Rheumatology - Introduction to rheumatological disease Flashcards

1
Q

What symptoms should be asked about in a rheumatological history?

A

Basic details - age, sex, height and weight (rheumatological conditions are more likely in women and the elderly)

Symptoms:

  • Pain - may be worse on usage (mechanical), after rest (inflammatory) or at night
  • Stiffness - early morning or disuse stiffness (inflammation); may be associated with weakness or deformity
  • Swelling, deformity
  • Symptoms of systemic illness - e.g. fever, weight loss, anorexia, fatigue

PMH - previous episodes of similar symptoms; autoimmune disease; dermatological diseases

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2
Q

What key features suggest inflammatory joint disease?

A

1) Symptoms:
- Stiffness: usually present after prolonged inactivity, early morning (> 1hr), easing as the day goes on
- Pain: inflammatory pain is usually present at rest as well as on movement

Both are generally relieved by NSAIDs.

2) Examination:
- overlying skin may be warm and red
- tenderness is elicited all across the joint line
- swelling is fluid in nature
- pain is elicited throughout the range of active and passive movements

3) Laboratory:
- ESR and CRP are both raised

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3
Q

What conditions cause an acute monoarthropathy?

A

Diagnosis is rheumatology depends on the distribution of inflammed joints + pattern of extra-articular involvement.

Monoarthropathy means that a single joint is involved.
DDx includes:
- trauma
- septic arthritis
- goat/ crystal arthropathy
- initial presentation of bilateral symmetrical polyarthritis (e.g. RA) but more likely an asymmetrical oligoarthritis (e.g. seronegative)

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4
Q

What type of joint distribution does RA produce?

A

RA is the classic bilateral symmetrical polyarthropathy. Polyarthritis means that multiple joints are involved, but may start with limited joint involvement. It typically affects the small joints of the hands and feet.

There are a number of extra-articular manifestations in RA:

  • lung + pleura - pleuritis, effusion, basal fibrosis
  • pericardium - pericarditis
  • blood vessel - vasculitis
  • nodules - e.g. elbow
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5
Q

What conditions produce an asymmetrical oligoarthritis?

A

The seronegative spongyloarthropathies usually produce an asymmetrical oligoarthritis. This is where there is 2-5 inflammed joints and extra-articular manifestations, including:

  • iritis
  • keratoderma
  • psoriatic plaques
  • enthesitis (inflammation where the tendon meets the muscle)
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6
Q

What pattern of joint involvement do connective tissue diseases show?

A

In these conditions (e.g. SLE) there is widespread involvement of many components of the musculoskeletal system and connective tissues which affects joints, skin and serosal surfaces as well as major organs such as the kidney and brain.

In SLE, this can include:

  • pericarditis
  • basal fibrosis, pleuritis
  • glomerulonephritis
  • myositis
  • nail-bed infarcts
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7
Q

What conditions are suggested by systemic extra-articular features?

A

High fever may suggest infection, Still’s disease or rheumatic fever but sometimes gout or SLE. Malaise and fatigue are very common but under-recognised features of inflammatory disorders. Weight loss may also occur.

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8
Q

What rheumatological conditions have skin changes?

A
Psoriasis
SLE
Vasculitis 
Scleroderma
Dermatomyositis 

All have characteristic skin changes

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9
Q

Mucosa changes in rheumatological disease

A

Oral ulcers in SLE, Crohn’s disease, and Behcets syndrome.

Mucosal dryness in Sjogrens syndrome.

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10
Q

What are Rheumatoid Factors? When are they useful and when do they occur?

A

Rheumatoid factors are autoantibodies against antigenic determinants of the Fc fragment of IgG.

  • they may be IgM, IgA or IgG class
  • only measurement of IgM RF is clinically useful
  • IgM RF is usually measured by agglutination tests and expressed as the serum dilution where agglutination still occurs (e.g. 1 in 40, 80, 160, 320 etc)
  • they occur in rheumatic diseases (e.g. 70% of RA, 40% of SLE, 30% systemic sclerosis) - in RA they are most useful for prognosis rather than diagnosis (high titre = adverse prognosis)
  • they are also found in: viral infections, chronic inflammatory diseases (e.g. TB), neoplasms, 5% of healthy individuals
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11
Q

What autoantibody is best used for the diagnosis of early RA?

A

Anti- CCP (anti-cyclic citrullinated peptide) are increasingly used for the early diagnosis of RA. The antibodies may be found months to years before the onset of clinical disease and may have a role in pathogenesis. They are also associated with erosive disease and may predict poor prognosis better than RF.

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12
Q

What are the approaches to managing rheumatic disease?

A

Treatment aims to relieve symptoms, maintain (restore) function and suppress underlying disease process. MDT approach is useful.

