Rheumatology Flashcards

1
Q

Causes of low back pain

A
  • Mechanical (soft-tissue lesion) back pain
  • Intervertebral disc lesions (e.g. prolapse, disc degeneration)
  • Facet joint disease (osteoarthritis, psoriatic arthritis)
  • Vertebral fracture
  • Paget’s disease
  • Axial spondyloarthritis
  • Spondylodiscitis
  • Spondylolisthesis
  • Bone metastases
  • Scheuermann’s disease
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2
Q

Features of mechanical low back pain

A
  • Time:
    • Often sudden
    • Recurrent episodes
  • Factors:
    • Precipitated by lifting or bending
    • Pain varies with physical activity (improved with rest)
  • Site: Limited to back or upper leg
  • No clear-cut nerve root distribution
  • No systemic features
  • Prognosis good (90% recovery at 6 weeks)
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3
Q

Back pain >>> Red flags for possible spinal pathology

A

History:

  • Age: presentation < 20 years or > 55 years
  • Character: constant, progressive pain unrelieved by rest
  • Location: thoracic pain
  • Past medical history:
    • Carcinoma
    • Tuberculosis
    • HIV
    • Systemic glucocorticoid use
    • Osteoporosis
  • Constitutional: systemic upset, sweats, weight loss (B symptoms like)
  • Major trauma

Examination:

  • Painful spinal deformity
  • Severe/symmetrical spinal deformity
  • Saddle anaesthesia
  • Progressive neurological signs/muscle-wasting (neurological)
  • Multiple levels of root signs (neurological)
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4
Q

Clinical features of radicular pain

A

Clinical features of radicular pain

  • Nerve root pain
  • Unilateral leg pain worse than low back pain
  • Pain radiates beyond knee
  • Paraesthesia in same distribution
  • Nerve irritation signs (reduced straight leg raising that reproduces leg pain)
  • Motor, sensory or reflex signs (limited to one or adjacent nerve roots)
  • Prognosis reasonable (50% recovery at 6 weeks)

Cauda equina syndrome

  • Difficulty with micturition
  • Loss of anal sphincter tone =/ faecal incontinence
  • Saddle anaesthesia
  • Gait disturbance
  • Pain, numbness or weakness affecting one or both legs
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5
Q

Clinical assessment of back pain

A

The main purpose: To differentiate the self-limiting disorder of acute mechanical back pain from serious spinal pathology

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6
Q

Mechanical back pain >>> frequency

A
  • It is the most common cause of Acute back pain in aged 20–55 >>> accounts for more than 90% of episodes
  • Low back pain is more common in → manual workers
    • Particularly those involve heavy lifting and twisting.
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7
Q

How to assess mechanical back pain

A
  • Presentation:
    • It is usually Acute
    • Associated with >>> lifting or bending.
    • Exacerbated by >> activity
    • Relieved by >>> rests
    • confined to the lumbar–sacral region, buttock or thigh
    • Asymmetrical
    • Does not radiate beyond the knee (which would imply nerve root irritation)
  • O/E:
    • Asymmetrical
    • Local paraspinal muscle spasm
    • Tenderness
    • Painful restriction of some, but not all, movements.
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8
Q

Mechanical back pain >>> prognosis

A
  • Generally good
  • After 2 days >>> 30% are better
  • By 6 weeks >>> 90% have recovered
  • Recurrences of pain may occur
  • About 10–15% of patients >>> go on to develop chronic back pain >>> that may be difficult to treat.
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9
Q

Factors that may cause transition of acute mechanical back pain to a chronic pain

A

Psychological elements, such as

  • job dissatisfaction
  • Depression
  • Anxiety
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10
Q

Back pain secondary to serious spinal pathology (Not mechanical) ⇒

Urgent investigation is needed if there is - ?

A
  • clinical evidence of spinal cord or nerve root compression
  • sepsis including tuberculosis, or
  • a cauda equina lesion
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11
Q

Spinal stenosis >>> presentation

A
  • Presents insidiously
  • Leg discomfort on walking
  • Relieved by >>>
    • Rest
    • Bending forwards (Thus may be more area is formed within)
    • Walking uphill
  • May adopt characteristic simian posture, with >>>
    • Forward stoop + slight flexion at hips and knees.
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12
Q

Spinal stenosis >>> the most common cause

A

The most common cause is:

Gadual development of coexisting contributing lesions such as >>>

  • Facet joint arthritis
  • Ligament flavum thickening or
  • Degenerative spondylolisthesis.
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13
Q

Degenerative disc disease is more common in -?

A

It is a common cause of chronic low back pain in middle-aged adults.

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14
Q

Prolapsed intervertebral disc >>> presentation

A

Prolapse of an intervertebral disc presents when >>> discs are still well hydrated

  • Young and early middle age >>> nerve root pain
  • Can be accompanied by >>>
    • A sensory deficit
    • Motor weakness
    • Asymmetrical reflexes
  • Examination may reveal > positive sciatic or femoral stretch test.
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15
Q

Prolapsed intervertebral disc >>> prognosis

A

About 70% of patients improve by 4 weeks.

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16
Q

Inflammatory back pain (IBP) >>> 2 important causes

A
  • Axial spondyloarthritis (axSpA)
  • Psoriatic arthrits (PsA)
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17
Q

Inflammatory back pain >>> presentations

[due to axial spondyloarthritis (axSpA) &

Psoriatic arthrits (PsA)]

A
  • Gradual onset
  • Almost always before the age of 40
  • Associated with morning stiffness
  • Improves with movement
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18
Q

Spondylolisthesis >>> presentation

A
  • Back pain
  • Typically aggravated by standing and walking

Occasionally, diffuse idiopathic skeletal hyperostosis >>>>> can cause back pain but it is usually asymptomatic.

