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MSK > Inflammatory Arthritis > Flashcards

Inflammatory Arthritis Flashcards

1
Q

What is rheumatoid arthritis?

A

Chronic inflammatory autoimmune disorder characterized by joint pain, swelling, and synovial destruction

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2
Q

What are the causes of rheumatoid arthritis?

A

Idiopathic autoimmune disorder, however believed to be multifactorial:
- 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)

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3
Q

Who is rheumatoid arthritis most common in?

A

Peaks 35-50 year old women

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4
Q

Describe pathophysiology of rheumatoid arthritis

A
  1. Non-specific inflammation affects the synovial tissue, which is then amplified by activation of T cells
  2. Leads to inflammatory joint effusion + synovial hypertrophy + progressive destruction and deterioration of cartilage and bone
  3. Inflammatory pannus (granulation tissue) forms which produces proteinases that destroy the cartilage extracellular matrix
  4. Tendon rupture and soft tissue damage can occur leading to joint instability and subluxation
  5. In the chronic phase this includes fibrosis + deformity
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5
Q

Describe the generation of auto-antibodies and activation of the immune response in rheumatoid arthritis

A
  1. Specific genes lead to the conversion of arginine (A) into citrulline (C) → protein will unfold due to loss of positive charge
  2. The unfolded protein acts as an antigen causing an autoimmune response mediated by auto CD4+ T cells
  3. Driven by a type IV hypersensitivity mechanism, but secondary type III hypersensitivity responses also occur
    - 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 leading to neutrophil infiltration and activation
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6
Q

What is the rheumatoid factor? Who has it?

A
  • An auto-antibody (IgM or IgA) that binds to Fc region of IgG
  • Found in ~80% of patients with RA
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7
Q

What is a high titre of RF an indication of?

A

Risk of extra-articular disease

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8
Q

When is anti-CCP present in body? What is it associated with?

A

Can be present for several years prior to articular symptoms
-Associated with erosive damage and current/previous smoking history

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9
Q

What do anti-CCP levels indicate?

A
  • Correlates with disease activity and levels remain positive despite treatment
  • Has low sensitivity so absence does not exclude disease
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10
Q

What are some 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 for MORE THAN 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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11
Q

What are some clinical signs of r. arthritis?

A
  • Symmetrical swelling of affected joints
  • 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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12
Q

What are some extra-articular manifestations of rheumatoid arthritis? Lungs, heart, skin, eye, other MSK?

A
  • Constitutional symptoms: low-grade fever, myalgia, malaise, fatigue, weight loss, night sweats
  • Lungs: interstitial fibrosis, pneuomconiosis (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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13
Q

What blood tests can you do for rheumatoid arthritis?

A
  • Raised inflammatory markers (CRP, plasma viscosity, ESR)
  • Autoantibodies: presence of Rheumatoid factor (60-70% specific) or anti-CCP antibodies (90-99% specific)
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14
Q

What will an X-Ray show in early r. arthritis? Late arthritis?

A
  • Early disease: can be normal, may show soft tissue swelling and periarticular oseopenia
  • Late disease: erosions, sublaxation
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15
Q

What can an USS show in r. arthritis?

A

Useful in detecting synovial inflammation if there is clinical uncertainty; good for treatment changes

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16
Q

When should you use MRI in rheumatoid arthritis?

A

Extremely sensitive but only use if diagnostic doubt

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17
Q

What can be used for symptomatic relief in r. arthritis?

A

Analgesics, NSAIDs and steroids

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18
Q

What do rheumatoid nodules not always respond to and what should you do?

A

DMARDs - excision if problematic but recurrence is high

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19
Q

What is the first line medication for r. arthritis? Examples

A

cDMARDs (conventional disease modifying anti-rheumatic drugs)
-E.g. oral methotrexate (first choice), subcutaneous methotrexate, leflunomide, or sulfasalazine

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20
Q

When should you aim to start patient on cDMARDs for r. arthritis?

A

Within 3 months of symptom onset

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21
Q

When should you administer bDMARDs?

A

Given if have tried 2 DMARDs and patient still has DAS28 score > 5.1

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22
Q

What is second line treatment for r. arthritis? Examples

A

bDMARDs (biological DMARDs)
- eg. anti-TNF agents and T cell receptor blockers

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23
Q

What other treatments can be used for r. arthritis?

