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Medicine Year 3 > Week 11 - Orthopaedics/Rheumatology > Flashcards

Week 11 - Orthopaedics/Rheumatology Flashcards

1
Q

What is rheumatoid arthritis? What are the complications of untreated RA?

A
  • Autoimmune disease
  • Results in chronic inflammation
  • If untreated
    • Joint destruction
    • Deformity
    • Loss of function
    • Extra-articular complications
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2
Q

Describe the pathophysiology of RA

A
  • Genetic predisposition? - HLA DR4 plus environmental precipitant (viral insult, bacteria, smoking?)
    • Smokers more likely to develop RA and respond less well to treatment
  • T and B cells involved, dendritic cells in circulation
  • Extended inflammatory response - cytokines amplify
  • Tissue damage
  • Synovitis
    • Synovium infiltrated with activated macrophages (stain red) with T cells and plasma cells (make rheumatoid factor)
    • Inflamed synovial tissue produces destructive enzymes (collagenases) and cytokines (interleukins, tumour necrosis factor etc.) made by macrophages in the lining layer
    • Site of damage to the joint is the junction between cartilage, overlaid with inflamed synovium = pannus, macrophages here erode through the cartilage into the underlying bone
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3
Q

Describe the epidemiology of RA

A
  • Around 690,000 people in the UK are living with RA (approx. 1% of the population)
  • 31,000 new cases every year
  • Female preponderance (3:1) - as with most autoimmune conditions
  • Age of onset usually between 30 & 60 but can affect anyone at any age
  • Disease is more aggressive in African American and Hispanic populations - Caucasians have less aggressive form
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4
Q

List the symptoms of RA

A
  • Pain
  • Stiffness
    • Early morning stiffness - feature of RA and osteoarthritis, RA lasts for at least an hour
    • Joint gelling - joints stiffen up when stop moving
  • Swelling - discreate swelling of individual joints
  • Small joint > large joint
  • Symmetrical
  • Persistent (>6 weeks)
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5
Q

List the signs of RA

A
  • Synovitis - joints feel spongey/boggy (rather than bony)
  • Hand deformity
    • Swan neck - DIP flexed, PIP hyperextended
    • Boutonniere (button hook) - DIP hyperextended, PIP flexed
    • Z-thumb
    • Ulnar deviation - fingers drift, chronic inflammation of MCP joint
  • Other relevant joint deformities
    • Loss of extension at the elbow
    • Damage to glenohumeral joint, in the shoulder
    • Atlanto-axial subluxation in the cervical spine causing pressure on spinal cord
    • Femoral head moves medially into weakened bone around acetabulum (protusio)
    • Foot - clawing of toes, dorsal dislocation of MTP joints
  • Rheumatoid nodules - extensors, fingers, in lung tissue
    • Found in 30-40%, only in seropositive patients
    • Indicate a more severe disease, often in association with other extra-articular features
    • If biopsied show macrophage giant cells and T cells surrounding an area of necrosis - local reaction to underlying vasculitis
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6
Q

What is the differential diagnosis for RA?

A
  • Polyarticular gout - acute onset (<24 hours), very painful
  • Psoriatic arthritis - 90% have psoriasis or have a first degree relative with psoriasis, DIP joints involved in psoriatic arthritis not RA (often also have nail disease)
  • Osteoarthritis - flares around menopause can be mistaken for RA, usually no synovitis (sometimes when joint healing, puffy/red)
  • SLE - presents as arthralgia more than arthritis, pain not inflammation
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7
Q

What investigations should be done in the diagnosis of RA?

A
  • Laboratory
    • Non-specific
      • CRP/ESR - acute phase response
      • FBC
        • Often anaemic in profound inflammatory response, unable to utilise iron
        • Thrombocytosis - high platelet count
        • Occasionally eosinophilia and lymphopaenia
      • Bone/urate - hypercalcaemia predisposes to pseudogout
      • Abnormal LFTs - alkaline phosphates and GGT commonly raised
    • Specific
      • Immunology - specialist
  • Imaging
    • Plain radiograph
    • Ultrasound
    • MRI
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8
Q

Describe the use of rheumatoid factor and CCP Ab in the diagnosis of RA

A
  • Rheumatoid factor
    • IgM antibody
    • Directed against Fc portion of IgG Ab
    • Found in
      • RA
      • SLE
      • Sjogren’s - often high
      • PBC
      • Hepatitis B and C
      • Bacterial endocarditis
      • Increasing age
    • Sensitivity around 70%
    • Specificity 80-85%
    • Positive in 100% of extra-articular manifestations
  • CCP Ab
    • Inflammation leads to cellular damage
    • Enzymatic process leads to the conversion of arginine residues to citrulline
    • Alteration of shape creates a foreign antigen from self - anti-citrullinated cyclic peptide antibodies
    • Sensitivity 66%
    • Specificity 90%
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9
Q

Describe the classification criteria for RA

A

EULAR 2010 classification criteria for RA

  • Joint involvement (tender/swollen)
    • 1 large joint - 0 points
    • 2-10 large joints - 1 point
    • 1-3 small joints (with or without large joints) - 2 points
    • 4-10 small joints (with or without large joints) - 3 points
    • >10 joints (at least one small joint) - 5 points
  • Serology
    • Negative RF/ACPA - 0 points
    • Low-positive RF/low-positive ACPA - 2 points
    • High-positive RF/high-positive ACPA - 3 points
  • Acute phase reactants
    • Normal CRP & ESR - 0 points
    • Abnormal CRP/ESR - 1 point
  • Duration of symptoms
    • <6 weeks - 0 points
    • >6 weeks - 1 point

Utilised in patients with at least one clinically synovitic joint, where the synovitis is not better explained by another disease.

A score of 6 or more would fulfil the classification criteria for RA

Don’t have to present with all at once - can be at different times

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10
Q

What is seen on X-ray in RA?

A
  • Early RA - X-rays likely to be normal
  • First changes
    • Peri-articular osteopaenia
    • Soft tissue swelling
  • Late changes
    • Erosion
    • Joint destruction
    • Subluxation (including A-A)
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11
Q

Is back pain seen in RA?

A

Not usually back pain but cervical vertebral destruction can occur - atlanto-axial joint instability (spinal cord at risk)

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12
Q

How can ultrasound be used in diagnosis of RA?

A
  • Diagnosis mostly clinical - history and examination
  • Potential to miss patients with subclinical disease - small joint ultrasound (offered to those with query of diagnosis/control of disease)
  • Can visualise thickness of synovium, extent of erosion, doppler for blood flow (synovitic joints have more blood supply)
  • MRI where ultrasound not as easily available or joints hard to ultrasound
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13
Q

What are the aims of treatment in RA?

A

Reduce inflammation

Maintain joint function

Prevent progression

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14
Q

What initial therapy is used in RA?

A

Reduce inflammation

  • NSAIDs - ibuprofen, naproxen, diclofenac
  • COX2 inhibitors e.g. Etoricoxib
    • Contraindicated in renal impairment and anti-coagulation
    • Unattractive in elderly patients and those with CV risk
  • Steroids
    • Oral e.g. prednisolone
    • Intramuscular - Depomedrone (methylprednisolone) or Kenalog (triamcinolone acetonide)
    • Intra-articular - Depomedrone or Kenalog
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15
Q

What is the first line treatment for RA?

A

Patients should be offered cDMARDs (conventional) first line and within 3 months of symptom onset

  • Methotrexate
  • Leflunomide
  • Sulfasalazine
  • Hydroxychloroquine if mild or palindromic disease
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16
Q

What tool is used for disease monitoring in RA?

A
  • Disease activity score - DAS28
    • >5.1 highly active
    • <3.2 low disease activity
    • <2.6 remission
  • Calculation - composite measure of swollen joints (28 joint count), tender joints, ESR and patient visual analogue score
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17
Q

Describe the use of bDMARDs in RA

A
  • Biologic DMARDs - target interleukins involved in pathophysiology of RA
  • Screening:
    • Viral hepatitis and HIV (including anti-core Ab)
    • Varicella
    • CXR and IGRA (TB) - how well treated? Latent TB destabilised by bDMARDs
    • Vaccination - influenza, pneumococcal
  • Contraindications
    • Active infection
    • Active or latent TB
    • Pregnancy - mostly safe until 2nd trimester
    • Malignancy
    • Diverticular disease (IL-6) - abscesses
  • Monitoring
    • Infections
    • Malignancy - risk of lymphoma, non-melanoma skin cancers
    • Bloods (FBC, LFTs)
    • Awareness with vaccination
  • Administration
    • IV - infliximab
    • Pens to inject subcutaneously at home
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18
Q

Who is involved in the MDT for RA?

A
  • OT
    • Activities of daily living
    • Grip strength
    • Splinting
    • Work assessment
  • Physio therapist
    • Joint protection
    • Injection
    • Exercises (ROM)
  • Nurses
    • Disease assessment
    • Monitoring
    • Helpline
  • Podiatry
    • Foot protection
    • Orthoses
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19
Q

Define compartment syndrome

A
  • Elevated interstitial pressure within a closed fascial compartment resulting in microvascular compromise
    • Increase in content/external pressure in a non-elastic closed compartment - raised pressure within the compartment
    • Blood flow compromised - ischaemia and cell death
  • Common sites - leg, forearm, thigh
    • Often when under influence of drugs/alcohol - lie on floor for long periods of time, buttocks affected
  • Orthopaedic emergency
    • Loss of function, limb or life (renal failure)
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20
Q

What causes compartment syndrome?

A
  • Increased internal pressure
    • Trauma - fracture, entrapment (bleeding)
    • Muscle oedema/myositis
    • Intercompartmental administration of fluids/drugs
    • Re-perfusion - vascular surgery
  • External compression
    • Impaired consciousness/protective reflexes
      • Drug/alcohol misuse
      • Iatrogenic - general anaesthetic (need padded operating table, no extremities on hard surfaces, pumps around limbs)
    • Positioning in theatre - lithotomy position used for gynaecological/urological surgery can cause compression of calves
    • Full thickness burns
  • Combination of several factors
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21
Q

Describe the pathophysiology of compartment syndrome

A
  • Pressure within the compartment exceeds pressure within the capillaries - reduced blood flow
  • Muscles become ischaemic and develop oedema through increased endothelial permeability (vicious cycle)
  • Autoregulatory mechanisms overwhelmed (relax smooth muscles, arteries vasoconstrict)
  • Necrosis begins in the ischaemic muscles after 4 hours, damaged muscles release myoglobin
  • Ischaemic nerves become neuropraxic, this may recover if relieved early, permanent damage may result after as little as 4 hours
  • Irreversible damage - loss of function, limb or life
  • Compromise of the arterial supply - late

Increased pressure –> reduced local blood flow

LBF = (Pa-Pv)/R, local blood flow = (arterial pressure - venous pressure)/resistance

Reduced tissue perfusion

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22
Q

How does an expansile compartment react to changes in compartment content/pressure vs a non-expansile compartment?

A
  • Expansile compartment
    • Increased compartment content
    • Temporary rise in pressure
    • Compartment expands and pressure stabilises
  • Non-expansile compartment
    • External compression
      • Pressure increases
      • Venous flow reduced, but arterial inflow continues
      • Pressure increases
    • Increased compartment contents
      • E.g. bleeding into compartment
      • Pressure increases
      • Venous flow reduced, but arterial inflow continues
      • Pressure increases
      • Ischaemia and permanent damage result
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23
Q

Describe the vicious cycle which occurs in the pathophysiology of compartment syndrome

A
  • Increased compartment pressure
  • Reduced venous outflow
  • Reduced blood flow
  • Ischaemia
  • Muscle swelling
  • Increased permeability
  • Increased compartment pressure
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24
Q

Describe the effects of ischaemia with time in compartment syndrome

A

1 hour

  • Nerve conduction normal, muscle viable

4 hours

  • Neuropraxia in nerves - reversible
  • Reversible muscle ischaemia

8 hours

  • Nerve axonotmesis and irreversible change
  • Irreversible muscle ischaemia and necrosis

Recognise and treat as soon as possible

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25
Q

What are the end-stage limb changes seen in compartment syndrome?

A
  • Stiff fibrotic muscle compartments
  • Impaired nerve function
  • Clawing of limbs
    • Clawed wrist and fingers - flexor compartment stronger than extensor
    • Calf muscle strongest in lower leg - permanent pointed foot
  • Loss of function
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26
Q

How is compartment syndrome diagnosed?

A
  • Clinical diagnosis
    • History
    • Examination
  • Impaired conscious level - e.g. drug misuse
    • Compartment pressure measurement
    • Normal pressure 0-4mmHg, 10mmHg with exercise
    • Diastolic BP - CP <30mmHg
    • CP >30mmHg
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27
Q

What are the clinical features of compartment syndrome?

A
  • Pain - out of proportion to that expected from the injury
  • Pain on passive stretching of the compartment
  • Pallor
  • Paresthesia
  • Paralysis
    • Paresthesia + paralysis - usually later, deep nerves affected first (e.g. 1st dorsal webspace)
  • Pulselessness
    • Pulses present (until late stages) unless associated vascular injury
  • Site
    • Forearm, leg, thigh
    • Hand, foot
  • Swelling
  • Shiny skin
  • Autonomic responses - sweating, tachycardia
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28
Q

How is compartment syndrome treated?

A
  • Treatment urgent
  • Open any dressings/bandages - reassess
    • Symptoms settle - observation
    • No improvement/deterioration - surgical release
      • >48 hours - delayed wound closure +/- plastic surgery/skin grafting
  • Surgical release
    • Full length decompression of all compartments
    • Excise any dead muscle
    • Leave wounds open
    • Repeat debridement until pressure down and all dead muscle excised
    • Wounds may not close - skin retracts, may need skin grafting
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29
Q

Describe the limb compartments

A
  • Forearm
    • Extensor (posterior)
    • Flexor (anterior)
    • Mobile wad of three
  • Leg
    • Anterior
    • Lateral
    • Superficial posterior
    • Deep posterior
  • Thigh
    • Anterior
    • Adductor
    • Posterior
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30
Q

What peri-operative management is required in compartment syndrome?

A
  • Adequate hydration
  • Fluid loss
  • Monitor and regulate electrolytes (K+)
  • Correct acidosis
  • Myoglobinuria - breakdown product of muscle
  • Renal function
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31
Q

What treatment is given in late presentation/diagnosis compartment syndrome?

A
  • Irreversible damage already present (>24 hours, longer if insidious)
  • Fasciotomy will predispose to infection
  • Non-operative treatment (NB renal failure)
  • Splint in position of function - hand splinted with fingers extended to stop clawing
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32
Q

List the functions of bone

A
  • Structural
    • Support
    • Protection of organs
    • Movement - muscle attachment and joints
    • Growth in early stages of development
  • Mineral Storage
    • Calcium (90% of bodies calcium in bones)
    • Phosphate (85% of bodies phosphate in bones)
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33
Q

Describe the types of bone

A
  • Cortical bone
    • Compact or tubular bone
    • 80% of the skeleton - long bones
    • Slow turnover rate/metabolic activity
    • Higher Young’s modulus (stiffer) and resistance to torsion and bending
  • Cancellous bone
    • Spongey or trabecular bone
    • Ends of long bone, cuboidal/flat bones
    • Higher turnover rate and undergoes greater remodelling
    • Lower Young’s modulus, and is correspondingly more elastic
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34
Q

Describe the composition of bone

A
  • Matrix
    • Organic components (40%) - collagen (mainly type 1), proteoglycans, non-collagenous proteins, mucopolysaccharides, growth factors and cytokines
      • Gives flexibility
    • Non-organic components (60%) - calcium hydroxyapatite and calcium phosphate (calcium, phosphorus)
      • Gives strength
  • Cells
    • Osteoprogenitor - differentiate into other cell types
    • Osteoblasts - produce new bone under influence of parathyroid hormone
    • Osteoclasts - bone resorption
    • Osteocyte - maintain bone tissue, 90% of the cells in mature bone
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35
Q

Describe the gross structure of long bones

A
  • Diaphysis (shaft)
  • Epiphysis (end)
  • Metaphysis (transitional flared area between diaphysis and epiphysis) - growth plate in embryonic development/childhood
  • Blood supply in through nutrient artery in diaphysis
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36
Q

What is the metaphysis?