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19
Q

Arachnoiditis

A

Rare cause of chronic severe low back pain

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20
Q

Arachnoiditis >>> cause

A
  • Chronic inflammation of the nerve root sheaths in the spinal canal >>> further, can complicate meningitis
  • Spinal surgery or
  • Myelography with oil-based contrast agents.
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21
Q

When is investigation needed in back pain?

A
  • Acute mechanical back pain > No investigation required
  • Persistent pain (> 6 weeks) OR red flags >>> need further investigation
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22
Q

Back pain >>> Investigation of choice (IOC)

A

MRI (Magnetic resonance imaging)

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23
Q

In back pain, MRI is the IOC >>> because?

A

Because, it can demonstrate >>>

  • spinal stenosis
  • cord compression
  • nerve root compression
  • inflammatory changes in axSpA
  • sepsis
  • malignancy
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24
Q

Investigations of back pain >>> imgaing modalities

A
  • MRI (MAgnetic resonance imaging) >>> IOC
  • Plain X-ray
  • Bone scintigraphy
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25
Q

Indications of ‘plain X-ray’ in back pain

A
  • Suspected vertebral compression fractures
  • OA (Osteroarthritis)
  • Degenerative disc disease
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26
Q

Indication of bone scintigraphy in back pain

A

If metastatic disease is suspected

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27
Q

Back pain >>> additional investigations

A
  • Routine biochemistry
  • CBC (= haematology)
  • ESR
  • CRP (to screen for sepsis and inflammatory disease)
  • Protein and urinary electrophoresis >>> for myeloma
  • HLA-B27 status >>> in IBP
  • PSA >>> for prostate carcinoma
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28
Q

Pateint with low back pain >>> indications of surgery

A
  • Progressive spinal stenosis
  • Spinal cord compression with nerve root compression
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29
Q

Management of back pain

A
  • Education is important in mechanical back pain. Eemphasise >>>
  • It is self-limiting condition
  • Exercise is helpful (rather than damaging)
  • Regular Analgesia and/or NSAIDs (may be required) >>> to improve mobility + to facilitate exercise.
  • Return to work and normal activity (ASAP)
    • Bed rest is NOT helpful >>> may increase the risk of chronic disability.
  • If a return to normal activities has not been achieved by 6 weeks >>> refer for physical therapy
  • Low-dose tricyclic antidepressant >>> may help pain, sleep and mood.

Other occasional treatment modalities >>>

  • Epidural and facet joint injection
  • Traction
  • Lumbar supports

(though there is limited RCT evidence to support their use)

  • Malignant disease, osteoporosis, Paget’s disease and SpAs >>>>> specific treatment of the underlying condition.
  • Surgery is required in less than 1% of patients with low back pain
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30
Q

Osteoarthritis: epidemiology

A
  • The prevalence rises progressively with age
  • At some point of life >>> 45% of all people develop knee OA and 25% hip OA
  • Although some are asymptomatic >>>>> the lifetime risk of having a total hip or knee replacement for OA in someone aged 50 is about 11% for women and 8% for men in the UK.
  • There are major ethnic differences in susceptibility:
  • The prevalence of hip OA is lower in Africa, China, Japan and the Indian subcontinent than in European countries, and that
    of knee OA is higher.
    • Higher prevalence of knee OA in the Indian subcontinent and East Asia might be accounted for by squatting.
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31
Q

Osteoarthritis: Risk factors

A

Genetics
• Skeletal dysplasias
• Polygenic inheritance (in most cases > polygenic; several genetic variants of small effects)

  • Heritability of OA ranges from >>>
    • Knee > 43%
    • Hip > 60%
    • Hand > 65%
  • OA can, however, be a component of multiple epiphyseal dysplasias >>>>> caused by mutations in the genes that encode components of cartilage matrix.

Developmental abnormalities (/structural abnormalities)
Cause:
presumably due to >>> abnormal load distribution across the joint
Developmental dysplasia of the hip
Slipped femoral epiphysis

>>> these are associated with a high risk of OA
(Similar mechanisms probably explain the increased risk of OA in patients with limb deformity secondary to Paget’s disease of bone)

Repetitive loading (due to ‘biomechanical factors’)
• Farmers >>> hip OA
• Miners >>> knee OA
• Elite or pofessional athelets >>> knee or ankle OA

Adverse biomechanics (who have had destabilising injuries)
• Meniscectomy
• Ligament rupture
• Paget’s disease

Obesity (strong association)

  • Particularly hip >>> thought to be,partly due to >>>
    • biomechanical factors
    • (also play a role) cytokines released from adipose tissue

Trauma
Hormonal
(Oestrogen appears to play a role)
• Oestrogen deficiency
• Aromatase inhibitors (for therapy of breast cancer) >>> flare of OA symptoms

Neutral factor: Participation in recreational sport >>> does not increase risk significantly

Protective factor: HRT; >>> women who use HRT have lower rates of OA

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32
Q

Osteoarthritis: main pathological process

A
  • Defining feature of OA: degenation of articular cartilage
  • Normally, chondrocytes are terminally differentiated cells
  • In OA >>> chondrocytes start dividing to produce >>> “nests of metabolically active cells”
  • Initially, matrix components are produced by these cells (at an increased rate)
  • At the same time >>> accelerated degradation of the major
    structural components of cartilage matrix, including aggrecan
    and type II collagen
  • Eventually, the concentration of aggrecan in cartilage matrix falls >>> makes the cartilage vulnerable to load-bearing injury >>> fissuring of the cartilage surface (‘fibrillation’) then occurs >>> leading to >>
    • the development of deep vertical clefts
    • localised chondrocyte death
    • decreased cartilage thickness.