A

-Physiotherapists, occupational therapists, podiatrists and orthotists
- Surgery for resistant disease, to control pain, or to improve/maintain function (synovectomy, joint replacement, joint excision, tendon transfers, arthrodesis and cervical spine stabilisation)

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24
Q

What can occur in long standing disease involvement of the cervical spine in r. arthritis?

A

Atlanto-axial subluxation → cervical cord compression

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25
Q

What are spondyloarthropathies?

A

A family of inflammatory arthritides characterised by involvement of both the spine and joints

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26
Q

Who are spondyloarthropathies more common in?

A

Principally in genetically predisposed (HLA B27 positive) individuals

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27
Q

What diseases are associated with the HLA B27 gene?

A

PAIR
-Psoriatic arthritis
-Ankylosing spondylitis
-IBS (+ enteropathic arthritis)
-Reactive arthritis

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28
Q

What people are more commonly HLA B27 positive?

A

Higher prevalence in the northern hemisphere, especially Scandinavian countries

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29
Q

What are 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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30
Q

What are 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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31
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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32
Q

Who is ankylosing spondylitis most common in?

A
  • Genetic predisposition - HLA B27 (90%)
  • More common in males (~4:1)
  • Typical age of onset is 20-40 years
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33
Q

Describe pathophysiology of ankylosing spondylitis?

A
  1. Inflammation of spine ligaments and joints, leading to remodelling
  2. Formation of syndesmophytes (bony outgrowths or spurs that develop at the edges of vertebrae in the spine
  3. Fusion of discs, causing ankylosis
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34
Q

What articular symptoms will someone with ankylosing spondylitis present with?

A
  • Spinal and neck pain (insidiuous and dull)
  • Morning stiffness > 30 mins that improves with activity
  • Peripheral arthritis (knee, shoulders, hips) - RARE
  • Exaggerated thoracic kyphosis and lumbar lordosis (‘question mark’ posture)
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35
Q

What extra- articular symptoms will someone with ankylosing spondylitis present with?

A
  • Eyes: anterior uveitis
  • Cardiac: aortic valve/root problem- aortic regurg
  • Lungs: upper lobe fibrosis
  • Gastro: Asymptomatic enteric mucosal inflammation
  • Other MSK: A-A sublaxation RARE
  • Amyloidosis (accumulation of protein fragments called amyloids)
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36
Q

What clinical signs show ankylosing spondylitis?

A
  • Schobers test: reduced lumbar spine flexion
    • In normal situations it should extend beyond 20cm
  • Reduced chest expansion
  • Occiput-to-wall (normal = 0)
  • Inflammatory enthesitis (sites where tendons or ligaments attach to bone, e.g. Achilles tendon, iliac crests) painful on palpation
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37
Q

What will blood tests show about ankylosing spondylitis?

A
  • Raised inflammatory markers
  • HLA B2
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38
Q

What imaging should you do for ankylosing spondylitis?

A
  • X-ray (common for X-rays to be normal at the time of presentation)
    • Bone density (normal early disease, reduced in later disease)
    • May show sclerosis and fusion of the sacroiliac joints
    • ‘Bamboo spine’ from syndesmophytes
    • Skinny corners
  • MRI - can detect sacroiliitis (active inflammation) and earlier changes such as bone marrow oedema and enthesitis of the spinal ligaments
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39
Q

What does the ASAS classification criteria for axial spondylarthritis (SpA) consist of?

A
  • Patients with ≳ 3 months back pain and age of onset <45 years
  • Sacrolitis on imaging and ≳1 SpA feature
  • OR HLA-B27 positive + ≳ 2 other SpA features (e.g. inflammatory back pain, arthritis, enthesitis, dactilitis, raised CRP)
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40
Q

What non-pharmacological treatments are there for ankylosing spondylitis?

A

Physiotherapy, occupational therapy, orthotics, chiropodist

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41
Q

What is the first line treatment for ankylosing spondylitis?

A

NSAIDs

42
Q

What treatment for symptomatic ankylosing spondylitis?

A
  • Corticosteriods/joint injections
  • Topical steriod eyedrops
43
Q

What treatment for severe ankylosing spondylitis?

A
  • Anti-TNF in severe disease unresponsive to NSAIDs and methotrexate
  • Consider other biologics if still unresponsive e.g. secukinumab (anti-IL17)
44
Q

When is surgery used for ankylosing spondylitis?

A

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

45
Q

What is psoriatic arthritis?

A

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

46
Q

Who is PsA common in?

A

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

47
Q

What are articular symptoms of PsA?

