Rheumatology Flashcards
Causes of low back pain
- 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
Features of mechanical low back pain
-
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)
Back pain >>> Red flags for possible spinal pathology
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)
Clinical features of radicular pain
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
Clinical assessment of back pain
The main purpose: To differentiate the self-limiting disorder of acute mechanical back pain from serious spinal pathology
Mechanical back pain >>> frequency
- 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.
How to assess mechanical back pain
-
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.
Mechanical back pain >>> prognosis
- 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.
Factors that may cause transition of acute mechanical back pain to a chronic pain
Psychological elements, such as
- job dissatisfaction
- Depression
- Anxiety
Back pain secondary to serious spinal pathology (Not mechanical) ⇒
Urgent investigation is needed if there is - ?
- clinical evidence of spinal cord or nerve root compression
- sepsis including tuberculosis, or
- a cauda equina lesion
Spinal stenosis >>> presentation
- 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.
Spinal stenosis >>> the most common cause
The most common cause is:
Gadual development of coexisting contributing lesions such as >>>
- Facet joint arthritis
- Ligament flavum thickening or
- Degenerative spondylolisthesis.
Degenerative disc disease is more common in -?
It is a common cause of chronic low back pain in middle-aged adults.
Prolapsed intervertebral disc >>> presentation
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.
Prolapsed intervertebral disc >>> prognosis
About 70% of patients improve by 4 weeks.
Inflammatory back pain (IBP) >>> 2 important causes
- Axial spondyloarthritis (axSpA)
- Psoriatic arthrits (PsA)
Inflammatory back pain >>> presentations
[due to axial spondyloarthritis (axSpA) &
Psoriatic arthrits (PsA)]
- Gradual onset
- Almost always before the age of 40
- Associated with morning stiffness
- Improves with movement
Spondylolisthesis >>> presentation
- Back pain
- Typically aggravated by standing and walking
Occasionally, diffuse idiopathic skeletal hyperostosis >>>>> can cause back pain but it is usually asymptomatic.
Arachnoiditis
Rare cause of chronic severe low back pain
Arachnoiditis >>> cause
- Chronic inflammation of the nerve root sheaths in the spinal canal >>> further, can complicate meningitis
- Spinal surgery or
- Myelography with oil-based contrast agents.
When is investigation needed in back pain?
- Acute mechanical back pain > No investigation required
- Persistent pain (> 6 weeks) OR red flags >>> need further investigation
Back pain >>> Investigation of choice (IOC)
MRI (Magnetic resonance imaging)
In back pain, MRI is the IOC >>> because?
Because, it can demonstrate >>>
- spinal stenosis
- cord compression
- nerve root compression
- inflammatory changes in axSpA
- sepsis
- malignancy
Investigations of back pain >>> imgaing modalities
- MRI (MAgnetic resonance imaging) >>> IOC
- Plain X-ray
- Bone scintigraphy
Indications of ‘plain X-ray’ in back pain
- Suspected vertebral compression fractures
- OA (Osteroarthritis)
- Degenerative disc disease
Indication of bone scintigraphy in back pain
If metastatic disease is suspected
Back pain >>> additional investigations
- 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
Pateint with low back pain >>> indications of surgery
- Progressive spinal stenosis
- Spinal cord compression with nerve root compression
Management of back pain
- 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
Osteoarthritis: epidemiology
- 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.
Osteoarthritis: Risk factors
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
Osteoarthritis: main pathological process
- 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
Osteoarthritis: defining feature
degenation of articular cartilage
Osteoarthritis: pathology in sub-chondral bone
Abnormalities in subchondral bone >>>
- sclerotic
- the site of subchondral cysts
Osteoarthritis >>> joint margin
At the joint margin >>> fibrocartilage is produced >>> undergoes endochondral ossification >> form osteophytes
Osteoarthritis >>> shape
- 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.
Osteoarthritis >>> BMD and osteoporosis
- 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.
