List I - Core Conditions Flashcards

1
Q

What is osteoarthritis?

A
  • Defined as a disorder of synovial joints which occurs when damage triggers repair processes leading to structural changes within a joint
  • Joint damage may occur through repeated excessive loading and stress of a joint over time or by injury
  • Damage to hyaline cartilage
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2
Q

What are the typical features altering the structure of the joint in osteoarthritis?

A
  • Localised loss of cartilage
  • Remodelling of adjacent bone and the formation of osteophytes (new bone at joint margins)
  • Mild synovitis (inflammation of the synovial membrane that lines the joint capsule
  • In some people these repair processes may alleviate symptoms but in others they cannot fully compensate for the joint damage, and symptoms of pain and stiffness may occur
  • Any synovial joint can be involved, most commonly peripheral joints are involved
  • Knees
  • Hips
  • Small joints of the hand
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3
Q

How common is osteoarthritis in the UK?

A
  • 18% of UK population aged over 45 years have sought treatment for osteoarthritis of the knee
  • 8% hip
  • 6% hand and wrist
  • Prevalence is higher in women than in men
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4
Q

What are the risk factors for developing osteoarthritis?

A
  • Genetic
  • Biological
  • Increasing age
  • Female sex - more common in the hip
  • Obseity
  • High bone density
  • Low bone density
  • Biomechanical
  • Joint injury and damage
  • Joint laxity and reduced muscle strength
  • Joint malalignment
  • Exercise stresses
  • Occupational stresses
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5
Q

What are the complications of osteoarthritis?

A
  • Joint deformity
  • Functional impairment and disability
  • Hand involvement may affect grip and pinch strength causing difficulty with activities such as opening jars, turning keys or door handles, lifting saucepans, fastening buttons and writing
  • Knee and hip involvement may cause difficulty walking, climbing stairs, dressing, driving
  • Psychosocial impact - may affect self confidence, self esteem, sleep quality, relationships and ability to self care for others
  • Occupational impact
  • Falls
  • Chronic pain syndrome
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6
Q

What is the prognosis of hand osteoarthritis?

A
  • Generally good
  • Interphalageal joint involvement usually becomes asymptomatic after a few years
  • Involvement of the 1st CMC joint generally has a poorer prognosis
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7
Q

What is the prognosis of hip osteoarthritis?

A
  • Poorer prognosis than hand or knee osteoarthritis

- Significant proportion of people require hip replacement within 5 years of diagnosis

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8
Q

What is the prognosis of knee osteoarthritis?

A
  • Knee involvement has a variable prognosis
  • Some people improve spontaneously
  • Some remain stable and some have progressively worsening symptoms and structural changes on x-ray which eventually require joint surgery
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9
Q

When should a diagnosis of osteoarthritis be suspected?

A
  • Suspect osteoarthritis if alternative conditions have been excluded and a person is 45 years or more with suggestive clinical features
  • Typical features include:
  • History:
  • Activity related joint pain - typically only one or a few joints are affected at a time, pain develops over months or years
  • No morning joint related stiffness
  • Functional impairment - hand may affect grip and pinch strength, knee and hip may cause difficulty walking
  • Examination:
  • Bony swelling and joint deformity
  • Joint effusions (uncommon except the knee)
  • Joint warmth and/or tenderness (may be synovitis)
  • Muscle wasting and weakness
  • Restricted and painful range of joint movement, crepitus (grating sound or sensation produced by friction between bone and cartilage)
  • Joint instability
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10
Q

How does osteoarthritis of the hand present?

A

Typically affects the first carpometacarpal (CMC) joint at the base of the thumb, distal interphalangeal (DIP) joint, and the proximal interphalangeal (PIP) joint

  • Pain can radiate distally towards the thumb or proximally to the wrist and distal forearm, and is often exacerbated by pinching actions or strong grip.
  • There may be wasting of the thenar muscles at the base of the thumb.
  • The CMC joint may develop a fixed flexion deformity, with hyperextension of the distal joints.
  • In advanced disease, there may be ‘squaring’ at the joint caused by subluxation (partial dislocation), formation of osteophytes, and remodelling of the bones.
  • Initially, there may be features of inflammation such as pain, warmth, redness, and swelling of affected DIP and PIP joints.
  • As disease progresses, there may be ulnar or radial deviation at affected joints

May have associated features such as:

  • Mucoid cysts (painful mucus-filled cysts) adjacent to the joint on the dorsum of the finger, which may cause longitudinal ridging of the nail.
  • Heberden’s and Bouchard’s nodes (bony nodules on the dorsum of the finger next to the DIP and PIP joints, respectively).
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11
Q

How does osteoarthritis of the hip present?

A

May present with:

  • Deep pain in the anterior groin on walking or climbing stairs, with possible referred pain to the lateral thigh and buttock, anterior thigh, knee, and ankle.
  • Pain which may occur at rest and may disturb sleep.
  • Painful restriction of internal rotation with the hip flexed.
  • An antalgic gait — a lurch towards the affected hip with less time spent weight-bearing on that side; the pelvis is held normally.

In advanced disease, there may be:

  • A Trendelenburg gait — a lurch towards the affected hip with less time spent weight-bearing on that side and the pelvis tilting down on the unaffected side, caused by wasting and weakness of the gluteal and anterior thigh muscles
  • A fixed flexion external rotation deformity, with compensatory increased lumbar lordosis and pelvic tilt. The lower limb can be significantly shortened.
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12
Q

How does osteoarthritis of the knee present?

A

Osteoarthritis of the knee:

  • Typically is bilateral and symmetrical, affecting the medial tibiofemoral, lateral tibiofemoral, or patellofemoral compartments, with pain localized to the affected compartment.
  • Unilateral osteoarthritis of the knee is usually secondary to predisposing trauma or disease.
  • Medial tibiofemoral involvement causes anteromedial pain, mainly on walking.
  • Lateral tibiofemoral involvement causes anterolateral pain, mainly on walking.
  • Patellofemoral involvement causes anterior knee pain worsened on inclines or stairs, particularly when going down; and progressive aching on prolonged sitting that is relieved by standing.
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13
Q

What are the associated features of OA of the knee?

A

May have associated features including:

  • Giving way — due to altered patella tracking, weak quadriceps muscles, severe patellofemoral involvement, and altered load-bearing mechanics. Note: weakness of the quadriceps is suggested if passive extension of the knee joint is greater than active extension.
  • Locking (inability to straighten the knee) — suggests loose meniscal cartilage in the joint.
  • Crepitus and tenderness along the joint line or with pressure on the patella.
  • Restricted flexion and extension.
  • Small-to-moderate effusions.
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14
Q

What are the features of OA of the knee in advanced disease?

A

In advanced disease, there may be:

  • Bony swelling of the femoral condyles and lateral tibial plateau.
  • Varus (bow-legged), or less commonly valgus (knock-knee), deformity.
  • An antalgic gait.
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15
Q

What are the typical radiological features of osteoarthritis?

A
  • Subchondral bone thickening and/or cysts; osteophyte formation (new bone formation at joint margins; loss or narrowing of the joint space (provides an estimate of the severity of cartilage damage)
  • Structural changes on x-ray may not correlate with reported symptoms and functional impairment
  • LOSS
  • Loss if joint space
  • Osteophytes
  • Subchondral sclerosis
  • Subchondral cysts
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16
Q

How should a person with osteoarthritis be initially managed in primary care setting?

