Osteoarthritis
OA primarily starts as a cartilage problem, later involving other structures. Once these are affected, the patient
starts to develop the pain characteristic of this condition.
Osteoarthritis
Cartilage Degradation: loss of matrix integrity
There is a role: cytokines, enzymes and nitric oxide
Risk factor :
Age (strongest)
Obesity
Injury muscle weakness
Knees and pelvis are the most common sites
Heberden and Bouchard Nodes
Mechanical pain, no systemic symptoms
Clinical Findings
The oncet is insidious
Articular stiffness < 15 minutes
Pain in motion
- Worse by activity / weight bearing
- relieved by rest
Deformity maybe absent or minimal
Bony enlargement of the interphallangeal occasionaly prominent
Limitation of motion of affected joint is common
Joint effusion and other articular signs of inflammation are mild
No systemic manifestation
Laboratory Findings :
Elevated sedimentation rate and other laboratory signs of inflammation are not present.
Imaging :
Radiographs may reveal :
Narrowing of the joint space
Sharpened articular margin
Osteophyte formation
Lipping of marginal bone
Thickened, dense subchondral bones
Bone cysts may also be present
Flow chart for Therapy of OA
Diagnosis
Physical measures
Patient Education
Medication
High Dose
Scheduled Opioids
NSAID
Surgery
Gout
Gout
Very painful episodes of arthritis
Intermittent, usually monoarticular in the toes, ankles
and knees
May develop into oligo or polyarthicular
Associated with the concentration of uric acid in the
plasma
Risk Factor
•Alcohol
•Dyslipidemia
•Hypertension
•Urolitiasis
• Drugs such as pyrazinamide, low-dose ASA
•Kidney illness
•Myeloproliferative Disorders
• Gout history in family
Gout
RHEUMATOID ARTHRITIS
(Auto immune Desease)
RHEUMATOID ARTHRITIS
(Auto immune Desease)