Osteoarthritis >>> the synovium
- 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
Osteoarthritis >>> the outer capsule
Outer capsule also thickens and contracts >>> usually retaining the stability of the remodelling joint.
Osteoarthritis >>> surrounding muscles
Around the joints >>> wasting of muscles + non-specific type II fibre atrophy
Osteoarthritis >>> Clinical features (signs & symptoms)
- *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.
Osteoarthritis >>> cause of joint pain
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)
Coarse crepitus in OA (palpable +/- audible) >>> cause?
Rough articular surfaces
Restricted movement in OA >>> cause?
due to capsular thickening or blocking by osteophyte
Osteoarthritis >>> the correlation between structural changes (assessed by imaging) & clinical features
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.
Generalised nodal OA: characteristics
- 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.
- the daughter of an affected mother has a 1 in 3 chance of
-
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
Generalised nodal OA >>> course of the disease
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
If generalised nodal OA involves first CMC (Carpo-metacarpal) joint >>> Sign and symptoms
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
Targeted area in Knee OA
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.
Knee OA >>> important risk factor in men
Trauma
>>> may cause unilateral OA
Knee OA >>> symptoms
- 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
Knee OA >>> signs (local examination findings)
- 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
Osteoarthritis >>> investigations
- 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
Importance of plain x-ray in OA
Importance:
It is of value in assessing the severity of structural change >>>
which is helpful if joint replacement surgery is being considered.
Probable X-ray findings in hand OA
In hand:
- Joint space narrowing affecting the PIP and DIP
- In some OA-affected joints >>> typical > Articular subchondral and ‘gullwing’ appearances
- Osteophyte formation
Probable X-ray findings in knee OA
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
Probable X-ray findings in hip OA
In hip:
- Superior joint space narrowing
- Subchondral sclerosis
- Osteophytes
- Cysts
Probable X-ray findings in spine OA
In spine:
- Disc narrowing
- Osteophytes
- Osteosclerosis at the apophyseal joints
- Cervical spondylosis
Unexplained early onset OA >>> investigations
- 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
Rheumatoid arthritis: what is it?
- 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
Rheumatoid arthritis >>> epidemiology
- 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
RA >>> pathophysiological chart
RA >>> HLA association
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.
RA >>> key factor in pathophysiology
TNF (Tumour necrosis factor)
So, anti-TNF is given in RA treatment
RA >>> genetic factors
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)
RA >>> environmental factors/trigger
-
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
RA >>> pathophysiology
-
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.
- Within these blood vessels >>> pro-inflammatory cytokines >>> activate
- 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.
- They consist of >>>
- Granulomatous lesions may occur in >>> the pleura, lung, pericardium and sclera.
Rheumatoid arthritis >>> Commonly affected joints
- Small joints of the hands (PIP, MCP)
- Feet and wrists
- Large joints
- Symmetrical involvement (= arthritis)
Rheumatoid arthritis >>> Features of the affected joints
- Pain
- Joint swelling (commonly of PIP, MCP or wrist joints)
- Soft tissue swelling
- Morning stiffness >1 hour
RA >>> examination of the joints typically reveals - ?
- Swelling
- Tenderness
- Erythema is unusual (Erythema suggests Co-existent sepsis)
Sometimes RA has >>> an acute onset + severe early morning stiffness + polyarthritis + pitting oedema.
This occurs more commonly in - ???
Older age
RA >>> Muscle-related another presentation
“Proximal muscle stiffness” mimicking >>> polymyalgia rheumatica
Risk factor (micriorganism) of RA
Proteus mirabilis is a (G-ve rod), causes UTI → predisposes susceptible patients to RA
RA >> time course (acute/chronic/intermittent)
- 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)
RA >>> hand deformities
(when and what)
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
RA >>> lower limb deformities
(when and what)
- *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).
More commonly, involved joints in RA, OA, PA
- PIP, MCP, Wrist >>> Rheumatoid arthritis
- DIP >>> Osteoarthritis, Psoriatic arthritis
- Base of the thumb >>> Osteoarthritis
Which patient group should be checked by ACR criteria of RA?
