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Musculoskeletal MBCHB > Inflammatory Arthritis > Flashcards

Inflammatory Arthritis Flashcards

1
Q

What is rheumatoid arthritis?

A

Inflammatory autoimmune disorder characterized by joint pain, swelling, and synovial destruction

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2
Q

What is the aetiology of rheumatoid arthritis?

A
  • Chronic inflammatory autoimmune disorder of unknown etiology
  • Hypotheses suggest the aetiology is multifactorial, with the following factors playing a role:
    • Genetic predisposition - seems to be associated with specific HLA types e.g. HLA DRB1 gene
    • Environmental triggers - infection and smoking increase anti-CCP
    • Hormonal factors - higher incidence in females (3:1)
  • Prevalence peaks 35-50 years of age
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3
Q

What is the pathophysiology of rheumatoid arthritis?

A
  • Initially, non-specific inflammation affects the synovial tissue, which is later amplified by activation of T cells
  • Triggers e.g. smoking, infection or trauma have been implicated
  • With time it may lead to inflammatory joint effusion and synovial hypertrophy as well as progressive destruction and deterioration of cartilage and bone
  • Inflammatory pannus (inflammatory granulation tissue) forms which produces proteinases that destroy the cartilage extracellular matrix
  • Tendon rupture and soft tissue damage can occur leading to joint instability and subluxation
  • Chronic phase - fibrosis, deformity
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4
Q

Explain the pathophysiology of the generation of auto-antibodies in rheumatoid arthritis?

A
  • Susceptibility genes lead to the conversion of arginine (A) into citrulline (C) → protein will unfold due to loss of positive charge
  • The unfolded protein acts as an antigen - autoimmune response mediated by auto-reactive CD4+ T cells
  • Involvement of pro-inflammatory CD4+ Th1 and Th17 effector cells and macrophages
  • Driven by a type IV hypersensitivity mechanism, but secondary type III hypersensitivity responses also occur as anti-citrullinated peptide antibodies (can be generated in the lungs from smoking) can form immune complexes with the citrullinated proteins produced in an inflamed synovium → neutrophil infiltration and activation
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5
Q

Explain the pathophysiology of rheumatoid factor?

A
  • IgM or IgA antibody that binds to Fc region of IgG
  • Found in ~80% of patients with RA (15% are negative for RF)
  • Patients with high titres of RF are more at risk of extra-articular disease
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6
Q

Explain the pathophysiology of anti-CCP.

A
  • Can be present for several years prior to articular symptoms
  • More likely to be associated with erosive damage
  • Associated with current/previous smoking history
  • Correlates with disease activity and levels remain positive despite treatment
  • Low sensitivity - absence does not exclude disease
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7
Q

What are the articular manifestations of rheumatoid arthritis?

A
  • Polyarthralgia
    • Symmetrical pain and swelling of affected joints
    • Rapid onset
    • Most commonly in the small joints of the hands and feet (PIPs/MCPs and MTPs)
    • Larger joints e.g. knees, shoulders, elbows and atlantoaxial joint can also be affected as the disease progresses
  • Early morning stiffness > 30 mins that usually improves with activity
  • Reduction in grip strength
  • Joint deformities (‘rheumatoid hand’)
    • Swan neck deformity: PIP hyperextension and DIP flexion
    • Boutonniere deformity: PIP flexion and DIP hyperextension
  • Atlanto-axial subluxation
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8
Q

What are the extra-articular manifestations of rheumatoid arthritis?

A
  • Systemic inflammation can cause extra-articular co-morbidities
  • Constitutional symptoms: low-grade fever, myalgia, malaise, fatigue, weight loss, night sweats
  • Lungs: interstitial fibrosis, pneumoconiosis (Caplan syndrome), rheumatoid lung nodules, pleuritis, pleural effusions
  • Heart: pericarditis, myocarditis, increased risk of CVD
  • Skin: pyoderma gangrenosum, Raynaud’s phenomenon, rheumatoid skin nodules
  • Eye: keratoconjunctivitis
  • Other MSK: osteopenia/osteoporosis, Sjogren syndrome
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9
Q

What is the typical presentation of rheumatoid arthritis?