A
  • In the presence of a diagnosis offer an individualised management plan based on the person’s expectations and goals:
  • Provide information - Arthritis Research UK
  • Advise on self care
  • Loose weight
  • Muscle strengthening
  • TENS
  • Simple analgesia - paracetamol and NSAIDs
  • Arrange regular review
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17
Q

If initial self management and/or drug treatments are ineffective or not tolerated, who can the person with osteoarthritis be referred to?

A
  • Physiotherapist
  • Occupational therapist
  • Podiatrist
  • Orthopaedic surgeon
  • Pain clinic
  • Psychology or mental health services
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18
Q

What are the surgical options for osteoarthritis?

A
  • Hips
  • Cemented hip replacement - metal femoral component is cemented into the femoral shaft, this is accompanied by a cemented acetabular polyethylene cup
  • Uncemented hip replacements are becoming increasingly popular, particularly in younger more active patients - they are more expensive than conventional hip replacements
  • Hip resurfacing is sometimes used where a metal cap is attached over the femoral head - often this is used in younger patients and has the advantage that the femoral neck is preserved which may be useful of conventional arthroplasty is needed later in life
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19
Q

How is recovery from arthroplasty for osteoarthritis managed?

A
  • Physiotherapy and a course of home exercises

* Walking sticks or crutches are usually used for up to 6 weeks after hip or knee replacement surgery

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20
Q

What is the advice to patients who have had hip replacement operation for osteoarthritis?

A
  • Advise to minimise the risk of dislocation
  • Avoid flexing the hip >90 degrees
  • Avoid low chairs
  • Do not cross legs
  • Sleep on back for the first 6 weeks
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21
Q

What are the complications associated with arthroplasty?

A
  • Wound and joint infection
  • Thromboembolism: NICE recommend patients receive 4 weeks LMWH following hip replacement
  • Dislocation
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22
Q

What is RA?

A
  • A chronic systemic inflammatory disease

* Early RA is defined as disease duration of 5 years or less from the onset of symptoms

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23
Q

How does RA present?

A
  • As inflammatory arthritis typically affecting the small joints of the hands and the feet and both sides equally and symetrically, any synovial joint can be affected
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24
Q

How common is RA?

A
  • Prevalence in the UK of RA is 1% - most common inflammatory arthritis
  • Peak onset is 30-50 years
  • 2-4 times more common in women than men
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25
Q

What are the possible complications of RA?

A
  • Amyloidosis
  • Anaemia
  • Dry eye syndrome (keratoconjunctivitis sicca), peripheral ulcerative keratitis
  • Felty’s syndrome - enlarged spleen and low WCC - affects less than 1% with RA
  • Fatigue
  • Increased mortality
  • Interstitial lung disease
  • Neuropathy
  • Orthopaedic problems including:
  • Carpal tunnel syndrome - 10-20%
  • Increased joint replacement surgery
  • Tendon rupture
  • Cervical myelopathy
  • Vasculitis, vasculitic ulcers, rheumatoid nodules
  • Weight loss
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26
Q

What are the comorbidities associated with severe RA disease?

A
  • Cardiovascular disease - Accelerated atherosclersis is the leading cause of death in RA
  • Pericarditis is present in 30-50% of people with RA but rarely leads to tamponade
  • Depression
  • Lymphomas - risk is double with RA
  • Serious infections
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27
Q

What are the complications of RA associated with drug treatment?

A
  • GI problems from NSAIDS
  • Infection - immunosuppressants and glucocorticoids
  • Liver toxicity - methotrexate related
  • Malignancy - TNF alpha inhibitor related
  • Osteoporosis - low dose dose glucocorticoid use in people with RA
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28
Q

When should a diagnosis of RA be suspected?

A
  • Persistent (lasting weeks rather than days) synovitis where no other underlying cause in obvious e.g. psoriatic arthritis
  • RA typically causes symmetrical synovitis of the small joints of the hands and feet

Clinical features include:

  • Pain - worse at rest
  • Swelling - around the joint (not bone swelling) giving a boggy feel on palpation
  • Stiffness - early morning usually lasting over 1 hour
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29
Q

When is a poorer prognosis of RA likely?

A
  • Greater number of joints affected
  • Swelling and tenderness in the affected joints
  • Proximal interphalangeal joints and metacarpophalangeal joints are affected and there is symmetry of joints affected
  • Positive metacarpophalangeal squeeze test - pain on squeezing the metacarpophalangeal or metatarsophalangeal joints together
  • Inability to make a fist or flex fingers is associated with an ability to diagnose RA from other diagnoses
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30
Q

What are the features in addition to joint synovitis that RA may present with?

A
  • Additional symptoms:
  • Rheumatoid nodules - hard, firm, swellings over extensor surfaces occur in a third of people with RA
  • Extra-articular features such as vasculitis or involvement of other body systems (eye, heart, lungs)
  • Systemic features of malaise, fatigue, fever, sweats and weight loss
  • Family history of RA

Presentation of RA is variable

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31
Q

What are the differential diagnoses for RA?

A

Other conditions that may cause synovitis such as:

  • Connective tissue disorders - SLE
  • Fibromyalgia - if numerous myofascial trigger points and somatic symptoms are present
  • Infectious arthritis - viral or bacterial
  • Osteoarthritis
  • Polyarticular gout
  • Polymyalgia rheumatica - suspect if the main symptoms are shoulder pain and stiffness
  • Psoriatic arthritis - commonly involves the small joints of the hands and feet, less often symmetrical, distal joints may be involved
  • Reactive arthritis - suspect this if a person has recently had viral or bacterial infection
  • Sarcoidosis - chest x-ray
  • Septic arthritis - suspect this if a single joint is hot and swollen and signs of fever
  • Seronegative spondyloarthritis
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32
Q

What are the necessary investigations for suspected rheumatoid arthritis?

A
  • Diagnosis is clinical - refer all people suspected of having RA for specialist assessment
  • Investigations are not necessary in primary care however will speed up the process
  • Rheumatoid factor - present in 60-70% of people with RA
  • anti-CCP if negative for RF - present in 80% of people
  • Arrange x-ray of hands and feet - help with diagnosis and determines disease severity
  • Consider the following tests to speed up the diagnostic process and act as a baseline measure prior to treatment:
  • Full blood count
  • U and E’s
  • LFT’s
  • CRP or ESR - elevated up to 40% in people with RA
  • USS or MRI
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33
Q

What is the referral requirements for a person with suspected RA (persistent synovitis with an unknown cause)?

A
  • Refer to a rheumatologist for an appointment (within 3 weeks) for specialist assessment
  • Refer urgently (within 3 working days) even with normal acute phase response, negative anti-CCP antibodies or rheumatoid factor if there are any of the following:
  • Small joints of the hand or feet are affected
  • More than one joint is affected
  • There has been delay of 3 months or longer between the onset of symptoms and the person seeking medical advice
  • Consider offering NSAID at the lowest effective dose until an rheumatology appointment is available
  • Do not prescribe a glucocorticoid in primary care before specialist assessment - it may mask clinical features
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34
Q

What drugs treatments are available in secondary care for confirmed rheumatoid arthritis?

A
  • cDMARD as monotherapy ideally within 3 months of the onset of symptoms - oral methotrexate, leflunomide or sulfasalazine
  • DMARD’s are myelosuppressive
  • Hydroxychloroquine may be used as an alternative for people with palindromic disease
  • Short term bridging treatment with glucocorticoids may be used when starting a new cDMARD to improve symptoms while waiting for it to take effect (2-3 months)
  • Additional cDMARDs can be used in combination
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35
Q

What is the role of primary care in the management of someone with confirmed rheumatoid arthritis?

