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Phase 3 > Week 11 - MSK > Flashcards

Week 11 - MSK Flashcards

1
Q

Define compartment syndrome. What are common sites?

A

Elevated interstitial pressure within a closed fascial compartment resulting in microvascular compromise.
Leg, forearm, thigh.

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2
Q

What causes compartment syndrome?

A

Internal pressure: Trauma (bleeding), muscle oedema, intracompartmental administartion of fluids/drugs, vascular surgery
or
External compression e.g. casts/bandages, full thickness burns, positioning in theature i.e. lithotomy.

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3
Q

Describe the pathophysiology of compartment syndrome.

A

Pressure within compartment exceeds pressure within the capillaries. Loss of perfusion and muscles become ischaemic and oedematous due to increased endothelial permeability. Necrosis begins in ischaemic muscles after 4 hours and ischaemic nerves become neuropraxic.

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4
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
Parasthesia (later stage)
Paralysis (later stage)
Pulselessness (later stage)
Limb may be swollen and the skin shiny.
Autonomic responses i.e. sweating, tachycardia may be present.

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5
Q

What compartment pressure indicates compartment syndrome and a need for fasciotomy?

A

> 30 mmHg

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6
Q

What is the treatment for compartment syndrome?

A 
Open any constricting dressings and bandages, 
Reassess
Surgical release - fasciotomy
Later wound closure
Possible skin grafting
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7
Q

What is the structure and function of tendons?

A

Parallel collagen fibrils with tenocytes, surrounded by sheath, largely avascular.
Function: transmits force from muscle to bone.

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8
Q

Describe the pathology of tendonopathy.

A

Chronic tendon injury of over use, degeneration and disorganisation of collagen fibres, increased cellularity, not a lot of inflammation, increased vascularity around tendon, IL-1, NO and PG release MMPs.

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9
Q

What are the risk factors for tendonopathy?

A

Age, chronic disease, diabetes, rheumatoid arthritis, adverse biomechanics, repetitive exercise, recent increase in exercise, quinolone antibiotics.

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10
Q

What are the clinical features of tendinopathy?

A

Pain, swelling, thickening, tenderness, provocative tests.

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11
Q

What imaging techniques are best for seeing tendinopathy?

A

Ultrasound, T1 MRI

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12
Q

What are some of the non-operative measures for tendinopathy?

A

NSAID’s, activity modification, physiotherapy, GTN patches, PRP injections, extracorporeal shock wave therapy, steroid injection.

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13
Q

What is the operative treatment for tendinopathy?

A

Debridement (excision of diseased tissue).

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14
Q

What are the functions of bone?

A

Structural: support, protection, movement.

Mineral storage: calcium, phosphate.

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15
Q

Describe 2 different types of bone tissue?

A

Outer cortical bone which is 80% of the skeleton, slow turnover rate, resistant to torsion and bending, small air spaces.
Inner cancellous bone, undergoes greater remodelling, more elastic, contains larger spaces with marrow and blood vessels.

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16
Q

Describe the composition of bone.

A

Cells - osteoclasts, osteoblasts, osteocytes, osteoprogenitor cells.
Matrix - inorganic - calcium, phosphorus. Organic - collagen type 1, mucopolysaccharides, non-collagenous proteins.

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17
Q

What are the different sections of a long bone?

A

Diaphysis (shaft)
Epiphysis (end)
Metaphysis (transitional flared area between diaphysis and epiphysis)

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18
Q

What are the steps of indirect fracture healing and the timescale of these steps?

A
  1. Fracture haematoma and inflammation.
    - 6-8 hours after injury
  2. Fibrocartilage (SOFT) callus formation.
    - lasts about 3 weeks
  3. Bony (HARD) callus formation.
    - after 3 weeks, lasts about 3-4 months.
  4. Bone remodelling - up to 2 years.
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19
Q

What is direct fracture healing?

A

Direct formation of bone WITHOUT the process of callus formation.

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20
Q

What different factors can compromise blood supply to bone?

A 
Surgical factors (iatrogenous)
Anatomical factors (certain fracture are just more prone to problems with blood supply) i.e. proximal pole of scaphoid, talar neck fractures, intracapsular hip fractures, surgical neck of humerus fractures.
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21
Q

What patient factors inhibit bone healing?