A
  • Unique feature of children’s bones
  • Responsible for skeletal growth
  • Allows remodelling of angular deformity after fracture
  • If physeal blood supply damaged, will lead to growth arrest (either partial or complete)
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37
Q

What are the methods of fracture healing?

A
  • Indirect healing (secondary)
  • Direct healing (primary)
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38
Q

What are the stages in indirect fracture healing?

A
  • Indirect healing (secondary, via callus formation)
  • Formation of bone via a process of differential tissue formation until skeletal continuity is restored
  • Inflammation, repair and remodelling
  1. Fracture haematoma and inflammation
  • Blood from broken vessels forms a clot
  • 6-8 hours after injury
  • Swelling and inflammation to dead bone cells at fracture site
  1. Fibrocartilage (SOFT) callus
  • Lasts about 3 weeks
  • New capillaries organise fracture haematoma into granulation tissue - ‘procallus’
  • Fibroblasts and osteogenic cells invade procallus
  • Make collagen fibres which connect ends together
  • Chondrocytes begin to produce fibrocartilage - gives stability
  1. Bony (HARD) callus
  • After 3 weeks and lasts about 3-4 months
  • Osteoblasts make woven bone
  1. Bone remodelling
  • Osteoclasts remodel woven bone into compact bone and trabecular bone
  • Often no trace of fracture line on X-rays
  • Remodelling a constant process
  • Clinical improvement in pain/stability long before
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39
Q

Why is movement important in indirect fracture healing?

A
  • Movement + weight bearing important - bone laid down in relation to stress put across it
  • A degree of movement is desirable to promote tissue differentiation
  • Excessive movement disrupts the healing tissue and affects cellular differentiation (need to stabilise)
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40
Q

Describe direct fracture healing

A
  • Unique ‘artificial’ surgical situation
  • Direct formation of bone, without the process of callus formation, to restore skeletal continuity
    • No callus formed
    • Inflammatory process then direct formation of bone via osteoclastic absorption and osteoblastic formation (cutting cones)
  • Fracture stable - no movement under physiological load
  • Relies upon compression of the bone ends

Process of direct fracture healing

  • No callus
  • Cutting cones cross fracture site
  • Lay down new osteones directly
  • Inititally randomly laid down then remodelled
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41
Q

Describe the blood supply of bone and how this affects fracture healing

A
  • Endosteal - inner 2/3rds
  • Periosteal - outer 1/3rd
  • Injured by a fracture
  • Further damaged by surgery
    • Nails into bone injures endosteal blood supply
    • Plates strip off periosteum
  • Compromise of blood supply
    • Surgical factors (iatrogenous)
    • Anatomical factors
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42
Q

How can a bone’s blood supply be compromised by anatomical factors?

A
  • Certain fractures prone to problems with union or necrosis (bone death) because of potential problems with blood supply
    • Proximal pole of scaphoid fractures - retrograde blood flow
    • Talar neck fractures
    • Intracapsular hip fractures
    • Surgical neck of humerus fractures
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43
Q

What patient factors can inhibit fracture healing?

A
  • Increasing age
  • Diabetes
  • Anaemia
  • Malnutrition
  • Peripheral vascular disease
  • Hypothyroidism
  • Smoking
  • Alcohol
  • Obesity
  • Medication
  • NSAIDs
  • Steroids
  • Bisphosphonates
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44
Q

How do NSAIDs affect fracture healing?

A
  • NSAIDs reduce local vascularity at fracture site - anti-inflammatory
  • Additional reduction in healing effect independent of flow
  • Evidence mainly from animal studies, but some surgeons do avoid their use post-operatively
  • COX-2 selective inhibitor NSAIDs inhibit fracture healing more than non-specific NSAIDs
  • Magnitude of effect is related to duration of treatment
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45
Q

How do bisphosphonates affect fracture healing?

A
  • Osteoporosis treatment - stress and microfractures, femoral neck fractures without trauma
  • Inhibit osteoclastic activity
  • Delay fracture healing as a result
  • Long half life
    • Takes years to get out of system
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46
Q

Define osteonecrosis

A
  • Osteonecrosis (bone death), also called avascular necrosis (AVN) refers to bone infarction (tissue death caused by an interruption of the blood supply) near a joint
  • The generic term ‘bone infarction’ is typically applied only to bone death that is not near a joint
  • Can be painful, main significance is that death of sub-chondral bone (i.e. bone under joint surface) can lead to collapse of the joint surface and end stage arthritis
  • Osteonecrosis is most common in the hip and shoulder
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47
Q

Describe the blood supply of the femoral head

A
  • Circumflex vessels form ring at base of neck of femur
  • Retinacular vessels up to femoral head
  • Anything disrupting the large or small vessels can cause osteonecrosis
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48
Q

Describe the clinical presentation of avascular necrosis

A
  • Can be asymptomatic - found incidentally on imaging
  • Most patients present because of pain, either from infarction itself or from arthritis
  • Patients with osteonecrosis of femoral head often complain of groin pain (typical of hip pathology) that worsens with weight-bearing and motion and less commonly complain of thigh and buttock pain
  • Rest pain occurs in about 2/3 of patients, while night pain occurs in about 1/3 of patients
  • Initial physical examination findings often non-specific, but after osteonecrosis progresses, joint function deteriorates and the patient with present with the findings of arthrosis
    • Limp
    • Tenderness around the affected bone
    • Restricted motion
  • In the femoral head, osteonecrosis causes particular limitation in internal rotation and abduction
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49
Q

Describe the epidemiology of osteonecrosis

A
  • Osteonecrosis accounts for more than 10% of the total hip replacements
  • Peak age of prevalence is 30s/40s
  • Osteonecrosis is bilateral in about 55% of cases and most common site is the hip
  • Overall prevalence of osteonecrosis in sickle cell anaemia is about 10%
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50
Q

Describe the pathophysiology of osteonecrosis

A
  • Oedema, haemorrhage, fibrilloreticulosis and hypocellularity may be present in bone marrow lesions
  • In AVN, the necrosis always involves the medullary bone first (the cortex may be spared because it has a collateral blood supply)
  • The overlying articular cartilage receives nutrition from the synovial fluid and remains viable
  • The dead bone has empty lacunae and is surrounded by necrotic adipocytes that often rupture and release their fatty acids
  • Fatty acids can bind calcium and form insoluble calcium soaps
  • During the healing process, osteoclasts resorb the necrotic trabeculae, while the remaining ones serve as scaffolding for the deposition of new bone (i.e. creeping substitution)
  • Nevertheless, the pace of creeping substitution may not be fast enough to be effective, and as a result, the necrotic cancellous bone collapses
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51
Q

What are the causes of an infarct which leads to mature osteonecrosis?

A
  • In some cases, the cause of the infarct is clear i.e. in sickle cell anaemia, mechanical blockage by rigid erythrocytes is likely
  • In others, the reason is less clear - vascular damage, increased intraosseous pressure and mechanical stresses are putative causes
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52
Q

How does osteonecrosis lead to arthritis?

A
  • If bone is deprived of its blood supply i.e. gets ischaemic, it dies
  • If bone dies, it does not remodel
  • Bone remodelling is the process by which osteoclasts secrete acid and proteolytic enzymes to digest the bone matrix and osteoblasts synthesise new organic matrix leading to the deposition of newer, better bone
  • If the bone does not remodel, micro-damage does not get repaired and the mechanical properties of the bone are impaired
  • If enough damage accumulates, the sub-chondral bone can be weakened to the point of collapse
  • If the sub-chondral bone collapses, the joint surface becomes irregular and no longer smooth
  • If one side of the joint surface is not smooth it will damage the other surface
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53
Q

How is imaging used in the diagnosis of osteonecrosis?

A
  • Plain radiograph may be normal for months after the onset of symptoms of osteonecrosis, but early findings may include mild density changes followed by sclerosis and cysts as it progresses
  • The pathognomonic crescent sign (subchondral radiolucency) precedes subchondral collapse
  • In the late stages of AVN, loss of sphericity and collapse of the femoral head and joint-space narrowing and degenerative changes in the acetabulum can be seen
  • MRI - 91% sensitivity
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54
Q

List the risk factors for osteonecrosis

A
  • History of trauma, especially a joint dislocation
  • Corticosteroid use or Cushing’s disease
  • Alcohol abuse
  • Sickle cell disease/haemoglobinopathies
  • Systemic lupus erythematosus
  • Antiphospholipid antibody syndrome
  • Metabolic diseases such as hyperlipidaemia
  • Renal failure (in renal transplantation, medication may be responsible)
  • HIV
  • Prior radiation therapy
  • Chemotherapy
  • Decompression sickness (diving)
  • Bisphosphonates (AVN of the jaw in particular with high dose in cancer treatment)
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55
Q

What risk prevention measures should be taken to prevent osteonecrosis?

A
  • Trauma (especially dislocation), steroid excess, alcohol abuse and sickle cell disease/haemoglobinopathies in particular important - patients with any of them need heightened scrutiny should they present with bone or joint pain and normal plain radiographs
  • To reduce risk of AVN, the minimum effective dose of systemic corticosteroids should be used and, if possible, steroid-sparing agents should be used
  • Patients at high risk of AVN (e.g. with prolonged corticosteroid use, haemoglobinopathies, renal transplant) should be educated about AVN and advised to report symptoms as soon as possible to facilitate treatment
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56
Q

What are the treatment options for osteonecrosis?

A
  • Depends on presence of any collapse
  • Reperfusion and healing of the infarcted area will not restore the joint surface
  • Partial weight bearing - limited evidence
  • Bisphosphonates - ironically and uncontrolled study
  • Core decompression with or without bone graft is appropriate in early stages - clear out necrotic bone
  • Total hip arthroplasty is appropriate in the late stages
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57
Q

What is Keinboch’s?

A
  • Breakdown of lunate bone due to avascular necrosis
  • Often history of trauma to wrist
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58
Q

What is osteoid? Where is it found?

A
  • New woven immature bone, produced by osteoblasts and maintained by osteocytes
  • Seen in foetal skeleton, after fracture or in bone tumour
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59
Q

What types of bone tumours are most common?

A
  • Secondary tumours in bone very common
  • Myeloma - commonest primary bone tumour
  • Primary bone tumours rare - specialist care
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60
Q

What types of secondary tumours are most prevelant in bone? Which bones are most commonly affected?

A
  • 60% of patients dying of cancer
  • Metastatic carcinoma
    • Bronchus, breast, prostate, kidney, thyroid (follicular)
  • Childhood
    • Neuroblastoma, rhabdomyosarcoma
  • Bones with good blood supply most commonly affected - long bones (femur, humerus, tibia), vertebrae
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61
Q

What are the effects of metastases on bone?

A
  • Often asymptomatic
  • Bone pain
  • Bone destruction
  • Long bones - pathological fracture
  • Spinal metastases - vertebral collapse, spinal cord compression, nerve root compression, back pain
  • Hypercalcaemia - thirst, abdominal pain
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62
Q

How are bone metastases detected?

A

PET-CT:

  • By combining PET with CT, anatomical detail can be achieved as well as functional data
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63
Q

Describe the types of bone metastases

A
  • Lytic or sclerotic
  • Majority are lytic - blackened area on X-ray
    • E.g. adenocarcinoma (probably bronchal) - bone replaced by adenocarcinoma, much more susceptible to fracture
    • Mechanism of bone destruction
      • Osteoclasts, not tumour cells
      • Stimulated by cytokines from tumour cells
      • Inhibited by bisphosphonates - reduce lysis
  • Sclerotic - white on X-ray
    • Cancer cells trigger cytokines to stimulate osteoblasts to produce more bone - woven, immature new bone (v cellular on histology)
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64
Q

Give examples of sclerotic bone metastases

A
  • Prostatic carcinoma - >60 y/o man w sclerotic metastases, likely to be primary prostatic carcinoma
  • Breast carcinoma
  • Carcinoid tumour - in lung/gut
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65
Q

Which cancers show solitary bone metastases? What are the features of solitary bone metastases?

A
  • Typically renal and thyroid carcinomas
  • Often long survival
  • Surgical removal often valuable - long term survival and cure
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66
Q

What is myeloma?

A
  • Commonest malignant primary bone tumour
  • Monoclonal proliferation of plasma cells (in bone marrow)
  • Solitary (plasmacytoma) or multiple myeloma
  • Orthopaedic consequences
  • ‘Medical’ consequences
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67
Q

What are the clinical effects of myelomas?

A
  • Bone lesions
    • Punched out lytic foci
    • Generalised osteopaenia leading to osteoporosis
  • Marrow replacement - pancytopaenia
    • Anaemia - RBC
    • Infections - WBC (leucopaenia)
    • Bleeding - platelets (thrombocytopaenia)
  • Immunoglobulin excess
    • ESR >100
    • Serum electrophoresis - monoclonal band
    • Urine - immunoglobulin light chains (Bence Jones protein)
  • Skeletal survey - X-rays of different bones
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68
Q

What is a typical radiological finding in myelomas?

A
  • Pepper pot skull
  • Punched out lytic foci of bone
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69
Q

What is seen histologically in myelomas?

A
  • Sheets of plasma cells - eccentric nuclei, paranuclear hof (clearing in cytoplasm where Golgi apparatus is)
  • Atypical plasma cells seen - multinucleated, mitoses
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70
Q

What diagnostic test can be done to confirm myeloma histologically?

A
  • In situ hybridisation to confirm all kappa or all lambda
    • Restriction of light chain - monoclonal proliferation only produces one light chain instead of both, tells you it is a tumour/reactive proliferation
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71
Q

What systemic medical effect do myelomas have?

A

Renal Impairment:

  • Myeloma kidney - precipitated light chains in renal tubules
  • Hypercalcaemia
  • Amyloidosis - acute phase reactive protein produced in infection, inflammation, malignancy, deposited in kidney
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72
Q

List the commonest primary bone tumours

A
  • Benign
    • Osteoid osteoma
    • Chondroma
    • Giant cell tumour
  • Malignant
    • Osteosarcoma
    • Chondrosarcoma
    • Ewing’s tumour
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73
Q

What is an osteoid osteoma?

A

Small, benign osteoblastic proliferation

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74
Q

Who is typically affected by osteoid osteomas? Which bones?

A
  • Common, any age especially adolescents, M:F 2:1
  • Any bones, especially long bones, spine
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75
Q

What are the symptoms of an osteoid osteoma?

A
  • Pain, worse at night, relieved by aspirin, scoliosis
  • Juxta-articular tumours - sympathetic synovitis
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76
Q

Describe the appearance of an osteoid osteoma

A
  • Tumour - well circumscribed nodule (nidus)
    • Nidus = proliferation of osteoblasts
  • Reactive bone around tumour = reactive sclerosis
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77
Q

How is an osteoid osteoma treated?

