OA & RA Flashcards

1
Q

Differences in features of OA and RA

A

OA

  • Affects DIP and PIP –> think herberdens nodes - DIP / Bouchards - PIP
  • bony swelling
  • limited stiffness

RA

  • Affects MCP, PIP and carpal bones, SPARES DIP
  • Soft tissue swelling
  • Stiffness prominent
  • Signs of systemic inflammation
  • Serology
  • Erosions - without osteophytes or sclerosis
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2
Q

What is OA?

  • Features
  • Epidemiology
  • RF
A
  • major cause of pain and disability in older people
  • characteristic distribution: hips, knees,
  • affects DIP and PIP –> think herberdens nodes - DIP / Bouchards - PIP
  • bony swelling
  • limited stiffness

Features:

  • focal loss of articular cartilage
  • Shelving ‘fibrillated’ cartilage
  • subchondral osteosclerosis
  • osteophyte formation at joint margin
  • remodelling of joint contour with enlargement of affected joints (increased surface area)
  • thickened capsule

Epidemiology

  • prevalence rises progressively with age
  • 45% knee / 25% hip
  • Spine > DIPJ > knee > hip

RF

  • age
  • gender (Women)
  • genetics
  • obesity - esp. associated with hip
  • previous injury to joint
  • chrondrocalcinosis
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3
Q

OA - pathophysiology

A

Genetic

  • heritability 43% knee, 60-65% hip
  • polygenic

Structural abnormalities

  • abnormal distribution of load across joint
  • slipped femoral epiphysis / development dysplasia of hip

Biomechanical factors
- occupations

Obesity

  • esp. associated with hip
  • cytokines released from adipose tissue and biomechanical factors
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4
Q

OA - what is the process of degeneration of articular cartilage?

A
  • chondrocytes - normally terminally differentiated cells
  • BUT in OA they divide to produce nests of metabolically active cells
  • they produce matrix components at increased rate
  • accelerate degradation of major structural components of cartilage matrix (aggrecans, type 2 collagen)
  • eventually level of aggrecan in cartilage matrix falls, leaving person vulnerable to load-bearing injury
  • fissuring of cartilage surface (fibrillation) –> deep vertical clefts, localized chondrocyte death and decreased cartilage thickness
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5
Q

What is the classification of OA?

A

Primary
- localized, generalized

Secondary

  • Congenital disorders
  • Trauma
  • Pagets disease
  • Inflammatory joint disease
  • avascular necrosis
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6
Q

Comparison of features in aging and OA:

  • keratan sulphate
  • water
  • protein/uronate
  • extractability of proteoglycans
A

OPPOSITE

OA

  • Decreased: keratan sulphate; protein/uronate
  • Increased: water; extractability of proteoglycans

AGING

  • Decreased: water; extractability of proteoglycans
  • Increased: keratan sulphate; protein/uronate
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7
Q

Clinical features of OA

A

Distribution: hips, knees, PIP and DIP joints of hands, neck,. lumbar spine

Restricted movement due to capsular thickening or blocking by osteophyte.

Palpable, sometimes audible, coarse crepitus due to rough articular surfaces.

Bony swelling around joint margins

Deformity - usually without instability

Joint-line or peri-articular tenderness

Muscle weakness and wasting

Symptoms:

  • insidious onset over months/years
  • pain - worse on use of joint, good days and bad days, mainly related to movement and weight-bearing, relieved by rest
  • only brief (<15mins) morning stiffness and brief (<5mins) ‘gelling’ after rest
  • usually only one or few joints painful
  • loss of movement (functional restriction)
  • pain on movement/restricted range
  • tenderness (articular/periarticular)
  • bony swelling
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8
Q

OA - investigations

A

Xray

  • assess severity of structural change
  • HIP: non-weight bearing postero-anterior view
  • KNEE - AP view - assess tibia-femoral cartilage loss
  • SPINE - plain xray
LOSS:
L - loss of joint space
O - osteophyte
S - Subchondral cysts 
S - subchondral sclerosis

If suspect nerve root compression or spinal stenosis –> MRI

Routine biochemistry, hematology and autoantibody tests - usually normal

synovial fluid from affected joint - viscous with low cell count

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9
Q

OA - treatment

A

Lifestyle
- education / self-management / weight loss / aerobic muscle strengthening / physio / orthoses

Pharma

(1) Topical NSAID, Paracetamol
(2) Oral NSAID
(3) Substitute compound analgesic for paracetamol
(4) Add gabapentin or low dose amitryptilline
(5) Consider tramadol and paracetamol
(6) Consider strong opioid instead of tramadol

Surgical

  • total joint replacements
  • osteotomy
  • fusions
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10
Q

