ARTHRITIS

Question 1

Arthralgia vs arthritis?

Answer 1

Arthralgia is pain in a joint
Arthritis is a diagnosis that involves articular inflammation

Question 2

Inflammatory vs non-inflammatory arthritis?

Answer 2

E.g. osteoarthritis is non-inflamamtory and RA is inflammatory
There is a degree of inflammation in the joint in osteoarthritis but no clinical signs of inflammation, little early morning stuffiness, normal or mild biochemical markers of inflammation compared to RA

Question 3

joint changes osteoarthritis vs rheumatoid arthritis

Answer 3

In OA - thinning of synovial membrane and friction between bones
In RA - synovial membrane is swollen, inflamed and there are bony erosions

Question 4

What is osteoarthritis?

Answer 4

A disorder of synovial joints which occurs when damage (i.e. from repeated excessive loading, injury or stress or a joint) triggers repair processes leading to structural changes within a joint

Question 5

Structural changes in the joint in osteoarthritis?

Answer 5

Localized loss of cartilage.
Remodelling of adjacent bone and the formation of osteophytes (new bone at joint margins).
Mild synovitis (inflammation of the synovial membrane that lines the joint capsule).

Question 6

Which joints are most commonly affected in osteoarthritis?

Answer 6

Weight bearing and axial skeleton
I.e. knees, hips, DIP joints in hands, CMC at base of thumb, lumbar spine and cervical spine

Question 7

Epidemiology of osteoarthritis?

Answer 7

The most common joint disease worldwide
Affects 10% of men and 18% of women >60
Risk develops with age
Prevlance is higher in women

Question 8

Risk factors for osteoarthritis?

Answer 8

Genetic
Increasing age
Female sex
Obesity
High bone density
Joint injury and damage
Joint laxity and reduced muscle strength e.g. hypermobility
Joint malalignment e.g. PHx of DDH, valgus knee deformity
Exercise stresses
Occupational stresses e.g. repetitive squatting

Question 9

Why does obesity increase the risk of osteoarthritis?

Answer 9

It increases the load on weight bearing joints
This increases the risk of developing knee osteoarthritis more than 3 fold

Question 10

Complications of osteoarthritis?

Answer 10

Joint deformity
Functional impairment and disability
Psychosocial issues
Occupation impact
Falls
Chronic pain sundrome

Question 11

Prognosis of osteoarthritis?

Answer 11

Quite often a progressive condition that leads to increased pain and functional impairment but not always! Hand involvement usually becomes asymptomatic after a few years
Hip involvement has poorest prognosis and a significant proportion of people require a hip replacement within 5 years of diagnosis

Question 12

General presentation of osteoarthritis?

Answer 12

Joint pain and stiffness that tends to worsen with activity and at the end of the day (if morning stiffness then it should not last >30 mins)
Bulky bony enlargements of the joint
Restricted range of motion
Weak grip
Crepitus on movement
Fluid around the joint
Muscle wasting
Joint instability

Question 13

Presentation of osteoarthritis of the hand?

Answer 13

Affects first Carpometacarpal joint at the base of the thumb, the DIP joint and PIP joint
Pain can radiate dismally towards thumb or proximally to wrist and distal forearm. Exacerbated by pinching or strong grip
Wasting of thenar muscles
CMC joint may develop a fixed flexion deformity
In advanced disease… Squaring of the joint caused by subluxation, formation of osteophytes and remodelling of bones, ulnar or radial deviation

Question 14

Presentation of osteoarthritis of the hip?

Answer 14

Deep pain in anterior groin on walking/climbing stairs with possible referred pain to the lateral thigh and buttock anterior thigh, knee and ankle
Pain may occur at rest and distrurb sleep
Painful restriction of internal rotation with the hip flexed
Antalgic gait

In advanced disease - trendelenburg gait and a fixed flexion external rotation deformity

Question 15

Presentation of osteoarthritis of the knee?