A
  • Primary care is part of the MDT
  • Ensures that all adults with RA have:
  • Rapid access to specialist care for flares
  • Information about when and how to access specialist care
  • Ongoing drug monitoring
  • DAS-28 for monitoring disease activity
  • Ensuring they have achieved treatment target
  • Offered annual review to assess the following:
  • Disease activity and damage
  • Check comorbidities
  • Assess for complications such as vasculitis and disease of cervical spine, lung or eyes
  • Organise appropriate cross referral
  • Assess need for surgery
  • Assess impact on the persons life
  • Identify and manage flares
  • Offer pneumococcal and yearly influenza vaccinations
  • Improve the person’s understanding of RA
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36
Q

What is the management of a flare of RA?

A
  • Exclude septic arthritis - single hot and swollen joint especially if there are signs of sepsis
  • Suspect a flare of RA if there are worsening:
  • Symptoms of stiffness, pain, joint swelling or general fatigue
  • Signs of joint synovitis, joint tenderness or loss of joint function
  • Inflammatory markers - CRP increase from previous
  • Seek specialist advice about management, offer a short term treatment with glucocortiocids either:
  • As a joint injection - methylprednisolone acetate or triamcinolone acetonide for a localized RA flare
  • Oral if IM not practical - reducing dose over 2-4 weeks
  • 2 week course of prednisolone 10 mg daily for 7 days then 5 mg daily for 7 days then stop
  • Consider offering an NSAID
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37
Q

When is referral to a surgeon indicated in rheumatoid arthritis?

A
  • Offer to refer people with RA for an early specialist surgical opinion if any of the following do not respond to optimal non-surgical management or before damage or deformity becomes irreversible:
  • Persistent pain due to joint damage or other soft tissue cause
  • Worsening joint function
  • Progressive deformity
  • Persistent localized synovitis
  • Imminent or actual tendon rupture
  • Nerve compression
  • Stress fracture
  • Urgent referral for people at risk of suspected or proven septic arthritis
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38
Q

How should management of RA vary when considering the possibility of COVID-19?

A
  • People with RA with suspected COVID-19
  • Be aware that immunosuppressant treatments may have atypical presentations - people taking prednisolone may not develop fever and those taking interleukin-6 inhibitors may not develop a rise in CRP
  • In people with RA with suspected COVID-19, they should:
  • Continue hydroychloroquine and sulfasalazine
  • Not suddenly stop prednisolone
  • Only have corticosteroids if there is significant disease and there are no alternatives
  • Temporarily stop other disease modifying antrheumatic drugs, JAK inhibitors and therapies, contact their rheumatology department for advice on when to restart
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39
Q

What is osteoporosis?

A
  • Disease characterised by low bone mass and structural deterioration of bone tissue with a consequent increase in bone fragility and susceptibility to fracture
  • Osteoporosis itself is asymptomatic and often remains undiagnosed until a fragility fracture occurs
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40
Q

What is an osteoporotic fracture?

A
  • A fragility fracture occurring as a result of osteoporosis
  • Characteristically occurs in the wrist, spine, and hip but can occur in the arm, pelvis, ribs and other bones
  • Fragility fracture is defined as a fracture following a fall from standing height or less, although vertebral fractures may occur spontaneously, or as a result of routine activities such as bending or lifting
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41
Q

According to the World Health Organisation, what is osteoporosis?

A
  • Osteoporosis is defined by a bone mineral density of -2.5 standard deviations below the mean peak mass (average of young healthy adults) as measured by a DEXA scan applied to the femoral neck and reported as a T-score
  • > -1.0 = normal
  • -1.0 to -2.5 = osteopenia
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42
Q

What is the problem with the BMD measurement?

A
  • BMD does not assess the structural deterioration in bone and consequently most osteoporotic fractures occur in women who do not have osteoporosis as defined by a T score equal to or less than -2.5
  • Z score is adjusted according to demographics - age, gender, ethinicity
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43
Q

What are the causes of osteoporosis?

A
  • Result of an imbalance in the normal process of bone remodelling by osteoclasts and osteoblasts
  • During normal ageing, bone breakdown by osteoclasts increases and is not balanced by new bone formation by osteoblasts, resulting in a combination of:
  • Reduced bone mineral density measured by DXA scanning
  • Changes in bone composition, architecture, size and geometry
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44
Q

Which factors influence the age at which osteoporosis becomes apparent?

A
  • Peak bone mass
  • Depends on genetics, levels of nutrition (calcium and vitamin D), sex hormone levels (androgens and oestrogens) and level of physical activity - reached in the third decade and starts to decline in the fifth decade, accelerates after the menopause for women
  • Rate of bone loss
  • Depends on oestrogen deficiency in women and decreased testosterone in men and hyperparathyroidism
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45
Q

What are the complications of osteoporosis?

A
  • Fragility fractures
  • Hip fractures - can impact their independence
  • Vertebral fractures - can cause back pain, loss of height, and kyphosis
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46
Q

How common is osteoporosis?

A
  • Women are at greater risk of osteoporosis due to the decrease in oestrogen production at the menopause which accelerates bone loss
  • Around 180000 of the fractures presenting in England and Wales each year are due to osteoporosis
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47
Q

What are the risk factors for getting an osteoporotic fracture?

A
  • Depends on the persons risk of falls and their bone strength determined by BMD and other risk factors - fracture risk increases as BMD decreases
  • Risk factors affecting bone strength include:
  • Endocrine diseases - DBM, hyperthyroidism, hyperparathyroidism
  • GI conditions - Crohn’s, UC, coeliac disease and chronic pancreatitis
  • CKD
  • Chronic liver disease
  • COPD
  • Menopause
  • Immobility
  • BMI <18.5 kg/m2
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48
Q

Which factors do not reduce BMD?

A
  • Age - risk increases with age and is at least partly independent of BMD
  • Oral corticosteroids - dose dependent
  • Smoking
  • Alcohol (3 units or more daily)
  • Previous fragility fracture
  • RA
  • Parental history of hip fracture
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49
Q

What are the risk factors for falls?

A
  • Impaired vision
  • Neuromuscular weakness and incoordination
  • Cognitive impairment
  • Use of alcohol and sedative drugs
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50
Q

Which patients should be identified to assess for fragility fractures?

A
  • All women over 65 years and over and all men aged 75 years and over
  • All women aged 50-64 years and all men aged 50-74 years who have any of the following risk factors:
  • Previous osteoporotic fragility fracture
  • Corticosteroid use present or past
  • History of falls
  • BMI <18.5 kg/m2
  • Smoker
  • Alcohol intake of >14 units per week
  • Secondary cause from previously identified risk factors
  • All people younger than 50 years of age with any of the following risk factors:
  • Current or frequent use of corticosteroids
  • Untreated premature menopause
  • Previous fragility fracture
  • People younger than 40 years of age with any of the following risk factors:
  • Current or frequent use of corticosteroids high dose >7.5 mg prednisolone daily for 3 months or more
  • Previous fragility fracture of the spine, hip, forearm or proximal humerus
  • History of multiple fragility fractures
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51
Q

How should a person be assessed for fragility fracture risk?

