ARTHRITIS

Jennilyn Bancifra and Bernadette M. Cid CFM JI April-May 2012

OSTEOARTHRITIS
caused by the breakdown and eventual loss of the cartilage of one or more joints a.k.a DEGENERATIVE JOINT DISEASE; occurs more frequently as a person ages

osteoarthritis

OSTEOARTHRITIS
Commonly affects hands, feet, spine and large weight bearing joints such as hips and knees Primary vs. Secondary

Causes of Primary OA
Age
Degeneration of the protein content of the cartilage

Repetitive use of joints

Incites irritation and inflammation of the cartilage

Inflammation of cartilage
Stimulates new bone growths (spurs)

Hereditary
Can be found in multiple members of the family

Causes of Secondary OA
Obesity Trauma or surgery to joint structures Congenital abnormalities Diabetes and other hormone disorders

Symptoms
Pain on affected joint/s after repetitive use
Usually more severe later in the day In complete loss of cartilage, pain may be present even at rest or with limited motion

Swelling, warmth and creaking of joints Stiffness of joints after prolonged inactivity Intermittent No systemic symptoms

Symptoms
OA of the knee Bow Legged Deformity Limping Irritation of spinal nerves from bony spurs of an arthritic spine numbness, tingling, pain

Symptoms
HEBERDENS NODE
Bony enlargements at the distal interphalengeal joint From bone spurs May not be painful but may limit motion

Symptoms
Bouchards Node
Bony enlargements at the proximal interphalangeal joint Also may not be painful but may limit motion

Diagnosis
Osteoarthritis Gout Rheumatoid Arthritis1

Key presenting symptoms

Pauciarticular. Pain with movement, improving with rest. Site of old injury (sport, trauma). Obesity. Occupation.

Monoarticular. Abrupt onset. Pain at rest and movement. Precipitating event (meal, physical stress). Family history.

Polyarticular. Gradual, symmetric involvement. Morning stiffness. Hands and feet initially involved more than large joints. Fatigue, poorly restorative sleep.

Diagnosis
Osteoarthritis Key physical findings Infrequent warmth, effusion. Crepitus. Enlargement/spur formation. Malalignment. Gout Podagra. Swelling, warmth. Exquisite pain with movement. Single joint (exceptionsplantar fascia, lumbar spine). Tophi. Synovial fluid with uric acid crystals. Elevated serum uric acid. 24 h urine uric acid. Rheumatoid Arthritis Symmetric swelling, tenderness. MCP, MTP, wrist, ankle usually before larger, proximal joints. Rheumatoid nodules. Elevated ESR/CRP. Rheumatoid factor. Anemia of chronic disease. Early erosions on x-ray, osteopenia at involved joints.

Key laboratory, x-ray Few characteristic findings (early). Loss of joint space, spur formation, malalignment (late).

Treatment
Goals of Treatment
Relief of Pain Restoration of Function Reduction of Disease Progression

Treatment
Pain Medications (NSAIDs, Capsaicin, Glucosamine+ Chondroitin) Physical Therapy Assistive devices Intraarticular injections Surgery

Adebajo, Ade (2012), BMC Family Practice

NON-STEROIDAL ANTI-INFLAMMATORY DRUGS FOR THE TREATMENT OF PAIN AND IMMOBILITY-ASSOCIATED OSTEOARTHRITIS: CONSENSUS GUIDANCE FOR PRIMARY CARE

ABSTRACT
Osteoarthritis is a common presentation in primary care, and non-selective non-steroidal anti-inflammatory drugs (sometimes also referred to as traditional NSAIDs or tNSAIDs) and selective cyclo-oxygenase 2 inhibitors (COX-2 inhibitors) are commonly used to treat it.

ABSTRACT
The UK's National Institute for Health and Clinical Excellence (NICE) recommends taking patient risk factors into account when selecting a tNSAID or a COX-2 inhibitor, but GPs have lacked practical guidance on assessing patient risk.

METHODS
Developing an evidence-based consensus statement with an accompanying flowchart that aimed at providing concise and specific guidance on NSAID use in osteoarthritis treatment

RESULTS
1. tNSAIDs are effective drugs in relieving pain and immobility associated with osteoarthritis. COX-2 inhibitors are equally effective 2. tNSAIDs and COX-2 inhibitors vary in their potential gastrointestinal, liver, and cardio-renal toxicity. This risk varies between individual treatments within both groups and is increased with dose and duration of treatment

RESULTS
3. COX-2 inhibitors are associated with a significantly lower gastrointestinal toxicity compared to tNSAIDs. Co-prescribing of aspirin reduces this advantage. 4. PPIs should always be considered with a tNSAID and with a COX-2 inhibitor in higher GI risk patients. An accompanying flowchart to guide management was also agreed.

CONCLUSION
Ascertaining individual patient risk is important when choosing treatment for patients with osteoarthritis.