Target population:
- Patient with At least 1 joint with clinical synovitis
- Patient with synovitis, not explained by any other disease
ACR (2010) criteria for diagnosis of Rheumatoid arthritis
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)
Systemic complications of rheumatoid arthritis
- Fever
- Susceptibility to infection
- Weight loss
- Fatigue
- Anorexia
RA >>> Respiratory complications
(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
RA >>> Cardiac complications
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
RA >>> Neurological complications
- Cervical cord compression
- Compression neuropathies
- Peripheral neuropathy
- Mononeuritis multiplex
RA >>> Psychiatric complication
Depression
RA >>> ocular complications
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
RA >>> musculoskleletal complications
- Osteoporosis (more common)
- Muscle-wasting (Cause: systemic inflammation + reduced activity)
- Tenosynovitis
- Bursitis
RA >>> vasculitis related complications
- Digital arteritis
- Visceral arteritis
- Ulcers
- Pyoderma gangrenosum
- Mononeuritis multiplex
RA >>> Haematological complications
- Anaemia (Due to NSAID induced GI blood loss → iron deficiency → microcytic anaemia)
- Thrombocytosis
- Eosinophilia
- In active disease → normochromic normocytic anaemia + thrombocytosis
RA >>> lymphatic complications
- 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
RA >>> nodules
- Subcutaneous nodules
- Sinuses
- Fistula
RA >>> a less common but important complication (mainly in poorly controlled RA)
Amyloidosis
Extra-articular features are more common in - ?
- 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
Subcutaneous nodules of RA occur in -?
Almost exclusively in RF or ACPA positive patients
Subcutaneous nodules of RA >> usual site ?
Extensor tendons
Subcutaneous nodules of RA >>> symptomatology
- Frequently asymptomatic
- Some may be complicated by >>> ulceration and secondary infection
Vasculitis in RA >>> features
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)
Risk of CVS disease in RA is increased due to - ?
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
RA >>> frequency of cervical cord compression
Rare
Cause of cervical cord compression in RA
Subluxation of the cervical spine
RA >>> level of cervical cord compression
At the atlanto-axial joint or at subaxial level
RA >>> course of cervical cord compression in RA
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
RA >>> cervical cord compression: clinical features
- 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 disease → reflexes and power can be difficult to assess; Therefore, sensory and upper motor signs are most important
RA >>> cervical cord compression: TOC ?
Urgently refer to neurosurgery → stabilisation and fixation
Rheumatoid arthritis: >>> Cause of Compression or entrapment neuropathy
Hypertrophied synovium or
Joint subluxation
RA >>> Examples of compression/ entrapment neuropathy
- *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)
Tarsal tunnel syndrome in RA
Entrapment of posterior tibial nerve in the flexor retinaculum → tarsal tunnel syndrome → burning, tingling and numbness* in the *distal soles and toes
Serositis in RA
- Asymptomatic; but may be –
- Pleural pain
- Pericardial pain
- Breathlessness
- Pericardial effusion (rare)
- Constrictive pericarditis (rare)
When does amyloidosis occur in RA?
If RA is poorly controlled
Amyloidosis >>> common features and findings
- Albumin: very low
- Creatinine: high
- Proteinuria (may be as nephrotic syndrome)
- Hepatomegaly
- Small joint Arthropathy
- Fatigue
- Weight loss
- Peripheral oedema
- Peripheral neuropathy
Secondary amyloid - >> ?
Extracellular accumulation of AA fibrils within tissue and organs (due to acute phase reactant, serum amyloid A)
Felty’s syndrome >>> risk factors
- Age of onset: _50-70_years
- Sex: Female > Male
- Race: Caucasians > Black
- Long standing RA
- Deforming + but inactive disease
- RF seropositive
Felty’s syndrome >>> common C/F
- Splenomegaly (MAIN)
- Lymphadenopathy
- Weight loss
- Skin pigmentation
- Keratoconjunctivitis sicca
- Vasculitis, leg ulcers
- Recurrent infections
- Nodules
Felty’s syndrome >>> lab findings
- Normochromic, normocytic anaemia (Like active RA)
- Neutropenia (MAIN)
- Thrombocytopenia
- Impaired T- and B-cell immunity
- Abnormal liver function
RA >>> IOC ?