A
  • Exlcude non-osteoporotic causes for fragility fractures
  • DEXA scan
  • Consider starting drug treatment for people with vertebral or hip fractures without undertaking DXA
  • For all other people with risk factors for osteoporosis, consider using the online risk calculators QFracture or FRAX which predict the absolute risk of hip fracture and major osteoporotic fractures (spine, wrist, hip, shoulder) over 10 years
  • Assess for vitamin D deficiency and inadequate calcium intake
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52
Q

How should a fragility fracture score be interpreted?

A
  • 10 year fracture risk of 10% is considered to be the threshold for arranging a DEXA scan in men and women
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53
Q

How is the QFracture risk score interpreted?

A

QFracture

  • High risk
  • Risk score is 10% or above
  • Intermediate risk
  • Risk score is close to but below 10%
  • Low risk
  • Risk score is below 10%
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54
Q

How is the FRAX score interpreted? (Assessment of risk of fragility fractures)

A

FRAX

  • High risk
  • Red zone of risk chart
  • Intermediate risk
  • Orange zone of risk chart
  • Low risk
  • Green zone of risk chart
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55
Q

How should high fragility risk scores be managed?

A
  • DEXA scan
  • Bone sparing drug treatment if the T score is -2.5 or less
  • If the T score is > -2.5, modify the risk factors where possible and treat any underlying conditions

(DEXA scan for those at intermediate fragility risk score, lifestyle modification for those at low risk of fragility fracture - do not offer drug treatment to these individuals)

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56
Q

What drug treatments can be prescribed to people at high risk of osteoporotic fracture?

A
  • Bisphosphonates such as alendronate 10 mg once daily or 70 mg once weekly or risedronate 5 mg once daily or 35 mg once weekly if there are no contraindications and after counselling to:
  • Post menopausal women and men over 50 with confirmed DEXA of -2.5 or less
  • If calcium intake is inadequate:
  • Prescribe 10 micrograms of vitamin D with at least 1000mg of calcium daily
  • Prescribe 20 micrograms of vitamin D with at least 1000 mg of calcium daily for elderly people who are house bound or in a nursing home
  • Consider prescribing HRT to women who have a premature menopause (before the age of 40)
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57
Q

What lifestyle advice should be given to manage the risk of osteoporotic fractures?

A
  • Take regular, tailored to the person, exercise to improve muscle strength
  • Eat a balanced diet
  • Stop smoking
  • Drink alcohol within recommended limits
  • Provide information - National Osteoporosis Society
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58
Q

How should a person at risk of osteoporotic fracture be followed up?

A
  • After bone sparing drug treatment, review the medication:
  • Ask about adverse effects of bisphosphonates such as GI dyspepsia or reflux, symptoms of atypical fracture, new onset of pains
  • Ask about adherence to treatment
  • People taking oral corticosteroids - advise to continue treatment with bisphosphonates and/or calcium and vitamin D until treatment with oral corticosteroids has stopped
  • For the remainder or people, review the need for continued treatment with bisphosphonates after 3-5 years
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59
Q

What is polymyalgia rheumatica?

A
  • A chronic, systemic rheumatic inflammatory disease characterised by aching and morning stiffness in the neck, shoulder and pelvic girdle in people older than 50 years of age
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60
Q

What causes polymyalgia rheumatica?

A
  • Unknown, although genetic and environmental factors are thought to contribute to the disease susceptibility and severity
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61
Q

What are the risk factors for developing PMR?

A
  • Older age - risk increases with age in both men and women - highest incidence is in people older than 65 years of age with peak in the 70-80 year old age group
  • Female gender
  • North European ancestry - PMR is most common this group
  • Infection - cyclic fluctuations and peaks in incidence have been observed in the winter months associated with mycoplasma, chlamydia pneumonia and paravovirus B19 infections
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62
Q

How common is PMR?

A
  • PMR is the most common inflammatory rheumatic disease in older people and one of the most common indications for long term corticosteroid treatment in the UK accounting for 22% of prescriptions
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63
Q

What are the complications of PMR?

A
  • Giant cell arteritis (GCA) and its complications can occur abruptly and without warning, early in the course of PMR
  • 15-20% of people with PMR develop GCA and 40-50% of people with GCA have symptoms of PMR
  • Complications of long term corticosteroid treatment
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64
Q

What is the prognosis of PMR?

A
  • Overall it is good - response to corticosteroids is rapid and dramatic with many symptoms resolving within 24-72 hours
  • 29-45% of people with PMR do not adequately respond to systemic corticosteroids within 3-4 weeks
  • Treatment for 1-2 years is often required
  • Relapse is common but responds to restarting or increasing the dose of corticosteroids
65
Q

When should a diagnosis of PMR be suspected?

A
  • Suspect PMR in a person over 50 years of age presenting with at least 2 weeks of the core symptoms of:
  • Bilateral shoulder and/or pelvic girdle pain - initially this may be unilateral but quickly becomes bilateral, is worse with movement and interferes with sleep
  • Shoulder pain may radiate to the elbows and is the presenting feature in 70-95% of people
  • Hip and neck pain is the presenting feature in 50-70% of people, hip pain may radiate to the knees
  • Stiffness lasting for at least 45 minutes after waking or periods of rest that may cause the person to have difficulty turning over in bed, rising from a bed or chair, or raising their arms above shoulder height
66
Q

What are the additional features of PMR that may accompany the core symptoms?

A
  • Low grade fever, fatigue, anorexia, weight loss and depression
  • Bilateral upper arm tenderness
  • Peripheral MSK signs include:
  • Carpal tunnel syndrome
  • Peripheral arthritis (knees and wrists) asymmetric and self limiting
  • Swelling with pitting oedema of hands, wrists, feet and ankles
  • Muscle strength is not usually impaired but pain may make testing difficult
67
Q

How is diagnosis of PMR made?

A
  • Identifying core features of the condition
  • Excluding conditions that mimic PMR by a positive response to oral corticosteroids
  • For a person with core symptoms of PMR who is over 50 years of age:
  • Request an ESR and/or CRP (raised inflammatory markers are supportive of a diagnosis of PMR)
  • Exclude:
  • GCA
  • Active infection or cancer
68
Q

Which tests are required before starting a patient on corticosteroids for PMR?

A
  • FBC
  • U and E’s
  • LFT’s
  • Calcium
  • ALP
  • Protein electrophoresis
  • TSH
  • Creatine kinase
  • RF
  • Urine dip
69
Q

What is the corticosteroid treatment required as a trial?

A

If PMR is the most likely diagnosis:

  • Prescribe a trial dose of oral prednisolone 15 mg daily and arrange follow up after 1 week to assess clinical response
  • After 3-4 weeks of treatment:
  • Consider reducing the dose of prednisolone
  • Recheck ESR/plasma viscosity and/or CRP to assess response to treatment
70
Q

Which atypical features of PMR should be indication for referral to a rheumatologist?

A
  • Younger than 60 years of age
  • Red flags such as weight loss, night pain or neurological features
  • Absence of core features of PMR including:
  • Bilateral shoulder or pelvic girdle aching
  • Stiffness lasting for at least 45 minutes after waking or periods of rest
  • Clinical features that are uncommon with PMR including people with:
  • Normal inflammatory markers or ESR more than 100 mm/hour or very high CRP
  • Chronic onset of symptoms
71
Q

When can a working diagnosis of PMR be made?

