Week 6 Nurse 530B

Week 6 Nurse 530B

Week 6 Nurse 530B

Arthritis refers to inflammation of one or more joints. Nonetheless, arthritis is classified as either inflammatory or non-inflammatory. Non-inflammatory, localized arthritis like osteoarthritis (OA) is not systemic, while systemic autoimmune joint diseases like rheumatoid arthritis (RA) are inflammatory. The purpose of this paper is to discuss osteoarthritis and rheumatoid arthritis, including their pathophysiology, clinical manifestations, evaluation, and treatment.


OA is a degenerative joint disease characterized by continuous deterioration and cartilage loss in one or more joints. As a person experiences joint trauma or ages, proteoglycans (a component of hyaline cartilage) decrease. The production of synovial fluid, which offers joint lubrication and nutrition, also decreases due to the reduced synthesis of hyaluronic acid and decreased body fluid in older adults (Yunus et al. 2020). The cartilage changes from its normal blue-white, translucent color to an opaque and yellow-brown appearance in early OA. As the cartilage and the bone underneath the cartilage start to erode, the joint space narrows, and osteophytes form. As OA advances, fissures, calcifications, ulcerations occur, and the cartilage thins. Inflammatory cytokines such as interleukin-1 increase this deterioration. As a result, the body’s normal repair process cannot overcome the fast process of degeneration (Yunus et al. 2020). In due course, the cartilage disintegrates, and pieces of bone and cartilage lie in the affected joint, causing crepitus, a grating sound attributed to the loosened bone and cartilage.


Clinical Manifestations

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OA presents with chronic joint pain and stiffness. In the early course of the disease, the joint pain diminishes after rest and exacerbates with activity. Later the joint pain occurs with slight motion and even during rest. The affected joint is often enlarged during examination due to bony hypertrophy and feels hard on palpation (Yunus et al. 2020). There is pain or tenderness on palpation or putting the joint through a range of motion (ROM). Crepitus is heard as the joint goes through ROM, and one or more joints are affected (Mora et al., 2018. Patients report joint stiffness lasting less than 30 minutes after a period of rest. Patients with hand involvement have Heberden’s nodes at the distal interphalangeal joints and Bouchard’s nodes at the proximal interphalangeal joints.


Evaluation of OA involves history taking, physical examination (inspection, palpation, and ROM exercises), and imaging assessment. Imaging assessments include x-rays to evaluate structural joint changes (Yunus et al. 2020). Magnetic resonance imaging (MRI) evaluates vertebral or knee involvement.


Treatment for OA aims to manage pain, prevent disability, and maintain and improve joint function. Drug therapy includes Acetaminophen, the drug of choice since OA is non-inflammatory (Yunus et al. 2020). Topical agents such as lidocaine 5% patches are used for temporary pain relief. NSAIDs are used if Acetaminophen is not effective. Non-pharmacologic treatment approaches include rest and joint protection by balancing rest and activity and using assistive devices. Besides, heat and cold applications temporarily alleviate pain and stiffness (Yunus et al. 2020). Nutritional therapy and exercises are recommended for weight loss to reduce the load on the joints and eventually increase joint mobilization.

Rheumatoid Arthritis

RA is a chronic, gradual, systemic inflammatory autoimmune disease that primarily affects the synovial joints. It is characterized by inflammation of connective tissue in the synovial joint. Since it is a systemic disease, it affects the body system, affecting several joints and other tissues. In RA, rheumatoid factors (RFs) are formed and attack healthy tissues, especially synovium, resulting in inflammation (Scherer et al., 2020). The disease then involves the articular cartilage, joint capsule, and surrounding ligaments and tendons. Various processes cause cartilage damage in RA.

CD4 T-helper cells and other immune cells in the synovial fluid promote the release of cytokine, mostly interleukin-1) and tumor necrosis factor, which attack the cartilage. Neutrophils and other inflammatory cells in the joint are triggered and break down the cartilage (Scherer et al., 2020). Immune complexes build up in the synovium, and osteoclasts get activated. In addition, B- and T-lymphocytes are triggered and increase the inflammatory response. Afterward, the synovium thickens and becomes hyperemic, fluid amasses in the joint space, and a pannus forms. The pannus is a vascular granulation tissue made of inflammatory cells. It wears down the articular cartilage, eventually destroying the bone (Scherer et al., 2020). Consequently, in late RA, bony ankylosis, fibrous adhesions, and calcifications occur, resulting in bone losing density and secondary osteoporosis.

Clinical Manifestations

Early clinical manifestations include joint inflammation, low-grade fever, fatigue, body weakness, anorexia, and paresthesias. Late manifestations include joint deformities, morning stiffness, and moderate to severe pain (Guo et al., 2018). Late systemic signs and symptoms include anemia, weight loss, severe fatigue, subcutaneous nodules, pericarditis, vasculitis, peripheral neuropathy, fibrotic lung disease, renal disease, and osteoporosis.


Diagnosis of RA includes history taking, physical examination, laboratory assessment, and imaging. Lab tests support the diagnosis of RA, but no individual or group of tests can confirm it. A positive Rheumatoid factor test or increase in RF indicates a possible RA. Other lab tests include Erythrocyte sedimentation rate (ESR), C – reactive protein, Serum complement, and white blood cell count (Guo et al., 2018). Imaging tests include plain x-ray, which visualizes the joint changes and deformities present in RA. A CT scan is used to evaluate the presence and extent of cervical spine involvement.


Drug therapy for RA includes NSAIDs, corticosteroid therapy, and Disease-modifying antirheumatic drugs (DMARDs). DMARDs have an anti-inflammatory action. Mild RA is treated with Plaquenil; Methotrexate is used for moderate to severe RA; and Gold Therapy for severe RA (Guo et al., 2018). Non-pharmacologic treatment approaches for pain management include proper positioning, adequate rest, and ice and heat applications.


OA is a non-inflammatory disease with local symptoms, while RA is an inflammatory disease with local and systemic symptoms. OA is a degenerative disease caused by aging and trauma, while RA is an autoimmune disease. In OA, symptoms are unilateral affecting, a single joint, while in RA, symptoms are bilateral, symmetric, and multiple joints are affected. OA’s drug therapy includes Acetaminophen and NSAIDs, while RA therapy includes NSAIDs and DMARDs. Non-pharmacological interventions are used in both diseases.


Guo, Q., Wang, Y., Xu, D., Nossent, J., Pavlos, N. J., & Xu, J. (2018). Rheumatoid arthritis: pathological mechanisms and modern pharmacologic therapies. Bone Research6, 15. https://doi.org/10.1038/s41413-018-0016-9

Mora, J. C., Przkora, R., & Cruz-Almeida, Y. (2018). Knee osteoarthritis: pathophysiology and current treatment modalities. Journal of pain research11, 2189–2196. https://doi.org/10.2147/JPR.S154002

Scherer, H. U., Häupl, T., & Burmester, G. R. (2020). The etiology of rheumatoid arthritis. Journal of autoimmunity110, 102400. https://doi.org/10.1016/j.jaut.2019.102400

Yunus, M., Nordin, A., & Kamal, H. (2020). Pathophysiological Perspective of Osteoarthritis. Medicine (Kaunas, Lithuania)56(11), 614. https://doi.org/10.3390/medicina56110614


Describe osteoarthritis (OA) and rheumatoid arthritis (RA), and discuss the pathophysiology, clinical manifestations, evaluation, and treatment for each.

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