A

Radiofrequency ablation using probe

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78
Q

What is an osteosarcoma?

A

A malignant tumour whose cells form osteoid or bone

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79
Q

Describe the epidemiology of osteosarcomas

A
  • Age - peak 10-25, second peak >70
    • In elderly only if pre-existing abnormality in bone e.g. Paget’s, avascular necrosis, radiotherapy
  • Site - metaphysis of long bones, 50% around knee
  • Sex - male preponderance, 3:2
  • Incidence - 2-3/million/year
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80
Q

How do osteosarcomas usually present?

A
  • Pain
  • Swelling
  • Loss of function
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81
Q

Describe the prognosis of osteosarcomas

A
  • Highly malignant
  • Early lung metastases (cannonball metastases) - haematogenous spread
  • 5 year survival - 15-20% pre-chemotherapy, 50-60% with chemotherapy
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82
Q

How are osteosarcomas managed?

A
  • Usually present to GP with pain, swelling, loss of function
  • Sent for X-ray
  • Referral to major centre when abnormality suspected on X-ray
  • Discussed at specialist MDT
  • Decision to biopsy by radiologist - biopsy to pathologist
  • MDT diagnosis
  • Neoadjuvant chemo for 8 weeks then surgical local control, take out affected bone and replace with customised prosthesis
    • Histological examination to determine what kind of osteosarcoma, if the margins are clear, how well the tumour responded to chemo
    • >90% death = good response, continue chemo
    • >10% tumour alive = poor response, change chemo regimen
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83
Q

What is seen histologically in osteosarcomas?

A
  • Features of malignancy - nuclear pleomorphism, abnormal mitotic activity
  • Bone deposition - pink
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84
Q

Which types of osteosarcoma have normal, better and worse prognoses?

A
  • Normal prognosis
    • Osteoblastic
    • Chrondroblastic
    • Fibroblastic
    • Telangiectatic
    • Small cell
    • Sclerotic
  • Worse prognosis
    • Paget’s
    • Multifocal
    • Post-irradiation
  • Better prognosis
    • Parosteal
    • Periosteal
    • Low grade central
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85
Q

What is an telangiectatic osteosarcoma?

A

Expanded lytic tumour, very little osteoid production - cystic cavities containing necrosis and haemorrhage

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86
Q

What is a forequarter amputation? When is it used?

A
  • Amputation of the arm including the scapula and humeral head
  • Used in tumours of the humerus which have extended into the soft tissue
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87
Q

Who is commonly affected by Paget’s disease?

A

Common in elderly, Anglo-Saxon origin

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88
Q

What is Paget’s disease?

A
  • Disorder of excessive bone turnover
  • Increased osteoclasis, increased bone formation, structurally weak bone
  • Disorganised bone architecture
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89
Q

Which bones are typically affected by Paget’s disease?

A

Vertebrae, pelvis, skull, femur

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90
Q

What are the symptoms/complications of Paget’s disease?

A
  • Bone pain
  • Deformity - bowing of long bones
  • Pathological fracture
  • Osteoarthritis
  • Deafness
  • Spinal cord compression
  • High cardiac output - cardiac failure
  • Paget’s sarcoma
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91
Q

Describe the features of Paget’s sarcoma

A
  • Second osteosarcoma peak in elderly
  • Usually lytic
  • Long bones > spine (c.f. Paget’s disease)
  • Very poor prognosis
  • Early metastases to long and bone
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92
Q

List common cartilaginous tumours

A
  • Enchondroma
  • Osteocartilaginous exostosis
  • Chondrosarcoma
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93
Q

What is an enchondroma?

A
  • Benign tumour of cartilage cells
  • Lobulated mass of cartilage within medulla of bone
  • Low cellularity, often surrounded by plates of lamellar bone
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94
Q

Who is typically affected by enchondromas? Which bones?

A
  • Common, any age
  • >50% hands and feet, long bones
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95
Q

What are the symptoms of enchondromas?

A
  • Often asymptomatic in long bones
  • Hands - swelling, pathological fractures
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96
Q

What is osteocartilaginous exostosis?

A
  • Benign outgrowth of cartilage with endochondral ossification
  • Usually benign but can become malignant (>1cm cap)
  • Probably derived from growth plate
  • Very common, usually in adolescence
  • Uncommonly multiple-diaphyseal aclasis, autosomal dominant
  • Metaphysis of long bones, not cranio-facial
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97
Q

What is a conventional chondrosarcoma?

A
  • De novo (primary) or from a pre-existing enchondroma or exostosis (secondary)
  • Central, within the medullary canal or peripheral on bone surface
  • 10% of malignant primary bone tumours
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98
Q

Who is typically affected by conventional chondrosarcomas? Which bones?

A
  • Predominantly middle aged and elderly
  • Males:females, 2:1
  • Axial skeleton, pelvis, rides, shoulder girdle, proximal femur and humerus, hands and feet rare
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99
Q

What is seen histologically in chondrosarcomas?

A

Cartilage cells in lacunae with aminoglycan matrix, v cellular, mitotic abnormalities

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100
Q

Describe the prognosis of chondrosarcomas

A
  • Chondrosarcoma much better prognosis than osteosarcoma - surgical removal, not likely to metastasise
  • Only fatal if in site not surgically available e.g. deep pelvis or skill (can recieve proton therapy but only outside UK)
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101
Q

Who is typically affected by Ewing’s sarcoma? Which bones?

A
  • Peak 5-15 years - paediatric tumour
  • Long bones (diaphysis or metaphysis)
  • Flat bones of limb girdles
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102
Q

Describe the prognosis of Ewing’s sarcoma

A
  • Early metastases to lung, bone marrow and bone - haematogenous spread
  • Historical 5 year survival 5%, modern 5 year survival 50-60%
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103
Q

Describe the histological appearance of Ewing’s sarcoma

A

Malignant small round blue cell tumour

CT99 marker positive

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104
Q

Describe the genetic abnormality associated with Ewing’s sarcoma

A
  • Specific translocation associated with Ewing’s sarcoma - 11:22
  • Diagnose on FISH/PCR
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105
Q

Which imaging modalities can be used in the musculoskeletal system? How are they used?

A
  • Radiographs – basic test, trauma, arthritis, congenital, tumour
  • Computed Tomography (CT) – bone detail, complex fractures,
  • Ultrasound (US) – small superficial lumps, tendons, joints, ligaments, synovitis,
  • Nuclear Medicine and PET scanning – cancer staging
  • Magnetic Resonance Imaging (MRI) – gold standard for assessing diseases of joints, soft tissues, bones
  • DEXA scanning - osteoporosis
  • Guided interventional Procedures – CT or US guided biopsy, drainage, Radiofrequency ablation
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106
Q

Describe the appearance of bone trauma on X-ray

A
  • Lucent - black
    • Gap between fracture ends
  • Sclerotic (dense) - white
    • Fracture lines overlapping
  • Important to have multiple views - fractures can be hidden depending on the angle
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107
Q

What is the typical outcome of a fall onto outstretched hands?

A
  • Scaphoid fracture
  • Sometimes can’t be seen on X-ray (better in angled up view), may need MRI if still have symptoms
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108
Q

Why is an X-ray needed following a shoulder dislocation?

A
  • Dislocation obvious clinically, do X-ray to see if there is associated fractures
  • Greater tuberosity of humerous often fractures as hits off glenoid of shoulder
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109
Q

List the types of fractures

A
  • Displaced - bone ends are not aligned
  • Angulated - fracture is at an angle
  • Rotated - rotation of the proximal portion in relation to the distal portion
  • Overriding - bone ends overlap, shortening of bone length
  • Distracted - gap between bone ends, widening of bone components
  • Comminuted - break into more than two fragments
  • Compound - fracture open to skin
  • Intra vs extra-articular
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110
Q

What is the significance of a fracture being intra- vs extra-articular?

A

Intra-articular more likely to develop post-traumatic osteoarthritis

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111
Q

What is the significance of a supracondylar fracture?

A
  • Fracture of distal humerus
  • Malunion will result in classic ‘gunstock’ deformity due to rotation or inadequate correction of medial collapse
  • Posterolateral displacement of the distal fragment can be associated with injury to the neurovascular bundle which is displaced over the medial metaphyseal spike
  • Nerve injury almost always results in neuropraxis that resolves in 3-4 months
  • Vascular injury usually results in a pulseless but pink hand
  • Conservative management and vascular intervention have the same outcome
  • A pulseless and white hand after reduction needs exploration
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112
Q

How are neck of femur fractures categorised?

A

Categorised as intra- or extra-capsular fractures

Intra-capsular fractures have risk of avascular necrosis of the femoral head

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113
Q

How are intra-capsular femoral neck fractures treated?

A
  • Older patient - hemiarthroplasty
  • Younger patient - full replacement
  • Fracture in intertrochanteric region - internal fixation/dynamic hip screw to preserve patients own hip joint
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114
Q

List the type of femoral neck fractures and how each is managed

A
  • Subcapital neck fracture - hip replacement
  • Transcervical neck fracture - hip replacement
  • Intertrochanteric fracture - internal rotation/dynamic hip screw
  • Subtrochanteric fracture - external/internal fixation
  • Fracture of the greater trochanter - bed rest/taping/casting/internal fixation
  • Fracture of the lesser trochanter - reduction/internal fixation
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115
Q

What causes Paget’s disease of bone?

A
  • Aetiology unknown - viral?
    • Racial predilection - more Caucasian’s affected
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116
Q

How many bones can be affected by Paget’s disease?

A

Monostotic or polystotic - one or multiple bones

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117
Q

What is seen biochemically in Paget’s disease?

A

Raised alkaline phosphate

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118
Q

How is the diagnosis of a bone tumour usually confirmed?

A
  • Biopsy of tumour under CT guidance
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119
Q

Describe the features of arthritis vs avascular necrosis on X-ray?

A
  • Osteoarthritis
    • Loss of joint space
    • Osteophytes
    • Subchondral sclerosis
    • Dense in acetabulum
    • Subchondral cysts
  • Avascular necrosis
    • Joint space maintained
    • Abnormality in femoral head - lucency below articular surface
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120
Q

Describe the classification of joint diseases

A
  • Degenerative - bone production (osteophytes)
  • Inflammatory (e.g. RA) - periarticular erosions
  • Depositional (e.g. gout)- periarticular soft tissue masses
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121
Q

List the features of reactive bone formation

A
  • Sub-chondral sclerosis
  • Osteophytosis
  • Periostitis - inflammation of periosteum
  • Occurs with age
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122
Q

List the types of bone erosions

A
  • Location
    • Peri-articular
    • Para-articular
  • Appearance
    • Ill-defined - active
    • Well defined - old
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123
Q

Which joint pathologies cause bone erosion?

A

Rheumatoid arthritis, gout

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124
Q

Describe the distribution of joint pathologies

A
  • Location within the skeleton
    • Mono/polyarthropathy
    • Symmetry
    • Which joints?
  • Location within the joint
    • Erosions
    • Joint space narrowing

RA - MCP/PIP joints, bilateral, symmetrical

OA - DIP joints, asymmetrical

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125
Q

How can joint space narrowing be diagnosed?

A

Joint space narrowing

  • Symmetric, erosions, soft tissue swelling = inflammatory
    • 1 joint - infection
    • >1 joint
      • Proximal, no bony proliferation - RA
      • Distal, bone proliferation - seronegative spondyloarthropathy
  • Asymmetric, osteophytes, sclerosis = degenerative
    • Typical osteoarthritis
    • Usual distribution, severity, age = atypical osteoarthritis
      • Trauma, crystal deposition, neuropathic, haemophilia
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126
Q

What is primary degenerative arthritis? What causes it?

A
  • Intrinsic degeneration of articular cartilage
  • Cause - excessive wear and tear
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127
Q

Which joints are most commonly affected by primary degenerative arthritis?

A
  • Most common - hips and knees
  • Uncommon - shoulders and elbows
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128
Q

What are the featues of primary degenerative arthritis on X-ray?

A
  • Narrowed joint space
  • Osteophytes
  • Subchondral sclerosis/cysts
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129
Q

Describe the involvement of the hands in osteoarthritis

A
  • F:M 10:1
  • DIP, PIP and 1st MCP joints affected
    • Sclerosis
    • Marginal osteophytes
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130
Q

What is secondary degenerative arthritis? How can it be identified?

A
  • Another process destroys articular cartilage e.g. developmental dysplasia of hip as child, previous infection of joint
  • Degenerative changes supervene
  • How to recognise
    • Atypical locations
    • Atypical appearance
    • Atypical age
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131
Q

What are the common and uncommon causes of secondary degenerative arthritis?

A
  • Common causes
    • Trauma
    • Infection
    • Avascular necrosis
    • Calcium pyrophosphate dihydrate disease (CPPD) - pseudogout
    • Rheumatoid arthritis
    • Haemophilia
  • Uncommon
    • Haemachromatosis
    • Acromegaly
    • Ochronosis
    • Wilson’s disease
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132
Q

What is seen on X-ray in rheumatoid arthritis with secondary degenerative changes?

A
  • Loss of joint space
  • Mild subarticular sclerosis
  • Lack of osteophytes
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133
Q

What causes calcium pyrophosphate dihydrate deposition disease (CPPD)?

A
  • Idiopathic or associated with
    • Hyperparathyroidism
    • Haemachromotosis
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134
Q

Describe the consequences and distribution of CPPD

A
  • Symmetrical
  • Similar to osteoarthritis but unusual distribution
  • Calcification of articular cartilage - chondrocalcinosis
    • Triangular fibrocartilage of wrist, knee, hip, shoulder, symphysis pubis
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135
Q

Describe the clinical presentation of CPPD

A
  • Sudden onset of pain/fever
    • Acute deposition of crystals into joints - sudden severe pain
  • Clinical - tender, swollen, red
  • May mimic septic arthritis
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136
Q

List the types of inflammatory arthritis

A
  • Infection
  • Rheumatoid (seropositive) arthritis
  • Seronegative arthropathies
    • Psoriatic arthritis
    • Reactive arthritis
    • Ankylosing spondylitis
    • Inflammatory bowel disease
  • Other connective tissue diseases
    • Systemic sclerosis (scleroderma)
    • Systemic lupus erythematosus
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137
Q

What factors predispose to infectious arthritis?

A
  • More common in adults
  • Usually local injury, surgery, vascular disease predispose
  • Fingers from bites, feet in diabetes, hips with total hip replacement (usually monoarticular)
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138
Q

What are the pathological consequences of infectious arthritis?

A
  • Destruction of cartilage and cortex
  • Soft tissue swelling
  • Rapid loss of joint space
  • +/- periosteal reaction
  • Osteoporosis
  • Later subluxation, OA, fusion
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139
Q

What are the typical causative organisms in infectious arthritis?

A

Staphylococcus, streptococcus, TB etc.

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140
Q

What are the radiographic findings in discitis as the disease progresses?

A
  • Normal 1-3 weeks
  • End plate erosion
  • Disc space narrowing
  • Bone destruction
  • Paravertebral mass
  • Late - sclerosis
  • Ankylosis - fusion of vertebrae after infection
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141
Q

How should discitis be imaged?

A

MRI - more sensitive

Shows oedema - fluid in joint space

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142
Q

Which joints are typically affected by RA?

A
  • Hands, feet
  • Elbows, knees, hips
  • Cervical spine
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143
Q

Describe the diagnostic criteria for RA

A

Old Criteria (4/6)

  • Morning stiffness
  • >2 joints
  • Hand and wrist joints
  • Rh nodules
  • RF positive
  • XR changes

Newer classification includes presence of bilateral wrist, MCP or PIP joint enhancement on MRI and leads to a more accurate diagnosis of early RA, symptoms >6 weeks.

