocular: keratoconjunctivitis sicca (most common), episcleritis, scleritis, corneal ulceration, keratitis, steroid-induced cataracts, chloroquine retinopathy
  • Depression
  • Osteoporosis
  • Vasculitis
  • Pericarditis
  • Peripheral sensory neuropathies: mononeuritis multiplex or symmetrical, peripheral – due to vasculitis of the vasa nervorum.
  • Felty’s syndrome (RA + splenomegaly + low white cell count)
  • Atlantoaxial subxalation
  • Amyloidosis
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8
Q

What are tests for Rheumatoid Arthritis?

A
  • Rheumatoid Factor
    • Rose-Waaler Test
  • Anti-CCP
    • USed if Rheumatoid Factor negative
  • X-Ray of hands and feet if suspected
    • Used as benchmark
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9
Q

What should be done one Rheumatoid is confirmed?

A
  • Measure anti-CCP antibodies unless already measure
  • X-ray of the hands to establish whter erosion present unless already done
  • Measure functioning ability using HAQ
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10
Q

What is the non-pharmocological management for Rheumatoid Arthritis?

A
  • Improve general fitness and regular exercise. Learn exercise for enhancing joint flexibility, muscle strength and managing other functional impairments
  • Short term pain relief
  • Occupational therapy
  • Podiatry if they have any problems with feet
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11
Q

What is the pharmacological management of Rheumatoid Arthritis?

A
  • 1st Line: DMARDs such as Methothrexate, Leflunomide
    • If not effective, add a second DMARD
  • Consider used Steroid Bridging therapy
  • Ig not managed by DMARDs still then can add monclonal antibody treatment such as Rituximab, Sarilumab
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12
Q

When is surgical management sought for Rheumatoid Arthritis?

A
  • Offer adults early specialist surgical opinion if any of following do not respond to optimal non-surgical management
    • Persistent pain due to joint damage or other identifiable soft tissue cause
    • Worsening joint function
    • Progressive deformity
    • Persistent localised synovitis
  • Offer to refer adults with any of following complications for specialist surgical opinion before damage or deformity becomes irreversible
    • Imminent or actual tendon rupture
    • Nerve compression
    • Stress fracture
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13
Q

What are the main expected benefits of surgical intervention?

A
  • Pain relief
  • Improvement or prevent of further deterioration of joint function and
  • Prevention of deformity
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14
Q

What is done if Cervical Myelopathy is suspected?

A
  • Request an urgent MRI scan and
  • Fer for specialist surgical opinion
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15
Q

What is Systemic Lupus Eythematosus?

A

An autoimmune disorder.

  • It typically presents in early adulthood and is more common in women and people of Afro-Caribbean origin
  • Characterized by remissions and flares.
  • Can be familial
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16
Q

What causes SLE?

A
  • When cells die by apoptosis, the cellular remnants appear on the cell surface as small blebs that carry self antigens.
  • These antigens include nuclear constituents (e.g. DNA and histones), which are normally hidden from the immune system.
  • In people with SLE, removal of these blebs by phagocytes is inefficient, so that they are transferred to lymphoid tissues, where they can be taken up by antigen-presenting cells.
  • The self antigens from these blebs can then be presented to T cells, which in turn stimulate B cells to produce autoantibodies directed against these antigens.
17
Q

Systemic Lupus: Immune factors activated?

A

Combination of availability of self-antigens and failure of the immune system to inactivate B cells and T cells that recognize these self-antigens (i.e. a breakdown of tolerance) leads to the following immunological consequences:

  • Development of autoantibodies that either form circulating complexes or deposit by binding directly to tissues.
  • Activation of complement and influx of neutrophils, causing inflammation in those tissues.
  • Abnormal cytokine production
18
Q

What are some aetiologies of SLE?

A
  • Genetics
  • Sex hormone status: pre-menopausal women are most frequently affected
  • Drugs: hydralazine, isoniazid, procainamide and penicillamine can induce form of SLE that is usually mild
  • Ultraviolet light: can trigger flares of SLE
  • Exposure to Epstein-Barr virus
19
Q

What type of Hypersentivity is SLE?

A

Type 3

20
Q

What is a Pnemonic to remeber symptoms of SLE?

A

SOAP BRAIN

  • S erositis - Pleurisy, pericarditis
  • O ral ulcers - usually painless; palate is most specific
  • A rthritis - small joints non-erosive
  • P hotosensitivity - or malar or discoid rash
  • B lood disorders - low WCC, lymphopenia, thrombocytopenia, haemolytic anemia
  • R enal involvement - glomerulonephritis
  • A utoantibodies (ANA positive in >90% cases)
  • I mmunologic tests e.g. low complements
  • N eurologic disorder - Seizures or psychosis
21
Q

What are all symptoms of SLE?

A
  • General features
    • Fatigue
    • Fever
    • Lymphadenopathy
  • Skin
    • Lesions may progress to become pigmented and hyperkeratotic before becoming atrophic
    • Raynaud’s phenomenon
    • Livedo reticularis
    • Non-scarring alopecia
  • Musculoskeletal
    • Arthralgia
    • Non-erosive arthritis
  • Cardiovascular
    • Pericarditis: the most common cardiac manifestation
    • Myocarditis
  • Respiratory
    • Pleurisy
    • Fibrosing alveolitis
  • Renal
    • Proteinuria
  • Neuropsychiatric
    • Anxiety and depression
    • Psychosis
    • Seizures
22
Q

What immunological tests are used to diagnosie SLE?

A
  • ANA positive (99% are )
    • anti-dsDNA: highly specific (> 99%), but less sensitive (70%)
    • anti-Smith: most specific (> 99%), sensitivity (30%)
  • Antiphospholipid antibodies
  • Complements
23
Q

What might you find in the full blood count of a patient with SLE?

A
  • Anaemia
  • Low white cell count
  • Low platelet count
24
Q

If there is evidence of haemolytic anaemia what test of the blood might help to confirm the autoimmune nature of the anaemia?

A

Coombs’ Test

25
Q

How is SLE monitored?

A
  • ESR: raised but CRP is normal
  • Complement levels (C3, C4) are low during active disease (formation of complexes leads to consumption of complement)
  • Anti-dsDNA titres can be used for disease monitoring (but note not present in all patients)
  • Urinalysis can be used for detecting renal diseas
  • Renal and Skin biopsy can be diagnostic
26
Q

What is the managment of Systemic Lupus Erythematosus?

A
  • Sun protection
    • UV light trigger SLE. Alters structure of DNA in dermis making it immunogenic
  • Advice on healthy lifestyle in view of cardiovascular risk
  • Hydroxychloroquine is helpful for rash and arthralgia
  • Mycophenolate mofetil, azathioprine and rituximab are commonly used
  • Short courses of prednisolone for flares
27
Q

What are features of Drug Induced SLE?

A
  • Symptoms
    • Arthralgia
    • Myalgia
    • Skin (e.g. malar rash) and Pulmonary involvement (e.g. pleurisy) are common
  • Immunology
    • ANA positive in 100%, dsDNA negative
    • Anti-histone antibodies are found in 80-90%
    • Anti-Ro, anti-Smith positive in around 5%
28
Q

What are common causes of Drug Induced Lupus?

A

Most common causes

  • procainamide
  • hydralazine

Less common causes

  • isoniazid
  • minocycline
  • phenytoin