Anti-CCP antibodies (= Anti-cyclic citrullinated peptide antibody = ACPA)
If suspected RA + but, rheumatoid factor negative >>> what next ?
(NICE recommendation)
test for anti-CCP antibodies → if it’s positive → Dx: RA
RA >>> top 3 main investigations
- 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
Ra >>> investigations to establish diagnosis
- 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
To monitor disease activity and drug efficacy in RA - ?
- Pain (visual analogue scale)
- Early morning stiffness (minutes)
- Joint tenderness
- Joint swelling
- DAS28 score
- ESR
- CRP
To monitor disease damage in RA - ?
- X-rays
- Functional assessment
To monitor drug safety in RA - ?
- FBC (Full blood count)
- Urine R/E (Urinalysis)
- Urea and creatinine
- Liver function tests (LFT)
- Chest X-ray
Anti- CCP antibodies (ACPA) >>> sensitivity and specificity
- 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)
Anti- CCP antibodies (ACPA) for detection of future development of RA
- 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”.
What is RF (Rheumatoid factor) ?
Circulating Ab (usually IgM) which reacts with Fc portion of patient’s own IgG
Methods of testing RF (Rheumatoid factor)
- Rose-waaler test: → sharp red cell agglutination
- Latex agglutination
RF >>> sensitivity and specificity to detect RA
- Sensitivity: 70% (these are also positive for ACPA)
- Less specific than ACPA
Dseases where RF is positive
- 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
X-ray findings in early RA
- Loss of joint space (seen in both RA and osteoarthritis)
- Juxta-articular osteoporosis
- Soft-tissue swelling
- Usually normal hand, wrist, feet
X-ray findings in late/advanced RA
- Periarticular erosions (osteopenia and osteoporosis) (periarticular osteoporosis and marginal joint erosions)
- Subluxation of joint
The main indication of X-ray in rheumatoid arthrits
Assessment of → painful joints → to determine >>> if any significant structural damage
In RA, if suspected atlantao-axial disease >>> investigations
Lateral X-rays (taken in flexion and extension) + MRI
In RA, if suspected Baker’s cyst >>> investigation
Ultrasound (may require)
Purpose of DAS28 scoring in RA
To assess >>> the need of:
- Disease activity
- Response to treatment
- Need for biological therapy
How is DAS28 scored and interpreted?
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
Change of RA during pregnancy
- 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
RA & conception or future pregnancy
- 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
RA in pregnancy >>> use of Analgesic
- Analgesic of choice: Paracetamol
-
Contraindicated → NSAIDs
- 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
RA is pregnancy >>> use of glucocorticoids
- Can be used to control disease flares
- Risks of: Hypertension, glucose intolerance, osteoporosis
- Short-term glucocorticoids is safe in lower dose in pregnancy
- If needed → TOC: Low –dose prednisolone
DMARDs that are safe (can be used) in RA + pregnancy
- Sulfasalazine (1st line)
- Hydroxychloroquine (1st line)
- Azathioprine (2nd line)
SHA
RA in pregnancy >>>
DMARDs that are contraindicated (must be avoided
- Methotrexate (also C.I in breast-feeding)
- Leflunomide (also C.I in breast-feeding)
- Cyclophosphamide (also C.I in breast-feeding)
- Mycophenolate
- Gold
RA in pregnancy >>> biological therapies
- Limited experience
- May be relatively safe during pregnancy
- The main theoretical risk → immunosuppression in the neonate
- *Except for** → Certolizumab → crosses the placenta in negligible amounts.
RA in pregnancy >>> treatment outline
- 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
Breast-feeding >>> anti-RA drugs that are contraindicated
- Methotrexate
- Leflunomide
- Cyclophosphamide
