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Year 3 Musculoskeletal > Arthritides > Flashcards

Arthritides Flashcards

1
Q

What is rheumatoid arthritis?

A

Chronic INFLAMMATORY systemic disease characterised by symmetrical deforming polyarthritis and extra-articular manifestations.

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2
Q

What is the aetiology of rheumatoid arthritis? Associations? (x2)

A

Unknown. Associated with other autoimmune phenomena including Raynoud’s syndrome and Sjogrens syndrome, and HLA DR-1 and DR-4 halotypes.

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3
Q

What is the pathophysiology of rheumatoid arthritis?

A

Inflammation of synovium and shows increased angiogenesis, cellular hyperplasia and migration of mononuclear inflammatory cells (T, B, macrophages and plasma cells). This leads to EROSION. Prominent cytokines include TNF, IL-1 and IL-6 which promote proliferation and metalloproteinase expression (thought to lead to joint destruction). NB: angiogenesis occurs to support the hypertrophic synovium.

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4
Q

What is the role of metalloproteinases?

A

Matrix enzymes that catalyse both collagen and proteoglycan degradation

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5
Q

What is the epidemiology of rheumatoid arthritis: Prevalence? Gender? Age?

A

1% prevalence. Three times more common in females. Peak incidence 50s years.

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6
Q

!!! What are the signs and symptoms of rheumatoid arthritis? Early signs? Late signs? (x8) Onset? Where?

A
  • Gradual onset. Associated with multiple peripheral joints, usually hands at MCP and PIP (although occasionally monoarticular), and symmetrically.
  • ARTICULAR: Joint pain and swelling, warm, morning stiffness, impaired function
  • Rheumatoid nodules: firm subcutaneous nodules on elbows, palms and over extensor tendons
  • EARLY SIGNS: spindling (swelling) of fingers at MCP and PIP.
  • LATE SIGNS: ulnar deviation of fingers as a result of subluxation at MCP, radial deviation of wrist, swan neck deformity, Boutonniere deformity, Z deformity of the thumb, trigger finger, wasting of the small muscles of the hand, palmar erythema
  • SYSTEMIC: fever, weight loss, fatigue
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7
Q

What is swan neck deformity?

A

MCP and DIP fixed flexion, PIP extension.

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8
Q

What is Boutonniere deformity?

A

MCP and DIP joint extension, PIP flexion (opposite of swan neck)

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9
Q

What is Z deformity of the thumb?

A

AKA hitchhiker thumb deformity; MCP flexion, IP exftension.

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10
Q

What is trigger finger?

A

Unable to straighten the finger and tendon sheath nodule palpable.

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11
Q

What are the investigations for rheumatoid arthritis? (x3)

A
  • Diagnosis clinical and laboratory/radiographic testing usually more important in providing prognostic information
  • BLOODS: anti-CCP antibodies (more specific), rheumatoid factor (monoclonal IgM against Fc portion of IgG; strong association with rheumatoid nodules and extra-articular manifestations), ANA (in 30%)
  • ACUTE PRESENTATION (rare): consider joint aspiration to exclude septic arthritis
  • X-RAYS: soft tissue swelling, angular deformity, periarticular EROSIONS and osteoporosis
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12
Q

What disease activity scores are there for rheumatoid arthritis? (x5)

A
  • Disease activity score (DAS)
  • 28-joint count version of disease activity score (DAS28)
  • Simplified disease activity index (SDAI)
  • Clinical disease activity index (CDAI)
  • Routine assessment patient index data (RAPID3)
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13
Q

What are the complications of rheumatoid arthritis? (x4 (x4, x4, x3, x3))

A
  • Vasculitis of skin leading to nail-fold infarcts (see photo), digital gangrene, ulcers, purpuric rash
  • Anaemia of chronic disease, megaloblastic anaemia (from increased folic acid demand), aplastic anaemia (from drugs), Haemolytic anaemia (in Felty’s syndrome; syndrome of RA, splenomegaly and neutropenia)
  • Pleural effusions, fibrosis, rheumatoid nodules in parenchyma
  • Pericarditis, myocarditis, conduction abnormalities
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14
Q

What is osteoarthritis?

A

Note this is different form osteoporosis. Age-related degenerative synovial joint disease when cartilage destruction exceeds repair causing pain and impaired function.

