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RHEUM Flashcards

1
Q

What are the 3 screening questions for musculo-skeletal disease?

A

1 Are you free of any pain or stiffness in your joints, muscles or back?
2 Can you dress yourself without too much difficulty?
3 Can you manage walking up and down stairs?
If yes to all 3, serious inflammatory muscle/joint disease is unlikely.

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2
Q

What bloods should you do to investigate rheumatological disease?

A

FBC, ESR, urate, U&E, CRP. Blood culture for septic arthritis. Consider rheumatoid factor, anti-CCP, ANA, other autoantibodies , and HLA B27 —as guided by presentation. Consider causes of reactive arthritis , eg viral serology, urine chlamydia PCR, hepatitis and HIV serology if risk factors are present.

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3
Q

X-ray features of osteoarthritis

A

Loss of joint space
Osteophytes
Subarticular sclerosis
Subchondral cysts

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4
Q

X-ray features of RA

A

Juxta articular ostopenia
Soft tissue swelling
Joint deformity
Loss of joint space

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5
Q

X-ray features of gout (1st MTPJ).

A

Peri-articular erosions
Normal joint space
Soft tissue swelling

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6
Q

Back pain: red flags

A

Aged <20yrs or >55yrs old
Acute onset in elderly people
Constant or progressive pain Nocturnal pain
Worse pain on being supine Fever, night sweats, weight loss  History of malignancy Abdominal mass
 Thoracic back pain Morning stiffness
 Bilateral or alternating leg pain Neurological disturbance (incl sciatica) Sphincter disturbance
Current or recent infection
 Immunosuppression, eg steroids/HIV
Leg claudication or exercise-related leg weakness/numbness (spinal stenosis)

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7
Q

Clinical tests for sacroiliitis?

A

direct pressure, lateral compression, sacroiliac stretch test (pain on adduction of the hip, with the hip and knee flexed).

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8
Q

Most likely cause of back pain in 15-30 yo px

A

Prolapsed disc, trauma, fractures, ankylosing spondylitis , spondylolisthesis (a forward shift of one vertebra over another, which is congenital or due to trauma), pregnancy.

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9
Q

Most likely cause of back pain in 30-50 yo

A

Degenerative spinal disease, prolapsed disc, malignancy (primary or secondary from lung, breast, prostate, thyroid or kidney ca).

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10
Q

Most likely cause of back pain >50yo

A

Degenerative, osteoporotic vertebral collapse, Paget’s , malignancy, myeloma, spinal stenosis.

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11
Q

Back pain Ix

A

FBC, ESR and CRP (myeloma, infection, tumour), U&E, ALP (Paget’s), serum/urine electrophoresis (myeloma), PSA.
X-rays can exclude bony abnormality but are generally not indicated.
MRI is the image of choice and can detect disc prolapse, cord compression, cancer, infection or inflammation (eg sacroiliitis).

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12
Q

OA Sx

A

tenderness, derangement and bony swelling (Heberden’s nodes at DIP, Bouchard’s nodes at PIP), reduced range of movement and mild synovitis

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13
Q

OA symptoms

A 
Localized disease (usually knee or hip): pain on movement and crepitus, worse at end of day; background pain at rest; joint gelling—stiffness after rest up to ~30min; joint instability. 
Generalized disease (primary OA): with Heberden’s nodes (‘nodal OA’, seen mainly in post-menopausal women), commonly affected joints are the DIP joints, thumb carpo-metacarpal joints and the knees.
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14
Q

OA Mx

A

Conservative:
•Exercise to improve local muscle strength and general aerobic fitness (irrespective of age, severity or comorbidity).
•Weight loss if overweight
•Use a multi- disciplinary approach, including physiotherapists and occupational therapists.
•Try heat or cold packs at the site of pain
•Walking aids
•Stretching/manipulation
Medical:
•Regular paracetamol ± topical NSAIDS. If ineffective use codeine or short-term oral NSAID (+PPI)
•Topical capsaicin (derived from chillies)
•Intra-articular steroid injections temporarily relieve pain in severe symptoms.
•Intra-articular hyaluronic acid injections (visco supplementation) are as effective as NSAIDS or steroid injection, but are much more expensive.
•TENS
•Glucosamine and chondroitin products are not recommended
Surgical:
•Joint replacement (hips, or knees) is the best way to deal with severe OA that has a substantial impact on quality of life.