>>>This is initially focal >>> mainly targeting the maximum load-bearing part of the joint >>> But eventually > large parts of the cartilage surface are damaged >>> in the abnormal cartilage, c__alcium pyrophosphate and basic calcium phosphate crystals often become deposited

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33
Q

Osteoarthritis: defining feature

A

degenation of articular cartilage

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34
Q

Osteoarthritis: pathology in sub-chondral bone

A

Abnormalities in subchondral bone >>>

  • sclerotic
  • the site of subchondral cysts
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35
Q

Osteoarthritis >>> joint margin

A

At the joint margin >>> fibrocartilage is produced >>> undergoes endochondral ossification >> form osteophytes

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36
Q

Osteoarthritis >>> shape

A
  • Bone remodelling + cartilage thinning >>> slowly alter the shape of the OA joint >>> increasing its surface area.
  • Homeostatic mechanism operative in OA >>> causes > enlargement of the failing joint >>> to spread the mechanical load over a greater surface area.
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37
Q

Osteoarthritis >>> BMD and osteoporosis

A
  • Higher BMD values (at sites distant from the joint) + particularly, associated with osteophyte formation.
  • Patients with OA are partially protected from developing osteoporosis and vice versa.
    • Why: the genetic factors that predispose to osteoporosis might be protective for OA.
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38
Q

Osteoarthritis >>> the synovium

A
  • in OA >>> the synovium is often hyperplastic
  • It may be the site of inflammatory change
    • But to a much lesser extent than in RA &other inflammatory arthropathies.
  • Osteochondral bodies commonly occur within the synovium, reflecting >>>
    • chondroid metaplasia or
    • secondary uptake and growth of damaged cartilage fragments
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39
Q

Osteoarthritis >>> the outer capsule

A

Outer capsule also thickens and contracts >>> usually retaining the stability of the remodelling joint.

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40
Q

Osteoarthritis >>> surrounding muscles

A

Around the joints >>> wasting of muscles + non-specific type II fibre atrophy

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41
Q

Osteoarthritis >>> Clinical features (signs & symptoms)

A
  • *Main presenting symptoms:** joint pain + functional restriction
  • *Characteristic distribution:** the hips, knees, PIP and DIP joints of the hands, neck and lumbar spine

Pain

  • Onset: insidious >>> over months or years
  • Nature: Variable or intermittent nature over time (‘good days, bad days’)
  • Mainly related to/increased by >>> movement and weight-bearing
  • Releived by >>> Rest
  • Only brief (<15 mins) morning stiffness and brief (<5 mins) ‘gelling’ after rest
  • Usually only one or a few joints painful

Clinical signs

  • Restricted movement
    • For many people, functional restriction of the hands, knees or hips is an equal, if not greater, problem than pain
  • Coarse crepitus: Palpable, sometimes audible
  • Bony swelling (Around joint margins)
  • Tenderness (Joint-line or periarticular)
  • Deformity (usually without instability)
  • Muscle weakness and wasting
  • Mild or absent synovitis
  • The clinical findings vary according to severity but are principally those of joint damage.
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42
Q

Osteoarthritis >>> cause of joint pain

A

The causes of pain in OA are not completely understood but may relate to >>>

  • increased pressure in subchondral bone (mainly causing night pain)
  • Trabecular microfractures
  • Capsular distension
  • Synovium >>> Low-grade synovitis
  • Bursitis (may also be)
  • Enthesopathy (Secondary to altered joint mechanics) (may also be)
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43
Q

Coarse crepitus in OA (palpable +/- audible) >>> cause?

A

Rough articular surfaces

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44
Q

Restricted movement in OA >>> cause?

A

due to capsular thickening or blocking by osteophyte

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45
Q

Osteoarthritis >>> the correlation between structural changes (assessed by imaging) & clinical features

A

The correlation between the presence of structural change (as assessed by imaging, and symptoms such as pain and disability)

Varies markedly according to site. The correlation >>>

  • Stronger at the hip (than that of knee)
  • Poor at small joints
    This suggests that >>>
    the risk factors for pain and disability may differ from those for
    structural change. >>>> for example >>>
    • At the knee, >>>>> reduced quadriceps muscle strength + adverse psychosocial factors (anxiety, depression) >>>> correlate more strongly with pain and disability [[than the degree of radiographic change]]
  • Radiological evidence of OA is very common in middle-aged and older people
  • The disease may coexist with other conditions, >>> so it is important to remember that >>> pain in a patient with OA may be due to another cause.
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46
Q

Generalised nodal OA: characteristics

A
  • Age: Peak onset in the middle age
  • Sex: Marked female preponderance
  • Genetics: Strong genetic predisposition;
    • the daughter of an affected mother has a 1 in 3 chance of
      developing nodal OA herself.
  • In hand:
    • Polyarticular >>> finger interphalangeal joint OA
    • Heberden’s (± Bouchard’s) nodes
  • Good functional outcome for hands
  • Predisposition to OA at other joints, especially knees
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47
Q

Generalised nodal OA >>> course of the disease

A

Some patients are asymptomatic …..
whereas, others >>> From 40 years onwards >>> at one or more PIP and DIP joints of the hands >>> pain + stiffness + swelling >>> gradually, these develop posterolateral swellings on each side of the extensor tendon >>> which slowly enlarge + harden >> become Heberden’s (DIP) and Bouchard’s (PIP) nodes.

