Joints

Question 1

Osteoarthritis

Answer 1

Osteoarthritis (OA) is the commonest joint condition.

onset typically >50yrs.

It is usually primary (generalized), but may be secondary to joint disease or other conditions (eg haemochromatosis, obesity, occupational).

Signs and symptoms: 
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 Heb erden’s nodes (‘nodal OA’, seen mainly in post-menopausal), commonly affected joints are the DIP joints, thumb carpo-metacarpal joints and the knees. There may be joint tenderness, derangement and bony swelling (Heberden’s nodes at DIP, Bouchard’s nodes at PIP), range of movement and mild synovitis. 

Assess effect of symptoms on occupation, family duties, hobbies and lifestyle expectations.

Tests:
Plain radiographs show: Loss of joint space, Osteophytes, Subarticular sclerosis and Subchondral cysts. CRP may be slightly elevated.

Core treatments:
Exercise to improve local muscle strength and general aerobic fitness (irrespective of age, severity or comorbidity). Weight loss if overweight. Analgesia: Regular paracetamol ± topical NSAIDS. If ineffective use
codeine or short-term oral NSAID (+PPI). Topical capsaicin (derived from chillies) may help.
Intra-articular steroid injections temporarily relieve pain in severe symptoms. Intra-articular hyaluronic acid injections (viscosupplementation) are as effective as NSAIDS or steroid injection, but are much more expensive.

Glucosamine and chondroitin products are not recommended.

Non-pharmacological:
Use a multidisciplinary approach, including physiotherapists and occupational therapists. Try
heat or cold packs at the site of pain, walking aids, stretching/manipulation or TENS.

Surgery: Joint replacement (hips, or knees) is the best way to deal with severe OA that has a substantial impact on quality of life.

Question 2

Ankylosing Spondylitis

Answer 2

Ankylosing spondylitis (AS) is a chronic inflammatory disease of the spine and sacroiliac joints, of unknown aetiology.
Prevalence: 0.25–1%. Men present earlier.
AS is 3 times more frequent in men than in women and begins most often between ages 20 and 40. It is 10 to 20 times more common among 1st-degree relatives of AS patients than in the general population.

Classification
Most patients with AS have predominantly axial involvement (called axial AS). Some have predominately peripheral involvement. Among those with axial involvement, some have no evidence of sacroiliitis on plain x-rays. Thus, some experts have classified AS as follows:

Axial AS: Has predominantly axial involvement and x-ray findings typical of sacroiliitis

Nonradiographic AS: Clinically similar to axial AS but without x-ray findings typical of sacroiliitis

Peripheral AS: AS with predominantly peripheral involvement

Symptoms and Signs
The most frequent manifestation is back pain, but disease can begin in peripheral joints, especially in children and women, and rarely with acute iridocyclitis (iritis or anterior uveitis). Other early symptoms and signs are diminished chest expansion from diffuse costovertebral involvement, low-grade fever, fatigue, anorexia, weight loss, and anemia.

Back pain—often nocturnal and of varying intensity—eventually becomes recurrent. Morning stiffness, typically relieved by activity, and paraspinal muscle spasm develop. A flexed or bent-over posture eases back pain and paraspinal muscle spasm; thus, kyphosis is common in untreated patients. Severe hip arthritis can eventually develop. In late stages, the patient has accentuated kyphosis, loss of lumbar lordosis, and fixed bent-forward posturing, with compromised pulmonary function and inability to lie flat. There may be peripheral potentially deforming joint involvement, sometimes involving the digits (dactylitis). Achilles and patellar tendinitis can occur.

Systemic manifestations occur in one third of patients. Recurrent, acute anterior uveitis is common and usually responds to local therapy; less commonly it becomes protracted and severe enough to impair vision. Neurologic signs occasionally result from compression radiculitis or sciatica, vertebral fracture or subluxation, or cauda equina syndrome. Cardiovascular manifestations can include aortic insufficiency, aortitis, angina, pericarditis, and cardiac conduction abnormalities (which may be asymptomatic). Dyspnea, cough, or hemoptysis can rarely result from nontuberculous fibrosis or cavitation of an upper lobe of the lung; cavitary lesions can become secondarily infected with Aspergillus. Rarely, AS results in secondary amyloidosis. Subcutaneous nodules do not develop.

Diagnosis
Lumbosacral spine imaging
Blood tests (ESR, C-reactive protein, and CBC)

Treatment
NSAIDs
Sulfasalazine, methotrexate, or TNF-α antagonists
Exercises and supportive measures

Question 3

Rheumatoid Arthritis

Answer 3

RA is a chronic systemic inflammatory disease, characterized by a symmetrical, deforming, peripheral polyarthritis.
Epidemiology: Prevalence is ~1% (higher in smokers).

Peak onset: 5th–6th decade.

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

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

Signs 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 fi ngers 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).
Extra-articular Nodules—elbows & lungs; lymphadenopathy; vasculitis; fibrosing alveolitis, obliterative bronchiolitis; pleural & pericardial effusion; Raynaud’s; carpal tunnel syndrome; peripheral neuropathy; splenomegaly; episcleritis, scleritis,
scleromalacia, keratoconjunctivitis sicca; osteoporosis; amyloidosis.

Investigations: 
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. X-rays show soft tissue swelling, juxta-articular osteopenia and decreased 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. 

Management:
Refer early to a rheumatologist (before irreversible destruction).

Question 4

Gout

Answer 4

Gout typically presents with an acute monoarthropathy with severe joint inflammation

> 50% occur at the metatarsophalangeal joint of the big toe (podagra).

Other common joints are the ankle, foot, small joints of the hand, wrist, elbow or knee. It can be polyarticular.

It is caused by deposition of monosodium urate crystals
in and near joints, precipitated, for example, by trauma, surgery, starvation, infection or diuretics. It is associated with raised plasma urate. In the long term, urate
deposits and renal disease (stones, interstitial nephritis) may occur.

Differential diagnoses:
Exclude septic arthritis in any acute monoarthropathy. Then consider haemarthrosis, CPPD (calcium pyrophosphate deposition) and palindromic RA.

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

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

Investigations:
Polarized light microscopy of synovial fluid shows negatively birefringent urate crystals. Serum urate is usually raised but may be normal. 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.

Treatment of acute gout:
Use high-dose NSAID or coxib (eg etoricoxib 120mg/24h
PO). Symptoms should subside in 3–5d.
NB: in renal impairment, NSAIDS and colchicine are
problematic. Steroids (oral, IM or intra-articular) may also be used. Rest and elevate the affected joint. Ice packs and ‘bed cages’ can be effective.

Prevention:
Lose weight. Avoid prolonged fasts, alcohol excess, purine-rich meats and low-dose aspirin.

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