A
  • Asymmetrical oligoarthritis
  • Predominantly affects joints of hands and feet (can be similar pattern to RA but some can have DIPJs)
  • 20% of cases involve sacro-iliac joints
48
Q

What are some extra-articular symptoms of PsA?

A
  • Eye disease
  • Nail involvement (pitting, onycholysis)
49
Q

Name 5 clinical subgroups of PsA

A
  • Confined to DIP joints hands/feet
  • Symmetric polyarthritis (similar to RA)
  • Spondylitis (spine involvement) +/- peripheral joint involvement
  • Asymmatric oligoarthritis with dactylitis
  • Arthritis mutilans (5% of patients have a particularly aggressive and destructive form of the condition)- usually occurs in the hands, involves the reabsorption of bone and collapse of soft tissue
50
Q

What will bloods show in PsA?

A

↑ inflammatory markers, negative RF

51
Q

What will X-Ray show in PsA?

A
  • Marginal erosions and ‘whiskering’
  • Osteolysis
  • Enthesitis
52
Q

What non-pharmacological treatments are there for PsA?

A

Physiotherapy, occupational therapy, orthotics, chiropodist

53
Q

What is first line in PsA?

A

NSAIDs

54
Q

What treatment for symptomatic PsA?

A
  • Symptomatic - corticosteriods/joint injections, topical steroid eyedrops
55
Q

What treatment for severe PsA?

A
  • Anti-TNF in severe disease unresponsive to NSAIDs and methotrexate
  • Consider other biologics if still unresponsive e.g. secukinumab (anti-IL17)
56
Q

What is enteropathic arthritis?

A

Occurs in patients with inflammatory bowel disease, involving inflammatory arthritis in the peripheral joints and sometimes the spine

57
Q

What are the causes of enteropathic arthritis?

A
  • 10-20% of IBD sufferers will have spine or joint problems (worse during flare ups)
  • 20% of patients with Crohn’s will have sacroiliitis
58
Q

Describe pathophysiology of enteropathic arthritis

A

Organisms with high lipopolysacharides in cell wall trigger immune reaction

59
Q

What are some symptoms of enteropathic arthritis

A
  • Arthritis in several joints (knees, ankles, elbows, and wrists, sometimes spine, hips, or shoulders)
  • GI - loose, watery stool with mucous and blood
  • Weight loss
60
Q

What are some clinical signs of enteropathic arthritis?

A
  • Low grade fever
  • Uveitis
  • Pyoderma gangrenosum
  • Enthesitis - archilles tendontitis, plantar fasciitis, lateral epicondylitis
  • Aphthous ulcers
61
Q

What investigations can you carry out for enteropathic arthritis?

A
  • Upper and lower GI endoscopy with biopsy showing ulceration/colitis
  • Joint aspirate - no organisms or crystals will rule out septic arthritis and crystal arthropathies
  • ↑ inflammatory markers
  • X-ray/MRI - sacroiliitis
  • USS - synovitis/tendosynovitis
62
Q

What treatment should you give for enteropathic arthritis?

A

-Treat both underlying condition and arthritis
- Management of the arthritis similar to other seropositive arthritis (physio, NSAIDs, DMARDs, anti-TNF etc.)

63
Q

What is reactive arthritis?

A

Infection induced systemic illness usually as an inflammatory synovitis from which viable microorganisms cannot be cultured

64
Q

What are causes of reactive arthritis?

A
  • Mostly urogenital (e.g. chlamydia, neisseria) and enterogenic (e.g. salmonella, campylobacter)
65
Q

Who is reactive arthritis common in?

A
  • Young adults (20-40)
  • Equal sex distribution
66
Q

Will reactive arthritis patients test positive for HLA B27?

A

Yes

67
Q

Describe the pathophysiology of reactive arthritis?

A

Occurs in response to an infection in another part of the body which triggers an autoimmune arthropathy
- Large joints e.g. the knee can become inflamed around 1‐3 weeks following the infection

68
Q

What are the symptoms of reactive arthritis?

A
  • Present 1-4 weeks after infection
  • General symptoms - fever, fatigue, malaise
  • Asymmetrical monoarthritis or oligoarthritis
  • Enthesitis
69
Q

What are some clinical signs of reactive arthritis?

A
  • Mucocutaneous lesions
    • Keratodema blenorrhagica
    • Circinate balanitis
    • Painless oral ulcers
    • Hyperkeratotic nails
  • Ocular lesions (uni or bilateral) - conjuntivitis, iritis
  • Vissceral manifestations - mild renal disease, carditis
  • Reiter’s syndrome: triad of urethritis, conjuctivitis/uveitis/iritis and arthritis
70
Q

What investigations should you carry out for 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)
71
Q

What are the treatments for reactive arthritis?