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144
Q

List the pathological features of RA

A
  • Hyperaemia
  • Soft tissue swelling
  • Synovitis
  • Effusion
  • Bone marrow oedema
  • Erosions, cysts
  • Joint space narrowing
  • Secondary degenerative changes
  • Loose bodies
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145
Q

Describe the hand involvement in RA

A
  • Symmetrical disease
  • MCP joint erosions
  • MCP ulnar deviation
  • Deformed thumbs
  • Erosions distal ulna
  • Erosive changes wrist
  • Secondary degenerative changes
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146
Q

Why is it important to consider the effects of RA on the cervical spine?

A
  • Atlanto-axial subluxation can lead to instability
  • Check before intubating patient
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147
Q

Describe the features of sero-negative inflammatory arthropathies in comparison to RA

A
  • Negative rheumatoid factor
  • Positive HLA-B27
  • Differ from RA by
    • Normal bone density
    • Periostitis
    • Ankylosis (fusion)
    • Asymmetrical pattern
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148
Q

How do patients with psoriatic arthritis usually present?

A
  • M = F, young adults
  • Usually skin and nail changes
  • DIP joints of hands > feet
  • Arthropathy may pre-date skin lesions in 20% of cases
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149
Q

What is seen on X-ray in psoriatic arthritis?

A

‘Pencil in cup’ deformity - resorption of distal phalanges

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150
Q

Who is typically affected by reactive arthritis?

A
  • M > F
  • 20-40 yrs
  • White > black
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151
Q

What causes reactive arthritis?

A

Chlamydia, salmonella, shigella

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152
Q

What conditions are associated with reactive arthritis?

A

Urethritis, arthritis (50%), conjunctivitis

Periositis, enthesopathy

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153
Q

Which joints are typically affected by reactive arthritis?

A

Lower limb, sacroiliac joint

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154
Q

Describe the natural progression of reactive arthritis

A
  • 1-3 weeks after infection (may not have been known infection) - inflammatory reaction in joint (infection is not within joint)
  • Can be self-limiting (most), recurrent, chronic or progressive
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155
Q

Who is typically affected by ankylosing spondylitis?

A
  • 3M:1F
  • 20-40 yrs
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156
Q

What are the symptoms of ankylosing spondylitis?

A
  • Low back pain
  • Stiffness
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157
Q

Which markers indicate ankylosing spondylitis?

A
  • HLA B27 +ve (8% of normal population)
  • RF negative
158
Q

What are the features of ankylosing spondylitis on X-ray?

A
  • Bilateral sacroilitis - symmetrical
  • Squaring of vertebral bodies
  • Romanus lesions - erosion of anterior and posterior vertebral endplates
  • Bamboo spine
  • Vertebral fractures
  • Peripheral large joint arthritis
  • Need MRI to identify and prevent further degeneration
159
Q

What causes gout?

A
  • Sodium urate crystal induced synovial inflammation
    • Occasional attacks or chronic arthropathy
    • Idiopathic, enzyme defects or secondary to myeloproliferative disorders
160
Q

Who is typically affected by gout?

A
  • Elderly males, hereditary
    • Young age suspect renal disease or myeloproliferative disorder
161
Q

Which joints are commonly affected by gout?

A
  • Aysymmetrical and monoarticularl
  • Foot - 1st MCP joint
  • Knee, hand, elhow
162
Q

What are the patholgoical conseuquences of gout?

A
  • Olecranon bursitis common
  • Para-articular erosions
  • Soft tissue mass
163
Q

Describe the diagnosis of gout

A
  • Several years before XR changes occur - long history between symptoms and XR changes
  • Sodium urate crystals by polarising microscope
164
Q

Describe the radiographic features of gout

A
  • Para-articular erosions
  • Sharply marginated with sclerotic rims
  • Overhanging edges
  • No joint space narrowing till late
  • Little or no osteoporosis
  • Soft tissue swelling
  • Tophi not usually calcified
165
Q

How does acute monoarthritis present?

A
  • Cardinal features of inflammation
    • Rubor, calor, dolor, tumour
  • +/- fever
  • +/- leukocytosis, raised CRP
  • Atypical presentations not uncommon
166
Q

What should acute monoarthritis be assumed to be? How can this be confirmed?

A

Acute monoarthritis is septic until proven otherwise - if in any doubt needle aspirate

167
Q

List the risk factors for septic arthritis

A

Previous arthritis

Trauma

Diabetes mellitus

Immunosuppression

Bacteraemia

Sickle cell anaemia

Prosthetic joint

168
Q

Describe the pathogenesis of septic arthritis

A
  • Bacteria enter joint and deposit in synovial lining
    • Haematogenous spread
    • Local invasion/inoculation
  • Rapid entry into synovial fluid
    • No basement membrane
    • Close relationship to blood vessels
169
Q

Which joints are most commonly involved in septic arthritis?

A
  1. Knee
  2. Polyarticular
  3. Hip
  4. Shoulder
  5. Wrist
  6. Ankle
  7. Elbow
  8. Other
170
Q

How does polyarticular septic arthritis differ from monoarthritis?

A
  • More likely to be over 60 years
  • Average of 4 joints
  • Knee, elbow, shoulder and hip predominate
  • High prevalence of RA
  • Often without fever and leukocytosis
  • Blood cultures + 75%
  • Synovial fluid cultures + 90%
  • Staph and strep most common
  • Poor prognosis
    • 32% mortality (compared to 4% with monoarticular disease)
171
Q

Describe synovial fluid in septic arthritis

A
  • Cell count >50,000 wbc/mm3
  • Differential >75% PMNs
  • Glucose low
  • Gram stain relatively insensitive test
  • Culture positive
172
Q

How should a joint aspirate be taken in suspected septic arthritis?

A

Always use a wide bore needle when you suspect infection, as pus may be very viscous and difficult to aspirate

173
Q

List the most common causes of infectious arthritis and the clinical clues which suggest each

A
  • Staphylococcus aureus - healthy adults, skin breakdown, previously damaged joint e.g. RA, prosthetic joint
  • Streptococcal species - healthy adults, splenic dysfunction
  • Neisseria gonorrhoea - healthy adults (particularly young, sexually active), associated tenosynovitis, vesicular pustules, late complement deficiency, negative synovial fluid and gram stain
  • Aerobic gram negative bacteria - immune compromised hosts, GI infection
  • Anaerobic gram negative bacteria - immune compromised hosts, GI infection
  • Mycobacterial species - immune compromised host, recent travel to or resistance in an endemic area
  • Fungal species (sporotrichosis, cryptococcus, blastomycosis) - immune compromised host
  • Spirochete (Borellia burgdorferi) - exposure to ticks, anteoedent rash, knee joint involvement
  • Mycoplasma hominis - immune compromised hosts with prior GI tract manipulation
174
Q

How is septic arthritis managed?

A
  • Joint aspiration
    • Daily or more frequently as required
  • Antibiotic therapy
    • Based on gram stain/culture and clinical factors
    • Duration is variable and depends on organism and host factors
  • Surgical intervention
    • Only necessary if patient is not responding after 48 hours of appropriate therapy - consult ortho if not improving
  • Serial synovial fluid analyses should be performed to document clearance of infection
175
Q

What are the risk factors for gout?

A
  • Non-modifiable
    • Age
    • Male gender
    • Race
    • Genetic factors
    • Impaired renal function
  • Modifiable
    • Obesity
    • Alcohol consumption
    • High-purine diet (meat and fish)
    • HFCS (high fructose corn syrup)
    • Certain medications
176
Q

What medications can be used to treat gout?

A
  • Aspirin
    • Bimodal effect
    • 75mg reduces UA excretion by 15%
  • Diuretics
  • Cyclosporin
  • Pyrazinamide and ethambutol
  • Nicotinic acid
177
Q

What is seen in the joint aspirate in gout?

A

Tophus - urate crystals

178
Q

How is gout diagnosed?

A
  • Joint aspirate - urate crystals
  • Presumptive dx of gout may be made in the absence of synovial fluid aspiration if
    • Typical presentation of podagra - gout affecting the metatarsophalangeal joint, recurrent acute joint inflammation (swelling over the big toe)
    • History of gout flares or hyperuricaemia
  • Raised sUA between attacks
179
Q

What is the differential diagnosis for gout?

A
  • Septic arthritis
    • Always have to consider with an acute monoarthritis
  • CPPD (pseudogout)
    • Less commonly 1st MTP
    • Most commonly seen in the knee, wrist and shoulde
180
Q

What are the goals of treatment in gout?

A
  • Acute attacks - relieve pain and reduce inflammation
    • Non-pharmacological (cold packs)
    • NSAIDs/Coxibs/Colchicine/Corticosteroids
  • Long-term
    • Prevent further acute attacks (62% within 1 year)
    • Prevent joint damage
    • Eliminate tophi
181
Q

What lifestyle modifications should be advised in the management of gout?

A
  • Diet
    • Reduce purine intake
    • Reduce fructose-containing drinks
    • Include skimmed milk, low fat yoghurt, vegetable protein and cherries every day
  • Weight loss
    • 1kg/month (avoid crash diets)
    • Avoid high protein diets
  • Moderate exercise
  • Reduce alcohol
182
Q

Which patients should be treated for gout?

A
  • Recurring attacks (>2 in 12 months)
  • Tophi
  • Chronic gouty arthritis
  • Renal impairment (eGFR <60 ml/min)
  • History of urolithiasis
  • Diuretic therapy use
  • Primary gout starting at a young age (under 40 years)
  • Very high serum urate >500 micromol/L
183
Q

What urate lowering therapies are available in the treatment of gout?

A
  • Allpurinol
    • Start at 100mg, increase in 100mg steps every 4 weeks target or max 900mg daily
  • Febuxostat
    • 80mg with option to increase to 120mg after 4 weeks if not at target urate
184
Q

How does calcium pyrophosphate deposition disease differ from gout?

A
  • Generally older age group
  • Associated chondrocalcinosis
  • Smaller, sparse rhomboid shaped crystals
185
Q

Describe the cause and development of reactive arthritis

A
  • One of the seronegative spondyloarthropathies
    • Seronegative for rheumatoid factor
    • Strong association with HLA-B27
  • Develops soon after an infection occurring elsewhere in the body
  • Viable organism cannot be recovered from the joint (so not a true septic arthritis)
186
Q

List the common organisms which cause reactive arthritis

A
  • Enteric infections
    • Salmonella
    • Shigella
    • Yersinia
    • Campylobacter
    • Clostridium
  • GU infections
    • Chlamydia trachomatis
    • Neisseria gonorrhoea
    • Mycoplasma genitalium
    • Ureplasma urealyticum
187
Q

Describe the prevalence of reactive arthritis

A
  • Unclear - underdiagnosed but incidence rising
  • Estimates for all chlamydial ReA 5 cases per 100K (1994)
  • SARA follows around 4% of all NGU
  • Male:female 10:1, age peak 20-40
  • Association with HLA-B27
    • 50 fold increased risk
      • Increased likelihood of developing ReA
      • Increased likelihood of persistence
188
Q

Describe the clinical picture of extra-articular vs articular reactive arthritis

A

Clinical Picture - Joints

  • Lower limb asymmetric oligoarthritis
  • Dactylitis (sausage digits)
  • Enthesopathy (achilles tendonitis, plantar fasciitis)
  • Inflammatory back pain

Clinical Picture- Extra-Articular

  • Conjunctivitis, iritis, keratitis, episcleritis
  • Keratoderma blennorhagica and nail dystrophy
  • Urethritis, prostatitis, cystitis, cervicitis
  • Circinate balanitis
  • Stomatitis, diarrhoea
  • Rarely cardiac involvement with aortitis
189
Q

Describe the pathogenesis of reactive arthritis

A
  • Unclear
  • May involve cross reactivity between bacterial antigen and joint tissues leading to a perpetuating Th2 cell mediated response
  • Persistence of antigenic material (heat shock proteins) due to failed clearance possibly due to polymorphisms of Toll-like receptors
190
Q

What investigations should be done in suspected reactive arthritis?

A
  • Joint aspiration to exclude sepsis
  • Swabs - urethral/cervical
  • Screen for other related infections
  • Inflammatory markers ESR and CRP
  • Chlamydia serology
  • HLA-B27 for prognostic not diagnostic reasons
191
Q

How is reactive arthritis managed?

A
  • Mild - NSAID and simple analgesia
  • Moderate - NSAID, joint aspiration and corticosteroid injection
  • Severe or prolonged - consider DMARD
  • Antibiotics
    • Initial treatment should be directed to underlying infections
    • Some evidence for Lymecycline in chronic chlamydia related SARA
    • Debate continues about late and prolonged courses of antibiotics - N.B some antibiotics have anti-inflammatory properties
192
Q

Describe the prognosis of reactive arthritis

A
  • 70% of cases of ReA are self limiting
  • Severity at onset does not predict outcome
  • HLA-B27 +ve more likely to develop chronic arthritis
  • Options for Sulfasalazine, Methotrexate and anti-TNF alpha antagonists but limited evidence base for treatment
193
Q

What is important to ask in a history for suspected osteoarthritis?

A
  • Presenting complaint
    • Pain - SOCRATES
    • MSK
      • Any other joints affected?
      • Any functional defect?
      • Does joint give way?
      • Joint swelling?
      • Joint locking/clicking?
      • Joint stiffness?
  • PMH
  • Drug history - painkillers?
  • Social history
    • Occupation
    • Home circumstances
    • Smoking/alcohol
  • Family history
    • History of arthritis/AI disease
194
Q

What are the likely findings on examination in an osteoarthritic hip?

A
  • Limp
  • Antalgic gait
  • Examination of hip - wasting of buttock muscles on right side, pain on internal rotation and flexion of hip, fixed flexion deformity (Thomas’ test)tenderness in joint crease over right hip
  • Restricted range of movements
195
Q

What are the typical features in the clinical presentation of osteoarthritis?

A
  • Cardinal feature is pain - aggravated by movement and relieve by rest, as time goes by relief is less complete
  • Pain usually aching character and poorly localised
  • Typically symptoms follow an intermittent course w periods of remission (may last months)
  • Later stages - pain may waken from sleep
  • Muscle spasm around joint may add to pain
  • Stiffness on waking in morning and after periods of inactivity e.g. sitting common, as joint moved patients feel better
  • Limitation of motion
  • Hip - loss of abduction and internal/external rotation, flexion contracture masked by postural adjustment of pelvis and lumbar spine
  • On examination -
    • Joint deformity
    • Wasting of associated muscles
    • Joint swelling
    • Localised tenderness
    • Palpable osteophytes
    • Crepitus
    • Reduced range of motion compared with normal extremity
    • Limp or antalgic gait due to pain
196
Q

What tests would you do to confirm a diagnosis of osteoarthritis?

A
  • X-ray
    • Loss of joint space
    • Subchondral sclerosis
    • Bone cysts
    • Osteophytes
  • Blood tests - to rule out other diagnoses (should be within normal limits in OA)
    • FBC
    • ESR, CRP
    • Rheumatoid factor, anti-nuclear factor, anti-CCP
    • Calcium, phosphate, alkaline phosphatase
197
Q

How should a patient with osteoarthritis be managed?