RA - History

A
  • joint pain stiffness and swelling in symmetrical distribution affecting wrists, MCP and PIP joints of hand and MTP joints of feet
  • large joints may also be affected
  • Early morning stiffness (typically >30 mins)
  • Inactivity gelling (stiffness after a period of inactivity)
  • Symptoms >6 weeks duration
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11
Q

RA - examination

A
  • Soft tissue swelling and tenderness of affected joints

- Pain on squeezing MCP and MTP joints (squeeze test)

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12
Q

RA - investigation

A

Bloods

  • FBC - may have anaemia
  • ESR raised
  • LFT

Serology

  • Anti-CCP antibodies - better sensitivity
  • RF - 75%; poor prognosis; not very specific (older people make more, fibrotic lung disease)

Xrays - hands (periarticular osteoporosis, erosions, joint subluxation, joint space narrowing)

  • L - loss of joint space
  • E - erosions
  • S - soft tissue swelling
  • S - soft bones (osteopenia)

MRI - sensitive imaging of synovitis

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13
Q

RA - Treatment

A

Initial - Treat symptoms with NSAIDs and/or analgesics pending clinic review. Avoid corticosteroids.

NSAIDs / Prednisolone / DMARDs / Biologics

Aim: treat with DMARD asap.

Front load with steroids:

  • corticosteroids - prednisolone (SE: osteoporosis, weight gain)
  • often given with bisphosphonates
  • intra-articular injections in flares

DMARD

  • target immune-mediated inflammatory activity
  • no immediate effect - may require 2-6 months to work

Methotrexate

  • Dihydrofolate reductase inhibitor (blocks DNA synthesis in proliferating cells)
  • take once a week, folic acid taken day later
  • SE: GI upset (vomiting, diarrhea, mouth ulcers), hair loss, skin rashes, teratogenic, Liver and pulmonary toxicity (fibrosis), bone marrow suppression
  • contraindications: pregnancy, immunosuppresino, liver disease
  • Regular monitoring: FBC and LFTs
  • need flu and pneumococcal vaccine

Hydroxychloroquine (also used for SLE and malaria)
- SE: retinal damage (blurred vision)

Sulphasalazine

  • aminosalicylate
  • anti-inflammatory, immunosuppressant
  • By mouth - 500mg - 2-3x daily
  • SE: rashes, GI upset, decreased WBCs and platelets / reversible azoospermia, anaphylaxis, photosensitivity, decreased folate

IF resistant to DMARDs, use biologics

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14
Q

What is RA?

A
  • Females > Males (3:1)
  • Often have long history - months -> years

May have started after giving birth to child (autoimmune disease) / fatigue, weight loss, depression due to excess inflammatory markers.

Chronic symmetrical, predominantly peripheral polyarthritis.
- joint pain stiffness and swelling in symmetrical distribution affecting wrists, MCP and PIP joints of hand and MTP joints of feet
Swelling confined to joint capsule.
Polyarticular 75%

  • Small and large synovial joints, upper and lower limbs
  • Early morning stiffness (typically >30 mins)
  • Inactivity gelling (stiffness after a period of inactivity)
  • Symptoms >6 weeks duration
  • Exacerbations and remissions
  • Erosions and deformities
  • Subcutanous nodules
  • +ve serological test for RF
  • Diffuse muscle wasting
  • Synovial thickening - feels like firm sponge (hyperplasia of synovial lining layer)

SPARES thoracolumbar spine and DIPs of fingers.

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15
Q

RA - risk factors

A
  • Smoking in anti-CCP and RF +ve RA (but not sero-negative) /former smokers have increased risk
  • Genetics -> FH
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16
Q

RA - outcomes

A
  • Premature mortality associated with accelerated atherosclerosis; change in lipoproteins, increased VWF
  • Incurable, progressive, auto-immune
  • 75% have erosions within 2 years

Morbidity:

  • twice more likely to have MI
  • 70% risk of stroke
17
Q

RA - deformities

A
  • less common now due to more aggressive treatments
  • Ulnar deviation
  • ‘Swan neck’ deformity
  • Boutonniere or button hole deformity
  • Z deformity of thumb
18
Q

RA - rare but severe spinal complication

A
  • Only C1 (atlas) can be affected in RA
    C2 = axis
  • Spinal cord compression due to subluxation of cervical spine at atlanta-axial joint or at subaxial level

Due to erosion of transverse ligament posterior to odontoid peg -> can lead to cord compression or sudden death following minor trauma
- Odontoid peg - not sitting stably on atlas -> can go through foramen magnum and push on brain -> causing death

Should be suspected if complain of new onset occipital headache, symptoms of paresthesia or electric shock in arms (shooting pains)

Urgent neurosurgical referral -> stabilisation and fixation

19
Q

RA - what does the disease activity score take into account? (DAS28)

A
  • tender joint count
  • swollen joint count
  • patient global activity (0-100)
  • ESR or CRP

Scores:
<2.6 = disease remission
<3.2 = low disease activity
>5.1 = high disease activity