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15
Q

What is the aetiology of osteoarthritis? (x1 and x4)

A
  • PRIMARY: unknown aetiology. Likely to be multifactorial, linked to age, genetics, female sex, menopause and obesity
  • SECONDARY: other disease can cause altered joint architecture and stability. Commonly associated diseases include developmental abnormalities (hip dysplasia, Perthes’ disease, slipped femoral epiphysis), previous trauma, inflammatory conditions (RA, gout, septic arthritis), metabolic (alkaptonuria, haemochromatosis, acromegaly)
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16
Q

What is slipped femoral epiphysis?

A

Occurs in teens and pre-teens who are still growing. For reasons that are not well understood, the ball at the head of the femur (thighbone) slips off the neck of the bone in a backwards direction.

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17
Q

What is alkaptonuria?

A

AKA black urine disease. Inherited disorder that prevents the body breaking down tyrosine and phenylalanine. It results in a build-up of homogentisic acid in the body which is excreted in the urine

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18
Q

How is osteoarthritis classified? (x5)

A
  • Based on distribution of affected joints.
  • Hand: commonly carpometacarpal (CMC; distal row of carpal bones to metacarpal bones) and trapeziometacarpal (thumb) joints, and wrist joint
  • Shoulder
  • Spine: spondylosis (different from spondylitis), commonly lumbar and cervical
  • Hip
  • Knee
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19
Q

! What is the pathophysiology of osteoarthritis? (x5 mechanisms)

A
  • There is failure in maintaining the balance between cartilage matrix synthesis and degradation:
  • Matrix metalloproteinases are found in increased concentrations in cartilage; Catabolic cytokine, IL-1, stimulates production of metalloproteinases; NO activates metalloproteinases; Anabolic cytokine levels such as IGF-1 are decreased; Mechanical loading harms chondrocytes and cartilage
  • These processes occur in cartilage (leading to fissuring (tears) and fibrillation (softening)) and other joint structures. The result is bone remodelling (subchondral sclerosis, osteophyte formation) and bone marrow lesions of subchondral bone (bone cysts).
  • Chronically, this can lead to alterations in the joint anatomy leading to increased and redistributed focal loading on joints e.g., varum and valgum in knee OA, which can potentiate further degeneration.
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20
Q

What is the epidemiology of osteoarthritis: Gender? Age? Ethnicity?

A

More common in females. Increasing age. More common in Caucasians and Asians.

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21
Q

What are the signs and symptoms of osteoarthritis? (x6)

A
  • Joint pain that is worse on use, and associated with stiffness/gelling after inactivity
  • Functional impairment
  • Crepitus during joint movement
  • Joint effusion (lack signs of inflammation such as warmth and redness)
  • Heberden’s nodes and Bouchard’s nodes
  • Malignment
  • No systemic features
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22
Q

What are Heberden’s nodes?

A

DIP swellings associated with osteophytes

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23
Q

What are Bouchard’s nodes?

A

PIP swellings associated with osteophytes

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24
Q

What are the investigations for osteoarthritis? (x2)

A
  • X-ray shows four classic features: joint space narrowing from cartilage loss, subchondral cysts, subchondral sclerosis and osteophytes.
  • BLOOD: normal ESR and CRP (differentiates from inflammatory arthritides)
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25
Q

What is ankylosing spondylitis?

A

Seronegative INFLAMMATORY arthropathy affecting preferentially the axial skeleton and sacroiliac joints.

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26
Q

What is the aetiology of ankylosing spondylitis? (x2)

A

Strong genetic linkage with HLA-B27. HLA-B27 may share molecular characteristics with bacterial epitopes, facilitating an autoimmune cross reaction with T cells. Infective triggers have also been suggested.

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27
Q

What is the pathophysiology of ankylosing spondylitis? Results? (x4)

A
  • In contrast to RA where the pathological processes are inflammation and erosion, AS has inflammation, cartilage erosion and subsequent repair (ossification)
  • Inflammation starts at the entheses (sites of attached of ligaments to vertebral bodies) and mediated by mononuclear cell infiltrates. This leads to erosion of cartilage.
  • Persistent inflammation leads to reactive ossification.
  • Changes start in the lumbar spine and progress up.
  • Result: squaring of vertebral bodies, formation of syndesmophytes (vertical ossifications bridging the margins of the adjacent vertebrae), fusions of syndesmophytes and facet joints (leading to ANKYLOSIS aka spinal immobility), and calcification of anterior and lateral spinal ligaments
  • Peripheral joints and extra-articular sites such as eye and bowel may be affected
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28
Q

What is the epidemiology of ankylosing spondylitis: Gender? Age?

A

Earlier presentation in males. Males 6x more common than females at 16 years, and 2x more common at 30 years. Peak incidence in late-teens and early-20s.