Answer 15

Presentation depends on where it affects…

Medial tibiofemoral involvement causes anteromedial pain, mainly on walking.
Lateral tibiofemoral involvement causes anterolateral pain, mainly on walking.
Patellofemoral involvement causes anterior knee pain worsened on inclines or stairs, particularly when going down; and progressive aching on prolonged sitting that is relieved by standing.

Others: giving way, locking, crepitus, tenderness, restricted flexion &extension
In advanced disease - bony swelling of femoral condyles, varus deformity and an antalgic gait

Question 16

Diagnosing osteoarthritis according to NICE?

Answer 16

NICE suggest a diagnosis can be made without any investigations if the patient id >45, has typical pain associated with activity and has no morning stiffness (or lasts <30 mins)

Question 17

Typical radiological features of osteoarthritis?

Answer 17

L – Loss or narrowing of joint space
O – Osteophytes (bone spurs)
S – Subarticular sclerosis (increased density of the bone along the joint line)
S – Subchondral cysts (fluid-filled holes in the bone)

Question 18

Heberden’s nodes vs Bouchard’s nodes?

Answer 18

Heberdens nodes are bony bumps on DIPs
Bouchards are on the PIPs

Question 19

Management of osteoarthritis?

Answer 19

Weight loss if overweight
Muscle strengthening and supervised therapeutic exercise and aerobic fitness training
Offer psychosocial support
Simple analgesia for symptom relied
Topical NSAIDs for knee osteoarthritis

If this doesn’t help…
Intra-articular injections for short-term benefits for knee and possibly hip
Consider referral to PT or local MSK clinic
Consider referral to OT
Consider referral to podiatry
Consider referral to orthopaedic surgeons for joint replacements in severe cases
Consider referral to pain clinic

Question 20

What is the Oxford Hip Score?

Answer 20

A self-assessment tool designed to assess function and pain in patients undergoing hip replacement surgery

Question 21

Complications of total hip replacement secondary to osteoarthritis ?

Answer 21

Perioperative - VTE, intraoperative fracture, nerve injury, surgical site infection
Leg length discrepancy
Posterior dislocation on extremes of hip flexion
Aseptic loosening - failure of joint prosthesis without infection
Prosthetic joint infection

Question 22

How long can intra-articular steroid injections work for in osteoarthritis?

Answer 22

2-10 weeks

Question 23

Post-op recovery from hip replacements?

Answer 23

patients receive both physiotherapy and a course of home-exercises
walking sticks or crutches are usually used for up to 6 weeks after hip or knee replacement surgery

Question 24

What basic advice should patients recieve to minimise the risk of dislocation following a hip replacement?

Answer 24

avoiding flexing the hip > 90 degrees
avoid low chairs
do not cross your legs
sleep on your back for the first 6 weeks

Question 25

Epidemiology of RA?

Answer 25

1% prevalence in the UK - most common inflammatory arthritis Occurs at any age but most commonly 30-50 2-4 times more common in women than men Approximately 1/3rd stop work within 2 years of its onset

Question 26

Complications of RA?

Answer 26

Amyloidosis Anaemia Ketatoconjunctivitis sicca, corneal ulceration, episcleritis, scleritis, keratitis Feltys syndrome Fatigue Increased mortality Interstitial lung disease, pleural effusion, fibrosis alveolitis Neuropathy Orthopaedic e.g. carpal tunnel, tendon ruptures, osteoporosis etc Vasculitis, ulcers, rheumatoid nodules Weight loss Severe - depression, CVD, lymphomas, serious infections

Question 27

What is feltys syndrome?

Answer 27

Rare extra-articulated manifestation of RA Causes presentation remembered as SANTA: Splenomegaly Anaemia Neutropenia Thrombocytopenia Arthritis

Question 28

Presentation of RA?

Answer 28

Presentation insidiously develops over a few months Symmetrical synovitis of the small joints of the hands and feet - pain, swelling, early morning stiffness lasting over 1 hour Rheumatoid nodules Positive squeeze test across metacarpal or metatarsal joints Swan neck and boutonnière deformities in late disease Extra-articular features Systemic features - malaise, fatigue, fever, sweats, weight loss

Question 29

What is palindromic rheumatism?