A
  • Pain relief - analgesics and anti-inflammatory agents
  • Increasing mobilisation - joint movement and muscle tone may be improved by physiotherapy
  • Reducing load - weight loss, walking stick
  • Surgical options - osteotomy, arthrodesis, joint replacement, excision arthroplasty
    • Realignment osteotomy can relieve pain - may change the mechanical axis of the joint to allow weight bearing on a part of the articular surface which is not affected
    • Arthrodesis best performed when adjacent joints relatively unaffected, because after joint is fused there is more demand on them, may be considered in younger patients where a joint replacement would be expected to fail after a relatively short time (demands higher)
    • Joint replacement is best treatment of established OA of the hip/knee, patient and surgeon must weight up benefits of pain relief and improved function and the risks of major surgery
    • Sometimes an excision arthroplasty can be performed where the affected joint is excised and the resulting space is allowed to fill with fibrous tissue
198
Q

What are the normal components of a synovial joint?

A
  • Parts of bone in contact with each other covered by smooth articular cartilage
  • Joints surrounded by connective tissue capsule
  • Joint cavity
  • Inner surface of capsule and non-articular surfaces of bones covered by synovial membrane
  • Capsule reinforced by ligaments
  • Joint capable of movement
199
Q

What features can be seen macroscopically in osteoarthritis?

A
  • Loss of articular cartilage with eburnation (polishing) of surface
    • May first appear as softening of the joint surface, followed by fissuring, flaking or complete loss of articular cartilage with exposed subchondral bone
    • Usually starts where load across the joint is greatest e.g. medial compartment of knee
  • Subarticular cyst formation
    • Due to raise intraarticular pressure
  • Osteophytes formation at the joint margins
    • Bony outgrowths with occur peripherally or centrally in affected joints
  • Sclerosis (thickening of the subchondral bone)
200
Q

What features can be seen microscopically and histologically in osteoarthritis?

A

Microscopically

  • Fissuring, flaking then full thickness loss of articular cartilage
  • Subarticular cysts
  • Nodules of reactive bone and cartilage (osteophytes) at the joint margins
  • Sclerosis of subchondral bone

Histologically

  • Normal articular cartilage - chondrocytes, manufacture and lie in a matrix of collagens, proteoglycans and non-collagenous proteins
  • Osteoarthritic cartilage characterised by increased water content, alterations in proteoglycans, collagen abnormalities and binding of proteins to hyaluronic acid, rate of synthesis of DNA, collagen and proteoglycans increased
201
Q

What changes are seen in the synovium in osteoarthritis?

A

Detritus synovitis

  • In OA the synovium is secondarily involved, with flakes of bone and cartilage broken off from the damaged joint embedding the synovium and causing mild villous hyperplasia and chronic inflammation
  • Villous hyperplasia and chronic inflammation visible around BVs as well as fragments of cartilage detritus
202
Q

What are the causes of osteoarthritis?

A
  • Primary osteoarthritis - wear and tear
  • Secondary osteoarthritis - many underlying causes
    • Intra-articular fracture
    • High intensity impact
    • Ligament injuries
    • Avascular necrosis
    • Acromegaly
    • Paget’s disease
    • Previous joint sepsis
    • Haemophilia - repeated haemarthroses
    • Haemochromatosis
    • Ochronosis
    • Pseudogout
    • Charcot’s joint
203
Q

What are the systemic effects of rheumatoid arthritis?

A
  • General manifestations
    • Malaise
    • Weight loss
    • Fever
  • Skin manifestations
    • Subcutaneous nodules in 20-30% - on elbows, finger joints, achilles tendon, bony prominences, more common in smokers
  • Vasculitis
    • Small vessel inflammation leads to micro-infarction in peri-ungual area
    • In fingers and toes can produce rheumatoid ulcers in lower limbs
  • Haematological
    • Anaemia, usually of chronic disease (normocytic, normochromic)
    • B12 deficiency may occur with pernicious anaemia
    • Folic acid deficiency may occur with poor diet
    • Iron deficiency may be dietary or secondary to blood loss
  • Felty’s syndrome
    • Lymphadenopathy, splenomegaly, leucopaenia, thrombocytopaenia
    • Increased risk of infection and lymphoproliferative disease
  • Pulmonary
    • Asymptomatic involvement found in 50% of patients at post mortem
    • Effusions are exudates with lymphocytes
    • Rheumatoid nodules can mimic bronchial Ca on X-ray
    • Nodules in coal miners (Caplan’s syndrome)
    • Pulmonary fibrosis with progressive alveolar scarring
    • Pulmonary artery hypertension can follow pulmonary fibrosis
  • Cardiac involvement
    • Nodule formation
    • Amyloidosis
    • Pericarditis
    • Valve fibrosis
  • Ocular involvement
    • Kerato-conjunctivitis sicca (secondary Sjogren’s syndrome) affect 35% - more common with longstanding RA
    • Scleromalacia - thinning of sclera
    • Scleritis - acute pain and redness, normal visual acuity
  • Neurological involvement
    • Vasculitis of vasa-nervorum causing peripheral neuropathy
    • If many nerves involved - mononeuritis multiplex
  • Amyloidosis
    • Rare, complication of longstanding poorly controlled arthropathy
    • Deposition in the kidney produces proteinuria and in the heart cardiac failure
    • May also involve liver, spleen, intestine and skin
  • Renal involvement
    • Has tended to be a complication of older therapies or of amyloidosis in long-standing disease
204
Q

Which tests should be done to rule out other diagnoses in RA?

A

Urate

Vitamin D

CK

TFTs

HLA B27

ANA

205
Q

Why should NSAIDs be used with caution?

A
  • All NSAIDs should be used with caution in patients w/ renal impairment, CV disease, asthma and gastric ulcer disease - use in lowest possible dose for shortest duration possible to help reduce toxicity
    • Patient’s at high risk of gastric ulcer disease - >65 y/o, previous ulceration, on other medications increasing risk (e.g. steroids), should also be prescribed PPI or H2 receptor antagonist
206
Q

What benefit do steroids have in RA?

A

Reduce inflammation - reduced symptoms of RA and erosion on XR

207
Q

What are the side effects of steroids?

A

Adrenal suppression, risk of infection from opportunistic infection, osteoporosis, diabetes mellitus, cataracts, bruising/thinning of skin, CVS disease and hypertension

208
Q

How should pain be treated in RA?

A
  • Simple analgesia should be used - follow analgesia ladder
    • Non-opioid, adjuvant
    • Opioid for mild-moderate pain
    • Opioid for moderate-severe pain
  • Consider nerve root pain, use e.g. carbamazepine, amitriptyline or gabapentin
  • TENS machines are an effective and non-toxic means of relieving pain in many patients
  • Non-pharmacological measures such as acupuncture can be employed by physiotherapists to aid pain relief
  • Pain may have psychological component
209
Q

What is the aim of DMARD therapy in RA?

A

Aim for aggressive control of inflammation, consequently symptom control and reduced radiological damage

210
Q

How are DMARDs monitored?

A

Require drug monitoring in the form of regular blood testing

211
Q

When are biologic DMARDs used?

A

Can be used in patients with high disease activity (DAS28 >5.1) despite treatment with at least two standard DMARD therapies including methotrexate

212
Q

What is the benefit of biologic DMARDs in RA?

A

Potent immunosuppressants, shown to be highly effective in reducing the signs and symptoms of RA and radiological progression/damage

213
Q

List the types of bDMARDs

A
  • Anti-TNF therapy e.g. etanercept, adalimumab, infliximab
  • Anti-B cell therapy e.g. rituximab
  • Inhibition of interleukins e.g. tocilizumab (IL-6 receptor), anakinra (IL-1)
  • Newer therapies targeting JAK2 inhibition are still undergoing trial, but show encouraging preliminary results
214
Q

Describe the holistic management of RA

A
  • Education - need to understand disease (leaflets, rheumatology specialise nurses, internet)
  • Psychosocial - support from specialist social worker, may have major effect on earning capacity, esp. if employment altered
  • Diet - adequate calcium, possible weight reduction
  • Depression - can be major hurdle in treatment, needs to be addressed and treated
  • Co-morbid disease - CVS risks e.g. smoking, hypertension, hypercholesterolaemia (RA independent CV risk factor), osteoporosis risk should be addressed and baseline densitometry considered
  • Fertility - need advice re fertility and contraception, disease often quiescent then flares post partum
    • Methotrexate contraindicated in male and female patients 6 months prior to conception due to teratogenic effects
  • Self-help groups
215
Q

What is vasculitis?

A
  • Primary vasculitides
    • Group of autoimmune conditions
    • 200-300/million population
  • Inflammation of blood vessels - BVs in different organs may be affected by typically affects:
    • Skin
    • Kidneys
    • Lungs and airways
    • Joints
    • Nerves
    • ENT
216
Q

Describe the pathogenesis of vasculitis

A
  • Combination of genetic and environmental factors leads to autoimmune reaction
  • Blood vessel inflammation cause symptoms
217
Q

Why is vasculitis important?

A
  • Granulomatosis with polyangiitis (type of vasculitis) - 30% all cause mortality at 5 years and 40% at 10 years
    • Mortality has decreased from 80% mortality at one year to 80% survival at 2 years with advances in treatment
  • Life threatening are life and organ threatening but extremely treatable with avoidance of end organ damage if diagnosed early
218
Q

List the types of vasculitis

A
  • Classified according to size of blood vessels involved
    • Large vessel vasculitis - giant cell arteritis most commonly encountered
    • Medium vessel vasculitis - seen very infrequently
    • ANCA-associated small vessel vasculitis - important
      • Refers to 3 conditions - granulomatosis with polyangiitis (previously referred to as Wegner’s), microscopic polyangiitis and eosinophilic granulomatosis with polyangiitis (Churg-Strauss)
    • Immune complex small vessel vasculitis
      • Cryoglobulimaemic vasculitis
      • IgA vasculitis (Henoch-Schonlein)
      • Hypocomplementemic uritcorial vasculitis (anti-C1q vasculitis)
219
Q

What is giant cell arteritis?

A

Systemic vasculitis that affects the aorta and its major branches

220
Q

Describe the prevalence of giant cell arteritis

A
  • Prevalence increases with advancing age
    • Rare below age 50 years
    • Peak incidence 70-79 years
  • Female:male ratio 2-3:1
  • Prevalence highest in Caucasians from Northern Europe and Northern US
    • Extremely uncommon in non-white populations
221
Q

Describe the clinical presentation of giant cell arteritis

A
  • Headache
    • Temporal headache with tenderness
    • Subacute onset
    • Constant
    • Little relief with analgesics
  • Visual symptoms
  • Jaw claudication - 50% of patients
    • Pain on chewing, relieved on stopping mastication - can be a cause of weight loss, often as problematic as headache
  • Polymyalgia rheumatica symptoms - seen in 50% of patients with biopsy proven GCA
    • Subacute onset of shoulder and pelvic girdle stiffness and pain with no alternate diagnosis
  • Constitutional upset
222
Q

What are the complications of giant cell arteritis?

A
  • Visual loss
    • GCA major cause of irreversible visual loss
    • 14-70% of GCA patients depending on the series
    • Acute ischaemic optic neuropathy
    • Sudden painless loss of vision, occasionally preceded by amaurosis fugax
    • Most common cause of visual loss in GCA is ischaemia of the optic nerve head due to vasculitis and interruption of blood flow in the posterior ciliary arteries
    • Visual loss can be sudden and complete or evolve within 24-48 hours
  • Large vessel vasculitis
    • Vascular stenoses and aneurysms
  • CVA
    • 3% GCA patients
    • Obstruction or occlusions of internal carotid artery or vertebral arteries
223
Q

How is giant cell arteritis diagnosed?

A
  • Clinical presentation
    • Typical headache
    • Appropriate age
    • No alternate diagnosis
    • Associated clinical features - jaw claudication, constitutional symptoms, PMR. (polymyalgia rheumatica)
  • Clinical examination findings
    • Temporal artery asymmetry, thickening, loss of pulsatility, tenderness
  • Acute phase response
    • ESR CRP
      • Acute phase reactants often elevated but not specific
      • Normal acute phase reactants have a high negative predictive value - ESR below 40mm/hr very unusual in GCA
  • Temporal artery biopsy - gold standard
    • Positive if interruption of the elastic laminae with mononuclear inflammatory cell infiltrate within vessel wall
    • Multinucleated cells are typical (40-60%) but their absence does not exclude a diagnosis
    • Affects vessels focally and segmentally - histological signs of inflammation may be missed in segments of arteries that are arteritis free, length of biopsy is important
224
Q

What initial treatment should be commenced in giant cell arteritis?

A

Due to risk of visual loss, TAB should be performed as soon as possible but patients should commence treatment with corticosteroids prior to undergoing definitive investigations - positive histological results in patients receiving corticosteroid therapy for 14-21 days before biopsy

225
Q

What imaging can be done in giant cell arteritis?

A
  • Temporal artery USS
    • Classic sign - halo sign, hypoechogenic mural thickening observed in inflamed temporal arteries
    • Quickly procedure and non-invasive
    • High specificity, in symptomatic patients USS negates need for TAB
    • If USS normal but high probability of GCA go on to have TAB, if low probability of GCA and negative USS can practically exclude GCA
  • MRI
    • Not commonplace
    • Used for follow up of GCA patients - may develop aneurysmal and stenotic complications
  • PET CT
    • Can show inflammatory cell infiltration of vessel wall - one of the earliest events in LVV
    • Not helpful in diagnosis of cranial GCA due to high background uptake of FDG in brain
    • No information on wall structure or luminal flow
226
Q

What is the treatment for giant cell arteritis?

A
  • Maintain prednisolone 60mg for 1 month
  • Taper to 15mg by 12 weeks
  • Aim to discontinue corticosteroids by 12-18 months
  • Corticosteroid sparing therapy in patients with disease relapse on steroid sparing
    • Mycophenolate Mofetil
    • Methotrexate
    • Tocilizumab (anti-II-6)
  • Relapse = clinical presentation and acute phase response markers
227
Q

What is the differential diagnosis in cutaneous (small vessel) vasculitis?

A
  • Idiopathic
  • Drugs
  • Infection - HCV, HBV, gonococcus, meningococcus, staph
  • Secondary RA/CTD/PBC/UC
  • Malignancy - haematological > solid organ
  • Manifestation of small/medium vessel ANCA associated vasculitis
228
Q

Describe the epidemiology of Henoch-Schonlein Purpura

A
  • More common in children 2-11 y/o
  • Observed in adults, mean age 43 y/o
  • Males > females
  • Frequently self limiting illness, 4-16 weeks
  • Good overall prognosis
  • Mortality 1-2%
229
Q

What are the symptoms/complications of Henoch-Schonlein Purpura?

A
  • Classic purpuric rash - buttocks, thighs > lower legs
  • Urticarial rash, confluent petechiae, ecchymoses, ulcers
  • Arthralgia, arthritis (lower limb) in 75%
  • Complications
    • GI - pain, bleeding, diarrhoea, rarely intussusception, more common in children
    • Renal - IgA nephropathy, more common in adults, 3-15% of cases
    • Urological - orchitis
    • CNS - very rare
230
Q

Describe the approach to management in Henoch-Schonlein purpura

A
  • Exclude secondary causes
    • History - multisystem disease, recent infections, recent drugs, lifestyle
    • Examination
    • Immunology - RF, ANA, ANCA, PR3, MPO
    • Virology
  • Assess extent of involvement
    • Urinalysis/urine PCR
231
Q

Describe the management and prognosis of Henoch-Schonlein purpura

A
  • Often no treatment required
  • Corticosteroids for certain complications - testicular torsion, GI disease, occasionally arthritis
  • Steroids in renal disease - evidence limited, steroids do not prevent development or progression of renal disease
  • HSP frequently self-limiting
  • Relapses in 5-10%, relapse tends to occur within 12 months
232
Q

Why is ANCA associated vasculitis important?