A
  • Swelling of affected joints
    • Synovial proliferation and reactive joint effusion cause soft tissue swelling - symmetrical synovitis (doughy swelling)
  • Positive compression tests of MCP and MTP joints
  • Bouchard’s nodes - bony swellings of proximal IPJ (also see in OA)
  • 25% of patients develop rheumatoid nodules, most commonly on extensor surfaces or sites of frequent mechanical irritation
    • Necrotising granulomas with a palisade of macrophages surrounding a central area of collagen necrosis
  • Synovial herniation - cysts e.g. Baker’s cyst
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10
Q

What are the investigations and their findings of rheumatoid arthritis?

A

Bloods

  • Raised inflammatory markers (CRP, plasma viscosity, ESR)
  • Autoantibodies: presence of Rheumatoid factor (60-70% specific) or anti-CCP antibodies (90-99% specific)

Imaging

  • X-ray of hands and feet - helps with diagnosis and determination of disease severity
    • Early disease: can be normal, may show soft tissue swelling and periarticular osteopenia
    • Late disease: erosions, subluxation
  • USS - may be useful in detecting synovial inflammation if their is clinical uncertainty (especially in early RA), useful in making treatment changes
  • MRI - extremely sensitive but only use if diagnostic doubt
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11
Q

What is the management of rheumatoid arthritis?

A

Symptomatic relief

  • Analgesics, NSAIDs and steroids can be used short term for symptomatic relief
  • Rheumatoid nodules don’t always respond to DMARDs - excision if problematic but recurrence is high

DMARDs (first line)

  • Conventional disease modifying anti-rheumatic drugs (cDMARDs) e.g. oral methotrexate (first choice), subcutaneous methotrexate, leflunomide, or sulfasalazine
  • Aim to start patients on DMARDs within 3 months of symptom onset

Biological disease modifying anti-rheumatic drugs (second line)

  • Given if have tried 2 DMARDs and patient still has DAS28 score > 5.1
  • Examples include anti-TNF agents and T cell receptor blockers
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12
Q

What are spondyloarthropathies?

A

family of inflammatory arthritides characterised by involvement of both the spine and joints, principally in genetically predisposed (HLA B27 positive) individuals

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13
Q

What is HLA B27?

A
  • Diseases associated with the HLA B27 subtype can be remembered with the mnemonic PAIR - psoriatic arthritis, ankylosing spondylitis, IBS (+ enteropathic arthritis), reactive arthritis
  • Higher prevalence in the northern hemisphere, especially Scandinavian countries
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14
Q

What are the shared rheumatological features of spondyloarthropathies?

A
  • Sacroiliac and spinal involvement
  • Inflammatory arthritis - oligoarticular, asymmetric, predominantly lower limb
  • Synovitis: inflammation of joint and tendon sheath linings
  • Enthesitis: inflammation at sites where ligaments and tendons attach to bones e.g. Achilles tendinitis, plantar fasciitis
  • Dactylitis (‘sausage’ digits): inflammation of the entire digit
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15
Q

What are the shared extra-articular features of spondyloarthropathies?

A
  • Ocular inflammation (anterior uveitis, conjunctivitis)
  • Mucocutaneous lesions
  • Rare aortic incompetence or heart block
  • No rheumatoid nodules
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16
Q

What is ankylosing spondylitis?

A

Chronic inflammatory disease of the axial skeleton that leads to partial or even complete fusion and rigidity of the spine

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17
Q

What is the aetiology of ankylosing spondylitis?

A
  • Genetic predisposition - HLA B27 (90%)
  • More common in males (~4:1)
  • Typical age of onset is 20-40 years
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18
Q

What is the pathophysiology of ankylosing spondylitis?