Typically, Each joint >>> goes through a phase of episodic symptoms (1–5 years)
>>> while the node evolves and OA develops >>>
Once OA is fully established >>>

  • Symptoms may subside + hand function often remains good
  • Due to osteophyte formation >>> affected joints are enlarged
  • characteristic lateral deviation (often showed) >>> reflecting the asymmetric focal cartilage loss of OA
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48
Q

If generalised nodal OA involves first CMC (Carpo-metacarpal) joint >>> Sign and symptoms

A

Involvement of the first CMC joint is also common, leading to >>>

  • Pain on trying to open bottles and jars
  • Functional impairment
    Clinically, it may be detected by >>>
    • The presence of crepitus on joint movement, and
    • Squaring of the thumb base
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49
Q

Targeted area in Knee OA

A

At the knee, OA principally targets >>>

  • the patello-femoral compartment
  • the medial tibio-femoral compartments

But eventually spreads >>> to affect the whole of the joint

It may be >>>

  • Part of generalised nodal OA or isolated OA
  • Most patients have bilateral and symmetrical involvement.
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50
Q

Knee OA >>> important risk factor in men

A

Trauma
>>> may cause unilateral OA

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51
Q

Knee OA >>> symptoms

A
  • Localised pain >>> in the anterior or medial aspect of the knee and upper tibia.
  • Patello-femoral pain >>> (usually) worse going up and down stairs or inclines.
  • If posterior knee pain >>> suggests >>> the presence of a complicating popliteal cyst (Baker’s cyst).
  • Difficulties in tasks, such as:
    • Prolonged walking
    • Rising from a chair
    • Getting in or out of a car
    • Bending to put on shoes and socks
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52
Q

Knee OA >>> signs (local examination findings)

A
  • Gait: A jerky, asymmetric (antalgic) gait + less time weightbearing on the painful side
  • Deformity:
    • Varus
    • Valgus (less commonly)
    • (and/or) fixed flexion deformity
  • Tenderness:
    • Joint-line and/or periarticular tenderness (secondary anserine bursitis + medial ligament enthesopathy) >>> causing tenderness of the upper medial tibia
  • Weakness and wasting of the quadriceps muscle
  • Restricted flexion and extension + coarse crepitus
  • Bony swelling around the joint line
  • In knee OA >>> CPPD crystal deposition is common
  • *This may result in** >>> more overt inflammatory component (stiffness, effusions) + super-added acute attacks of synovitis >>> which may be associated with >>> more rapid radiographic and clinical progression
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53
Q

Osteoarthritis >>> investigations

A
  • A Plain X-ray of the affected joint >> often will show one or more typical features of OA
  • For hip >>> Do non-weight beraingX-ray pelvis PA view
  • For knee >>> Do stan**dingX__-ray knee AP view >>> to assess >>> tibio-femoral cartilage loss
    • A flexed skyline view >>> to assess patello-femoral involvement.
  • For spine >>> Plain X-ray spine
    • If suspected spinal stenosis or nerve root compression >>> Do MRI
  • Routine biochemistry: normal
  • CBC/haematology: normal
  • Autoantibody tests: usually normal
  • Acute phase response: moderate
  • Synovial fluid (aspirated from an affected joint)
    • viscous
    • A low cell count
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54
Q

Importance of plain x-ray in OA

A

Importance:
It is of value in assessing the severity of structural change >>>
which is helpful if joint replacement surgery is being considered.

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55
Q

Probable X-ray findings in hand OA

A

In hand:

  • Joint space narrowing affecting the PIP and DIP
  • In some OA-affected joints >>> typical > Articular subchondral and ‘gullwing’ appearances
  • Osteophyte formation
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56
Q

Probable X-ray findings in knee OA

A

In knee:

  • Advanced OA >>> almost complete loss of joint space >>> affecting both compartments
  • Sclerosis of subchondral bone
  • In severe patello-femoral OA >>> almost complete loss of joint space + lateral displacement of the patella
  • If marked medial tibio-femoral OA >>>>> typical varus knee deformity
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57
Q

Probable X-ray findings in hip OA

A

In hip:

  • Superior joint space narrowing
  • Subchondral sclerosis
  • Osteophytes
  • Cysts
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58
Q

Probable X-ray findings in spine OA

A

In spine:

  • Disc narrowing
  • Osteophytes
  • Osteosclerosis at the apophyseal joints
  • Cervical spondylosis
59
Q

Unexplained early onset OA >>> investigations

A
  • If unexplained early-onset OA >>> Do additional investigation:
    Guided by the suspected underlying condition.
  • In acromegaly >>> X-ray shows:
    • Dysplasia or
    • Vascular necrosis
    • Widening of joint spaces
  • In haemochromatosis >>> X-ray shows
    • Multiple cysts
    • Chondrocalcinosis
    • MCP joint involvement in haemochromatosis
  • In neuropathic joints >>> X-ray shows
    • Disorganised architecture
60
Q

Rheumatoid arthritis: what is it?

A
  • A common form of inflammatory arthritis
  • It occurs throughout the world and in all ethnic groups
  • Chronic disease
  • Characterised by a clinical course of exacerbations and remissions
  • A complex disease >>> both genetic and environmental components
61
Q

Rheumatoid arthritis >>> epidemiology

A
  • Age: Peak onset = 30-50 years, although occurs in all age groups
  • Sex: Female: Male ratio = 3:1 (Female has more ratio than male)
  • Prevalence in the UK = 1% (= 1 in 100 = 1000 in 100,000)
  • Prevalence in Europe & in the Indian subcontinent = 0.8-1.0%
  • Prevalence in the south-east Asia = 0.4% (lower)
  • Prevalence in Pima Indians = 5% (highest in the world)
  • Some ethnic differences e.g. High in Native Americans
62
Q

RA >>> pathophysiological chart

A
63
Q

RA >>> HLA association

A

HLA-DR4 (especially Felty’s syndrome)
The strongest association is with variants in the HLA region.