A
  • If there is patient reported response of global improvement of 70% or more within a week and normalisation of inflammatory markers within 4 weeks
  • If there is a lesser response, consider increasing the dose of prednisolone to 20mg and reassess the response
  • If still response is less than 70% reconsider the diagnosis and refer for specialist assessment
72
Q

Which other conditions can present similarly to PMR?

A
  • Degenerative disorders
  • Cervical and lumbar sponylosis
  • Osteoarthritis
  • Bilateral adhesive capsulitis (frozen shoulder)
  • Endocrine disorders
  • Thyroid disease
  • Parathyroid disease
  • Infection
  • Viral illness
  • Chronic osteomyelitis
  • Tuberculosis
  • Infective endocarditis
  • Inflammatory disorders
  • RA
  • Spondyloarthropathy
  • Remitting seronegative symmetric synovitis with pitting oedema (rare)
  • Polymyositis/dermatomyositis
  • SLE
  • Cancer
  • Multiple myeloma
  • Acute leukaemia
  • Lymphoma
  • Lung carcinoma
  • Drug related
  • Myalgia due to statins
  • PMR like syndrome due to quinidine
  • Others
  • Osteomalacia
  • Fibromyalgia
  • Chronic fatigue syndrome
73
Q

How should a person with PMR have their corticosteroid regime reduced ?

A

Reduce the dose of corticosteroids when the symptoms are fully controlled as follows:

  • Typically treatment is required for 1-2 years
  • For people who are well controlled on 15 mg prednisolone daily:
  • Continue 15 mg daily until symptoms are fully controlled (usually 3 weeks)
  • Reduce dose to 12.5 mg each day for 3 weeks then
  • Reduce dose to 10 mg each day for 4-6 weeks then
  • Reduce dose by 1 mg every 4-8 weeks until treatment is stopped
  • PPI cover 20 mg omeprazole
  • Ensure the person is provided with a blue steroid card and discuss potential adverse effects of corticosteroids
74
Q

In addition to the reducing regime, what other advice should be given to a person with PMR?

A
  • Advise them:
  • Not to stop taking prednisolone abruptly and to seek advice if they are experiencing problems taking it
  • Avoid close contact with people who have chickenpox, shingles or measles if they do not have immunity and seek advice if exposed
  • Provide written information about PMR (PMRGCA UK)
  • Arrange routine review once week after any change in dose and at least every 3 months in the first year following diagnosis (earlier if symptoms worsen or are not controlled)
  • Assess and manage osteoporotic fracture risk
75
Q

In addition to monitoring the effects of reducing corticosteroid treatment, what else needs to be monitored?

A
  • Blood pressure
  • Glucose

(FBC and/or U and E’s if required e.g. GI bleed or prednisolone and diuretic use)

76
Q

What is rheumatoid factor (RF)?

A
  • Circulating antibody (usually IgM) which reacts with the Fc portion of the patients own IgG
77
Q

How can RF be measured?

A
  • Rose-Waaler test: sheep red cell agglutination

* Latex agglutination test (less specific)

78
Q

How useful is RF as a marker of rheumatoid arthritis?

A
  • RF is positive in 70-80% of patients with rheumatoid arthritis, high titre levels are associated with severe progressive disease (but NOT a marker of disease activity)
79
Q

What other conditions are associated with a positive RF?

A
  • Sjorgren’s syndrome (100%)
  • Felty’s syndrome (100%)
  • Infective endocarditis (50%)
  • SLE (20-30%)
  • Systemic sclerosis (30%)
  • General population (5%)
  • Rarely: TB, HBV, EBV, leprosy
80
Q

What is the value of anti-cyclic citrullinated peptide antibody?

A
  • Anti-CCP may be detectable up to 10 years before the development of rheumatoid arthritis
  • It may therefore play a key role in the future of rheumatoid arthritis, allowing early detection of patients suitable for aggressive anti-TNF therapy
  • It has a similar sensitivity to rheumatoid factor (around 70%) with much higher specificity of 90-95%
81
Q

What is the NICE guidance regarding testing for rheumatoid arthritis?

A
  • Patients with suspected RA who are RF negative should be tested for anti-CCP antibodies
82
Q

What is gout?

A
  • A disorder of purine metabolism characterised by a raised uric acid level in the blood (hyperuricaemia) and the deposition of urate crystals in joints and other tissues such as soft connective tissues or the urinary tract
  • Monosodium urate
83
Q

What is gouty arthritis?

A
  • Due to urate crystals in joints
  • Natural history of gout can occur in 3 distinct phases:
  • Long period of asymptomatic hyperuricaemia
  • Period during which acute attacks of gouty arthritis are followed by variable intervals (months to years) when there are no symptoms
  • Final period of chronic tophaceous gout, where people have nodules affecting joints
  • Gout may present with hyperuricaemia, and hyperuricaemia may occur without gout
84
Q

What is the mechanism for the development of gout?

A
  • Uric acid is the end product of the break down of purines and exists as sodium urate at a physiological pH
  • 70% of urate is excreted by the kidneys and 30% by the GI tract
  • Hyperuricaemia is the single most important risk factor for developing gout - level of urate directly correlates with risk of disease
85
Q

What are the primary and secondary causes of hyperuricaemia?

A

Primary causes
* Hyperuricaemia is usually due to impaired renal excretion of urate, 90% of people with hyperuricaemia are under excretors of urate, about 10% are over producers of urate and some people are both under excretors and over producers of urate

Secondary causes
* Hypertension, hyperparathyroidism, Down’s syndrome, lead nephropathy, sarcoidosis, medication, chronic renal disease, volume depletion, glycogen storage diseases, lymphoproliferative/myeloproliferative disorders, carcinomatosis, polycythaemia and severe psoriasis

86
Q

What are the other lifestyle risk factors for the development of gout?

A
  • Age
  • Male gender
  • Menopause
  • Renal disease
  • Obesity
  • Metabolic syndrome
  • Dyslipidaemia
  • Drugs - diuretics
  • Trauma
  • Genetics
87
Q

Why does gout tend to affect the joints in the extremities?

A
  • Due to temperatures in the hands and feet being low enough to precipitate urate from plasma, thus tophi typically forms in the helix of the ear, fingertips, olecranon bursae and other cooler anatomical sites
88
Q

How common is gout?

A
  • Gout is the most common inflammatory arthritis and is increasing in prevalence worldwide
  • More common in men and prevalence increases with age plateauing at around 80 years of age
89
Q

What are the complications of gout?

A
  • Tophi can occur in 50% of people with untreated gout after 10 years
  • Tophi can create problems with activities of daily living, become inflammed, exude tophaceous material, or develop secondary infection and adversely impact on quality of life
  • Urinary stones are found in around 14% of people with gout
  • Gout is an independent risk factor for CKD, MI and CVD mortality
90
Q

What is the prognosis of a patient with gout?

A
  • Acute attacks are self limiting and usually completely resolve within 1-2 weeks without treatment
  • Attacks have been reported to recur in 62% of people within a year - recurrent acute episodes and the development of chronic gout lead to progressive joint damage, pain and disability
91
Q

How is a person with suspected gout assessed from their history?