Answer 29

Self-limiting relapsing/remitting episodes of monoarthritis of different large joints with joints appearing normal between episodes

Question 30

Risk factors for RA?

Answer 30

Female - due to oestrogen Smoking FHx - HLA DR4

Question 31

Which gene is most commonly associated with RA?

Answer 31

HLA DR4

Question 32

Most commonly affected joints in RA?

Answer 32

MCP PIP Wrist MTP

Question 33

Hand signs in RA?

Answer 33

Z-shaped deformity to the thumb Swan neck deformity (hyperextended PIP and flexed DIP) Boutonniere deformity (hyperextended DIP and flexed PIP) Ulnar deviation of the fingers at the MCP joints

Question 34

What causes Boutonnière deformity in RA?

Answer 34

caused by a tear in the central slip of the extensor components at the PIP joint. The central slip connects to the middle phalanx at the PIP, and the lateral bands go around the PIP and connect to the distal phalanx. When the patient tries to straighten their finger, the lateral bands pull on the distal phalanx, causing the DIP joint to hyperextend and the PIP joint to flex.

Question 35

What is atlantoaxial subluxation?

Answer 35

A potential complication of RA where synovitis and ligament damage around the odontoid peg of the axis (C2) allows it to shift within the atlas (C1) This can cause spinal cord compression and is an emergency

Question 36

How common are ocular manifestations of RA? What are the common types?

Answer 36

25% have ocular manifestations - keratoconjunctivits sicca is most common. Others are episcleritis, scleritis, corneal ulceration and keratitis. Iatrogenic - steroid-induced cataracts and chloroquine retinopathy

Question 37

What are some examples of extra-articular manifestations of RA?

Answer 37

Ocular manifestations Pulmonary fibrosis, bronchiolitis obliterans Feltys syndrome Sjögren’s syndrome Anaemia CVD Rheumatoid nodules - elbows and fingers Lymphadenopathy Carpal tunnel syndrome Amyloidosis

Question 38

How do we diagnose RA?

Answer 38

If its suspected clinically investigations are not necessary You may consider doing: - rheumatoid factor blood test - measure anti-CCP - x-ray of hands and feet You may also consider the following tests to acts as a baseline measure prior to Tx: - FBC, U&Es, LFTs - CRP or ESR - US or MRI of joints

Question 39

Discuss the sensitivity and specificity of rheumatoid factors for RA?

Answer 39

RF is positive in up to 80% of pt with RA and high levels are associated with severe progressive disease RF can be positive in feltys syndrome, Sjögren’s syndrome, infective endocarditis, SLE, systemic sclerosis It can also be seen in 5% of general population

Question 40

What tests can be done to detect rheumatoid factor for diagnosing RA?

Answer 40

Rose-Waaler test: sheep red cell agglutination Latex agglutination test (less specific)

Question 41

Discuss the sensitivity and specificity of anti-CCP for RA?

Answer 41

May be detectable up to 10 years before the development of RA Present in 70% of pt with RA Specificity is 90-95% (Because the specificity is much higher… if pt are suspected RA but get a negative RF test they should then be tested for anti-CCp)

Question 42

X-ray changes you may see in RA?

Answer 42

loss of joint space juxta-articular osteoporosis soft-tissue swelling periarticular erosions subluxation and disclocation e.g. ulnar deviation at MCPJs

Question 43

Scoring systems for RA?

Answer 43

Health Assessment Questionnaire (HAQ) - measures functional ability which should be done at baseline to assess response to treatment Disease Activity Score 28 joints (DAS28) - used to monitor disease activity and response to treatment

Question 44

Management of RA?

Answer 44

DMARD monotherapy +/- a short-course of bridging prednisolone E.g. methotrexate, leflunomide, sulfasalazine Hydroxychloroquine for palindromic disease

Question 45

How should you monitor response to treatment in RA?

Answer 45

CRP and disease activity e.g. using a score like DAS28

Question 46

How do you manage flares of RA?