A
  • Associated with the most morbidity and mortality
  • Has also seen the most therapeutic advances in recent years, most likely to benefit from early diagnosis
  • Collective group of conditions which share many manifestations
233
Q

List the types of ANCA associated vasculitis

A
  • Granulomatosis with polyangiitis (GPA) - formerly called Wegner’s
  • Microscopic polyangiitis (MPA)
  • Eosinophilic granulomatosis with polyangiitis (EGPA) - formerly called Churg Strauss vasculitis
234
Q

Describe the epidemiology of granulomatosis with polyangiitis

A
  • Incidence 2-12 per million population
  • Higher incidence in Northern European countries
235
Q

Describe the clinical features of granulomatosis with polyangiitis

A
  • Characterised by granulomatous necrotising inflammatory lesions of the upper and lower respiratory tract and often a pauci-immune glomerulonephritis
  • Classic triad of disease
    • Upper airway ENT
      • Rhinitis
      • Chronic sinusitis
      • Chronic otitis media
      • Saddle nose deformity
      • Nasal septal perforation
    • Lower respiratory
      • Parenchymal nodules +/- cavitation
      • Alveolar haemorrhage
    • Renal
      • Rapidly progressive pauci immune glomerulonephritis
  • Constituational symptoms
    • Fatigue
    • Weight loss
    • Fever/sweats
    • Myalgia/arthralgia
    • Failure to thrive in elderly
236
Q

List the organ specific features of granulomatosis with polyangiitis

A
  • Oral cavity - ulcerations throughout oral mucosa
  • Eye - psudeotumours, conjunctivitis
  • Nose - stuffiness, nosebleeds, saddle nose
  • Lungs - cavities, bleeds, lung infiltrates
  • Heart - pericarditis
  • Skin - nodules on the elbow, purpura
  • Kidneys - glomerulonephritis
  • Foot drop
237
Q

Describe the general approach to vasculitis care

A
  1. Make the correct diagnosis
  2. Assess disease severity
  3. Treat
  4. Assess disease activity and manage complications
238
Q

When should vasculitis be considered as a diagnosis?

A
  • Classical presentation
  • Constitutional symptoms
    • Loss of appetite, weight loss, malaise, night sweats, fevers
  • Multi-system disease (detailed systemic enquiry)
  • Repeated GP/hospital attendances
  • Disease not behaving as expected or ‘as it should’
239
Q

What tests are done to diagnose vasculitis?

A
  • Immunology
    • Immunological blood tests - ANCA, MPO, PR3
  • Pathology
240
Q

What are ANCA? How are they tested for?

A
  • Autoantibodies directed against the cytoplasmic constituents of neutrophils and monocytes
  • Should always be tested by 2 methods
    • Indirect immunofluorescence - gives p or cANCA staining patterns
    • ELISA for PR3/MPO - most commonly observed antigens
241
Q

How useful is ANCA?

A
  • Diagnosis
    • ANCA as a screening tool is unhelpful - many cases of false positive ANCA
  • Prognostic information
  • Assess response to treatment
  • Monitoring for early signs of relapse
242
Q

How should ANCA test results be interpreted?

A
  • Must be done in correct clinical setting
  • cANCA with PR3 very suggestive of GPA
  • pANCA with strong MPO suggestive of MPA (or EGPA)
  • Positive ANCA by indirect immunofluorescence but negative PR3/MPO is of doubtful significance and does not support a diagnosis of AAV
  • Not all AAV has a +ve ANCA
243
Q

How is vasculitis treated?

A
  • Remission induction - switch off vasculitis activity to induce remission
    • Drugs used tend to be associated with significant toxicity - higher dose = higher toxicity
    • Time pressure - longer to induce remission, higher likelihood of vasculitis induced organ damage and even death
    • 3-6 months
  • Remission maintenance
    • Prevent relapse
    • Lower drug toxicities
    • More prolonged therapy (2+ years)
244
Q

Describe drugs for remission induction in vasculitis

A

Prednisolone AND

  • Severe disease (life or organ threatening)
    • Cyclophosphamide (oral/IV)
      • Risks include infection, cytopaenias, malignancy, infertility
    • Rituximab, anti-B cell biologic agent
      • As effective as cyclophosphamide (better in relapsing disease)
      • Safer for repeated treatments - less malignancy
      • No risk of infertility
  • Moderate disease severity (not life or organ threatening)
    • Methotrexate
    • Mycophenolate
245
Q

Describe drugs for remission maintenance in vasculitis

A
  • Azathioprine
  • Methotrexate
  • Mycophenolate mofetil (less good - higher relapse rates
246
Q

Give examples of causes of abnormal and normal inflammation

A
  • Abnormal inflammation
    • Inflammatory arthropathies
    • Ulcerative colitis/Crohn’s
    • Psoriasis
  • Unwanted normal inflammation
    • Solid organs transplants
    • Bone marrow grafts
247
Q

Why are steroids good immunosuppressants?

A
  • Steroids are excellent immunosuppressants
    • Rapid onset (within hours)
    • Easy to administer
    • Able to treat wide variety of inflammatory conditions
  • Limited by intolerable adverse effects, especially at high dose
248
Q

What are the side effects of steroid sparing agents?

A
  • Weight gain and fluid retention
  • Glaucoma
  • Osteoporosis
  • Infection
  • Hypertension and hypokalaemia
  • Peptic ulceration and GI bleed
  • Psychological/psychiatric symptoms
249
Q

List non-steroid immunosuppressant drugs

A
  • Inhibitors of DNA synthesis
    • Methotrexate
    • Azathioprine
    • Mycophenolate
  • Lymphocyte signalling inhibitors
    • Cyclosporin
    • Tacrolimus
    • Sirolimus
    • Leflunomide
250
Q

How is methotrexate used in high and low doses?

A

High dose - cytotoxic chemotherapy agent

Low dose - immunosuppressant

251
Q

Describe the mechanism of action of corticosteroids

A
  • Block transcription factor binding sites to stop inflammatory protein genes being turned on
  • Cause transcription of anti-inflammatory protein by binding to anti-inflammatory protein genes
252
Q

Describe the mechanism of action of methotrexate

A
  • Blocks dihydrofolate reductase, thymidylate synthetase and ATIC to prevent DNA synthesis
  • Arrest of cells in the S-phase
253
Q

Describe the other actions of methotrexate

A
  • Folate antagonism
    • Similar structures of folate and methotrexate
  • Adenosine signalling
  • Methyl donors
  • Eicosanoids and MMPs
  • Cytokines
  • Adhesion molecules
254
Q

What are the adverse effects of methotrexate?

A
  • GI
    • Nausea, vomiting, diarrhoea
    • Hepatitis
    • Stomatitis
  • Haematological
    • Leucopaenia
  • Others
    • Frequent infections
    • Pulmonary fibrosis
255
Q

How is the toxicity of methotrexate reduced?

A

Folic acid used to reduce methotrexate toxicity - folic acid 5mg usually given 4 days after MTX

256
Q

What are the indications for methotrexate?

A
  • Most commonly used for rheumatological disease
    • Rheumatoid arthritis
    • Psoriasis and psoriatic arthropathy
  • Steroid sparing agent in giant cell arteritis
257
Q

Describe the clinical use of methotrexate

A
  • Given once a week with folic acid usually 4 days later
  • Normally given orally but can be given s/c if significant GI toxicity
  • Takes several weeks for effect to become apparent
  • Patients need regular monitoring bloods
258
Q

Describe the mechanism of action of azathioprine

A
  • Converted within cells into a nucleoside analog
  • Incorporated into DNA and RNA chains leading to termination of nucleic acid strands
  • Cell growth and metabolism halts
  • Preferential action of lymphocytes as other cells have purine salvage pathway
  • Other actions
    • Azathioprine given at too low a dose to prevent immune responses through cytotoxic effect
    • Other mechanisms must be required to inhibit immune response
    • Evidence that azathioprine inhibits T-cell co-stimulation through interference with CD28
259
Q

What are the adverse effects of azathioprine?

A
  • GI
    • Nausea, vomiting, diarrhoea
    • Hepatitis and cholestasis
  • Haematological
    • Leucopaenia
    • Thrombocytopaenia
  • Others
    • Frequent infections
    • Rapid onset alopecia
260
Q

Describe azathioprine metabolism

A
  • TPMT enzyme vital in reducing active drug in cells
  • Around 0.2-0.6% of individuals lack TPMT
  • Without TPMT there is accumulation of the most active metabolites of azathioprine within cells and development of severe toxicity
  • Checking TPMT activity prior to treatment with azathioprine prevents this problem
261
Q

What are the indications for azathioprine?

A
  • Most commonly used for inflammatory bowel diseases
    • Ulcerative collitis
    • Crohn’s disease
  • Other severe autoimmune disease
    • Myaesthenia gravis
    • Eczema
262
Q

Describe the clinical use of azathioprine

A
  • Given orally on a daily basis
  • Effects take several weeks to become evident
  • Need monitor bloods on a monthly basis
263
Q

Describe the mechanism of action of cylosporin

A
  • Small molecule inhibitor of calcineurin
  • Effect of inhibiting signalling transduction from the activated TCR complex
  • Profound in inhibition of T-cell activation
264
Q

What are the adverse effects of azathioprine?

A
  • Nephrotoxicity
  • Hypertension
  • Hepatotoxicity
  • Anorexia and lethargy
  • Hirsutism
  • Paraesthesia
  • Does not cause bone marrow suppression
265
Q

Compare tacrolimus (FK506) to cyclosporin

A

Tacrolimus is different class of drug to cyclosporin but similar mechanism of action

More potent activity

Very similar use to cyclosporin but may be a little better tolerated

266
Q

What are the indications for cyclosporin?

A
  • Usually given for organ transplantation
    • Liver
    • Kidney
    • Heart/lung
  • Sometimes used for inflammatory conditions
  • Can be used topically i.e. to skin or eye
267
Q

Describe the clinical use of cyclosporin

A
  • Given orally on a daily basis
  • Dose established using therapeutic drug monitoring
  • Many drug interactions through cytochrome P450 enzyme
  • Need to monitor blood tests regularly
268
Q

What are the disadvantages of immunosuppressants?

A
  • Effectiveness
    • Immunosuppressants often insufficient to control inflammatory disease with subsequent progression
    • Usually have slow rate of onset limiting usefulness in acute severe disease
  • Toxicity
    • Even at low dose, immunosuppressants have significant toxicity
    • Class effects include
      • Bone marrow suppression
      • Frequent infections
269
Q

What is biologic therapy?

A
  • Therapeutic agents synthesised biologically rather than chemically
  • Able to target specifically designated components of the immune system
  • Able to do so with minimal off target effects
  • Usually delivered by parenteral route
  • Relatively favourable side effect profile
270
Q

What types of agent is infliximab? What is its target?

A
  • Monoclonal ab
  • Target - soluble cytokine
271
Q

What type of agent is etanercept? What is its target?

A
  • Soluble receptor
  • Target - soluble cytokine
272
Q

What type of agent is Rituximab? What is its target?

A
  • Monoclonal ab
  • Target - surface marker
273
Q

What are the side effects of biologic therapies?

A
  • Adverse effects
    • Hypersensitivity reactions
    • Infusion reactions
    • Mild gastrointestinal toxicity
  • Infections
    • Much less frequent with most biologics than anticipated
    • In general infectious complications have not been significantly higher than placebo in clinical trials
274
Q

What infections are associated with anti-TNF therapy?

A
  • Increased risk of TB, particularly disseminated TB
  • Need to screen for latent TB before prescribing
  • Also increased risk of salmonella and listeria
275
Q

What infections are associated with rituximab (anti-CD20)?

A
  • Generalised increased risk of serious infection
  • High risk of hepatitis B reactivation, need to screen and prophylaxis if necessary
276
Q

Which infections are associated with Anti-IL1 therapy?

A

Increased risk of respiratory tract infection and pneumonia

277
Q

Which infections are associated with abatacept (anti-CD86)?

A

Increased risk of pneumonia and respiratory tract infection

Increased risk of TB but less than TNF blockade

278
Q

Describe the risk of TB with anti-TNF therapy

A
  • High risk of TB with anti-TNF therapy
  • Patients often have defective granuloma formation and disseminated disease
  • Need to screen for latent TB infection prior to treatment
    • Use an interferon gamma release assay (IGRA)
    • Treat for latent TB if required
279
Q

Describe the burden of back pain on the NHS and for UK businesses

A
  • 60-80% of adults experience back pain at some point in their lives
  • 6-9% adults see GP about back pain in UK each year
  • UK business loses 4.9 million work days per year
    • £1.6 billion direct costs
    • 75-85% workers absenteeism
280
Q

Describe the burden of back pain on patients personally

A
  • Financial
    • Work
    • Out of pocket expenses
  • >50% of patients with chronic back pain = insomnia
  • Psychological effects (including uncertainty about diagnosis)
    • Emotional stress
    • Relationship breakdowns
    • Severe emotional distress for partners
    • Limitations in fulfilling family tasks
281
Q

Compare acute and chronic back pain

A
  • Most acute back pain settles spontaneously
  • 7% –> chronic back pain >3 months
  • Most chronic back pain ‘mechanical’, ‘wear and tear’ but differential diagnosis includes
    • Medical and surgical emergencies
    • Life-threatening cancers
    • Treatable conditions
282
Q

Why is the source of back pain hard to diagnose?

A
  • Back pain = symptom, not diagnosis
  • Source of pain difficult to determine
    • ? Ligament, facet joint, paravertebral muscles and fascia, discs, spinal nerve roots (all implicated as pain generators)
  • Poor correlation of pain and imaging
  • Even after thorough work up - >85% isolated back pain unexplained
283
Q

What are the broad differential diagnoses for back pain?

A
  • Mechanical (97%) - non-specific low back pain (NSLBP)
  • Systemic
    • Infection
    • Malignancy
    • Inflammatory
  • Referred i.e. no pathology in back
284
Q

List the features of non-specific low back pain

A
  • Onset at any age, variable rate
  • Generally worsens with movement or prolonged standing
  • Better with rest
  • Early morning stiffness <30 mins
285
Q

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

A
  • Lumbar strain/sprain
    • Most common cause
    • Muscle spasms usually settle 24-48 hours
  • Degenerative disc disease (‘spondylosis’)
    • Many - asymptomatic disc disease
    • Increase with flexion, sitting, sneezing
  • Degenerate facet joint disease
    • More localised
    • Increase with extension
  • Disc prolapse, spinal stenosis
  • Compression fractures
286
Q

How is non-specific LBP managed?

A
  • Keep diagnosis under review
  • Reassurance
    • Careful with terminology used
  • Education, promote self-management
    • Advise to stay active
  • Exercise programme and physiotherapy
  • Analgesics as appropriate (avoid opiates)
  • Also acupuncture

NOT injections, traction, lumbar supports

287
Q

How does a prolapsed disc develop?

A
  • IVD - fibrous outer ring (annulus fibrosus) and middle nucleus pulpsosus
  • Part of the softer middle disc bulges through the fibrous outer ring and presses on the nerve as it leaves the spinal cord
288
Q

What are the clinical effects of disc prolapse?