A

Ask about the following:

  • Current and previous attacks:
  • Which joints involved
  • Most commonly 56-78% in the first metatarsophalangeal joint (big toe), also common in the midfoot, ankle, knee, fingers wrist and eolbow joints (usually monoarticular but can be oligoarticular or rarely polyarticular)
  • Symptoms and rapidity of onset
  • Frequency and duration of attacks
  • Previous drug interventions
  • Ability to mobilise and impact on functioning
  • Age of onset
  • Possible risk factors
  • Alcohol
  • Diet - purines e.g. red meat and seafood and high intake of fructose
  • Use of drugs that can raise urate plasms such as ACE inhibitors, beta-blockers, ciclosporin, diuretics, pyrazinamide, ritanovir, tacrolimus and lead exposure
  • Family history of gout
  • Associated co-morbidities
92
Q

What should you look for on examination of a person with suspected gout?

A
  • Arthritis - swelling, redness, warmth and pain on passive movement, typically 1st MTP although any joint can be affected
  • Lower limb joints more frequently
  • Examine all joints to assess for subtle signs in other joints
  • If septic arthritis is suspected, refer for emergency joint aspiration and culture
  • Tophi - firm, white nodules under translucent skin
  • Usually take 10 years after the first attack of gout for tophi to develop, although in atypical cases, tophaceous disease can be the initial presentation without any flares
  • Tophi over extensor joint aspects such as the elbow or knee, or achilles tendon - can occur in other areas such as the helix of the ears or dorsum of the hands or feet
  • Usually pain free but can become inflammed, infected or ulcerated or discharge white material
93
Q

According to the American College of Rheumatology criteria for the diagnosis of acute gouty arthritis, how is diagnosis made?

A
  • Gold standard is microscopy of urate crystals in synovial fluid or tophi - however testing for this is not always practical
  • Negatively birefringent, needle shaped crystals
  • Serum urate can be raised but can also be normal
94
Q

What investigations for gout should be considered?

A
  • If there are typical gout like symptoms and no suspicion of other conditions such as septic arthritis, no initial investigations are required
  • If there is doubt, the following can be considered:
  • Joint fluid microscopy and culture - presence of urate crystals or tophi in synovial fluid is diagnostic
  • Serum uric acid can be measured 4-6 weeks after an attack of gout to confirm hyperuricaemia - deposition of monosodium urate crystals occur when levels are persistently above 380 micromo/L (normal level does not exclude the diagnosis)
  • Joint x-ray - often normal, although there can be non specific soft tissue swelling and subcortical cysts may be present, advanced disease may demonstrate bone erosion
  • Screen for CVD risk factors and renal disease - if diagnosis of gout is made - assess cardiovascular risk and any concomitant renal disease
95
Q

What are the differential diagnoses for gout?

A
  • Septic arthritis
  • Bursitis, cellulitis, tenosynovitis
  • Non-urate crystal induced arthropathy such as pseudogout
  • Osteoarthritis
  • Psoriatic arthritis
  • Reactive arthritis
  • Rheumatoid arthritis
  • Haemochromatosis
  • Trauma
96
Q

What self care treatment is recommended in acute gout?

A
  • Should be treated as early as possible (as soon as the attack occurs)
  • Rest and elevate the limb
  • Avoid trauma to the affected joint
  • Keep the joint exposed and in a cool environment
  • Ice pack
  • Discuss weight loss, exercise, diet, alcohol consumption and fluid intake
97
Q

What is the pharmacological management recommended in acute gout?

A
  • NSAIDs or colchine are first line
  • Maximum dose of NSAID should be prescribed until 1-2 days after the symptoms have settled
  • PPI cover required
  • Colchine has a slower onset of action - main side effect is diarrhoea
  • Oral steroids may also be considered if the first line management is contrindicated
  • Dose of prednisolone is 15 mg/day
  • Intra-articular injection can also be used
  • If the patient is already taking allopurinol, this should be continued
98
Q

What are the radiological features of gout ?

A
  • Joint effusion is an early sign
  • Well defined ‘punched out’ erosions with sclerotic margins in a juxta-articular distribution, often with over hanging edges
  • Relative preservation of joint space until late disease
  • Eccentric erosions
  • No periarticular osteopenia (in contrast to rheumatoid arthritis)
  • Soft tissue tophi may be seen
99
Q

What are the indications for urate lowering therapy?

A
  • Urate lowering therapy is recommended to all patients after their first attack of gout
  • ULT is particularly recommended if:
  • 2 gout attacks in 12 months
  • Tophi
  • Renal disease eGFR <60
  • Uric acid renal stones
  • Prophylaxis if on cytotoxics or diuretics
  • Young age onset of primary gout
100
Q

What is the guidance regarding urate lowering therapy?

A
  • Allopurinol is first line
  • Start low dose, titrate upwards every 4 weeks until serum uric acid is below 300 micromol/L
  • Traditionally not started until 2 weeks after the attack of gout when the patient is not in pain to make the decision
  • Initial dose is 100 mg od with the dose titrated every few weeks to aim for a serum uric acid of < 300 mmol/l - lower if the patient has a reduced eGFR
  • Colchicine cover / NSAIDs should be considered when starting allopurinol
  • Febuxostat (also a xanthine oxidase inhibitor) is second line
  • Uricase (urate oxidase) can be tried for refractory cases - it is an enzyme that catalyzes the conversion of urate to the degradation product allantoin
  • Pegloticase (polyethylene glycol modified mammalian uricase) can be used for rapid urate lowering therapy in patients with persistent symptomatic and severe gout
101
Q

What is Lesch-Nyhan syndrome?

A
  • Hypoxanthine-guanine phosphoribosyl transferase (HGPRTase) deficiency
  • x-linked recessive therefore only seen in boys
  • Features include: gout, renal failure, neurological deficits, learning difficulties, self-mutilation
102
Q

What is the standard dosing of colchicine for the treatment of acute gout?

A
  • 500 micrograms 2-4 times per day until pain relief is achieved or diarrhoea/vomiting prevents
  • Do not exceed a total dose of 6 mg of colchicine
103
Q

What is pseudogout?

A
  • Form of microcrystal synovitis caused by the deposition of calcium pyrophosphate dihydrate crystals in the synovium
  • Positively birefringent rhomboid calcium pyrophosphafe crystals
104
Q

What are the risk factors for pseudogout?

A
  • Haemochromatosis
  • Hyperparathyroidism
  • Acromegaly
  • Low magnesium, low phosphate
  • Wilsons disease
105
Q

What are the clinical features of pseudogout?

A
  • Knee, wrist and shoulders most commonly affected
  • Joint aspiration - weakly positively birefringent rhomboid shaped crystals
  • X-ray - chondrocalcinosis
  • Can be seen as liner calcifications of the meniscus and articular cartilage
106
Q

What is the management of pseudogout?

A
  • Aspiration of joint fluid for exclusion of septic arthritis
  • NSAIDs or intra-articular, IM or oral steroids as for gout
107
Q

What is vasculitis?

A
  • Group of conditions characterised by inflammation of the blood vessel walls
  • Can lead to compromised vessel integrity
108
Q

What types of vasculitis affect the aorta and its branches?

A
  • Takayasu’s artertitis
  • Buerger’s disease
  • Giant cell arteritis
109
Q

What types of vasculitis affect the large and medium sized arteries?

A
  • Buerger’s disease
  • Giant cell arteritis
  • Polyarteritis nodosa
110
Q

What types of vasculitis affect the medium sized muscular arteries?

A
  • Polyarteritis nodosa

* Wegener’s granulomatosis

111
Q

What types of vasculitis affect the small muscular arteries?

A
  • Wegener’s granulomatosis

* Rheumatoid vasculitis

112
Q

What are the features of Takayasu’s arteritis?