Answer 46

Oral, IM or intraarticular glucocorticoids

Question 47

How should you manage RA if there is inadequate response to at least 2 DMARS, 1 of which being methotrexate?

Answer 47

TNF inhibitors can be tried e.g. etanercept, infliximab or adalimumab

Question 48

Biological therapies that can be tried for RA?

Answer 48

Tumour necrosis factor (TNF) inhibitors (e.g., adalimumab, infliximab, etanercept, golimumab and certolizumab) Anti-CD20 on B cells (e.g., rituximab) Anti-interleukin-6 inhibitors (e.g., sarilumab and tocilizumab) JAK inhibitors (e.g., upadacitinib, tofacitinib and baricitinib) T-cell co-stimulation inhibitors (e.g., abatacept)

Question 49

What must be monitored whilst on methotrexate?

Answer 49

FBC, U&Es and LFTS every 1-2 weeks until therapy is stabilised and then 2-3 months after that - risk of myelosuppression and liver cirrhosis Advise pt to report all symptoms suggesting infection, particularly sore throat

Question 50

Side effects of methotrexate?

Answer 50

Mouth ulcers and Mucositis N&v&d Liver toxicity Bone marrow suppression and leukopenia Pneumonitis Teratogenic and needs to be avoided 3-6 months before conception in both women and men

Question 51

RA sympotms in pregnancy?

Answer 51

Tend to improve in pregnancy but likely to have a flare following delivery and post-breastfeeding!

Question 52

Management of RA in pregnancy?

Answer 52

Sulfasalazine and hydroxychloroquine are three safest drugs NSAIDs can be used until 32/40 - risk of early closure of ductus arteriosus

Question 53

Side effects of hydroxychloroquine?

Answer 53

Bull’s eye retinopathy which may result in severe and permenant visual loss Blue-grey skin pigmentation Hair bleaching

Question 54

Main risk of anti-TNF medications?

Answer 54

Reactivation of TB

Question 55

How does hydroxychloroquine work?

Answer 55

It suppresses the immune system by interfering with Toll-like receptors, disrupting antigen presentation and increasing the pH in the lysosomes of immune cells

Question 56

How does sulfasalazine work?

Answer 56

a prodrug for 5-ASA which works through decreasing neutrophil chemotaxis alongside suppressing proliferation of lymphocytes and pro-inflammatory cytokines.

Question 57

Cautions for starting sulfasalazine?

Answer 57

G6PD deficiency allergy to aspirin or sulphonamides (cross-sensitivity)

Question 58

Possible adverse effects of sulfasalazine?

Answer 58

oligospermia = male infertility Stevens-Johnson syndrome pneumonitis / lung fibrosis myelosuppression, Heinz body anaemia, megaloblastic anaemia may colour tears → stained contact lenses Rashes May cause orange urine

Question 59

Leflunomide SE?

Answer 59

Liver impairment Interstitial lung disease Hypertension

Question 60

Poor prognostic factors for RA?

Answer 60

RF positive anti-CCP antibodies poor functional status at presentation X-ray: early erosions (e.g. after < 2 years) extra articular features e.g. nodules HLA DR4 insidious onset

Question 61

what are seronegative spondyloarthropathies?

Answer 61

A family of rheumatological disorders which are RF and anti-CCP antibody are negative and have an association with the HLA B27 antigen Types: - psoriatic arthritis - ankylosis spondylitis - reactive arthritis - enteropathic arthritis - associated with IBD

Question 62

What % of patients with psoriasis develop psoriatic arthritis?

Answer 62

10-20%

Question 63

Patterns of psoriatic arthritis?

Answer 63

Symmetrical polyarthritis like RA - most commonly (40%) asymmetrical oligoarthritis where it usually affect 1-4 joints on 1 side of the body - 30% Sacroiliitis - axial skeleton DIP-predominant joint disease - 10% Arthritis mutilans

Question 64

What is arthritis mutilans?

Answer 64

severe deformity fingers/hand, 'telescoping fingers'

Question 65

How can you distinguish between psoriatic arthritis and RA just based on joint affected?