A

Increasing age, smoking, alcohol intake, diabetes, anaemia, malnutrition, peripheral vascular disease, hypothyroidism.

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22
Q

Name 3 types of medication that can affect bone healing.

A

NSAIDs (reduce local vascularity at fracture site) steroids, bisphosphonates.(inhibit osteoclast activity)

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23
Q

Secondary tumours in the bone are very common. Which primary cancers commonly lead to bone metastases?

A

Bronchus, breast, prostate, kidney, thyroid.

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24
Q

Which childhood cancers often lead to metastases of the bone?

A

Neuroblastoma, rhabdomyosarcoma.

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25
Q

Which bones are often affected by metastases?

A

Those with good blood supply i.e. long bones, vertebrae.

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26
Q

How can bone metastases present?

A

Often asymptomatic
Bone pain (typically unremitting and worse at night)
Swelling
Systemic symptoms i.e. weight loss, malaise
Pathological fractures
Hypercalcaemia
Spinal metastases: vertebral collapse, spinal cord compression, nerve root compression, back pain.

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27
Q

What investigations could be performed for suspected bone tumours?

A

Skeletal isotope scan, x-rays, MRI, PET-CT.

Serum alkaline phosphatase, hypercalcaemia.

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28
Q

Name 3 benign primary bone tumours and 3 malignant.

A

Benign:
Osteoid osteoma
Chondroma
Giant cell tumour

Malignant:
Osterosarcoma
Chondrosarcoma
Ewing’s tumour

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29
Q

What age group, sex and part of the skeleton is most commonly affected by osteoid osteoma?

A

Adolescents
Males
Any bone, especially spine and long bones.

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30
Q

What age group, sex and part of the skeleton is most affected by osteosarcoma?

A

Age 10-25
Males
Metaphysis of long bones, especially knee.

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31
Q

Where does osteosarcoma commonly metastsize to? Which variant has a worse prognosis?

A

The lung.

Paget’s osteosarcoma.

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32
Q

What is an enchondroma? Which bones does it commonly affect?

A

A lobulated mass of cartilage within in the medulla.

Hands and feet, long bones.

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33
Q

What is Osteocartilaginous Exostosis? Which age group does it normally affect? Where in the bone is it normally found?

A

Benign outgrowth of cartilage with endo-chondral ossification.
Adolescence
Metaphysis of long bones.

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34
Q

What age group, sex and part of the skeleton is commonly affected by chondrosarcoma?

A

Middle aged and elderly
Males
Axial skeleton i.e. ribs, pelvis, shoulder.

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35
Q

Which age group is normally affected by a Ewing’s sarcoma? Where does it often metastasize to? Which bones does it normally affect? Which sex does it normally affect?

A

5-15 year old
Lung, bone, bone marrow.
Flat bones of limb girdles.
Females

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36
Q

How are bone tumours managed?

A
  • analgesics and anti-inflammatory drugs
  • local radiotherapy
  • chemotherapy
  • bisphosphonates for symptoms.
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37
Q

Describe the aetiology of rheumatoid arthritis.

A

HLA-DR4 and other genetic factors.
Smoking
Infection i.e. EBV, TB
Pregnancy? (female preponderance)

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38
Q

Describe the epidemiology of rheumatoid arthritis.

A

Female:male ration 3:1
Affects 1% of caucasians
30-50 years old at presentation.

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39
Q

Describe the pathophysiology of rheumatoid arthritis.

A

Synovitis - infiltration of inflammatory cells to synovium.
Pannus, a layer of chronically inflamed tissue extends across the cartilage, destroying it.
This results in bone destruction and joint deformities.

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40
Q

What are the clinical features of rheumatoid arthritis?

A

Synovitis - any synovial joint
Symmetrical
Small joints of hands and feet early on, shoulder and hip at onset rare.
MCPs/PIP/wrists
Inflammatory - pain, erythema, swelling,
Tenosynovitis, bursitis, CTS
Constitutional symptoms i.e. fatigue, weakness, low grade fever, weight loss, anorexia.

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41
Q

Name 3 extra-articular signs of RA.

A

pleural effusion, lung fibrosis, peripheral neuropathy.

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42
Q

How would RA be investigated?