A
  • Inflammatory, obliterative arteritis affecting the aorta and branches
  • M>F
  • Can present with upper limb claudication
  • Diminished or absent pulses
  • ESR affected during the acute phase
113
Q

What are the features of Buerger’s disease?

A
  • Segmental thrombotic occlusions of the small and medium sized lower limb vessels
  • Commonest in young male smokers
  • Proximal pulses usually present, but pedal pulses are lost
  • Acute hypercellular occlusive thrombus is often present
  • Tortuous corkscrew shaped collateral vessels may be seen on angiography
114
Q

What are the clinical features of Giant cell arteritis?

A
  • Systemic granulomatous arteritis that usually affects large and medium sized vessels
  • F>M
  • Temporal arteritis is the commonest type
  • Granulomatous lesions may be seen on biopsy (50% are normal)
115
Q

What is the presentation of polyarteritis nodosa?

A
  • Systemic necrotising vasculitis affecting small and medium sized muscular arteries
  • Most common in populations with high prevalence of hepatitis B
  • Renal disease is seen in 70% of cases
  • Angiography may show saccular or fusiform aneurysms and arterial stenoses
116
Q

What is the clinical presentation of Wegener’s granulomatosis?

A
  • Mainly affects small and medium sized arteries
  • Systemic necrotising granulomatous vasculitis
  • Cutaneous vascular lesions may be seen (ulceration, nodules and purpura)
  • Sinus imaging may show mucosal thickening and air fluid levels
117
Q

What is the main advice to a patient with Buerger’s disease?

A
  • Stop smoking - markedly improves the disease
118
Q

What are most vaculitides treated with?

A
  • Immunosuppressants
119
Q

How is lower back pain defined?

A
  • Pain in the lumbo-sacral area of the back between the bottom of the ribs and the top of the legs
120
Q

What are the specific causes of low back pain?

A
  • Sciatica
  • Vertebral fracture
  • Intra-abdominal pathologies
  • Ankylosing spondylitis (rare)
  • Cancer
  • Infection
121
Q

What are the non-specific causes of low back pain?

A
  • Not attributed to a specific cause

* Trauma or musculo-ligamentous strain in many cases

122
Q

How common is low back pain?

A
  • 20% of people each year consult their GP about it
  • 3-4% of young adults <45yrs are chronically disabled by low back pain
  • 5-7% of older adults >45yrs are chronically disabled due to lower back pain
123
Q

What are the risk factors for the development of non-specific low back pain?

A
  • Obesity
  • Physical inactivity
  • Occupational factors (heavy lifting)
  • Depression and other psychological conditions
124
Q

What is the prognosis of low back pain?

A
  • Most resolve within 4 weeks
  • People at higher risk of long term pain and functional disability include those with:
  • Pain longer than 12 weeks
  • Psychosocial distress
  • Maladaptive coping strategies such as avoidance of work, movement or other activities
  • Pain coping characterised by excessively negative thoughts
125
Q

What are the complications of low back pain?

A
  • Development of chronicity and depression

* Time off work, reduced productivity and loss of employment

126
Q

How should the history and examination be taken from the patient about back pain?

A
  • SOCRATES pain
  • Observe gait, posture, skin and any bruising, skin changes, rashes, deformity or swelling of the back
  • Perform a neurological examination looking for loss of sensation, changes to reflexes, limitation or range of movement including straight leg raising, tenderness and fever and loss of anal tone
127
Q

What are the red flags to rule out in the assessment of back pain?

A
  • Cauda equina syndrome
  • Cancer of the spine
  • Spinal fracture due to trauma or osteoporotic collapse
  • Spinal infection
128
Q

What are the other causes of lower back pain to keep in mind when assessing a patient?

A
  • GI
  • GU
  • Ankylosing spondylitis (particularly if they are under 40 years old)
  • Pain at night not relieved when supine
  • Stiffness in the morning relieved with movement/exercise
  • Gradual onset of symptoms
  • Osteoporosis - non-specific pain or a vertebral fracture
  • Shingles - unilateral pain and dermatomal rash distribution
  • Sciatica if the pain radiates below the knee to the foot or toes
  • Suspect non-specific lower back pain if the person’s pain varies with posture and time
129
Q

What is the general management for a person with low back pain?

A
  • If red flag symptoms - admit or refer urgently
  • If an underlying cause has been identified manage according to the specific diagnosis
  • If non-specific low back pain is suspected assess the person using a risk stratification tool such as the STarTBack to identify modifiable risk factors
  • Offer self management advice
  • Offer analgesia to manage pain - NSAID’s, if spasm consider a short course of benzodiazepines such as 2 mg x 3 per day for up to 5 days
  • Advise the person to seek follow up if symptoms persist or are worsening after 3-4 weeks
130
Q

What is the management for lower back pain for people who are assessed at higher risk of a poor outcome?

A
  • Offer referral to a group exercise programme
  • Consider offering referral to a physiotherapist for manual therapy
  • Promote and facilitate return to work or normal ADL’s
131
Q

What is the STarT Back Screening Tool?

A
  • Simple prognostic questionnaire to identify modifiable risk factors (biomedical, psychological and social) for back pain disability
  • Stratifies patients into low, medium or high risk categories
  • Each category has a matched treatment package
  • Has been shown to reduce back pain related disability and be cost effective
132
Q

What is the self management advice to people with low back pain?

A
  • Address any specific concerns the person has about the cause of their pain and their expectations of treatment
  • Provide information on self-help measures to relieve symptoms
  • Encourage the person to stay active, resume normal activities, and return to work as soon as possible
  • Prolonged bed rest is not recommended
  • Person does not need to be pain free before returning to normal activities or work
133
Q

How is sciatica different from low back pain (without radiculopathy)?

A
  • Sciatica is the term for symptoms of pain, tingling, and numbness which arise from nerve root compression or irritation in the lumbosacral spine.
  • Symptoms of sciatica typically extend to below the knee — from the buttocks, across the back of the thigh, to the outer calf, and often to the foot and toes
134
Q

What are the potential causes of sciatica?

A
  • A herniated intervertebral disc — in about 90% of cases.
  • Spondylolisthesis.
  • Spinal stenosis
135
Q

What is ankylosing spondylitis?

A
  • (Radiographic axial spondyloarthritis) is axial spondyloarthritis characterised by sacroiliitis on x-ray
  • Can occur in the absence of x-ray changes and this is classified as non-radiographic axial spondyloarthritis (although changes may be visible on MRI)
136
Q

What are the presenting features of ankylosing spondylitis?

A
  • Chronic back pain (often inflammatory in nature) and stiffness that improves with exercise, not rest
  • Sacroiliac joint and spinal fusion
  • New bone formation leads to sacroiliac joint ankylosis and the formation of syndesmophytes (bone growths in intervertebral joint ligaments) in the spine
  • Arthritis and enthesitis - most common peripheral manifestations (predominently in the lower limbs with asymmetrical distribution)
  • Dactylitis (swelling of a finger or toe)
  • Fatigue
  • Extra-articular manifestations (for examples anterior uveitis, psoriasis, inflammatory bowel disease
137
Q

What causes ankylosing spondylitis?

A
  • More than 90% heritability has been estimated for axial spondylitis
  • Most important genetic risk factor is HLA B27 which usually reflects the prevalence of axial spondyloarthritis within a population but varies considerably between different populations
138
Q

How common is ankylosing spondylitis?