Answer 65

Psoriatic arthritis tends to affect the DIP joints and axial skeleton RA tends to affect MCP, PIP abd wrist

Question 66

Symptoms of psoriatic arthritis?

Answer 66

Arthritis most commonly symmetrical but can have other patterns Psoriatic skin lesions Periarticular disease e.g. tenosynovitis, dactylitis or enthesitis Nail changes - pitting or oncholysis

Question 67

What is enthesitis?

Answer 67

Inflammation of the entheses which are the points of insertion of tendons into bone E.g. Achilles tendinitis and plantar fasciitis

Question 68

What is dactylitis?

Answer 68

Inflammation of an entire finger

Question 69

What screening tool can be used for psoriatic arthritis for pt with psoriasis?

Answer 69

Psoriasis epidemiological screening tool - PEST It involves questions about joint pain, swelling, history of arthritis and nail pitting. A high score leads to a rheumatology referral

Question 70

Classic x-ray changes in psoriatic arthritis?

Answer 70

Periostitis - thickened, irregular outline of the bone Ankylosis Osteolysis Dactylitis Pencil-in-cup appearance in digits - central erosion of the bones on one side of the joint - this is associated with arthritis mutilans

Question 71

Management of psoriatic arthritis?

Answer 71

Mild disease may be treated with just NSAID Mod-severe disease - methotrexate Other treatments that can be tried - monoclonal antibodies and apremilast

Question 72

Prognosis of psoriatic arthritis vs RA?

Answer 72

Psoriatic arthritis has a better prognosis than RA

Question 73

What % of pt with psoriatic arthropathy have nail changes?

Answer 73

80-90%

Question 74

Nail changes seen in psoriasis and psoriatic arthropathy?

Answer 74

pitting onycholysis (separation of the nail from the nail bed) subungual hyperkeratosis loss of the nail

Question 75

What is gout?

Answer 75

A type of arthritis caused by monosodium urate crystals forming inside and around joints causing sudden flares of severe pain, heat and swelling

Question 76

Which joints are most commonly affected in gout?

Answer 76

Most commonly MTP, CMC at base of thumb and wrist But can also affect larger joints e.g. knee and ankle

Question 77

4 clinical phases of gout?

Answer 77

Asymptomatic hyperuricaemia — the risk of developing gout increases with the degree of hyperuricemia. Acute gout — in almost all initial episodes a single peripheral joint is affected, most commonly the metatarsophalangeal joint. Intercritical gout — after resolution of the first attack the second attack may occur within one year and chronic symptoms develop within 10 years. Chronic tophaceous gout — large crystal deposits (tophi) produce irregular firm nodules and chronic joint damage.

Question 78

What is urate?

Answer 78

A metabolite of purines The ionised form of uric acid

Question 79

How is urate excreted?

Answer 79

70% by kidneys and 30% by GIT

Question 80

Risk factors for gout?

Answer 80

Hyperuricaemia Risk factors for hyperuricaemia: CKD, hypertension, DM, hyperlipidaemia, osteoarthritis, myeloproliferative disorders (high cell turnover), severe exfoliative psoriasis High purine diet - excess alcohol, sugary drinks, meat, seafood Obesity FHx Genetics e.g. glycogen storage disease Males Post-Menopausal women Older age Some meds e.g. diuretics, low-dose aspirin, Ciclosporin

Question 81

Pathophysiology behind gout?

Answer 81

Hyperuricaemia is caused in 90% of cases by under-excretion of urate 10% is caused by over-producers of urate

Question 82

Epidemiology of gout?

Answer 82

More common in men >30 and women post-menopause Prevalence increases with age - rare in under 40s Higher prevalence in Oceania, North America, indignious populations

Question 83

Complications of gout?

Answer 83

Chronic arthritis Joint damage Reduced QOL Renal stones Tophi which may create their own problems e.g. infection Hyperuricaemia is associated with an increased risk of: CVD CKD

Question 84

Prognosis of gout?

Answer 84

Acute attacks are self-limited and will resolve spontaneously over 5-15 days If not taking urate-lowering therapies, risk of recurrence is 62% in the first year, 78% in second year and 84% in third year following

Question 85

What are tophi?