A
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19
Q

What are the articular symptoms of ankylosing spondylitis?

A
  • Spinal and neck pain
    • Gradual onset of dull pain that progresses slowly
  • Morning stiffness > 30 mins that improves with activity
  • Peripheral arthritis (knee, shoulders, hips) - rare
  • Late AS - loss of lumbar kyphosis with pronounced cervical lordosis (‘question mark’ posture)
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20
Q

What are the signs of ankylosing spondylitis?

A
  • Schober’s test: used to measure lumbar spine flexion
    • Involves measuring 5cm below the posterior superior iliac crests and 10cm above, whilst the patient is upright, then asking them to bend forwards and remeasuring the distance
    • In normal situations it should extend beyond 20cm
  • Reduced chest expansion
  • Occiput-to-wall (normal = 0)
  • Inflammatory enthesitis e.g. of the Achilles tendon, iliac crests - painful on palpation
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21
Q

What are the extra-articular features of ankylosing spondylitis?

A
  • Anterior uveitis
  • Cardiovascular involvement (aortic valve/root - aortic regurg)
  • Pulmonary involvement (upper lobe fibrosis)
  • Asymptomatic enteric mucosal inflammation
  • Neurological involvement (rarely A-A subluxation)
  • Amyloidosis
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22
Q

What is seen in blood tests for ankylosing spondylitis?

A
  • Raised inflammatory markers
  • HLA B27
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23
Q

What is seen in imaging in ankylosing spondylitis?

A
  • X-ray
    • Bone density (normal early disease, reduced in later disease)
    • May show sclerosis and fusion of the sacroiliac joints
    • Bony spurs from the vertebral bodies (syndesmophytes) can bridge the intervertebral disc resulting in fusion, producing a ‘bamboo spine’
    • Skinny corners
    • Common for X-rays to be normal at the time of presentation
  • MRI - can detect sacroiliitis (active inflammation) and earlier changes such as bone marrow oedema and enthesitis of the spinal ligaments
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24
Q

What is the ASAS classification for ankylosing spondylitis?

A
  • In patients with ≳ 3 months back pain and age of onset <45 years
  • Sacroiliitis on imaging and ≳1 SpA feature OR HLA-B27 positive and ≳ 2 other SpA features (e.g. inflammatory back pain, arthritis, enthesitis, dactylitis, raised CRP)
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25
Q

What is the non-pharmacological management for ankylosing spondylitis?

A

Physiotherapy, occupational therapy, orthotics, chiropodist

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26
Q

What is the pharmacological management for ankylosing spondylitis?

A
  • NSAIDs - first line
  • Symptomatic - corticosteroids/joint injections, topical steroid eyedrops
  • DMARDs e.g. methotrexate, sulfasalazine, leflunomide
  • Anti-TNF in severe disease unresponsive to NSAIDs and methotrexate
  • Consider other biologics if still unresponsive e.g. secukinumab (anti-IL17)
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27
Q

What is the surgical management for ankylosing spondylitis?

A

Mainly reserved for hip and knee arthritis, kyphoplasty is controversial and carries considerable risk

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28
Q

What is psoriatic arthritis?

A

Inflammatory arthritis associated with psoriasis, but 10-15% of patients can have PsA without psoriasis

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29
Q

What is the aetiology of psoriatic arthritis?

A

Occurs in up to 30% of people affected by skin psoriasis

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30
Q

What are the articular symptoms of psoriatic arthritis?

A
  • Usually an asymmetrical oligoarthritis but can affect the hands in a similar pattern to RA
  • Predominantly affects joints of hands and feet
  • 20% of cases involve sacro-iliac joints
  • Some patients have a predilection for arthritis of the DIP joints of the fingers and/or toes
  • Spondylitis, actylisis and enthesitis commonly occur
31
Q

What are the extra-articular symptoms of psoriatic arthritis?