A
  • Treatment the underlying infectious cause and symptomatic relief, including IA or IM steroid injections
  • 90% resolve within 6 months
  • Remaining 10% - chronic progressive erosive disease, requiring DMARDs
72
Q

What is gout?

A

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

73
Q

What is the cause of gout?

A

Usually due to high serum uric acid levels (hyperuricaemia)

74
Q

What are the two causes of hyperuricaemia?

A
  • Increased urate production
  • Reduced urate excretion
75
Q

What causes increased uric acid production?

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
76
Q

What causes reduced uric acid excretion?

A
  • Chronic renal impairement
  • Volume depletion e.g. heart failure
  • Hypothyroidism
  • Diuretics
  • Cytotoxins e.g. cyclosporin
77
Q

Who is at most risk for gout?

A
  • Age 20-80
  • More common in men than women
  • Very rare in women before the menopause (oestrogen is protective)
  • Some evidence for a genetic predisposition
78
Q

What are recurrent gout flares due to? Chronic gouty arthritis?

A
  • 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
79
Q

What places are commonly affected by gout?

A
  • Any joint can be affected, but the first metatarsalphalangeal (MTP) joint is the classic site of disease
    • Ankle and knee also common
80
Q

Describe pain, onset, and length of time of gout

A
  • 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
81
Q

What is chronic tophaceous gout?

A

Prior to the development of tophi, individuals with chronic tophaceous gout typically experience recurrent gout attacks which develops over time into the presence of tophi

82
Q

What are gouty tophi

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
83
Q

What can chronic gout lead to?

A

Destructive erosive arthritis

84
Q

What will blood tests show in gout?

A
  • Serum uric acid raised
    • May be normal during acute attack (~40%)
  • Raised inflammatory markers
  • Renal function (ACR and GFR) - cause or effect
85
Q

What will aspiration of synovial fluid show?

A
  • Polarised microscopy - needle shaped, negative birefringent crystals
  • Gram stain and culture to rule out septic arthritis in acute gout
86
Q

What will X-Ray show in gout?

A

Erosion may be visible in long-standing gout

87
Q

What treatment do you use for acute 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
88
Q

How should prophylactic therapy be taken for gout?

A
  • Prophylaxis should be started 4-6 weeks after acute attack, with NSAIDs for first 6 months (or colchicine/steroids) as rapid reduction in uric acid level may result in further exacerbation of gout
  • WHO target for serum uric acid is 300-360µmol/L
    • Monitor every 4-6 weeks
89
Q

Who is prophylactic therapy indicated for?

A

-2+ acute attacks despite lifestyle modification
- Presence of gouty tophi
- Heart failure when unable to stop diuretics

90
Q

What drugs are used for prophylaxis in 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
91
Q

What is pseudogout?

A

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

92
Q

Who is pseudogout most common in? Why?

A

Most common in the elderly (chondrocalcinosis increases with age)

93
Q

What is chondrocalcinosis?

A

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

94
Q

What do pseudogout and chondrocalcinosis fall under?

A

Calcium Pyrophosphate Deposition disease (CPPD)

95
Q

What does pseudogout affect?

A

Fibrocartilage - knees, wrists, ankles

96
Q

What is pseudogout associated with?

A
  • Hyperparathyroidism
  • Familial hypocalciuric hypercalcaemia
  • Haemochromatosis
  • Wilson’s disease
  • Haemosiderosis
  • Hypophosphatasia
  • Hypomagnesemia
  • Hypothryoidism
  • Gout
  • Neuropathic joints
  • Amyloiosis
  • Trauma
97
Q

What are symptoms of pseudogout?

A
  • Monoarthritis - swollen, painful, warm joint
  • Knee most commonly affected
98
Q

What will a blood test show for pseudogout?

A

Rise in inflammatory markers

99
Q

What will aspiration of synovial fluid show?

A

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

100
Q

How do you treat pseudogout?

A
  • Treat acute episodes appropriately - NSAIDs, colchicine, steroids, rehydration
  • No prophylactic management
101
Q

What is Hydroxyapatite Deposition Disease/Acute Calcific Tendonitis

A

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

102
Q

Who is HDD most common in?

A

Most common in females, 50-60 years

MSK (12 decks)

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