Answer 85

Subcutaneous uric acid deposits - typically seen on hands, elbows, ears They are firm, white nodules under translucent skin. They are usually pain-free but can become inflamed or infected They typically affect 50% of people after 10 years

Question 86

Presentation of gout?

Answer 86

Rapid onset (often overnight) severe pain with redness and swelling - most commonly in MTP

Question 87

How do we diagnose gout?

Answer 87

Measure serum urate level - 360 or more confirms diagnosis If serum urate level is <360 but high suspicion of gout, repeat serum urate measurement in 2-4 weeks after flare has settled If diagnostic uncertainty: Joint aspiration and microscopy of synovial fluid - Synovial fluid analysis will show needle-shaped negatively birefringent monosodium urate crystals under polarised light X-ray may also be done

Question 88

X-ray findings of a joint affected by gout?

Answer 88

joint effusion well-defined 'punched-out' erosions with sclerotic margins in a juxta-articular distribution, often with overhanging edges relative preservation of joint space until late disease Para-articular erosions i.e. slightly away from the joint margins unlike in RA or OA no periarticular osteopenia (in contrast to rheumatoid arthritis) soft tissue tophi may be seen

Question 89

What can cause increased production of uric acid?

Answer 89

Severe psoriasis High protein turn over e.g. Myeloproliferative or lymphoproliferative disorders Cytotoxic drugs Purine rich diet

Question 90

Management of acute gout?

Answer 90

NSAIDs or colchicine (if both contraindicated: short course of oral corticosteroid) If not effective then intra-articular or IM corticosteroid injection can be done

Question 91

How does colchicine work?

Answer 91

It inhibits microtubular polymerization by binding to tubulin, interfering with mitosis It also inhibits neutrophil motility and activity

Question 92

Caution for colchicine use for treating gout?

Answer 92

In renal impairment Reduce dose if eGFR is 10-50 Avoid if eGFR is <10

Question 93

Main SE of colchicine?

Answer 93

Diarrhoea

Question 94

Indications for urate-lowering therapy after first attack of gout?

Answer 94

It is now recommended for everyone! Particularly important it >=2 attacks in 12 months, there are tophi, renal disease, uric acid renal stones or if on cytotoxics/diuretics

Question 95

When should urate-lowering therapy be started after a first attack of gout?

Answer 95

2 weeks after the attack

Question 96

What therapies do we offer for urate-lowering in gout?

Answer 96

Allopurinol Second line - febuxostat In refractory cases: uricase or pegloticase

Question 97

How does allopurinol work? What should be used alongside it?

Answer 97

It’s a xanthine oxidase inhibitor. Xanthine oxidase is the enzyme that converts hypoxanthine to xanthine and xanthine to uric acid Recommended to use NSAIDS or colchicine alongside for the first 6 months as starting urate lowering therapy can trigger attacks!

Question 98

Lifestyle modifications for gout?

Answer 98

reduce alcohol intake and avoid during an acute attack lose weight if obese avoid food high in purines e.g. Liver, kidneys, seafood, oily fish (mackerel, sardines) and yeast products Increasing vitamin C intake may also decrease serum uric acid levels

Question 99

What is pseudogout?

Answer 99

A crystal arthropathy caused by calcium pyrophosphate crystals collecting in joints causing synovitis It is also known as acute calcium pyrophosphate crystal deposition disease

Question 100

Who does pseudogout occur in?

Answer 100

Strongly associated with increasing age Pt who develop pseudogout <60 usually have an underlying risk factors e.g. haemachromatosis, hyperparathyroidism, low magnesium, low phosphate, acromegaly or Wilson’s disease

Question 101

Presentation of pseudogout?

Answer 101

Knee, wrist and shoulders are the most commonly affected Many pt are asymptomatic Others present with chronic pain and stiffness in multiple joints. Can be hot and swollen

Question 102

Diagnosing pseudogout?