Recent studies have shown that >>> the association with HLA is determined by >>>

  • Variations in 3 amino acids in the HLA-DRβ1 molecule (positions 11, 71 and 74)
  • Single variants HLA-B (at position 9)
  • HLA-DPβ1 (at position 9)

The non-HLA loci generally lie within or close to genes involved in regulating the immune response.

64
Q

RA >>> key factor in pathophysiology

A

TNF (Tumour necrosis factor)

So, anti-TNF is given in RA treatment

65
Q

RA >>> genetic factors

A

The importance of genetic factors is demonstrated by >>>

  • Higher concordanceof RA in monozygotic (12–15%) compared
    with dizygotic twins (3%)
  • increased frequency of disease in the first-degree relatives
  • Nearly 100 loci that are associated with the risk of developing RA (detected by genome wide association studies)
66
Q

RA >>> environmental factors/trigger

A
  • Infection
    • In a genetically susceptible host >>> through processes like citrullination >>> modify host proteins >>> triggers autoimmunity >>> becomes immunogenic
    • NO single specific pathogen has been identified
  • Cigaretter smoking
    • Associated with more severe disease
    • Reduced responsiveness to treatment
67
Q

RA >>> pathophysiology

A
  • infiltration of the synovial membrane with >>>
    • CD4+ T -lymphocytes (interacts with other cells of the synovium)
    • B lymphocytes (interacts with other cells of the synovium)
    • Plasma cells
    • Dendritic cells
    • Macrophages
  • >>> Lymphoid follicles form within the synovial membrane >>> in which T- and B-cell interactions occur >>> causing >
    1. Activation of T cells >>> to produce cytokines (+)
    2. Activation of B cells >>> to produce autoantibodies, (including RF and ACPA)
  • The Positive feedback loop:
    • T cells produce TNF and interferon gamma (IFN-γ) >>> they activate synovial macrophages
    • Macrophages produce several pro-inflammatory cytokines, including >>> TNF, IL-1 and IL-6 >>> which act on synovial fibroblasts >> produce further cytokines >>> set up a positive feedback loop
  • Synovial fibroblasts proliferate, causing >>> synovial hypertrophy >>> producing matrix metalloproteinases + the proteinase ADAMTS-5 >>> which degrade soft tissues and cartilage.
  • Within ithe inflammed synovium >>> Prostaglandins and nitric oxide produced >>> cause > vasodilatation >> swelling + pain.
  • Systemic release of IL-6 triggers production of acute phase proteins by the liver.
  • At the joint margin >>> the inflamed synovium (pannus) >>> directly invades bone and cartilage >> cause joint erosions.
  • A key pathogenic factor in bone erosions and periarticular osteoporosis is osteoclast activation, stimulated by <<<
    • the production of M-CSF by synovial cells and RANKL by activated T cells
  • New blood-vessel formation (angiogenesis) occurs >>> causing > the inflamed synovium to become >>> highly vascular
    • Within these blood vessels >>> pro-inflammatory cytokines >>> activate
      endothelial cells >>> support recruitment of yet more leucocytes >>>
      perpetuate the inflammatory process.
  • Later, fibrous or bony ankylosis may occur.
  • Adjacent miscles to inflamed joints >>> atrophy + (may be) infiltrated with lymphocytes >>> leads to >>> progressive biomechanical dysfunction >>> may further amplify destruction
  • Rheumatoid nodules occur in patients who are RF or ACPA positive >>> primarily affect extensor tendons.
    • They consist of >>>
      • A central area of fibrinoid material
      • Surrounded by a palisade of proliferating mononuclear cells.
  • Granulomatous lesions may occur in >>> the pleura, lung, pericardium and sclera.
68
Q

Rheumatoid arthritis >>> Commonly affected joints

A
  • Small joints of the hands (PIP, MCP)
  • Feet and wrists
  • Large joints
  • Symmetrical involvement (= arthritis)
69
Q

Rheumatoid arthritis >>> Features of the affected joints

A
  • Pain
  • Joint swelling (commonly of PIP, MCP or wrist joints)
  • Soft tissue swelling
  • Morning stiffness >1 hour
70
Q

RA >>> examination of the joints typically reveals - ?

A
  • Swelling
  • Tenderness
  • Erythema is unusual (Erythema suggests Co-existent sepsis)
71
Q

Sometimes RA has >>> an acute onset + severe early morning stiffness + polyarthritis + pitting oedema.

This occurs more commonly in - ???

A

Older age

72
Q

RA >>> Muscle-related another presentation

A

“Proximal muscle stiffness” mimicking >>> polymyalgia rheumatica

73
Q

Risk factor (micriorganism) of RA

A

Proteus mirabilis is a (G-ve rod), causes UTIpredisposes susceptible patients to RA

74
Q

RA >> time course (acute/chronic/intermittent)

A
  • It is Mainly chronic disease
  • Sometimes RA has >>> An acute onset + severe early morning stiffness + polyarthritis + pitting oedema. (This occurs more commonly in old age)
  • Occasionally >>> the onset is palindromic + with relapsing and remitting episodes of pain, stiffness and swelling (that last for only a few hours or days)
75
Q

RA >>> hand deformities

(when and what)

A

When they develop: Long-standing uncontrolled disease in older people

Although these have become less common over recent years with more aggressive management in young age