A
  • Eye disease
  • Nail involvement (pitting, onycholysis)
32
Q

What are the clinical subgroups of psoriatic arthritis?

A
  • Confined to DIP joints hands/feet
  • Symmetric polyarthritis (similar to RA)
  • Spondylitis (spine involvement) +/- peripheral joint involvement
  • Asymmetric oligoarthritis with dactylitis
  • 5% of patients have a particularly aggressive and destructive form of the condition known as arthritis mutilans - usually occurs in the hands, involves the reabsorption of bone and collapse of soft tissue
33
Q

What are the investigations for psoriatic arthritis?

A
  • Bloods - ↑ inflammatory markers, negative RF
  • X-ray
    • Marginal erosions and ‘whiskering’
    • Osteolysis
    • Enthesitis
34
Q

What is the non-pharmacological management for psoriatic arthritis?

A

Physiotherapy, occupational therapy, orthotics, chiropodist

35
Q

What is the pharmacological management for psoriatic arthritis?

A
  • NSAIDs - first line
  • Symptomatic - corticosteroids/joint injections, topical steroid eyedrops
  • DMARDs e.g. methotrexate, sulfasalazine, leflunomide
  • Anti-TNF in severe disease unresponsive to NSAIDs and methotrexate
  • Consider other biologics if still unresponsive e.g. secukinumab (anti-IL17)
36
Q

What is enteropathic arthritis?

A

Refers to an inflammatory arthritis involving the peripheral joints and sometimes the spine, occurring in patients with inflammatory bowel disease

37
Q

What is the aetiology of enteropathic arthritis?

A
  • 10-20% of IBD sufferers will experience spine or joint problems
  • 20% of patients with Crohn’s will have sacroiliitis
  • Worsening of symptoms during flare-ups of IBD
38
Q

What is pathophysiology of enteropathic arthritis?

A

Organisms with high lipopolysaccharides in cell wall trigger immune reaction

39
Q

What is the presentation of enteropathic arthritis?

A
  • Patients present with arthritis in several joints, especially knees, ankles, elbows, and wrists, sometimes spine, hips, or shoulders
  • GI - loose, watery stool with mucous and blood
  • Weight loss
  • Low grade fever
  • Uveitis
  • Pyoderma gangrenosum
  • Enthesitis - Achilles tendonitis, plantar fasciitis, lateral epicondylitis
  • Aphthous ulcers
40
Q

What are the investigations for enteropathic arthritis?

A
  • Upper and lower GI endoscopy with biopsy showing ulceration/colitis
  • Joint aspirate - no organisms or crystals (rules out septic arthritis and crystal arthropathies)
  • ↑ inflammatory markers
  • X-ray/MRI - sacroiliitis
  • USS - synovitis/tendosynovitis
41
Q

What is the management of enteropathic arthritis?

A
  • Usually involves finding mediation to manage both the underlying condition and the arthritis
  • Management of the arthritis similar to other seropositive arthritis (physio, NSAIDs, DMARDs, anti-TNF etc.)
42
Q

What is reactive arthritis?

A

Infection induced systemic illness characterised primarily by an inflammatory synovitis from which viable microorganisms cannot be cultured

43
Q

What is the aetiology of reactive arthritis?

A
  • Most common preceding infections are urogenital (e.g. chlamydia, neisseria) and enterogenic (e.g. salmonella, campylobacter)
  • HLA B27 positive
  • Young adults (20-40)
  • Equal sex distribution
44
Q

What is the pathophysiology of reactive arthritis?

A
  • Occurs in response to an infection in another part of the body
  • Large joints e.g. the knee become inflamed around 1‐3 weeks following the infection
  • The infection triggers an autoimmune arthropathy
45
Q

What is the presentation of reactive arthritis?