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29
Q

What are the signs and symptoms of ankylosing spondylitis? (x7 +5)

A
  • Lower back: SLEEP DISTURBANCE, worse in morning, improves on activity, returns with rest.
  • Unilateral buttock pain from inflammation of a sacroiliac joint
  • Progressive loss of spinal movement including reduced spinal flexion
  • Symptoms of asymmetrical peripheral arthritis
  • Thoracic kyphosis in later stages (leading to question-mark posture)
  • Enthesitis: most commonly lower limbs: heel, knee, ischial tuberosities.
  • Pleuritic chest pain (caused by costovertebral joint involvement) and associated with reduced chest expansion (dyspnoea)
  • EXTRA-ARTICULAR: anterior uveitis (common), apical lung fibrosis, reduced chest, aortic regurgitation, IBD
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30
Q

What tests can be used to assess spinal mobility in ankylosing spondylitis? (x2)

A
  • OCCIPUT-WALL DISTANCE: increased distance between back of head and wall
  • SCHOBER’S TEST: mark is made on the skin of the back in the middle of a line drawn between the posterior iliac spines. A mark 10cm above this is made and patients asked to bend forwards. The distance between the two marks should increase by at least 5cm, but is reduced in AS.
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31
Q

What does x-ray show in ankylosing spondylitis? (x3)

A
  • Pelvic x-ray requested in all patients to identify sacroiliitis (blurring of joint margins, followed by erosions, sclerosis and SI joint fusion in later disease)
  • Lateral radiographs of spine may show erosions, squaring, sclerosis, syndesmophytes, and used to calculate the modified Stoke Ankylosing Spondylitis Spinal Score (mSASSS), which quantifies the degree of structural damage in the spine. Late disease may show bamboo spine.
  • CXR: apical fibrosis
32
Q

What is bamboo spine?

A

Fusion of syndesmophytes.

33
Q

What other investigations are there for ankylosing spondylitis? (x4)

A
  • HLA-B27: not diagnostic but present in 90%
  • FBC: anaemia of chronic disease, raised ESR and CRP
  • USS: to assess enthesitis
  • MRI: for early detection of AS
34
Q

What other seronegative spondyloarthropathies are there? Note about genetics?

A

Psoriatic arthritis, enteropathic arthritis (related to IBD), and reactive arthritis – each also have an association with the gene HLA-B27.

35
Q

What is reactive arthritis?

A

Characterised by a STERILE arthritis occurring after an extra-articular infection (commonly GI or urogenital).

36
Q

What is the aetiology of reactive arthritis? (x2)

A
  • Associated with infections of the GI tract (mostly dysenteric diseases): Salmonella, Shigella, Yersinia, Campylobacter; and urogenital tract: Chlamydia trachomatis (most common cause). Typically GRAM NEGATIVE bacteria
  • HLA-B27 identified in 80% of patients – autoimmune cross-reactivity is a proposed theory related to HLA-B27
37
Q

What is the pathophysiology of reactive arthritis?

A

Initial activation of the immune system (by infective trigger) is followed by an autoimmune reaction of the JOINTS, SKIN and EYES. In HLA-B27 susceptible patients, this may be due instead to the arthritogenic peptide theory (proposes that HLA-B27 presents arthritogenic bacterial material to T cells, eliciting an autoimmune response).

38
Q

What is the epidemiology of reactive arthritis: Gender? Age?

A

Male:female ratio is 20:1. Age of onset is 20-40.

39
Q

What is Reiter’s syndrome?

A

Triad of reactive arthritis, urethritis and conjunctivitis, and classic presentation of reactive arthritis.

40
Q

What are the signs and symptoms of reactive arthritis? (x8)

A
  • ARTHRITIS: asymmetric oligoarthritis affecting mostly the large joints of the lower limb, and lower back (sacroiliitis).
  • ETHESITIS: typically affecting heels
  • Patients may also have dactylitis (inflammation of whole finger arising from flexor tenosynovitis)
  • CONJUNCTIVITIS or ANTERIOR UVEITIS
  • SKIN LESIONS: including circinate balanitis and keratoderma blenorrhagica
  • ORAL ULCERATION: painless
  • Fever
  • Nail hyperkeratosis and onycholysis (detachment from bed)
41
Q

What is oligoarthritis?

A

2-4 joints.

42
Q

What is circinate balanitis?

A

Scaling red patches which may evolve, encircling the glans penis

43
Q

What is keratoderma blenorrhagica?