A
  • May be acute, increase cough
  • Typically leg > back pain, ‘sciatica’, ‘radiculopathy’
  • Leg pain = dermatomal distribution
  • Straight-leg raising test +ve
  • Reduced reflexes
289
Q

How is a disc prolapse managed?

A
  • Most resolve spontaneously within 12 weeks
  • Wait with investigations –> MRI (X-ray)
  • <10% need surgery (helps leg, not back pain)
    • Surgery better outcomes at 6 weeks than conservative
    • But no clear benefit at 1 year
290
Q

What are the symptoms of cauda equina syndrome?

A
  • Neuropathic symptoms
    • Bilateral sciatica
    • Saddle anaesthesia
  • Bladder or bowel dysfunction
    • Reduced anal tone
291
Q

What usually causes cauda equina syndrome?

A

Large prolapsed disc

292
Q

How should cauda equina be managed?

A

Urgent neurosurgical review

293
Q

What is spinal stenosis?

A
  • Anatomical narrowing spinal cord
    • Congenital and/or degenerative
    • Often presents with ‘claudication’ legs/calves
      • Worse walking, rest in flexed position
    • Natural history variable, includes improvement
294
Q

What investigations should be done in spinal stenosis?

A

X-ray, MRI

Imaging only if diagnosis uncertain or will alter management

295
Q

Should surgery be done in spinal stenosis?

A

Surgery generally high risk

296
Q

What is spondylolisthesis?

A

‘Slip’ of one vertebrae on one below

297
Q

What are the symptoms of spondylisthesis?

A
  • 3-6% population = pars interarticularis defect, asymptomatic in most
  • Pain may radiate to posterior thigh
  • Increase with extension
298
Q

How should spondylisthesis be managed?

A

Rarely needs surgery (if severe)

299
Q

Which patients are most vulnerable to vertebral compression fractures?

A

Elderly patients

Associated osteoporosis - risk of recurrence high

300
Q

What are the symptoms of a vertebral compression fracture?

A
  • Often sudden onset, severe
  • Radiates in ‘belt’ around chest/abdomen
  • Most pain settles in 3/12, chronic mechanical and kyphosis
301
Q

Which investigations should be done in suspected vertebral compression fractures?

A

X-ray, DEXA scan

302
Q

How are vertebral compression fractures treated?

A
  • Conservative (analgesia)
  • Calcitonin
  • Vertebroplasty (cement) or kyphoplasty (balloon)
303
Q

Describe the location of bone fractures due to spinal osteoporosis by age

A
  • 60 y/o = thoracic
  • 65 y/o = thoracic, upper lumbar
  • 75 y/o = thoracic, upper and lower lumbar
304
Q

What can cause referred pain in the back?

A

Retroperitoneal Structures

  • Aortic aneurysms
    • CVS features (BP, increased HR), collapse, pulsating abdominal mass
  • Acute pancreatitis
    • Epigastric pain, relief lean forwards, unwell
  • Peptic ulcer disease (duodenal)
    • Epigastric pain (meals), history PUD, vomit, blood/melaena
  • Acute pyelonephritis/renal colic
    • History UTI/stones, unwell, radiation, haematuria, frequency
  • Endometriosis/gynae
305
Q

What are the systemic causes of back pain?

A

Infection - discitis, osteomyelitis, epidural abscess

Malignancy

Inflammatory

306
Q

Which patients are at high risk of infective discitis?

A

Immunosuppressed, diabetes, IV drug use

307
Q

What are the systemic symptoms of infective discitis?

A

Fever (may be PUO), weight loss

308
Q

Describe the back pain in infective discitis

A

Constant back pain - rest, night-pain

309
Q

Which investigations should be done in the diagnosis of infective discitis?

A
  • Blood tests - FBC, ESR, CRP, blood cultures
  • Imaging - X-ray (end-plate/vertebral destruction), MRI
  • Radiology guided aspiration
310
Q

What is the most common causative organism of infective discitis?

A

Staph aureus

311
Q

How is infective discitis managed?

A

IV antibiotics +/- surgical debridement

Look for source

312
Q

What can be a complication of untreated infective discitis?

A

Soft tissue extension - paravertebral abscess

313
Q

What would give a high index of suspicion for malignancy in back pain

A
  • History of malignancy
    • Lung, prostate, thyroid, kidney, breast
  • Onset age >50 years
  • Constant pain, often worse at night
  • Systemic symptoms, primary tumour signs and symptoms
314
Q

What imaging should be done in suspected malignancy in back pain?

A

X-ray (lytic/destructive), MRI, bone scan

Look for primary

315
Q

Describe typical inflammatory back pain

A
  • Onset <45 years (often teens)
  • Early morning stiffness >30 mins
  • Back stiff after rest and improves with movement
  • May wake 2nd half night, buttock pain
316
Q

How prevalent is inflammatory back pain?

A

Of all patients with chronic LBP (>3 months)

  • 10-15% have inflammatory symptoms (i.e. inflammatory back pain = symptom complex, not a diagnosis)
  • 1% have condition = ankylosing spondylitis or axial spondylarthritis (axSpA)
317
Q

How should back pain be approached diagnostically?

A
  • History (RED flags)
  • Examination - back, neurology, abdomen
  • Most = non-specific LBP - no further investigation
  • Keep diagnosis under review - investigate if unusual/new features
  • Imaging = X-ray, MRI
  • Bloods - if suspect infective/inflammatory, myeloma screen
318
Q

List the symptoms/signs in back pain that are red flags

A

Symptoms:

  • New onset age <16 or >50
  • Following significant trauma
  • Previous malignancy
  • Systemic - fevers/rigors, general malaise, weight loss
  • Previous steroid use
  • IV drug abuse, HIV or immunosuppressed
  • Recent significant infection
  • Urinary retention
  • Non-mechanical pain (worse at rest ‘night pain’)
  • Thoracic spine pain

Signs:

  • Saddle anaesthesia
  • Reduced anal tone
  • Hip or knee weakness
  • Generalised neurological deficit
  • Progressive spinal deformity
319
Q

What are the yellow flags in back pain?

A

Biopsychosocial model = patients likely to develop chronicity:

  • Attitudes - towards the current problem
  • Beliefs - misguided belief that they have something serious
  • Compensation - awaiting payment for an accident/RTA
  • Diagnosis - inappropriate communication, patients misunderstanding what is meant, examples being ‘your disc has popped out’ or ‘your spine is crumbling’
  • Emotions - other emotional difficulties e.g. depression/anxiety
  • Family - either over bearing or under supportive
    • Work/relationships
320
Q

Compare the features of mechanical and inflammatory back pain

A
  • Age of onset
    • Mechanical - any age
    • Inflammatory - usually <40 years
  • Onset
    • Mechanical - variable, may be acute
    • Inflammatory - insidious
  • Morning stiffness
    • Mechanical - <30 mins
    • Inflammatory - >30 mins
  • Exercise
    • Mechanical - may worsen pain
    • Inflammatory - improves pain (stiffness)
  • Rest
    • Mechanical - often improves
    • Inflammatory - no improvement
  • Night
    • Mechanical - may improve
    • Inflammatory - may wake during second half of night
321
Q

Describethe criteria for ankylosing spondylitis

A

Modified New York Criteria for Ankylosing Spondylitis (1984)

  • Clinical criteria
    • Low back pain and stiffness for more than 3 months which improves with exercise, but is not relieved by rest
    • Limitation of motion of the lumbar spine in both the sagittal and frontal planes
    • Limitation of chest expansion relative to normal values correlated for age and sex
  • Radiological criterion
    • Sacroiliitis grade >2 bilaterally or grade 3-4 unilaterally

Definite ankylosing spondylitis if the radiological criterion is associated with at least 1 clinical criterion.

322
Q

Describe the spectrum of axial spondyloarthritis

A
  • Non-radiographic axSpA - X-ray negative
  • Radiographic axSpA - X-ray positive sacroilitis
  • X-ray positive sacroilitis and/or spinal changes
323
Q

Describe the pathological features of spondylarthritis

A
  • Enthesitis and dactylitis
  • Axial involvement
  • New bone formation/ankylosis
  • Extra-articular manifestations
  • Heterogeneity
324
Q

Describe the classification criteria for axial SpA

A

ASAS Classification Criteria for Axial SpA:

  • In patients with >3 months back pain and age onset <45 years and -
    • Sacroiliitis on imaging plus >1 SpA features
      • Inflammatory back pain
      • Arthritis
      • Enthesitis (heel)
      • Uveitis
      • Dactylitis
      • Psoriasis
      • Crohn’s/colitis
      • Good response to NSAIDs
      • Family history for SpA
      • HLA-B27
      • Elevated CRP
    • OR HLA-B27 plus >2 other SpA features

Sacroiliitis on imaging

  • Active (acute) inflammation on MRI highly suggestive of sacroiliitis associated with SpA
  • Definite radiographic sacroiliitis according to mod NY criteria
325
Q

What are the differences between classification and diagnostic criteria?

A
  • Classification criteria
    • Diagnosis is already known
    • Aim for homogenous population for trials
    • Do not have step to ‘exclude’ other potential causes
  • Diagnostic criteria
    • Diagnosis not known
    • Require exclusion of other potential causes for symptoms/results
326
Q

How is axSpA diagnosed?

A

Clinical diagnosis

  • Context
  • Pre-test likelihood
  • Exclude other causes
327
Q

Describe the epidemiology of axSpA and AS

A
  • Onset <45 years
  • Many in late teens-early adulthood 15-35 years
  • AS = mainly male
  • axSpA =approaching 1:1 gender split
  • AS prevalence = 0.05-0.5% population
  • axSpA = limited data, 0.5-1.5% population
328
Q

List the symptoms of axSpA

A
  • Inflammatory back pain
  • Fatigue
  • Arthritis in other joints - hips, knees
  • Enthesitis - achilles tendon, plantar fasciitis
  • Inflammation outside joints - extra-articular
    • Eye - uveitis
    • Skin - psoriasis
    • Bowel - Crohn’s disease/ulcerative colitis
    • Other - heart, lungs, osteoporosis
  • Family history of above
329
Q

What imaging is recommended for axSpA?

A
  • X-rays
    • Pelvis AP films (sacroilitis)
    • Lumbar spine films in ankylosing spondylitis
      • Sclerosis - shiny corners of vertebral bodies
      • Syndesmophytes (and spondylophytes)
      • Bridging syndesmophytes
  • MRI allows earlier identification of sacroilitis
    • Beware of mimics - infective sacroilitis, insufficiency fracture
330
Q

How can MRIs be misleading in the diagnosis of AS and axSpA?

A

MRI changes may reflect normal biomechanics:

  • Positive MRI - bone marrow oedema of sacroiliac joints
    • Chronic low back pain - 21%
    • Postpartum - 63%
    • Healthy - 23%
    • Post-partum deep/extensive bone marrow oedema, axSpA/post-partum only - 57%
    • Recreational runners - 30-35%
    • Elite ice hockey players - 41%
  • No erosions
  • Clinical context key
331
Q

How are AS and axSpA diagnosed?

A

Remains a clinical diagnosis

  • Suggestive symptoms (including IBP)
  • Imaging
  • Associated features
    • Family history of AS/axSpA
    • Extra-articular - psoriasis, colitis, uveitis
  • Other investigations
    • HLA-B27 status
    • CRP/ESR (usually normal)
  • Exclude other causes or explanations
332
Q

What causes axSpA and AS?

A
  • Genetics = susceptibility
    • HLA-B27+ >75% AS vs 8% Caucasian population
    • Lots of other mutations - overlap with other diseases
      • Esp. IL-23R, Th17 response
  • Environment
    • ?infection
    • Microbiome in gut and skin
  • Biomechanics
  • IL-23/17 Pathway Implicated in Enthesitis and axSpA:
333
Q

What are the treatment options for axSpA?

A
  • NSAIDs
  • Education, exercise, physical therapy, rehabilitation, patient associations, self help groups
  • Analgesics
  • Surgery
  • Biologic drugs
334
Q

What can patients with axSpA do to help manage their condition?

A
  • Exercises - ‘back to action’
  • Stop smoking
    • Higher rates of AS
    • Higher disease activity
    • Worse physical function
    • Poorer quality of life
    • More X-ray progression
    • Less likely to respond to biologics
  • Self management strategies
  • Health - diet and sleep
335
Q

Which biologic drugs are used in axSpA?

A
  • TNF inhibitors
  • IL-12A inhibitors
336
Q

Describe the pathogenesis of osteoarthritis

A
  • Joint gets destroyed
  • The surface of the joint becomes eroded
  • Cartilage wears away
  • Osteophytes may form
  • Subchondral changes happen
  • Joint stops functioning as normal
  • Surrounding tissues - capsule, ligaments, tendons, muscles, adjacent joints, mobility are affected
337
Q

Describe the pathology of osteoarthritis

A
  • Proteolytic breakdown of cartilage matrix from an increased production of enzymes, such as metalloproteinases
  • The proteoglycan and collagen fragments released into the synovial fluid as the disease progresses
  • Erosion to the cartilage roughens surface and fibrillation which narrows the joint space
  • Increased production of synovial metalloproteinases, cytokines and TNF that can diffuse back into the cartilage to destroy soft tissue around the knee
338
Q

Describe the typical history in a patient presenting with osteoarthritis

A
  • Pain
  • Stiffness
  • Swelling
  • Clicks/crepitus
  • Deformity
  • Impacts
    • Mobility
    • Walking/support/instability
    • Sleep
    • Functioning
    • Normal activities
    • Recreational activities
339
Q

What examination should be done in a patient presenting with osteoarthritis?

A
  • General examination, incl. gait
  • Systemic examination
  • Specific joint examination
  • Look/feel/move/special tests
  • Neurovascular status distally
  • Leg length measurement - shortening in arthritis of knee/hip
340
Q

Which investigations should be done in a patient presenting with osteoarthritis?

A
  • Radiographic
  • Blood
  • Urine
  • Aspirate
341
Q

Describe the grading of osteoarthritis on X-ray

A
  • Grade 0 - no radiographic features of OA are present
  • Grade 1 - doubtful joint space narrowing (JSN) and possible osteophytic lipping
  • Grade 2 - definite osteophytes and possible JSN on anteroposterior weight-bearing radiograph
  • Grade 3 - multiple osteophytes, definite JSN, sclerosis, possible bony deformity
  • Grade 4 - large osteophytes, marked JSN, severe sclerosis and definite bony deformity
342
Q

How is mild high riding congenital hip dislocation managed?

A

Stage 1 (minor)

  • If patient not predisposed to OA, no special therapeutic treatment for stage 1 (symptoms minimal if any)
  • Lifestyle considerations e.g. regular exercise may be helpful, weight loss if obese slows progression
  • Supplements e.g. glucosamine and chondroitin may be recommended by some but no hard evidence to support their use
  • Role of prophylactic surgery is controversial and is not generally recommended
  • Future - genetic/biological therapy
343
Q

How is mild high riding congenital hip dislocation managed?

A

Stage 2 (mild) -

  • Physiotherapy - different nonpharmacologic therapies to help relieve pain and discomfort
  • Many recommended a strict regimen of exercise and strength training for increased joint stability and weight loss
  • Additionally, braces, knee supports or shoe inserts may be used to protect knee from stress
  • Analgesia as required
  • Role of prophylactic surgery controversial and is not generally recommended
  • Future - genetic/biological therapy
344
Q

How is moderate high riding congenital hip dysplasia managed?