  • Ulnar deviation of the fingers
  • Swan neck deformity
  • Boutonnière or ‘button hole’ deformity
  • Z deformity of the thumb
  • Dorsal subluxation of the ulna at the distal radio-ulnar joint (may be) >>> contribute to Rupture of the fourth and fifth extensor tendons.
  • If nodules in the flexor tendon sheaths >>> Triggering of fingers
76
Q

RA >>> lower limb deformities

(when and what)

A
  • *When they develop:** Long-standing uncontrolled disease in older people
  • Although these have become less common over recent years with more aggressive management in the young age*
  • Subluxation of the MTP joints (meta-tarso-phalangeal joints) of the feet >>> (may result) in ‘cock-up’ toe deformities, causing:
    • Pain on weight-bearing on the exposed MTP heads
    • Development of secondary adventitious bursae and callosities
  • In the hind foot >>> damage to the ankle and subtalar joints >>> valgus deformity of the calcaneus
    • Associated with loss of the longitudinal arch (flat foot) <<< due to rupture of the tibialis posterior tendon
  • In patients with knee synovitis >>> Popliteal (Baker’s) cysts may occur
    • Here, synovial fluid communicates with the cyst but is prevented from returning to the joint by a valve-like mechanism (NOT specific to RA)
    • Rupture may be induced by knee flexion >>> leading to >> calf pain + swelling >>> may mimic a deep venous thrombosis (DVT).
77
Q

More commonly, involved joints in RA, OA, PA

A
  • PIP, MCP, Wrist >>> Rheumatoid arthritis
  • DIP >>> Osteoarthritis, Psoriatic arthritis
  • Base of the thumb >>> Osteoarthritis
78
Q

Which patient group should be checked by ACR criteria of RA?

A

Target population:

  1. Patient with At least 1 joint with clinical synovitis
  2. Patient with synovitis, not explained by any other disease
79
Q

ACR (2010) criteria for diagnosis of Rheumatoid arthritis

A

Diagnosis by scale:

  • Add score of categories A to D: If score ≥ 6/10 >>> Dx: Rheumatoid arthritis
  • For not missing any criteria >>> Check through the criteria (from high score to low score) (= 5 to 0, 3 to 0, 1 to 0)
80
Q

Systemic complications of rheumatoid arthritis

A
  • Fever
  • Susceptibility to infection
  • Weight loss
  • Fatigue
  • Anorexia
81
Q

RA >>> Respiratory complications

A

(above downwards)

  • Bronchiolitis obliterans
  • Pulmonary fibrosis → often asymptomatic; sometimes, risk is increased by anti-TNF therapy
  • Pulmonary nodules
  • Methotrexate pneumonitis (A complication of drug therapy)
  • Fibrosing alveolitis
  • Pleural effusion
  • Pleurisy
  • Caplan’s syndrome >>> massive fibrotic nodules (= pneumoconiosis) (due to occupational coal dust exposure)
  • Infection (possibly atypical) secondary to immunosuppression
82
Q

RA >>> Cardiac complications

A

RA patients have an increased risk of IHD

  • IHD (Ischaemic Heart Disease) (more common)
  • Pericarditis
  • Myocarditis
  • Endocarditis
  • Conduction defects
  • Coronary vasculitis
  • Granulomatous aortitis
  • Rare: heart block, cardiomyopathy, coronary artery occlusion, aortic regurgitation
83
Q

RA >>> Neurological complications

A
  • Cervical cord compression
  • Compression neuropathies
  • Peripheral neuropathy
  • Mononeuritis multiplex
84
Q

RA >>> Psychiatric complication

A

Depression

85
Q

RA >>> ocular complications

A

Fron to back

  • Keratoconjunctivitis sicca (most common)d__ry, burning, gritty eyes
    • Cause: Secondary Sjogren’s syndrome
  • Episcleritis → redness
  • Scleritis → redness + pain → uncommon, but most serious sight-threatening
    • If so → urgent refer to ophthalmology, artificial tear, antibiotics
  • Keratitis (peripheral ulcerative keratitis) → redness + pain → uncommon, but most serious sight-threatening
  • Corneal ulceration
  • Steroid-induced cataracts
  • Scleromalacia
  • Chloroquine retinopathy
86
Q

RA >>> musculoskleletal complications

A
  • Osteoporosis (more common)
  • Muscle-wasting (Cause: systemic inflammation + reduced activity)
  • Tenosynovitis
  • Bursitis
87
Q

RA >>> vasculitis related complications

A
  • Digital arteritis
  • Visceral arteritis
  • Ulcers
  • Pyoderma gangrenosum
  • Mononeuritis multiplex
88
Q

RA >>> Haematological complications

A
  • Anaemia (Due to NSAID induced GI blood loss → iron deficiency → microcytic anaemia)
  • Thrombocytosis
  • Eosinophilia
  • In active disease → normochromic normocytic anaemia + thrombocytosis
89
Q

RA >>> lymphatic complications

A
  • Felty’s syndrome (RA + splenomegaly + low white cell count/ neutropaenia)
  • Splenomegaly
  • Localised or generalised lymphadenopathy can occur in patients with active disease
  • But persistent lymphadenopathy → may indicate >>> the development of lymphoma >>> more common in long-standing RA
90
Q

RA >>> nodules

A
  • Subcutaneous nodules
  • Sinuses
  • Fistula
91
Q

RA >>> a less common but important complication (mainly in poorly controlled RA)

A

Amyloidosis

92
Q

Extra-articular features are more common in - ?

A
  • Patient with long-standing seropositive erosive disease
  • Occasionally. They can occur At presentation (especially In men)
  • Most are due to
    • Serositis
    • Granuloma
    • Nodule formation
    • Vasculitis
93
Q

Subcutaneous nodules of RA occur in -?