A 
Bloods:
FBC, U&Es, LFTs, ESR/CRP, RF (rheumatoid factor), ACPA (anti-citrillunated peptide antibody), ANA (anti-nuclear antibody).
X-ray 
USS
MRI
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43
Q

What are the potential differentials for a diagnosis of rheumatoid arthritis?

A 
OA
SLE/other connective tissue disease
PMR (polymyalgia rheumatica)
Psoriatic arthropathy
Sponyloarthropathies
Reactive arthritis
Sarcoid
CPPD (calcium pyrophosphate)
Lyme’s
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44
Q

What are the different treatments for RA?

A

Non-pharmacological:
OT/PT
Pharmacological:
Symptomatic - NSAIDs, analgesia
Disease modifying - DMARDS - i.e. methotrexate, sulfasalazine
Glucocorticoids
Biologics i.e. anti-TNF - etanercept, infliximab. Anti-CD20 i.e. rituximab

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45
Q

What does biological therapies in RA increase your risk of? What precautions should be made?

A

Infection i.e. TB, varicella zoster.

Determine vaccine status and vaccinate against influenza and pneumococcal annually.

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46
Q

What are the indications for immunosuppressant drugs?

A

Abnormal inflammation - inflammatory arthropathies, ilcerative colitis/crohn’s, psoriasis.
or
Unwanted normal inflammation -
Solid organ transplants, bone marrow grafts

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47
Q

Name some side effects of steroids.

A 
Weight gain + fluid retention
Glaucoma
Osteoporosis 
Infection 
Hypertension + hypokalaemia 
Peptic ulceration and GI bleed 
Psychiatric symptoms
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48
Q

Name 3 non-steroid immunosuppressant drugs.

A

Methotrexate
Azathioprine
Cyclosporin

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49
Q

What is the mechanism of action of methotrexate?

A

Stops the action of the enzyme dihydrofolate needed for production of DNA.

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50
Q

What are the adverse effects of methotrexate? How is methotrexate toxicity reduced?

A

GI - hepatitis, stomatitis
Haematological - leukopenia
Others: frequent infections, pulmonary fibrosis.
Folic acid.

51
Q

What are the common indications for methotrexate?

A

Rheumatoid arthritis
Psoriasis
Psoriatic arthropathy

52
Q

What is the mechanism of action of azathioprine?

A

Blocks purine synthesis mainly in lymphocytes.

53
Q

What are the adverse effects of azathioprine?

A

GI - hepatitis, cholestasis
Haematological - leukopenia, thrombocytopenia
Others - frequent infections

54
Q

What must be done before giving someone azathioprine?

A

Check their TPMT activity because if they lack it, azathioprine will be toxic.

55
Q

What are the common indications for azathioprine?

A

IBD i.e. Ulcerative colitis
Crohn’s disease
Other severe autoimmune i.e. myasthenia gravis, eczema

56
Q

What is the mechanism of action of cyclosporin?

A

Inhibits calcineurin and therefore inhibits T cell activation.

57
Q

What are the adverse effects of cyclosporin?

A 
Nephrotoxicity 
Hypertension 
Hepatotoxicity 
Anorexia and lethargy 
Hirsutism 
Paraesthesia
58
Q

What are the common indications for cyclosporin?

A

Organ transplantation - i.e. liver, kidney, heart/lung.

Topically for inflammatory conditions i.e. skin or eye.

59
Q

What are some of the disadvantages to immunosuppressants?

A

Sometimes insufficient to control inflammatory disease with subsequent progression, slow rate of onset.
Toxicity even at a low dose.
Bone marrow suppression, frequent infections.

60
Q

Generally, how do biologic therapies work?

A

Target specific components of the immune system with minimal off target effects.

61
Q

What are some of the adverse effects of biologic therapies?

A

Hypersensitivity reactions
Infusion reactions
Mild gastrointestinal toxicity
Infection (but less risky than typical immunosuppressants).

62
Q

Give 4 examples of increased risk of infections with biologic therapies.

A

Anti-TNF - increased risk of TB
Rituximab - risk of Hep B reactivation
Abatacept and anti-IL-1 therapy - incresaed risk of respiratory tract infections and pneumonia.

63
Q

What is it important to screen for before commencing anti-TNF therapy?

A

Latent TB (with interferon gamma release assay).

64
Q

What is giant cell arteritis? What is the epidemiology?