Answer 102

Exclude septic arthritis and gout - usually symptoms are much milder Pseudogout more likely to affect proximal joints more than gout e..g knee and wrist Joint aspiration to confirm the disease - will show calcium pyrophoshate crystals which are rhomboid-shaped and weakly-positively birefringent of polarised light XR - will show chondrocalcinosis which are calcium deposits which show up in a thin white line in the middle of the joint space. Can also show same XR changes as osteoarthritis “LOSS”

Question 103

Management of pseudogout?

Answer 103

Note this is not fully treatable but you can manage symptoms. Symptoms will usually resolve spontaneously over several weeks but symptomatic management options include: NSAIDs is first line Or intra-articulate, IM or oral steroids

Question 104

Septic arthritis mortality rate?

Answer 104

10%

Question 105

Cause of septic arthritis?

Answer 105

Most commonly staph aureus Young adults who are sexually active - neisseria gonorrhoea is the most common The most common cause is haematogenous spread e.g. from distance bacterial infections Be aware 1% of all joint replacements end in infection

Question 106

Presentation of septic arthritis?

Answer 106

Affects a single joint usually (commonly the knee) Rapid onset of: Hot, red, swollen, painful joint Stiffness and reduced range of movement Systemic symptms - fever, lethargy, sepsis

Question 107

Investigations for septic arthritis?

Answer 107

FBC, ESR, CRP Synovial fluid sampling before antibiotics - gram staining, crystal microscopy, culture Blood cultures as commonly hameatogenous spread Joint imaging may be done

Question 108

Management of septic arthritis?

Answer 108

IV antibiotics which cover gram-positive cocci - flucloxacillin (or clindamycin if penicillin allergic) for 4-6 weeks ( usually switched to oral antibiotics after 2 weeks) (Ceftriaxone is used for gonococcal infection) Needle aspiration to decompress the joint Arthroscopic lavage may be required

Question 109

What is reactive arthritis?

Answer 109

A seronegative spondyloarthropathies associated with HLA-B27 Formerly called Reiter’s syndrome Classic triad - urethritis, conjunctivitis and arthritis Defined as an arthritis that develops following an infection where the organism cannot be recovered from the joint

Question 110

Organisms most commonly associated with reactive arthritis?

Answer 110

Chlamydia trachomatis - particularly in men Shigella, salmonella, yersinia, campylobacter

Question 111

Presentation of reactive arthritis?

Answer 111

Within 4 weeks of initial infection… Bilateral conjunctivitis (non-infective) or anterior uveitis Urethritis (non-gonococcal) Circinate balanitis (dermatitis of the head of the penis) Arthritis - asymmetrical oligoarthritis of lower limbs Dactylitis “Can’t see, can’t pee, can’t climb a tree”

Question 112

Management of reactive arthritis?

Answer 112

Septic arthritis most likely will need to be ruled out first using joint aspiration! symptomatic: treat triggering infection, NSAIDS, intra-articular steroid injections or systemic steroids sulfasalazine and methotrexate are sometimes used for persistent disease

Question 113

Prognosis of reactive arthritis?

Answer 113

Most cases rarely last >12 months

Question 114

What is ankylosing spondylitis?

Answer 114

A HLA-B27 associated seronegative spondyloarthropathy affecting the axial skeletal causing progressive stiffness and pain Aka axial spondyloarthritis

Question 115

Who does ankylosing spondylitis typically affect?

Answer 115

Men 20-30 years old Men:women 3:1 and men are more likely to get severe disease

Question 116

Presentation of ankylosing spondylitis?

Answer 116

Gradual development over at least 3 months of pain and stiffness in the lower back and sacroiliac pain Pain and stiffness is worse with rest and improves with movement. Stiffness takes at least 30 minutes to improve in the am May have night pain Other features may include chest pain, enthesitis (e.g. Achilles tendinitis or plantar fasciitis), dactylitis, vertebra fractures and SOB

Question 117

Clinical examination findings of ankylosing spondylitis?

Answer 117

Reduced lateral flexion Reduced forward flexion - Schober’s test Reduced chest expansion

Question 118

What are the associated conditions of ankylosing spondylitis?