A
  • Prevalence of 0.05% to 0.23%
  • M>F 2:1
  • Most commonly begins between 20 and 30 years of age, with 90-95% of people aged less than 45 years at disease onset
139
Q

What are the extra-articular associations of ankylosing spondylitis?

A
  • Uveitis
  • Psoriasis
  • Inflammatory bowel disease
140
Q

What are the complications of axial spondyloarthritis?

A
  • Ankylosis or spinal fusion
  • Spinal fractures
  • Hip involvement
  • Anterior uveitis (iritis)
  • Osteoporosis
  • Cardiac complications
  • Lung involvement
  • Neurological involvement
  • Adverse effects from drugs - NSAIDS and DMARDS
  • Decreased quality of life and work productivity
141
Q

What is the prognosis of ankylosing spondylitis?

A
  • Variable - damage is progressive and irreversible
  • Axial spondyloarthritis is often characterised by persistent or fluctuating axial inflammation (on MRI) and structural progression (on x-ray). Both the inflammation and new bone formation (if inflammation is ongoing) affect quality of life due to pain, reduction in mobility and function
  • Prognosis of ankylosing spondylitis also depends on the presence of extraspinal manifestations (for example uveitis, psoriasis, inflammatory bowel disease), the person’s age at diagnosis, and the choice of treatment
142
Q

How can a working diagnosis of ankylosing spondylitis be made?

A

Suspected ankylosing spondylitis in anyone with chronic or recurrent low back pain, fatigue, stiffness especially if:

  • Person is 45 years of age or younger
  • Back pain present for more than 3 months
  • Back pain and stiffness is inflammatory (rather than mechanical) and worse in the morning (lasting for more than 30 minutes) improving with movement
  • Current or previous:
  • Buttock pain - uni lateral, may change sides
  • Pain in the thoracic or cervical spine
  • Arthritis
  • Enthesitis (inflammation of the entheses, the sites where tendons or ligaments insert into the bone)
  • Anterior uveitis
  • Psoriasis or IBD or UTI
  • Waking up at night due to symptoms
  • Symptoms respond to a course of NSAIDS within 48 hours
  • Family history of ankylosing spondylitis
143
Q

What are the diagnostic criteria used by rheumatology for ankylosing spondylitis?

A
  • Modified New York criteria
  • ASAS classification criteria (for people with back pain for 3 months or longer who were < 45 years old at the onset of the back pain)
144
Q

What is the modified New York criteria for AS?

A
  • Clinical criteria:
  • Low back pain; present for more than 3 months; improved by exercise but not relieved by rest. Limitation of lumbar spine motion in both the sagittal and frontal planes. Limitation of chest expansion relative to normal values for age and sex.
  • Radiological criteria : sacroiliitis on x-ray
  • Definite ankylosing spondylitis if the radiological criterion is present plus at least one clinical criterion. Probable ankylosing spondylitis if three clinical criteria are present alone, or if the radiological criterion is present but no clinical criteria are present.
145
Q

What is the ASAS classification criteria of AS (for people with back pain for 3 months or longer who were < 45 years old at onset of back pain)?

A
  • Sacroilitis on imaging plus 1 or more spondyloarthritis features

or

  • HLA-B27 plus 2 or more other spondyloarthritis features
146
Q

What investigations can be done when considering a diagnosis of AS?

A
  • ESR and/or CRP - should not be ruled out if normal
  • X-rays - AS is suggested by x-ray changes of the sacroiliac joints and spine including sacroiliitis, sclerosis (thickening of bone) erosions and partial or total ankylosis (fusion of joints)
  • MRI - in some people inflammation of the sacroiliac joints can be detected on MRI despite an absence of changes on x-ray
  • More sensitive for early disease
  • HLA-B27 - only if a person has 3 referral criteria
147
Q

When should a person with suspected AS be referred to rheumatology?

A
  • Refer to rheumatology if a person has low back pain starting before the age of 45 years and lasting longer than 3 months, plus 4 or more of the following criteria:
  • Low back pain starting before the age of 35 years.
  • Symptoms which wake them during the second half of the night.
  • Buttock pain.
  • Improvement when moving.
  • Improvement within 48 hours of taking a nonsteroidal anti-inflammatory drug (NSAID).
  • Spondyloarthritis in a first-degree relative.
  • Current or past arthritis.
  • Current or past enthesitis.
  • Current or past psoriasis
  • If exactly 3 of the additional criteria are present, perform an HLA-B27 test. If the test is positive, refer the person to a rheumatologist for a spondyloarthritis assessment
  • Refer same day to ophthalmology if anterior uveitis is suspected
148
Q

When should anterior uveitis be suspected?

A
  • Suspect acute anterior uveitis when an eye becomes red and acutely painful especially if there is also photophobia or blurred vision
149
Q

What are the differential diagnoses for AS?

A
  • Degenerative or mechanical problems (most common) — for example degenerative disc disease, spondylosis, congenital vertebral anomalies, degenerative changes in the intevertebral (facet) joints, osteoarthritis of sacroiliac joints.
  • Fractures.
  • Infectious sacroiiitis.
  • Bone metastasis.
  • Primary bone tumours.
  • Spinal stenosis.
  • Hypermobility
150
Q

What treatment can be given to a patient with suspected AS while waiting for referral?

A
  • NSAID - lowest effective dose
151
Q

What is the ongoing management for AS?

A
  • Encourage regular exercise such as swimming
  • NSAID are first line treatment
  • Physiotherapy
  • DMARD’s are used to treat RA (such as sulphasalazine) but only really useful if there is peripheral joint involvement
  • EULAR guidelines suggest - Anti-TNF therapy should be given to patients with persistently high disease activity despite conventional treatments
152
Q

What are the features seen on x-ray for a patient with AS?

A
  • Sacroiliitis: subchondral erosions, sclerosis
  • Squaring of lumbar vertebrae
  • ‘bamboo spine’ (late & uncommon)
  • Syndesmophytes: due to ossification of outer fibers of annulus fibrosus
  • Chest x-ray: apical fibrosis
153
Q

What is reactive arthritis?

A
  • Defined as an arthritis that develops following an infection where the organism cannot be recovered from the joint.
154
Q

What is associated with reactive arthritis?

A
  • HLA-B27
  • Reiter’s syndrome
  • Triad of urethritis, conjunctivitis and arthritis
  • Post dysenteric
  • Post STI - sexually acquired reactive arthritis SARA
155
Q

Which organisms are commonly associated with post-dysenteric form of reactive arthritis?

A
  • Shigella flexneri
  • Salmonella typhimurium
  • Salmonella enteritidis
  • Yersinia enterocolitica
  • Campylobacter
156
Q

Which organisms are commonly associated with post STI reactive arthritis?

A
  • Chlamydia trachomatis
157
Q

What is the approach the management of reactive arthritis?

A
  • Symptomatic: analgesia, NSAIDS, intra-articular steroids
  • Sulfasalazine and methotrexate are sometimes used for persistent disease
  • Symptoms rarely last more than 12 months
158
Q

What are the clinical features of reactive arthritis?

A
  • Typically develops within 4 weeks of initial infection - symptoms generally last around 4-6 months
  • Arthritis is typically an asymmetrical oligoarthritis of lower limbs
  • Dactylitis
  • Symptoms of urethritis
  • Eye: conjunctivitis (seen in 10-30%), anterior uveitis
  • Skin: circinate balanitis (painless vesicles on the coronal margin of the prepuce), keratoderma blenorrhagica (waxy yellow/brown papules on palms and soles)