Athritis, Kelainan Regional Jaringan Ikat Sendi, Infeksi Sendi dan Kelainan Metabolik Tulang dan Sendi

Prof. dr. Hermansyah, SpPD-KRUntuk mahasiswa kedokteran 2009

I. ArthritisA. Karena inflamasi sendi, akibat inflamasi outoimun, proses degeneratif, maupun kelainan metabolik (asam urat) - Rhematoid Arthritis autoimun

- Osteroarthritis proses degeneratif - Gout Arthritis asam urat B. Infeksi - Septik Arthritis

Arthritis symptomsl l l l l l

pain swelling stiffness deformity instability loss of function

II. Kelainan Regional Jaringan Ikat Sendi (Penyakit Reumatik Ekstra Artikular)Biceps Tendinitis Tenis Elbow/ Golf Elbow Tendinitis pergelangan tangan Trigger Finger Tendinitis Achilles Plantar fascitis

III. Kelainan Metabolik Tulang degeneratif (Osteoporosis)

Rhematoid Arthritis Synovial joints: Normal Anatomy 1. Bone: 2. Cartilage: 3. Synovium

1. Cartilage 2. Bone 3. Synovium

Synovial joints: Normal physiology 1. Relatively friction free movement of cartilage on cartilage 2. Lubricated by synovial fluid 3. Maintained by synovial membrane

Rhematoid Arthritis Etiology: autoimmune (complex) Prevalence: 1 to 2% of population Onset: age 30 to 50 3:1 female to male ratio

RA: pathophysiology1. Synovitis secondary to deposition of immune complexes

RA: pathophysiology2. Proliferation of invasive granulation tissue: pannus formation

RA: pathophysiology3. Enzymatic destruction of cartilage and bone spreading to capsule and ligaments with loss of range of motion

Rhematoid Arthritis

Rheumatoid arthritis: diagnosis (four or more for diagnosis of RA) Morning stiffness (>1 HR) 3 or more joint areas affected Hand joint arthritis Symmetric arthritis Rheumatoid nodules Serum rheumatoid factor (auto Ab 85%) Radiographic changes

RA: managment Goals: decrease inflammation and swelling decrease pain and stiffness increase or maintain normal function Education / rest / exercise and physical therapy

RA: management NSAIDs: ASA, etc. Steroids: prednisone Immunosuppressive therapy: methotrexate, cyclophosphamide TNF alpha inhibitors: etanercept and infliximab

Osteoarthritis Osteoarthritis is an idiopathic disease Characterized by degeneration of articular cartilage Leads to fibrillation, fissures, gross ulceration and finally disappearance of the full thickness of articular cartilage

Normal Cartilage Avascular, alymphatic and aneural tissue Smooth and resilient Allows shearing and compressive forces to be dissipated uniformly across the joint

Factors responsible Ageing Genetics Hormones Mechanics

Pathologic lesions Primary lesion appears to occur in cartilage Leads to inflammation in synovium Changes in subchondral bone, ligaments, capsule, synovial membrane and periarticular muscles

Gout Arthritis Gout can also occur as a result of overproduction of uric acid Gout is an attack of uric acid deposits in joints Usually found in joints of feet and legs

What is Gout Arthritis Purines are not properly processed in our body Excreted through kidneys and urine Hyperuricemia- buildup of uric acid in body and joint fluid

The Four Stages of Gout Asymptomatic Acute Intercritical Chronic

ASYMPTOMATIC A- meaning without indicates that there are no symptoms associated Patient will be unaware of what is happening Gout can only be determined with the help of a physician

ACUTE Sever and sudden onset Involve one or a few joints Frequently starts nocturnally Joint is warm, red, and tender

INTERCRITICAL More concentration of uric acid crystals Typically no need for drug intervention at the time.

CHRONIC Continuous or persistent over a long period of time Treatment required Not easily or quickly resolved

SYMPTOMS Joint pain Affects one or more joints : hip, knee, ankle, foot, shoulder, elbow,wrist, hand, or other joints Great toe, ankle and knee are most common

Swelling of Joint Stiffness Warm and red Possible fever

Skin lump which may drain chalky material

Diagnosing Gout X-rays Arthrocentesisextraction of joint fluid Examination of joint Patient medical history

TREATMENT Colchicine- reduces pain, swelling, and inflammation; pain subsides within 12 hrs and relief occurs after 48 hrs Allopurinol- decreases the production of uric acid Probenecid and sulfinpurazone- prevent absorption of uric acid in the tubules of kidney Reduce alcohol intake Increase water intake Watch diet for food rich in purines