A

Systemic vasculitis that affects the aorta and its major branches.
Prevalence increases with age, female more common, caucasians more common.

65
Q

What are the clinical features of giant cell arteritis (GCA)?

A

Headache - temporal headache, constant, subacute onset, little relief with analgesics.
Visual symptoms
Jaw claudication
Polymyalgia rheumatica symptoms

66
Q

What are the complications of GCA?

A

Visual loss, large vessel vasculitis, CVA.

67
Q

How is GCA diagnosed?

A
  1. clinical presentation
  2. clinical examination findings i.e. temporal artery assymetry, thickening, lack of pulsality
  3. acute phase response i.e. ESR/CRP
  4. further investigations i.e. temporal artery biopsy, USS, MRI, PET-CT.
68
Q

How is giant cell arteritis treated?

A

Prednisolone. If clinical suspicion treat.

69
Q

What are the potential causes of cutaneous vasculitis?

A 
Idiopathic 
Drugs 
Infection i.e. hep B, hep C
Inflammatory conditions i.e. RA, UC
Malignancy
70
Q

What are the clinical signs of Henoch Schonlein Purpura (HSP)?

A

Classic purpuric rash - buttocks, thighs, lower legs.
Urticarial rash, confluent petechiae, ecchymoses, ulcers.
Arthralgia/arthritis (lower limb) in 75%

71
Q

What are some of the complications of HSP?

A

Gastrointestinal - pain, bleeding, diarrhoea.
Renal - IgA nephropathy.
Urological - orchitis

72
Q

How is HSP managed?

A

Frequently self limiting, corticosteroids for certain complications i.e. testicular torsion, GI disease, occasionally arthritis.

73
Q

What is granulomatosis with polyangiitis (GPA) pathologically characterised by?

A

Granulomatous necrotising inflammatory lesions of the upper and lower respiratory tract and often a pauci-immune glomerulonephritis.

74
Q

What is the classic triad of disease seen in GPA? What constitutional symptoms may be present?

A

Upper airway/ENT - rhinitis, chronic sinusitis, chronic otitis media, saddle nose deformity, nasal septal perforation.
Renal - (rapidly progressive) pauci-immune glomerulonephritis
Lower respiratory - parenchymal nodules +/- cavitation, alveolar haemorrhage.
Constitutional - fatigue, weight loss, fever/sweats, myalgia/arthralgia, failure to thrive in elderly.

75
Q

How to you assess for ANCA autoantibodies in ANCA associated vasculitis?

A

Indirect immunofluorescence

ELISA for PR3/ MPO

76
Q

How would you bring about remission induction in a patient with vasculitis?

A

Prednisolone

+ cyclophosphamide or rituximab in severe (life or organ threatening disease)

+ methotrexate in moderately severe disease (not life or organ threatening).

77
Q

What treatments should a patient remain on after vasculitis to maintain remission?

A

Azathioprine

Methotrexate

78
Q

What are the risk factors for septic arthritis?

A 
Rheumatoid/osteoarthritis 
bDMARDS
joint prostheses/surgery 
Low socioeconomic status 
IV drug abuse
Alcoholic liver disease
Diabetes
Previous IA corticosteroid injection 
Cutaneous infection/ulcers
79
Q

What are the potential differential diagnoses for an acute hot joint?

A
  • septic arthritis
  • crystal arthropathy
  • trauma/hemarthrosis(bleeding into joint spaces).
  • early presentation of polyarthropathy (RA/PsA/AS/ReA)
80
Q

What are the principles of managing septic arthritis?

A

Synovial fluid must be aspirated, gram-stained and cultured prior to antibiotics.
Short history of acute hot, swollen and tender joint should be regarded as SA until proven otherwise.

Blood cultures should always be taken.
Polarised light microscopy should be carried out on synovial fluid obtained.

81
Q

What pathogen commonly septic arthritis?

A

Staphylococcus aureas (most commonly)
MRSA
Gram negatives

82
Q

How is septic arthritis managed?

A

IV antibiotics for 2 weeks or until signs improve and then orally for 4 weeks after.
If a prosthetic joint, usually 6+ weeks IV and prosthesis may need to be removed.

83
Q

What is reactive arthritis?

A

A sterile inflammatory arthritis following a distal mucosal infection (classically GU or GI).

84
Q

What are the clinical features of reactive arthritis?