A
  • Present 1-4 weeks after infection
  • General symptoms - fever, fatigue, malaise
  • Asymmetrical monoarthritis or oligoarthritis
  • Enthesitis
  • Mucocutaneous lesions
    • Keratoderma blennorrhagia
    • Circinate balanitis
    • Painless oral ulcers
    • Hyperkeratotic nails
  • Ocular lesions (uni or bilateral) - conjuntivitis, iritis
  • Visceral manifestations - mild renal disease, carditis
46
Q

What is Reiter’s syndrome?

A

triad of urethritis, conjunctivitis/uveitis/iritis and arthritis

47
Q

What are the investigations of reactive arthritis?

A
  • Bloods - ↑ inflammatory markers, FBC, U+Es, LFTs, HLA B27 (rarely necessary)
  • Cultures - blood, urine, stool
  • Joint fluid analysis - rule out infection (aspirate should be negative)
  • X-ray of affected joints
  • Ophthalmology opinion
48
Q

What is the management of reactive arthritis?

A
  • Treatment is aimed at the underlying infectious cause and symptomatic relief, including IA or IM steroid injections
  • Most cases self-limiting - 90% resolve spontaneously within 6 months
  • Remaining 10% - chronic progressive erosive disease, requiring DMARDs
49
Q

What is gout?

A

Potentially disabling and erosive inflammatory arthritis caused by the deposition of monosodium urate crystals into joints and soft tissues

50
Q

What are the causes of increased urate production -> causes of hyperuricaemia?

A
  • High dietary purine intake (red meat, seafood, corn syrup)
  • Alcohol
  • Inherited enzyme defects
    • Usually idiopathic - 90% unknown enzyme deficiency
    • HGPRT enzyme deficiency impairs purine nucleotide salvage pathway → degraded to urate
  • Myeloproliferative/lymphoproliferative disorders
  • Psoriasis
  • Haemolytic disorders
51
Q

What are the causes of reduced urate excretion -> causes of hyperuricaemia?

A
  • Chronic renal impairment
  • Volume depletion e.g. heart failure
  • Hypothyroidism
  • Diuretics
  • Cytotoxics e.g. cyclosporin
52
Q

What are the risk factors of gout?

A
  • Age - rare under 20, decreases after age 80
  • More common in men than women
  • Very rare in women before the menopause (oestrogen is protective)
  • Some evidence for a genetic predisposition
53
Q

What is the pathophysiology of gout?

A
  • Uric acid is the final compound in the breakdown of purines (A+G) in DNA metabolism
  • Recurrent gout flares are the result of the acute inflammatory response to deposited MSU crystals
  • Chronic gouty arthritis and tophaceous gout is the result of a chronic granulomatous inflammatory response to deposited crystals
    • Histology of gouty tophi - amorphous eosinophilic debris and inflammation (giant cells)
54
Q

What is the presentation of acute gout?

A
  • Although any joint can be affected the first metatarsal phalangeal (MTP) joint is the classic site of disease
    • Ankle and knee are the other most commonly affected joints
  • Severe pain, hot swollen joint which may mimic a septic arthritis
  • Abrupt onset, often overnight
  • Settles in about 10 days without treatment, 3 days with treatment
55
Q

What is the presentation of chronic tophaceous gout?

A
  • Gouty tophi are painless white accumulations of uric acid which can occur in the soft tissues and occasionally erupt through the skin
  • Often diuretic associated
  • May get acute attacks
  • Chronic gout can result in a destructive erosive arthritis
56
Q

What are the investigations of gout?

A

Bloods

  • Serum uric acid raised
    • May be normal during acute attack (~40%)
  • Raised inflammatory markers
  • Renal function (ACR and GFR) - cause or effect

Aspiration of synovial fluid

  • Polarised microscopy - needle shaped, negative birefringent crystals
  • Gram stain and culture to rule out septic arthritis in acute gout

X-rays

  • Erosion may be visible in long-standing gout
57
Q

What is the acute management of gout?