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15
Q

What is an emergency you MUST consider when presented with an acute joint?

A

Consider septic arthritis in any acutely inflamed joint, as it can destroy a joint in under 24h. Inflammation may be less overt if immunocompromised (eg from medication) or if there is underlying joint disease. The knee is affected in >50% cases

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16
Q

Septic arthritis RF

A
  • Pre-existing joint disease (especially rheumatoid arthritis)
  • Diabetes mellitus
  • Immunosuppression
  • Chronic renal failure
  • Recent joint surgery
  • Prosthetic joints (where infection is particularly difficult to treat)
  • IV drug abuse
  • Age >80yrs
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17
Q

Septic arthritis Ix

A

Urgent joint aspiration for synovial fluid microscopy and culture is the key investigation as plain radiographs and CRP may be normal. The main differential diagnoses are the crystal arthropathies. Blood cultures may be helpful for guiding antibiotic choice later.

Ask yourself “How did the organism get there?” Is there immunosuppression, or another focus of infection, eg from indwelling IV lines, infected skin, or pneumonia (present in up to 50% of those with pneumococcal arthritis)

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18
Q

Common causative organisms for septic arthritis

A
  • Staph. Aureus
  • Streptococci
  • Neisseria gonococcus
  • Gram –ve bacilli.
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19
Q

Management of septic arthritis

A
  • If in doubt start empirical IV antibiotics (after aspiration) until sensitivities are known.
  • Follow local guidelines for antibiotic choice.
  • If HIV +ve, look for atypical mycobacteria and fungi.
  • Antibiotics are required for a prolonged period but there is no consensus on which route or for how long they should be continued (eg ~2 weeks IV, then 2–4 weeks PO)—ask a microbiologist.
  • Ask for orthopaedic advice for consideration of arthrocentesis, lavage and debridement, especially if there is a prosthetic joint involved.
  • This may be done arthroscopically (eg for knee) or open under GA (eg for hip; this allows for biopsy— helpful in TB).
  • Splint for ≤48h, give adequate analgesia and consider physiotherapy.
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20
Q

What antibiotics are given for septic arthritis?

A

Consider flucloxacillin 1g/6h IV (clindamycin if penicillin allergic)
•Vancomycin 1g/12h IV if MRSA (or history of MRSA); or
•Cefotaxime 1g/8h IV if gonococcal or Gram –ve organisms suspected

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21
Q

NSAIDs SE

A

GI bleeding (!gastrointestinal damage may occur without dyspeptic symptoms) and renal impairment

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22
Q

When are NSAIDs contraindicated?

A

severe cardiac failure

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23
Q

When on NSAIDs, what factors increase side effects?

A
  • prolonged use
  • ^age
  • Polypharmacy
  • history of peptic ulcers and renal impairment (review before and after starting therapy)
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24
Q

Which NSAID has the lowest GI risk?

A

Ibuprofen

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25
Q

How long do the anti-inflammatory effects of NSAIDs fully take place?

A

3 weeks

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26
Q

When are NSAIDs to be avoided?

A

Avoid giving NSAIDS to patients on aspirin and do not use in active GI ulceration.

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27
Q

What must you tell patients on NSAIDs?

A

“Take the lowest possible dose for the shortest possible time”
Drugs are to relieve symptoms: on good days, don’t take any.
In rheumatoid arthritis, cod liver oil (eg 10g/d) reduces reliance on NSAIDS by 30%.
Abdominal pain may be a sign of impending GI problems: stop the tablets, and come back for more advice if symptoms continue.
Report black stools ± faints at once.
Don’t supplement prescribed NSAIDS with ones bought over the counter (eg ibu-
profen): mixing NSAIDS can increase risks 20-fold.
Smoking and alcohol increase NSAID risk

28
Q

Cardiovascular side effects of NSAIDS

A

a small increased risk of MI and stroke (independent of cardiovascular risk factor or duration of use). Specifically implicated are celecoxib (any dose), diclofenac (>150mg/24h) and ibuprofen (>1200mg/24h)

29
Q

Gout: DDx

A

Exclude septic arthritis in any acute monoarthropathy Then consider haemarthrosis, CPPD and palindromic RA

30
Q

Epidemiology of RA

A

Prevalence is ~1% (increases in smokers). F:M >2:1. Peak onset: 5th–6th decade.
HLA DR4/DR1 linked (associated with increased severity).