A

Hot, swollen, tender, restricted joint.
Common in knees, feet, toes, hips and ankles.
Some people get dactylitis, keratoderma blennorrhagicum (skin lesions on palms and soles), mouth ulcers, conjuctivits/uvitis, circinate balanitis (skin manifestation on penis), inflammatory back pain).

85
Q

What is gout?

A

Gout is a syndrome characterised by high levels of urate crystals and deposition causing attacks of acute inflammatory arthritis, tophi around the joints and possible joint destruction. Most commonly affects the first toe, foot, ankle, knee, fingers, wrist, elbow but can affect any joint.

86
Q

What is the clinical features of gout?

A

Rapid onset pain, swelling, tenderness of the joint. Hyperuricaemia. Crystals present in aspirated fluid.

87
Q

What are the treatments for acute gout?

A

NSAIDs (+co prescription of PPI for gastric protection.)
Colchicine - works best within 24 hours of onset of attack, don’t commence after 36 hours. (look out for drug interactions)
Corticosteroids

88
Q

What is the long term treatment of gout?

A

Urate lowering therapy i.e.
Allopurinol (xanthase oxidase inhibitor)
Lifestyle alterations to reduce risk factors.

89
Q

What are the clinical features of osteoarthritis?

A

Pain, stiffness, swelling, clicks/crepitus, deformity, reduced mobility, trouble sleeping, difficulty walking, doing normal activities.
Altered gait, signs seen on joint examination and special tests.

90
Q

What are some secondary causes of OA?

A

Other joint problems, nearby joint problems, back problems, systemic problems, long term medicines, family history, allergies -metals, treatment history, previous surgery, social history/personal habits.

91
Q

Describe the pathophysiology of OA.

A

Proteolytic breakdown of the cartilage matrix from increased production of enzymes such as metalloproteinases. Proteoglycan and collagen fragments released into synovial fluid. Erosion to the cartilage narrows the joint space.

92
Q

Describe the pathology of a joint with OA.

A

Thickened articular capsule, loss of cartilage, inflamed synovium, thickened crunched up bone with no cartilage covering, osteophytes, joint space narrowing, bone angulation deformity.

93
Q

What are the signs of OA on an X-ray?

A

Osteophytes, joint space narrowing, subchondral sclerosis, bony deformity.

94
Q

What is the management of OA?

A

Minor - lifestyle changes, supplements i.e. glucosamine and chondroitin.
Mild - physiotherapy, analgesia as required, knee supports, braces, shoe inserts as required.
Moderate - Analgesics and possibly stronger ones i.e. oxycodone, codeine. Acupuncture, heat and cold therapy, massage, local anti-inflammatory gels. Intra-articular injections of steroid/hyaluronic acid.
Severe - Surgery - joint replacement, realignment, excision, fusion.

95
Q

What would be the indications for a joint replacement surgery?

A

Stage 4 osteoarthritis - joint stiffness, extreme pain or walking or running, tenderness.

96
Q

What are the potential complications of joint replacement surgery?

A

General - PE, DVT, neurovascular damage, infection, respiratory, cardiac compromise, death.

Specific hip - dislocation, fracture, leg length discrepancy.
Specific knee - stiffness, fracture, ligament or tendon damage.

97
Q

What are the features of mechanical back pain? List some of the causes behind mechanical back pain.

A 
Variable age of onset
Generally worsens with movement or prolonged standing 
Better with rest 
Early morning stiffness <30 mins 
Lumbar strain or sprain (common cause)
Degenerative disc disease
Degenerative facet joint disease
Compression fractures
98
Q

How is non specific lower back pain managed?

A
  • keep diagnosis under review
  • Reassurance (careful with terminology)
  • Education, promotion of self management
  • Exercise programme and physiotherapy
  • analgesics as appropriate (avoid opiates)
  • Not injections, traction, lumbar support.
99
Q

Define spinal stenosis.

A

Anatomical narrowing of the spinal canal.

100
Q

What are the clinical features of cauda equina syndrome? What causes it? How should it be managed?

A 
Bilateral sciatica 
Saddle anaesthesia 
Bladder or bowel dysfunction 
Reduced anal tone 
Usually caused by a large prolapsed disc. 
URGENT neurosurgical review.
101
Q

Define spondylolisthesis.