A

Stage 3 (moderate) -

  • Over the counter NSAIDs or pain-relief therapies may be prescribed
  • If not effective stronger pain medicine e.g. codeine and oxycodone etc.
  • If don’t respond to physical therapy, weight loss, use of NSAIDs, brace, acupuncture, head/cold therapy, massage, local intra-inflammatory gels
  • May require intra-articular injections of steroid/hyaluronic acid into the joint
  • Not curative but can give short-midterm relief of symptoms - risk of infection/repetition/shortening effect
  • Some may consider prophylactic realignment surgery
345
Q

How is high riding congenital hip dysplasia managed?

A

Stage 4 (severe) -

  • If do not respond to analgesia, physical therapy, weight loss, use of NSAIDs, brace, acupuncture, heat/cold therapy, massage, local anti-inflammatory gels
  • Surgery
    • Realignment
    • Replacement - most common
    • Excision
    • Fusion
    • Biological - future
346
Q

Describe the staging of knee osteoarthritis

A
  • Stage 1
    • Symptoms
      • No pain
      • Bones not rubbing or scraping each other
    • Treatment
      • No treatment
      • Exercise
      • Healthy lifestyle
      • Knee osteoarthritis brace
  • Stage 2
    • Symptoms
      • Minor pain after walking or running
      • Joint stiffness
      • Bones not rubbing or scraping each other
      • Tenderness
    • Treatment
      • Exercise
      • Healthy lifestyle
      • Over the counter medications
      • Knee osteoarthritis brace
  • Stage 3
    • Symptoms
      • Minor pain after walking or running
      • Joint stiffness
      • Tenderness
      • Bones rubbing/scraping each other
    • Treatment
      • Exercise
      • Healthy lifestyle
      • Prescribed medications
      • Injections
      • Knee osteoarthritis brace
  • Stage 4
    • Symptoms
      • Joint stiffness
      • Extreme pain after walking or running
      • Tenderness
    • Treatment
      • Healthy lifestyle
      • Prescribed medications
      • Injections
      • Surgery
      • Knee osteoarthritis brace
347
Q

Which joints can be replaced?

A
  • Knee - total knee replacement, uni-compartmental, patello-femoral replacement
  • Hip
  • Ankle
  • Shoulder
  • Elbow
  • Wrist
  • Finger
  • Toe
  • Disc
348
Q

What are the basic principles of joint replacement?

A
  • Take away the diseased surface
  • Replace with artificial material that needs to stick to bone
349
Q

Which materials can be used in joint replacement?

A
  • Titanium, molybdenum, vanadium alloys
  • Cobalt chrome alloys
  • Ultra high molecular weight polyethylene
  • Ceramics
  • Coated implants - porous/hydroxyapatite/tantalum etc.
  • Polished implants
350
Q

List the modes of fixation in joint replacement

A
  • Uncemented - usually coated
    • Primary fixation by Pressfit, secondary by bone growth
  • Cemented - usually polished
    • Primary and secondary fixation with cement (polymethyl methacrylate)
  • Hybrid
    • Cup uncemented, stem cemented
  • Reverse hybrid
    • Cup cemented, stem uncemented
351
Q

Describe the surgical procedure involved in joint replacement

A
  1. Positioning
  2. Exposure
  3. Bone preparation
  4. Implantation
  5. Reduction
  6. Assessment
  7. Closure
  8. Post-op checks
  9. Rehabilitation
352
Q

Describe the important muscular relationships of the posterior hip

A
  • Superiorly - piriformis muscle (sciatic nerve runs under)
  • Superior and inferior gemelli muscles with obturator muscle between
  • Quadraceps femoris inferiorly
353
Q

List the methods of navigation in joint replacement

A
  • Reamer navigation
  • Computer navigation - shown on screen
  • Navigated rasping of shaft
354
Q

List the methods of canal preparation in hip replacement

A
  • Straight reamers
  • Femoral broaches
355
Q

How is joint replacement evaluated post-operatively?

A

X-ray

356
Q

Describe post-op rehabilitation in joint replacement

A
  • Mobilisation
  • Discharge
  • Home exercise program
  • Removal of clips/sutures if needed
357
Q

What modern development has allowed quicker rehabilitation after joint replacement surgery?

A

Early Recovery Program

  • Preop education
  • Preop exercise
  • Joint school - physiotherapist, occupation therapist, discharge planning
  • Minimal soft tissue dissection surgery
  • Faster rehab and discharge post-op
  • 2 weeks to 1-4 days
358
Q

What modern surgical techniques have developed in joint replacement surgery?

A
  • Computer assisted navigation
  • Robotics
359
Q

What are the advantages of total hip replacement?

A
  • Cup - orientation
  • Stem - orientation
  • Assessment
  • More insight
  • May better surgical technique
  • MIS/patient demands
  • Better anatomic positioning? Long term results
  • Consistency with planning
  • Leg length and offset
  • Reduces the ceramic on ceramic noise
360
Q

What are the potential complications of hip and knee replacement surgery?

A
  • General (with both TKR and THR) - DVT/PE, infection, neurovascular damage, swelling, stiffness, non/partial relief/recurrence, anaesthetic problems, renal, gastric, respiratory, cardiac, cerebral compromise, death, failure of procedure, revision
  • Specific hip - dislocation, fracture, leg length discrepancy, hip noise, implant breakage/failure
  • Specific knee - stiffness, fracture, ligament or tendon damage, kneeling difficultly, failure, revision, dissatisfaction rates (10-20%)
361
Q

What are the aims in hip arthroplasty?

A
  • To achieve a stable, well functioning hip with well balanced tissues that lasts forever
    • Component fixation - surgeons choice?
    • Bearing surfaces - surgeons choice?
    • Leg length - surgical technique
    • Offset - surgical technique
    • Centre of rotation - surgical technique
    • Orientation of cup and femur - surgical technique
  • Accuracy and precision in THR
    • Highly desirable
    • Less than half of cups are in desired position
362
Q

How does navigation compare to robotics in joint replacement?

A
  • Navigation is the guidance system
    • Intra-operative feedback
    • Surgeon performs and is in control
  • Robotics
    • Pre-op 3D planning
    • Types
      • Active - drives itself, autopilot (ROBODOC)
      • Semi-active (haptic) - Mako
        • Defines boundaries - surgeon still in control but robot restricts for surgeon errors
363
Q

What are the operative steps in total knee replacement?

A
  • Exposure
  • 3 bony cuts - distal femoral, rotational femoral (AP), proximal tibial
  • Soft tissue balancing - ROM, collateral balancing (medio lateral soft tissue release), patellar tracking
  • Assessment
  • Closure
364
Q

What are the consequences of incorrect alignment, position and rotation of a joint prosthesis?

A
  • Compromised function
  • Abnormal wear
  • Premature loosening
  • Patellofemoral problems
365
Q

What are the benefits of computer navigated total knee arthroplasty?

A
  • Studies have shown navigated total knee arthroplasty better functional outcomes than conventional total knee arthroplasty
  • Well proven
  • Component alignment in all three planes
  • Contact stress reduction
  • Reduced fat embolism
  • Reduced blood loss
  • MIS surgery
  • Kinematics
  • Soft tissue releases
  • Longevity
366
Q

How satified are patients following total knee replacement?

A
  • At 1 year out:
    • Very satisfied 88%
    • Satisfied 7%
    • Unsure 4%
    • Dissatisfied 1%
367
Q

How risky is joint replacement compared to other surgeries?

A
  • Surgeon >7 year experience, does >75 cases/year
  • Use any implant in top group
  • Unconstrained, uncemented
  • Effective infection control
  • Computer assisted navigation - improves outcomes further, lower revision rates
368
Q

What is the role of a rheumatology clinical nurse specialist?

A
  • Advanced level nurses offering specialist care in a specific field
  • Education/self management
  • Support - referrals to other MDT
  • Clinical role e.g. mediation r/v, joint aspiration/injection, ultrasound
  • Patient helpline management
  • Research/audit
369
Q

What common helpline calls are made to rheumatology clinical nurse specialists?

A
  • Medication advice
  • Flare
  • Vaccination advice
  • Joint injection
  • GP advice abnormal bloods
  • Family planning
  • Biologic advice
  • Drug administration
  • Travel advice
  • Allergy advice
  • PIP appeal support
  • External support group (NRAS, arthritis UK)
  • Appointments
  • General disease advice
  • Unrelated medical advice
370
Q

What monitoring should be done with hydroxychloroquine treatment?

A

No blood monitoring required

Yearly eye tests at opticians as can cause retinal toxicity

371
Q

Describe the dosing of commonly used DMARDs

A
  • Methotrexate - taken once weekly (same day)
    • Starting dose - varies depending on severity of disease, co-morbidities
    • Dosing 7.5mg-30mg, option to switch to s/c preparation
  • Sulphasalazine - taken daily
    • Dosing - 40mg/kg, 500mg tablets - start 1 daily and increase
  • Hydroxychloroquine - taken daily
    • Dosing - >62kg = 400mg daily, >46kg <62kg = 200mg/400mg alternate days, <46kg >31kg = 200mg daily
372
Q

How is DAS28 used to determine RA treatment?

A

Scores of >5.1 on two occasions is the minimum criteria for eligibility of biologic therapies

Drop of at least 1.2 points is required for continuation of treatment

373
Q

Which DMARDs are used in psoriatic arthritis?

A

Methotrexate

Sulphasalazine

Leflunomide

Cyclosporin

IM gold

374
Q

How is psoriasis severity assessed?

A

Psoriasis area and severity index - PASI

375
Q

List the disease assessment tools used in ankylosing spondylitis

A

BASDAI – Bath Ankylosing Spondylitis Disease Activity Index

BASFI – Bath Ankylosing Spondylitis Functional Index

BASMI – Bath Ankylosing Spondylitis Metrology Index

376
Q

Describe the use of BASDAI in ankylosing spondylitis

A
  • Gold standard for measuring and evaluating disease activity
  • 6 questions of 5 major symptoms
    • Fatigue
    • Spinal pain
    • Areas of localised tenderness (enthesis)
    • Morning stiffness duration
    • Morning stiffness severity
  • Scale from 1 to 10 (1 for no problem, 10 for worst problem)
  • Scores: 4 or greater – suboptimal control of the disease
377
Q

Describe the use of BASFI in ankylosing spondylitis

A
  • Assess the function of a person with Ankylosing Spondylitis
  • From easy to impossible

BASFI questions:

  • Putting on socks or tights without help or aid
  • Bending from the waist to pick up a pen from the floor without aid
  • Reaching up to a high shelf without help or aids
  • Getting up from an armless chair without your hands or any other help
  • Getting up off the floor without help from lying on your back
  • Standing unsupported for 10 mins without discomfort
  • Climbing 12-15 steps without using a handrail or walking aid
  • Looking over your shoulder without turning your body
  • Doing physically demanding activities (e.g. physiotherapy, exercises, gardening or sports)
378
Q

Describe the use of BASMI in ankylosing spondylitis

A

Measures spinal mobility

Series of measurements carried out by physiotherapists

379
Q

What are the criteria for biologic agents in RA, psoriatic arthritis and ankylosing spondylitis?

A
  • RA - DAS-28 > 5.1
    • 3 or more tender joint and 3 or more swollen joints
    • Failed trials of two DMARDs, including MTX (unless contraindicated).
  • PsA - 3 or more tender joint and 3 or more swollen joints
    • Failed trials of two DMARDs, including MTX (unless contraindicated) ( CASPAR guidelines)
  • AkSpa – failed two NSAIDs
    • 2 consecutive BASDAI > 4 – taken 4 weeks apart
380
Q

List the biologic therapies used for RA, psoriatic arthritis and ankylosing spondlyitis

A
  • Etanercept - RA, PsA, AkSpA
  • Adalimumab - RA, PsA, AkSpA
  • Certolizumab - RA, PsA, AkSpA
  • Golimumab - RA, PsA, AkSpA
  • Rituximab - RA
  • Tocilizumab - RA
  • Secukinumab - PsA, AkSpA
  • Ustekinumab - PsA
  • Infliximab - RA, PsA
381
Q

Describe the common overlap of roles between physios and OTs

A
  • Education and self management
    • Educate - patient condition and flare management, behaviour modification and graded activity planning to facilitate better joint management
    • Enable - addressing any difficulties to particular functions/activities at home or work
    • Empower - giving patients confidence to know how to manage their condition long term, awareness of who can be involved in their management and services to support them and how to access them
382
Q

Describe the role of physiotherapy in rheumatology assessment

A
  • Identify patient condition and how if affects them physically and to what degree an individuals function is affecting mobility, posture etc.
  • Examine MSK system to get baseline of current status
  • Consider other body systems e.g. neuro, cardiovascular etc.
  • Any special equipment requirements
  • Identify the patients current self management and coping strategies
  • What physiotherapy interventions are needed
  • Discuss our assessment findings with the patient and in conjunction with them devise a goal orientated treatment plan
383
Q

What do the guidelines say about the role of physiolotherapy in RA?

A
  • SIGN management of RA
    • Principles of management - patient education, MDT working includes access to PT (among others)
    • Role of the MDT included high level evidence that highlights specific exercise therapy
  • NICE guidelines in RA
    • Access to specialist PT to - improve general fitness and encourage regular exercise, learn exercises to enhance joint flexibility, muscle strength and management of other functional impairments
384
Q

What are the benefits of manual and exercise therapy in rheumatological conditions?

A
  • Joints - swelling, ROM, pain
  • Muscles - joint stability, strength
  • Bone - bone density, cachexia
  • Sleep
  • Mood
  • Function - including ability to stay in work
  • Co-morbidities - CV fitness, metabolic syndrome, respiratory etc.
  • Supported by inflammatory exercise classes, hydrotherapy
385
Q

What pain management strategies can be used by physiotherapists in rheumatological diseases?

A
  • Supports - taping, splinting, walking aids
  • Acupuncture
  • Central sensitisation inventory

In conjunction with other therapies to allow rehabilitation to progress

386
Q

What is the role of occupational therapy in rheumatology?

A
  • Supporting self managment
    • Lifestyle management courses
      • Fatigue management
      • ‘Looking After Your Joints’
      • NRAS self management
  • Assisstive devices
  • Managing fatigue
  • Vocational rehabilitation
387
Q

How are assisstive devices used in rheumatology?

A
  • Use to accommodate a physical/functional limitation
  • Promote good posture during an activity - related to joint protection
  • Equipment more accessible
  • Consider contra-indications
  • Assessment and advice required to prevent inappropriate use/cost
388
Q

How do OTs help manage fatigue in rheumatological conditions?

A
  • Sleep hygiene
  • Pacing, planning, prioritising
  • Physical activity
  • Goal setting
  • Activity diaries
389
Q

How do OTs help with vocational rehabilitation in rheumatological conditions?

A
  • Ergonomic advice
  • Self management at work
  • Workplace assessment
  • Advice on work adjustments
  • Signposting to other agencies
390
Q

Describe the splinting techniques used in rheumatological conditions

A
  • Splinting of the thumb
    • Orfit thumb spica
    • Elastic thumb support
    • Neoprene thumb support
  • Splinting MCPJ/PIPJ
    • Range of splints that can be used for Ulnar deviation
    • Resting splint
    • Oval 8
    • Oedema glove
391
Q

What are the aims of hand exercises in rheumatological conditions?

A
  • Consider patients occupation and activity levels
  • Consider disease progression
  • Maintain ROM
  • Improve flexibility
  • Increase muscle strength
392
Q

What hand exercises are done in rheumatological conditions?

A
  • Ulnar deviation
  • Exercising the thumb
  • Using theraputty

Medicine Year 3 (15 decks)

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