Osteoarthritis.pptx

Osteoarthritis for D.Pharm students, etiology of osteoarthritis, pathophysiology of osteoarthritis, management of osteoarthritis.

1. MUSCULOSKELETAL DISORDERS OSTEOARTHRITIS A PRESENTATION BY AMAN KUMAR LECTURER GCRG COLLEGE OF PHARMACY

2. DEFINITION Osteoarthritis= Osteo + Arthron + Itis. Osteo= bone. Arthron= Joint. Itis= Inflammation. "Osteoarthritis is a degenerative disease of joints characterized by loss of cartilage with proliferation of new bone and remodelling (reshaping) of joint . ” OR "It is a chronic joint disorder characterized by degeneration of joint cartilage and adjacent bone followed by bony overgrowth leading to joint pain and stiffness (hardness)." Osteoarthritis is also known as degenerative joint disease (DJD) or degenerative arthritis. It occurs when the protective cartilage on the ends of the bones wears (lost) down over the time. Cartilage is the slippery tissue that cover the ends of the bones in a joint. Healthy cartilage absorbs the shock of movement. When cartilage is lost, the bones rub together and over time this can permanently damage the joint. Since in this disease, the cartilage wears and tears (broken and deformed), this disease is also known as wear and tear arthritis.

3. ETIOLOGY OF OA Factors that can increase the risk of osteoarthritis include: Older Age: The risk of osteoarthritis increases with age. Gender: Women are more likely to develop osteoarthritis. Obesity: Carrying extra body weight contributes to osteoarthritis in several ways, and the more you weigh, the greater your risk. Increased weight adds stress to weight- bearing joints, such as your hips and knees. Joint Injuries: Injuries, such as those that occur when playing sports or from an accident, can increase the risk of osteoarthritis. Even injuries that occurred many years ago and seemingly healed can increase your risk of osteoarthritis. Repeated Stress on the Joint: If your job or a sport you play places repetitive stress on a joint, that joint might eventually develop osteoarthritis. Genetics: Some people inherit osteoarthritis due to their family history. Bone Deformities: Some people are born with malformed joints or defective cartilage. This may lead to OA.

4. PATHOPHYSIOLOGY OF OA Release of Inflammatory chemicals like Interleukins. Interleukins activates chondrocytes and synovial cells. Chondrocytes and Synovial cells synthesizes enzyme Matrix metallo proteinases (MMPs). These MMPs are primary enzymes which degrades cartilage around bones. Degradation of cartilage results in OA.

5. CLINICAL MANIFESTATIONS OF OA Joint pain. Swelling. Morning stiffness. Locking. Loss of flexibility. Reduced motion. Slowness in motion.

6. DIAGNOSIS OF OA X-ray. Blood test. Joint fluid analysis. Physical examination.

7. TREATMENT OF OA Non-pharmacological treatment: Use of moist heat at joint. Weight reduction. Mild exercise. Pharmacological treatment: NSAIDs: To reduce inflammation and pain. Example- Ibuprofen, Aspirin, Diclofenac sodium. Corticosteroids: To reduce pain. Example- Prednisone. Chondroprotective drugs: These drugs inhibits the MMPs enzymes which are responsible for cartilage destruction. Examples- Rumalon , Pentosan . Surgery: This method is used when all other methods of treatment are failed. In this method, the patient undergoes joint replacement surgery.

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