A
  • NSAIDs e.g. naproxen
  • Colchicine if NSAIDs not suitable e.g. patients with heart failure, chronic kidney disease
    • Side effect: diarrhoea
  • Steroids (third line) - orally, IM or intra-articular into joint
  • Lifestyle modification is usually enough to prevent further flares
58
Q

What is the prophylactic therapy of gout?

A
  • Prophylaxis should be started 4-6 weeks after acute attack and requires cover with NSAIDs for first 6 months (or colchicine/steroids) as rapid reduction in uric acid level may result in further exacerbation of gout
  • Indications include 2+ acute attacks despite lifestyle modification, presences of gouty tophi and heart failure when unable to stop diuretics
  • WHO target for serum uric acid is 300-360µmol/L
    • Monitor every 4-6 weeks
59
Q

What are the other treatment options of gout?

A
  • Xanthine oxidase inhibitors - allopurinol (first line), febuxostat (if allopurinol not tolerated/contraindicated)
  • Others:
    • Uricosuric drugs - sulfinpyrazone, probenecid
      • Can worsen renal impairment
    • IL-1 inhibitors - canakinumab
60
Q

What is pseudogout?

A

Deposition of calcium pyrophosphate in the joints and soft tissues leads to inflammation

61
Q

What is chondrocalcinosis?

A

calcium pyrophosphate deposition occurs in cartilage and other soft tissues in the absence of acute inflammation

62
Q

What is the aetiology of pseudogout?

A
  • Most common in the elderly
    • Chondrocalcinosis increases with age
  • Both pseudogout and chondrocalcinosis come under the umbrella of Calcium Pyrophosphate Deposition disease (CPPD)
  • Related to osteoarthritis - calcium deposition can occur in some cases of OA
  • Affects fibrocartilage - knees, wrists, ankles
63
Q

What are risk factors of pseudogout?

A
  • Hyperparathyroidism
  • Familial hypocalciuric hypercalcaemia
  • Haemochromatosis
  • Wilson’s disease
  • Hemosiderosis
  • Hypophosphatasia
  • Hypomagnesemia
  • Hypothyroidism
  • Gout
  • Neuropathic joints
  • Amyloidosis
  • Trauma
64
Q

What is the presentation of pseudogout?

A
  • Monoarthritis - swollen, painful, warm joint
  • Knee most commonly affected
65
Q

What are the investigations for pseudogout?

A

Aspiration of synovial fluid

  • Polarised microscopy - calcium pyrophosphate crystals are envelope shaped, mild positively birefringent

Bloods

  • Marked rise in inflammatory markers
66
Q

What is the management of pseudogout?

A
  • Treat acute episodes appropriately - NSAIDs, colchicine, steroids, rehydration
  • No prophylactic management
67
Q

What is hydroxyapatite deposition disease?

A

Deposition of basic calcium phosphate in the joints and soft tissues leads inflammation; the shoulder is the most frequently involved site (‘Milwaukee shoulder’)

68
Q

What is the aetiology of hydroxyapatite deposition disease?

A

Most common in females, 50-60 years

69
Q

What is the pathophysiology of hydroxyapatite deposition disease?

A
  • Hydroxyapatite crystal deposition in the supraspinatus tendon
  • Release of collagenases, serine proteinases and IL-1
  • Acute and rapid deterioration
70
Q

What is the presentation of hydroxyapatite deposition disease?

A

Acute onset of severe shoulder pain

71
Q

What are the investigations for hydroxyapatite deposition disease?

A

X-ray - calcification can be seen just proximal to the greater tuberosity

72
Q

What is the management of hydroxyapatite deposition disease?

A
  • NSAIDs, subacromial steroid and local anaesthetic injections for pain relief
  • Usually self limiting - pain eases as calcification resorbs
  • Physiotherapy
  • Surgical removal of calcifications may be appropriate for cases refractory to other attempts of conservative treatment
  • Last line - partial or total arthroplasty
73
Q

What is seen on this xray?

A

Calcification -> Hydroxyapatite deposition disease

Musculoskeletal MBCHB (21 decks)

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