31
Q

How does RA typically present?

A

symmetrical swollen, painful, and stiff small joints of hands and feet, worse in the morning. This can fluctuate and larger joints may become involved.

32
Q

What are some less common presentations of RA?

A
  • Sudden onset, widespread arthritis;
  • Recurring mono/polyarthritis of various joints (palindromic RA);
  • Persistent monoarthri- tis (often knee, shoulder or hip); •Systemic illness with extra-articular symptoms, eg fatigue, fever, weight loss, pericarditis and pleurisy, but initially few joint problems (commoner in men); •Polymyalgic onset—vague limb girdle aches;
  • Recurrent soft tissue problems (eg frozen shoulder, carpal tunnel syndrome, de Quervain’s tenosynovitis).
33
Q

Sx of RA

A
  • Early (inflammation, no joint damage): swollen MCP, PIP, wrist, or MTP joints (often symmetrical)
  • Look for tenosynovitis or bursitis
  • Later (joint damage, deformity): ulnar deviation of the fingers and dorsal wrist subluxation. Boutonnière and swan-neck deformities of fingers or Z-deformity of thumbs occur.
  • Hand extensor tendons may rupture. Foot changes are similar.
  • Larger joints can be involved.
  • Atlanto-axial joint subluxation may threaten the spinal cord (rare).
34
Q

Extra articular features of RA

A
  • nodules—elbows & lungs;
  • lymphadenopathy;
  • vasculitis;
  • fibrosing alveolitis,
  • obliterative bronchiolitis;
  • pleural & pericardial effusion;
  • Raynaud’s; carpal tunnel syndrome; peripheral neuropathy;
  • splenomegaly (seen in 5%; only 1% have Felty’s syndrome: RA + splenomegaly + neutropenia); episcleritis, scleritis, scleromalacia, keratoconjunctivitis sicca; osteoporosis; amyloidosis
35
Q

RA: Ix

A
  • Rheumatoid factor (RhF) is positive in ~70% . A high titre is associated with severe disease, erosions and extra-articular disease.
  • Anticyclic citrullinated peptide antibodies (ACPA/anti-CCP) are highly specific (~98%) for RA.
  • There is often anaemia of chronic disease.
  • Inflammation causes increased platelets, ESR, CRP
36
Q

RA: imaging

A
  • X-rays show soft tissue swelling, juxta-articular osteopenia and narrow joint space.
  • Later there may be bony erosions, subluxation or complete carpal destruction
  • Ultrasound and MRI can identify synovitis more accurately, and have greater sensitivity in detecting bone erosions than conventional X-rays.
37
Q

RA: Mx conservative

A

Offer specialist physio- and occupational therapy, eg for aids and splints. There is increased risk of cardiovascular and cerebrovascular disease, as atherosclerosis
is accelerated in RA. Manage risk factors.
Smoking also increases symptoms of RA.

38
Q

RA: Rx

A 
• Early use of DMARDS and biological agents improves long-term outcomes 
• Steroids rapidly reduce symptoms and inflammation. Avoid starting unless appropriately experienced. They are useful for treating acute exacerbations (‘flares’), eg IM depot methylprednisolone 80–120mg. Intra-articular steroids have a rapid but short-term effect 
Oral steroids (eg prednisolone 7.5mg/d) may control difficult symptoms, but side-effects preclude routine long-term use. 
• NSAIDS are good for symptom relief, but have no effect on disease progression. Paracetamol and weak opiates are rarely effective.
39
Q

RA: is there a role for surgery?

A

Surgery may relieve pain, improve function and prevent deformity.

40
Q

What is one of the keys in managing RA as a GP?

A

!!!! Refer early to a rheumatologist (before irreversible destruction).

41
Q

How is disease activity measured in RA?

A

Disease activity is measured using the DAS28. Aim to reduce score to <3.

42
Q

What is the key biological event in RA?

A

Over-produced cytokines and cellular processes erode cartilage and bone, and produce the systemic effects seen in RA

43
Q

Key pharmacological management of RA-what is first line?

A

Disease-modifying antirheumatic drugs (DMARDS) are 1st-line for treating RA

44
Q

When should DMARDS be started? How long do they take to provide symptomatic benefit?

A

within 3 months of persistent symptoms.

They can take 6–12 weeks for symptomatic benefit.