A

Brownish-red macules, vesico-pustules and yellowish-brown scales on soles or palms

44
Q

What is nail hyperkeratosis?

A

Accumulation of scales under the distal portion of the nail plate, with nail thickening and uplifting

45
Q

What are the investigations for reactive arthritis? (x5)

A
  • There is no specific diagnostic test. Rather, group of tests is used to confirm suspicion
  • BLOOD: raised ESR/CRP, HLA-B27, anaemia of chronic disease
  • STOOL/URETHERAL SWABS/CULTURES: may be negative by the time of development of arthritis
  • URINE: screen for Chlamydia trachomatis
  • X-RAYS: useful in chronic disease; erosions at entheses (Achilles, plantar spurs, sacroiliitis), asymmetrical syndesmophytes
  • JOINT ASPIRATION: exclude septic and crystal-associated arthritis
46
Q

What is septic arthritis?

A

AKA infective arthritis. Joint inflammation resulting from intra-articular infection.

47
Q

What is the aetiology of septic arthritis? (x3)

A
  • Systemic infection allowing for haematogenous spread
  • Recent orthopaedic procedures
  • Contiguous spread (across a border): from cutaneous ulcers or osteomyelitis
48
Q

What are the risk factors for septic arthritis? (x6)

A
  • Immunosuppression
  • Diabetes
  • HIV
  • Alcoholism
  • Prosthetic joint
  • Foreign travel: tick exposure are vectors for bacterial aetiology
49
Q

What are the common organisms in septic arthritis? (x6, x4 and x1)

A
  • BACTERIA: Staphylococcus aureus, Mycobacterium tuberculosis in all ages. Strep. pneumoniae, Strep. pyogenes and Neisseria meningitidis in less than 4 years. Mainly Neisseria gonorrhoea in 16-40 years.
  • VIRUSES: rubella, mumps, HBV, parvovirus B19
  • FUNGI: candida
50
Q

What is the epidemiology of septic arthritis: Age?

A

Most common in children and elderly. Peak age of incidence is over 80s.

51
Q

What are the signs and symptoms of infective arthritis? (x3) Onset? Where?

A
  • Sudden onset (less than 2 weeks), unless in TB arthritis.
  • Excruciating joint pain: redness, swelling
  • Loss of function
  • Usually affecting single large joint (polyarthritis in immunosuppressed). Most commonly affected joint is knee, followed by hip, ankle, elbow.
  • Fever
52
Q

What are the investigations for septic arthritis? (x5)

A
  • JOINT ASPIRATION (first investigation): grossly purulent synovial fluid. Send for cytology, microscopy, C&S, and PCR if suspected viral aetiology
  • BLOOD CULTURES: detect aetiology; usually septic arthritis is caused by haematogenous spread
  • BLOODS: ESR, CRP and WCC MAY be elevated. U&Es and LFTs to assess for end-organ damage from sepsis
  • X-RAY: as baseline
  • May also want to do investigations for other infective aetiologies such as urine dipstick and swabs from other sources
53
Q

What is the investigation pathway when someone presents with a hot, swollen, acutely painful joint with movement restriction?

A

Treat as septic arthritis until proven otherwise, even in the absence of fever and irrespective of microbiology and blood test results.

54
Q

What is crystal arthropathy?

A

Deposition of crystals in joint cartilage causing acute attacks of INFLAMMATORY arthritis.

55
Q

What are the types of crystal arthropathy? (x2)

A

Gout and pseudogout.

56
Q

What is gout?

A

Disorder or uric acid metabolism causing recurrent bouts of acute arthritis caused by deposition of monosodium urate crystals in joints, as well as in soft tissues and kidneys.

57
Q

What is the aetiology of gout? (x3, x3 and x5)

A
  • INCREASD URATE INTAKE or PRODUCTION: increased dietary uptake (protein foods), increased nucleic acid turnover e.g., lymphoma, leukaemia, psoriasis (urea is a metabolite of purine), and Lesch-Nyhan syndrome (increased synthesis)
  • DECREASED RENAL EXCRETION: idiopathic, drugs, renal dysfunction.
  • Acute attacks may be precipitated by trauma, infection, alcohol, starvation, introduction/withdrawal of hypouricemic agents.
58
Q

What drugs cause decreased renal excretion of urea?

A

CAN’T LEAP: ciclosporin, alcohol (especially beer), nicotinic acid, thiazides, loop diuretics, ethambutol, aspirin, pyrazinamide.

59
Q

What is the pathophysiology of gout?