Answer 118

Remembers the As Anterior uveitis Aortic regurgitation AV block Apical lung fibrosis Anaemia of chronic disease Achilles tendinitis Amyloidosis And caudal equina syndrome

Question 119

What is schobers test?

Answer 119

a line is drawn 10 cm above and 5 cm below the back dimples (dimples of Venus). The distance between the two lines should increase by more than 5 cm when the patient bends as far forward as possible This is reduced in ankylosing spondylitis

Question 120

Investigations for ankylosing spondylitis?

Answer 120

ESR and CRP are raised HLA-B27 is of little use Plain XR of sacroiliac joints - If XR is negative for sacroiliac joint involvement but suspicion remains high then obtain MRI which may show early inflammation signs e.g. bone marrow oedema Spirometers may show a restrictive defect due to combination of pulmonary fibrosis, kyphosis and ankylosis of costovertbral joints

Question 121

XR findings of sacroiliac joints in ankylosing spondylitis?

Answer 121

Sacroiliitis - subchondral erosions and sclerosis Squaring of lumbar vertebrae Syndesmophytes due to ossification of outer fibers of annulus fibrosus Bamboo spine - late &uncommon sign

Question 122

Management of ankylosing spondylitis?

Answer 122

Encourage regular exercise e.g. swimming First line - NSAIDs + PT Second line - If very resistant to treatment then anti-TNF therapy can be tried DMARDs are only used if peripheral joint involvement Intra-articular steroid injections may be considered for specific joints

Question 123

Oligoarthritis vs polyarthritis?

Answer 123

Oligoarthritis means less than 5 joints affected Polyarthritis is >5 joints

Question 124

What is chondrocalcinposis?

Answer 124

Presence of calcium deposits in the cartilage of a joint Seen in calcium pyrophosphate deposition disease aka pseudogout This can also be present in up to 1/3rd of healthy 65-75 year olds

Question 125

Pathophysiology of rheumatoid arthritis?

Answer 125

Trigger -> macrophages release TNF alpha, IL1 and IL6 -> Synovial membrane is inflamed + fibroblast-like synoviocytes are stimulated, activated and proliferate -> activation of osteoclasts = bone erosion Proteases are also released which causes cartilage degradation T cells secrete IL17 which promotes macrophage activity and stimulates fibroblast-like synoviocytes and help stimulate osteoclasts Plasma cells assist in inflammation through cytokines and antibodies In the synovial fluid we find neutrophils which produce proteases and ROS = bone and cartilage degradation Immune complexes are also found in this synovial fluid The fibroblast-like synoviocytes can migrate from joint to joint = this is why we get symmetrical arthritis

Question 126

Pathophysiology of osteoarthritis?

Answer 126

Chondrocytes in articular cartilage and inflammatory cells in surrounding tissues break down collagen and proteoglycans, destroying articular cartilage. The exposure of the underlying subchondral bone results in sclerosis, followed by reactive remodelling which leads to the formation of ostephytes and subchondral bone cysts The joint space is progressively lost over time

Question 127

What % of patients with axial spondyloarthritis have HLA-B27?

Answer 127

90%

Question 128

How long do joint replacements typically last?

Answer 128

15-20 years

Question 129

What is enteropathic arthritis?

Answer 129

a type of arthritis that occurs with inflammatory bowel disease

Question 130

Complications of ankylosing spondylitis?

Answer 130

Ankylosis or spinal fusion Apical fibrosis and other lung involvement - this is due to costovertebral involvement decreasing vital capacity Joint damage - hips and knees due to change of gait to accommodate stiffness Anterior uveitis Osteoporosis and spinal fractures CVD Decreased QOL and work productivity Risk of cauda equina

Question 131

Prognosis of gout and why?

Answer 131

It will continue to return and worsen This is because as we age our renal function worsens

Question 132

What skin conditions are likely with reactive arthritis?

Answer 132

circinate balanitis (painless vesicles on the coronal margin of the prepuce) keratoderma blenorrhagica (waxy yellow/brown papules on palms and soles)