A

Pars interarticularis defect resulting in a ‘slip’ of one vertebra on the one below.

102
Q

Name some causes of referred pain in the back.

A 
Aortic aneurysm 
Acute pancreatitis 
Peptic ulcer disease
Acute pyelonephritis/renal colic 
Endometriosis/gynae
103
Q

What are the features, natural history and treatment of acute disc prolapse?

A 
Acute onset, increase cough 
Leg pain in dermatomal distribution 
Reduced reflexes
Most spontaneously resolve in 12 weeks 
Wait for investiagtions - MRI and Xray 
<10% need surgery
104
Q

What are red flag symptoms when approaching back pain?

A 
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
105
Q

What are the red flag signs when assessing back pain?

A

Saddle anaesthesia, reduced anal tone, hip or knee weakness, generalised neurological deficit, progressive spinal deformity.

106
Q

Define spondylosis.

A

Degeneration of the intervertebral discs.

107
Q

Define tendinopathy.

A

Chronic tendon injury of overuse.

108
Q

Describe the pathology of tendinopathy.

A

Degeneration, disorganisation of collagen fibres, increased cellularity, inflammatory mediators IL-1, NO, PGs release MMPs, increased vascularity.

109
Q

What are some of the risk factors for tendinopathy?

A

Age, chronic disease, diabetes, rheumatoid arthritis, adverse biomechanics, repetitive exercise, recent increase in activity, quinilone antibiotics.

110
Q

How is tendinopathy diagnosed?

A

Ultrasound

MRI - T1

111
Q

What are some of the non-operative treatments for tendinopathy?

A 
NSAIDs
Activity modification 
Physiotherapy 
GTN patches
PRP injections 
Extra-corporeal shock wave therapy
112
Q

What would the operative treatment involve for tendinopathy?

A

Debridement, excision of disease tissue.

113
Q

What is osteonecrosis? How does it present?

A

Spontaneous death of some of the bone due to bone infarction.

Presents incidentally on imaging or with pain from the infarction itself or from arthritis.

114
Q

What are the risk factors for osteonecrosis?

A

History of trauma, especially joint dislocation, corticosteroid use or cushing’s disease, alcohol abuse, sickle cell disease.

115
Q

What is commonest malignant primary bone tumour? What do the lesions look like?

A

Myeloma

Punched out lytic foci, generalised osteropenia.

116
Q

What is the most common clinical features of SLE? What would blood results show?

A

Arthralgia and rash

FBC - may show leucopenia, thrombocytopenia, anaemia of chronic disease.
Autoantibodies - ANA, anti-phospolipid antibodies, Anti-Ro, Anti-Sm, Anti-La, anti-dsDNA
U&E - raised in renal disease
CRP - usually normal but may be raised when patient has arthritis or lupus pleuritis.

117
Q

What would be the treatment of SLE?

A

Mild - topical therapies for skin disease. MSK - NSAIDs and IA/IM steroid, low dose oral prednisolone, methotrexate.
Moderate disease - oral prednislone, DMARDs i.e. methotrexate, azathioprine, ciclosporin.
Biological therapies i.e. rituximab.
Severe disease - High dose steroid, DMARDs, B cell therapy, cyclophosphamide, IVIG. Plasmaphoresis.

118
Q

Describe the aetiology of Rheumatoid Arthritis?

A

Genetics + environment
HLA-DR4 and other genetic factors
Smoking
Infection - EBV, TB

119
Q

Describe the pathophysiology of RA?

A

Synovitis - immune cells invading a noramally relatively acellular environment in the form of a pannus, a hyperplastic invasive tissue leading to cartilage breakdown and erosions. Involves TNF alpha and anti-citrullinated peptide antibody.

120
Q

What autoantibodies can indicate RA?

A

RF, anti-CCP/ACPA, ANA

121
Q

What are the treatments for RA?

A

OT, PT

Symptomatic - NSAIDs + analgesia
Disease modifying - DMARDs i.e. methotrexate, gold, Glucocorticoids, Biologics i.e. anti-TNF such as infliximab, etanercept

122
Q

What is the gene for Ankylosing Spondylitis?

A

HLA-B27

123
Q

Define juvenile idiopathic arthritis.

A

Disease of childhood onset characterised by arthritis persisting for at least 6 weeks and currently having no cause.

Phase 3 (14 decks)

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