45
Q

What are some examples of DMARDS? Which provide best results

A

Best results are often achieved with a combination of methotrexate, sulfasalazine and hydroxychloroquine. Other DMARDS include leflunomide and IM gold (now rarely used). The role of penicillamine, azathioprine and ciclosporin is less clear

46
Q

What is a potentially fatal side effect of dmards? How can you monitor this?

A

!!Immunosuppression is a potentially fatal SE of treatment (especially in combination with methotrexate) which can result in pancytopenia, increases susceptibility to infection and neutropenic sepsis. Regular FBC monitoring is required.

47
Q

Side effects of Methotrexate

A

•Methotrexate—pneumonitis (get urgent respiratory help), oral ulcers, hepatotoxicity

48
Q

Side effects of Sulfalazine

A

• Sulfasalazine—rash, reduced sperm count, oral ulcers

49
Q

Side effects of leflunomide

A

teratogenicity(M&F), oral ulcers, increased BP, hepatotoxicity

50
Q

Side effects of Hydroxychloroquine

A

Hydroxychloroquine—irreversible retinopathy (request annual ophthalmology review)

51
Q

What does NICE guidance say about biological agents?

A

There are 4 approaches, which should be initiated under specialist supervision

52
Q

What are the four approaches to biological agents?

A

TNF-a inhibitors
B cell depletion
IL-1 and IL-6 inhibition
Disruption of T cell function

53
Q

For each biological agent mechanisms, provide an example.

A

TNF-a inhibitors:
Infliximab , etanercept, adalimumab, certolizumab- pegol and golimumab.

B cell depletion, eg Rituximab

IL-1 and IL-6 inhibition, eg Tocilizumab (IL-6 receptor blocker)

Disruption of T cell function, eg Abatacept

54
Q

When are TNF-a inhibitors recommended?

A

All are approved by NICE (usually in combination with methotrexate) as 1st-line biological agents for active RA after failure to respond to 2 DMARDS and with a DAS28 >5.1.

55
Q

Which drugs can be used instead of methotrexate when it is contraindicated?

A

adalimumab and etanercept can be used as monotherapy

56
Q

When is Rituximab used?

A

Rituximab, used in combination with methotrexate and ap- proved by NICE for severe active RA where DMARDS and a TNF-a blocker have failed

57
Q

When is Tocilizumab used?

A

ocilizumab (IL-6 receptor blocker), approved by NICE in combination with methotrexate for patients where both a TNF-a blocker and rituximab have failed (or are contraindicated)

58
Q

Causes of gout

A

Hereditary, high dietary purines, alcohol excess, diuretics, leukaemia, cytotoxics (tumour lysis)

59
Q

Which conditions is gout associated with?

A

Cardiovascular disease, hypertension, diabetes mellitus and chronic renal failure
Gout is a marker for these, therefore seek out and treat if needed.

60
Q

Gout Ix

A

Polarized light microscopy of synovial fluid shows negatively bi- refringent urate crystals
Serum urate is usually raised but may be normal.
X-ray.

61
Q

Gout: how do X-rays look?

A

Radiographs show only soft-tissue swelling in the early stages. Later, well-defined ‘punched out’ erosions are seen in juxta-articular bone There is no sclerotic reaction, and joint spaces are preserved until late

62
Q

Management of Gout

A

Conservative:
•Rest and elevate the affected joint.
•Ice packs and ‘bed cages’ can be effective.

Medical
• Use high-dose NSAID or coxib (eg etoricoxib 120mg/24h PO) Symptoms should subside in 3–5d.
•If CI (eg peptic ulcer; heart failure; anticoagulation), colchicine (0.5mg/6–12h PO) is effective but slower to work (note new BNF guidelines of max 6mg per course).
•NB: in renal impairment, NSAIDS and colchicine are problematic. Steroids (oral, IM or intra-articular) may also be used.

63
Q

What advice can you give to patients on preventing gout?

A

Lose weight. Avoid prolonged fasts, alcohol excess, purine-rich meats and low-dose aspirin ( increased serum urate).

64
Q

Gout prophylaxis: when should this be initiated and what does this aim to do?

A

Start if >1 attack in 12 months, tophi or renal stones. The aim is to reduce attacks and prevent damage caused by crystal deposition.

65
Q

Pharmacological prophylaxis of gout

A

Use allopurinol and titrate from 100mg/24h, increasing every 2 weeks until plasma urate <0.3mmol/L (max 300mg/8h).

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