1) Conservative:
- education, physio, activity modification, weight loss, exercise, smoking cessations
- intra articular oer peri-articular steroid injection

2) Medical:
- NSAIDs, DMARDs (e.g. methotrexate, sulphasalazine for RA; cyclophosphamide for SLE, renal disease and vasculitis)
- biologic therapies - e.g. anti-cytokine receptor therapies and anti-adhesion B cell molecule therapies, antitumour necrosis factor therapy (esp RA)

3) Surgery:
- joint fusion, replacement, synovial resection
- carefully selected patients

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13
Q

What are the clinical features of OA?

A

OA is non inflammatory, degenerative joint disease which is usually secondary to other pathologies (rarely primary). It is common in the elderly, and patients report:

  • polyarticular involvement
  • chronic
  • symptoms worse with use (cf. RA where symptoms are worse with disuse)
  • < 1 hr morning stiffness
  • loss of function (e.g. can’t button up shirts, open jars etc)
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14
Q

What are the examination findings in OA?

A

OA is not an inflammatory joint disease, so the joints are not red or warm with only mild tenderness.

Hand examination typically shows:

  • Heberden’s nodes - DIPJ
  • Bouchard’s nodes - PIPJ
  • squaring of the thumb (due to arthritis at the first carpo-metacarpal joint)
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15
Q

Investigations in OA

A

OA is normally a clinical diagnosis and so investigations are not normally performed. If they were they would show normal inflammatory markers and negative RhF and ANA.

X rays show:

  • Loss of joint space
  • Osteophytes
  • Subchondral sclerosis
  • Subchondral cysts
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16
Q

How should OA be managed?

A

1) Conservative
- education, activity modification, physio/ OT (if necessary), weight loss

2) Medical
- NSAIDs
- analgesia (paracetamol, codeine)

3) Surgery
- major joint replacement

17
Q

What is gout?

A

Gout is a crystal arthropathy caused by accumulation of uric acid in the joint space.

It is painful, red and swollen often with acute exacerbations (flare ups), and commonly involves the first MTP joint.

Gout can also be chronic, with tophi present across a number of small joints which appear red and swollen.

18
Q

Investigations in gout

A

During an acute attack the ESR and CRP will be raised but will be normal in between.

Renal function should also be checked as impairment reduces urate excretion.

Joint or nodule aspiration is the gold standard for diagnosing gout and the fluid is looked at using polarised light. Fluid aspirate is typically turbid and shows NEGATIVELY birefringent needle shaped crystals on polarised light microscopy.

19
Q

What causes gout?

A

Uric acid accumulates either because patients are over producers (as occurs classically in high turnover states such as treatment of leukaemia) or under excretion.

Under excretion is more common and can be due to family history, drugs (e.g. thiazide diuretics) or alcohol.

20
Q

How is gout managed?

A

Risk factors for gout should be managed alongside the condition itself.

Acute exacerbations are treated with NSAIDs (except aspirin), Colchicine, and intra-articular injections.

Maintenance therapy with Allopurinol or febuxostat can be considered in patients who have had 3+ exacerbations, have loss of joint space or tophaceous deposits. These agents lower uric acid levels.

21
Q

What crystals are present in pseudogout?

A

Calcium pyrophosphate dihydrate.

Pseudogout shows POSITIVELY birefringent rhomboid crystals on light microscopy following joint aspiration

22
Q

What is fibromyalgia? How is it diagnosed?

A

Fibromyalgia is a chronic pain disorder of unknown cause, and is a diagnosis of exclusion (i.e. no other cause can be identified).

The American College of Rheumatologists (ACR) 1990 diagnostic criteria state:

  • chronic widespread pain, on both sides of the body, above and below the waist
  • minimum duration of 3 months
  • tenderness to palpation on 11/18 tender points

Patients often have additional associated symptoms - e.g. sleep disturbance, fatigue and anxiety, depression, GIT disturbance

23
Q

What are the risk factors for fibromyalgia?

A

1) Yellow flags = psychosocial factors for developing chronic persistent pain and long term disability
- belief that activity is harmful
- sickness behaviour
- social withdrawal
- emotional disturbances

2) female sex
3) low SES
4) middle age

24
Q

Investigations in fibromyalgia

A

It is important not to over investigate fibromyalgia, but positive ACR/ clinical history should guide investigations.

Investigations are usually ALL normal, but it is important to exclude hypothyroidism and hypocalcaemia.

Fibromyalgia should not be confused with PMR which IS an inflammatory condition.

25
Q

How should fibromyalgia be managed?

A
  • MDT approach is helpful
  • be supportive and reassure the patient
  • drugs - low dose amitryptaline (25-75mg nocte) may help with sleep; SSRI may help with anxiety, analgesia
  • be aware of yellow flags
  • moderate intensity aerobic exercise