A

Hyperuricaemia leads to hyper-saturation and crystal formation. Urate crystals in the joint trigger an acute inflammatory response by inducing TNF-alpha, leading to neutrophil influx, metalloproteinase and NO production, and subsequent synovitis and erosion. Spontaneous resolution occurs from clearance by phagocytes, coating the crystals with proteins and neutrophil apoptosis.

60
Q

What is the epidemiology of gout: Gender? Age?

A

10x more common in men. Increased incidence with age. Rare in childhood and pre-menopausal women.

61
Q

What are the types of gout? (x3)

A

Acute attack, inter-critical gout, chronic tophaceous gout

62
Q

What are the signs and symptoms of an acute attack of gout? Disease progression?

A
  • Symptoms peak at 24 hours and resolve in 7-10 days. Attacks are often recurrent.
  • Sudden excruciating monoarticular pain, usually the MTP joint of the great toe, though can affect any joint. Worse in the morning. May be oligoarthritic.
  • Swelling and joint effusion reflecting inflammatory process
  • May present with cellulitis, polyarticular or periarticular involvement
63
Q

What is inter-critical gout?

A

Asymptomatic intervals between acute attacks of gout.

64
Q

What is chronic tophaceous gout? Symptoms? (x2)

A

Follows repeated acute attacks. Persistent low-grade fever, polyarticular pain with painful tophi (urate deposits) over extensor joint surfaces – usually most evident on tendons of hands and feet and pinna of the ear.

65
Q

What are the complications of gout? (x2)

A

Urate urolithiasis, secondary infection or ulceration of tophi.

66
Q

What are the investigations for gout? (x3)

A
  • ARTHROCENTESIS OF SYNOVIAL FLUID ASPIRATE: presence of monosodium urate crystals which are NEEDLE-SHAPED and NEGATIVELY BIREFRINGENT under polarised light (relates to refraction). Diagnostic test. You can also exclude septic arthritis in the aspirate
  • BLOOD: serum urate levels (may be normal in acute episodes so should be collected two weeks after attack resolves). May also see raised WCC
  • PLAIN X-RAY: peri-articular ‘rat-bite’ erosions (punched-out erosions with sclerotic and overhanging margins – see photo)
67
Q

How do uric acid renal stones present on x-ray?

A

Radiolucent (black).

68
Q

What is pseudogout?

A

INFLAMMATORY arthritis associated with deposition of calcium pyrophosphate dihydrate (CPPD) crystals in joint cartilage. Can be acute and chronic forms.

69
Q

What is the aetiology of pseudogout? (x5) Precipitating factors? (x3)

A
  • Previous joint damage: osteoarthritis, trauma
  • Haemochromatosis
  • Hyperparathyroidism
  • Hypomagnesaemia
  • Hypophosphatasia (autosomal recessive disease characterised by reduced bone mineralisation and decreased serum alkaline phosphatase, which can lead to rickets and recurrent fractures)
  • Provoking factors include recurrent illness, surgery, local trauma.
70
Q

What is the pathophysiology of pseudogout?

A

Excessive cartilage pyrophosphate production from atypical chondrocytes, leading to local calcium pyrophosphate supersaturation and CPPD crystal formation and deposition. Shedding of crystals into the joint cavity precipitates inflammation and catabolic effects on articular tissues.

71
Q

What is the epidemiology of pseudogout: Gender? Age?

A

Females are 2x more likely to get pseudogout. More common in elderly (over 60 years)

72
Q

What are the signs and symptoms of an acute attack of pseudogout? (x3)

A
  • Painful, swollen monoarthritic large joint, usually knee, ankle, shoulder, elbow, or wrist. There is overlying erythema and warmth
  • Restricted range of movement
  • Fever
73
Q

How do signs and symptoms differ in chronic pseudogout? (x4)

A

Similar to osteoarthritis, associated with bony swellings, crepitus, deformity (varus in knees), and polyarthritic.

74
Q

What are the investigations for pseudogout? (x3)

A
  • ARTHROCENTESIS OF SYNVOLIAL FLUID ASPIRATE: diagnostic; microscopy shows RHOMBOID BRICK-SHAPED crystals with weak POSITIVE BIREFRINGENCE under polarised light. Can also exclude infective arthritis.
  • BLOOD: raised WCC, ESR.
  • X-RAY: chondrocalcinosis (linear calcification of cartilage), signs of osteoarthritis (in chronic pseudogout; loss of joint space, osteophytes, subchondral cysts, sclerosis)
75
Q

SUMMARY: What are the differences between gout and pseudogout?

A

.

Year 3 Musculoskeletal (9 decks)

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