A

Almost exclusively in RF or ACPA positive patients

94
Q

Subcutaneous nodules of RA >> usual site ?

A

Extensor tendons

95
Q

Subcutaneous nodules of RA >>> symptomatology

A
  • Frequently asymptomatic
  • Some may be complicated by >>> ulceration and secondary infection
96
Q

Vasculitis in RA >>> features

A

This is uncommon but may occur in seropositive patients.

The presentation is with →

  • systemic symptoms, such as
    • fatigue
    • fever
    • nail-fold infarcts
  • Rarely,
    • cutaneous ulceration
    • skin necrosis
    • mesenteric, renal or coronary artery occlusion (may occur)
97
Q

Risk of CVS disease in RA is increased due to - ?

A

A combination of >>> conventional risk factors, such as:

  • High cholesterol
  • Smoking
  • High BP (HTN)
  • Low physical activity
  • NSAIDs
  • Glucocorticoids
  • The effects of inflammatory cytokines on vascular endothelium
98
Q

RA >>> frequency of cervical cord compression

A

Rare

99
Q

Cause of cervical cord compression in RA

A

Subluxation of the cervical spine

100
Q

RA >>> level of cervical cord compression

A

At the atlanto-axial joint or at subaxial level

101
Q

RA >>> course of cervical cord compression in RA

A

Course: Due to erosion of the transverse ligament posterior to the odontoid peg. >> atlanto-axial subluxation →can lead to >>> cord compression OR following minor trauma/manipulation → sudden death

102
Q

RA >>> cervical cord compression: clinical features

A
  • Suspect if – paraesthesia or electric shock in the arms
  • Insidious onset
  • Subtle loss of function→ may initially be attributed to active disease

In patients with extensive joint diseasereflexes and power can be difficult to assess; Therefore, sensory and upper motor signs are most important

103
Q

RA >>> cervical cord compression: TOC ?

A

Urgently refer to neurosurgery → stabilisation and fixation

104
Q

Rheumatoid arthritis: >>> Cause of Compression or entrapment neuropathy

A

Hypertrophied synovium or

Joint subluxation

105
Q

RA >>> Examples of compression/ entrapment neuropathy

A
  • *The most common:** median nerve compression → present as: bilateral carpal tunnel syndrome
  • *others:** ulnar nerve (at elbow or wrist), lateral popliteal nerve (at fibular head)
106
Q

Tarsal tunnel syndrome in RA

A

Entrapment of posterior tibial nerve in the flexor retinaculum → tarsal tunnel syndrome → burning, tingling and numbness* in the *distal soles and toes

107
Q

Serositis in RA

A
  • Asymptomatic; but may be –
  • Pleural pain
  • Pericardial pain
  • Breathlessness
  • Pericardial effusion (rare)
  • Constrictive pericarditis (rare)
108
Q

When does amyloidosis occur in RA?

A

If RA is poorly controlled

109
Q

Amyloidosis >>> common features and findings

A
  • Albumin: very low
  • Creatinine: high
  • Proteinuria (may be as nephrotic syndrome)
  • Hepatomegaly
  • Small joint Arthropathy
  • Fatigue
  • Weight loss
  • Peripheral oedema
  • Peripheral neuropathy
110
Q

Secondary amyloid - >> ?

A

Extracellular accumulation of AA fibrils within tissue and organs (due to acute phase reactant, serum amyloid A)

111
Q

Felty’s syndrome >>> risk factors

A
  • Age of onset: _50-70_years
  • Sex: Female > Male
  • Race: Caucasians > Black
  • Long standing RA
  • Deforming + but inactive disease
  • RF seropositive
112
Q

Felty’s syndrome >>> common C/F

A
  • Splenomegaly (MAIN)
  • Lymphadenopathy
  • Weight loss
  • Skin pigmentation
  • Keratoconjunctivitis sicca
  • Vasculitis, leg ulcers
  • Recurrent infections
  • Nodules
113
Q

Felty’s syndrome >>> lab findings

A
  • Normochromic, normocytic anaemia (Like active RA)
  • Neutropenia (MAIN)
  • Thrombocytopenia
  • Impaired T- and B-cell immunity
  • Abnormal liver function
114
Q

RA >>> IOC ?

A

Anti-CCP antibodies (= Anti-cyclic citrullinated peptide antibody = ACPA)

115
Q

If suspected RA + but, rheumatoid factor negative >>> what next ?

(NICE recommendation)

A

test for anti-CCP antibodies → if it’s positive → Dx: RA

116
Q

RA >>> top 3 main investigations

A
  • IOC: Anti-CCP antibodies (= Anti-cyclic citrullinated peptide antibody = ACPA)
  • Rheumatoid factor (RF)
    • NICE recommendation: If suspected RA + but, rheumatoid factor negative → test for anti-CCP antibodies → if it’s positive → Dx: RA
  • X-ray of the joints
117
Q

Ra >>> investigations to establish diagnosis

A
  • Clinical criteria
  • ESR and CRP → raised (but normal level do NOT exclude RA, especially if few joints are involved)
  • USG or MRI
    • Not routinely required
    • Indication: clinical uncertainty about the presence of →synovitis
  • Anti-CCP (NICE recommended IOC)
  • RF
118
Q

To monitor disease activity and drug efficacy in RA - ?

A
  • Pain (visual analogue scale)
  • Early morning stiffness (minutes)
  • Joint tenderness
  • Joint swelling
  • DAS28 score
  • ESR
  • CRP
119
Q

To monitor disease damage in RA - ?

A
  • X-rays
  • Functional assessment
120
Q

To monitor drug safety in RA - ?

A
  • FBC (Full blood count)
  • Urine R/E (Urinalysis)
  • Urea and creatinine
  • Liver function tests (LFT)
  • Chest X-ray
121
Q

Anti- CCP antibodies (ACPA) >>> sensitivity and specificity

A
  • Sensitivity = 70-80% (similar to RF)
    • Means, among the ‘Patients with RA’ → ACPA & RF can detect 70-80% of them
  • Specificity = 90-95% (higher than RF)
122
Q

Anti- CCP antibodies (ACPA) for detection of future development of RA

A
  • Detectable up to 10 years before the development of RA
  • Play a key role in the future RA → allows early detection of patients >>> suitable for “aggressive anti-TNF therapy”.
123
Q

What is RF (Rheumatoid factor) ?

A

Circulating Ab (usually IgM) which reacts with Fc portion of patient’s own IgG

124
Q

Methods of testing RF (Rheumatoid factor)

A
  • Rose-waaler test: → sharp red cell agglutination
  • Latex agglutination
125
Q

RF >>> sensitivity and specificity to detect RA

A
  • Sensitivity: 70% (these are also positive for ACPA)
  • Less specific than ACPA
126
Q

Dseases where RF is positive

A
  • Rheumatoid arthritis (70%)
  • Sjogren’s syndrome (100%)
  • Felty’s syndrome (100%)
  • Infective endocarditis (50%)
  • SLE (20-30%)
  • Systemic sclerosis (30%)
  • General population: 5%
  • Rarely: TB, leprosy, HBV, EBV
127
Q

X-ray findings in early RA

A
  • Loss of joint space (seen in both RA and osteoarthritis)
  • Juxta-articular osteoporosis
  • Soft-tissue swelling
  • Usually normal hand, wrist, feet
128
Q

X-ray findings in late/advanced RA

A
  • Periarticular erosions (osteopenia and osteoporosis) (periarticular osteoporosis and marginal joint erosions)
  • Subluxation of joint
129
Q

The main indication of X-ray in rheumatoid arthrits

A

Assessment of → painful joints → to determine >>> if any significant structural damage

130
Q

In RA, if suspected atlantao-axial disease >>> investigations

A

Lateral X-rays (taken in flexion and extension) + MRI

131
Q

In RA, if suspected Baker’s cyst >>> investigation

A

Ultrasound (may require)

132
Q

Purpose of DAS28 scoring in RA

A

To assess >>> the need of:

  • Disease activity
  • Response to treatment
  • Need for biological therapy
133
Q

How is DAS28 scored and interpreted?

A

Count “the number” of “swollen and tender joints” in the upper limbs and knees >>> combine this with >>> the ESR + the patient’s assessment of the activity of their arthritis (on a visual analogue scale**: where, 0 indicates no symptoms and 100 the worst symptoms possible) → enter into a calculator (online) → generate a numerical score.

Interpretation: The higher the value → the more active the disease

134
Q

Change of RA during pregnancy

A
  • Old prior diagnosed RA improves (may remission) in pregnancy
  • Often has a flare after delivery (or often first presents post-partum)
  • *Why:** immunosuppression in pregnancy + hormonal changes
135
Q

RA & conception or future pregnancy

A
  • If early RA or poorly controlled (= unstable) RA→ defer conception until disease is stable
  • Stop methotrexate (at least) 3 months before pregnancy
  • Stop Leflunomide (at least) 24 months before pregnancy
136
Q

RA in pregnancy >>> use of Analgesic

A
  • Analgesic of choice: Paracetamol
  • ContraindicatedNSAIDs
    • NSAIDs & selective COX-2 inhibitors → can be used up to 32weeks of pregnancy (Davidson says upto* *20 weeks)
    • NASIDs can cause early closure of ductus arteriosus
137
Q

RA is pregnancy >>> use of glucocorticoids

A
  • Can be used to control disease flares
  • Risks of: Hypertension, glucose intolerance, osteoporosis
  • Short-term glucocorticoids is safe in lower dose in pregnancy
  • If neededTOC: Low –dose prednisolone
138
Q

DMARDs that are safe (can be used) in RA + pregnancy

A
  • Sulfasalazine (1st line)
  • Hydroxychloroquine (1st line)
  • Azathioprine (2nd line)

SHA

139
Q

RA in pregnancy >>>

DMARDs that are contraindicated (must be avoided

A
  • Methotrexate (also C.I in breast-feeding)
  • Leflunomide (also C.I in breast-feeding)
  • Cyclophosphamide (also C.I in breast-feeding)
  • Mycophenolate
  • Gold
140
Q

RA in pregnancy >>> biological therapies

A
  • Limited experience
  • May be relatively safe during pregnancy
  • The main theoretical riskimmunosuppression in the neonate
  • *Except for** → Certolizumabcrosses the placenta in negligible amounts.
141
Q

RA in pregnancy >>> treatment outline

A
  • First line: Sulfasalazine or Hydroxychloroquine (Safe in pregnancy)
  • Second line: Azathioprine (If first line fails to control
    • Before Azathioprine → check TMPT deficiency
  • Oral analgesic of choice in pregnancy: Paracetamol
  • Short-term glucocorticoids (Low –dose prednisolone) is safe in lower dose in pregnancy
  • In obstetric anaesthesia of RA patient → check the risks of atlanto-axial subluxation
142
Q

Breast-feeding >>> anti-RA drugs that are contraindicated

A
  • Methotrexate
  • Leflunomide
  • Cyclophosphamide
143
Q
A