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Understanding the pathophysiology of rheumatoid arthritis

Understanding the pathophysiology of rheumatoid arthritis

Rheumatoid Arthritis is a long-term autoimmune disease that causes chronic inflammation of the joints, as well as the tissue surrounding the joints and other organs. Huether and McCance (2008) RA is the most common autoimmune inflammatory disease in adults; it can affect children and adolescents, but it is less common. This condition affects 0.5-2% of the adult population. This potentially debilitating disease affects approximately 1.5 million men and women. Rheumatoid arthritis is more common in women, affecting nearly three times as many women as men. In most cases, the onset occurs between the ages of 30 and 60 for women and later in life for men. Although extensive research has been conducted on the causes of rheumatoid arthritis, the etiology remains unknown. Although RA is not hereditary, hormones, genetics, and environmental factors all play a role in the likelihood of developing this autoimmune disease. It is most likely a combination of genetic and inflammatory mediators. Huether and McCance (2008) Many RA patients have the genetic marker (HLA DR4 32). This marker increases the likelihood that the body’s immune system will attack healthy joints and tissues. Some cases occur when the immune system incorrectly attacks the joint tissues. Allergies, bacteria, viruses, and genetic factors have all been proposed as factors contributing to or initiating destructive inflammation. 2017 (Martini & Bartholomew)

System(s) of the Body Involved

Rheumatoid arthritis develops when antibodies attack the connective tissues surrounding the joints (Martini & Bartholomew, 2017). Fingers, feet, wrists, elbows, ankles, and knees are the most commonly affected joints, but the shoulders, hips, and cervical spine may also be affected, as well as tissues of the lungs, heart, kidneys, eyes, throat, and skin (Huether & McCance, 2008). This is why RA is referred to as a systemic disease. RA can cause interstitial lung disease in lung tissues, which is caused by increased scarring of the lung tissue and can impair one’s ability to breathe. RA can cause pericardial effusion, which is inflammation of the heart’s outer lining, in the heart. This can result in other heart problems, such as myocarditis, which is inflammation of the heart muscle. Finally, the patient is at high risk for congestive heart failure with both of these conditions (CHF). Rheumatoid nodules, which are firm subcutaneous nodules commonly found on pressure points or extensor surfaces of the body’s bony prominences, such as the fingers, are common in RA patients. The most common visual deformity seen in RA patients is rheumatoid nodules. Most patients are considered terminal once their RA has progressed to the point where it has affected major organs.

Affected major body systems’ normal anatomy

One of the most common joints in the human body is the synovial joint. Synovial joints are any freely movable joints; diarthrosis is another term for these types of joints. The following structures are found in a typical synovial joint: articular cartilage, joint capsule, synovial membrane, synovial fluid, bursae, and supporting ligaments (Herlihy, B., 2011). They permit movement and a wide range of motion. Synovial joints are most commonly found at the ends of long bones, such as the arms and legs. Under normal circumstances, the bony surfaces do not come into contact because they are covered with articular cartilage, which forms a smooth surface within the joint. A joint capsule, also known as an articular capsule, encloses the joint in a sleeve-like covering. Synovial fluid is secreted into the joint cavity by the synovial membrane, which lines the joint capsule. Synovial fluid in the joint cavity lubricates the joint’s moving surfaces. As a result, the friction within the joint is reduced. Bursae are small sacs of synovial fluid that exist between the joint and the tendons that cross over the joint in many synovial joints. 2017 (Martini & Bartholomew) B. Herlihy (2011).

Normal physiology of affected body systems

The primary function of synovial fluid is to cushion and lubricate joints. (E. Konstantakos, MD, 2016) Synovial fluid in the joint cavity lubricates and reduces friction on moving surfaces in the joint. 2017 (Martini & Bartholomew) The synovial membrane of a joint produces albumin and hyaluronic acid, which give synovial fluid its viscosity and slickness. Furthermore, synovial fluid delivers nutrients to and removes waste from the cartilage. When a joint is at rest, some of the synovial fluid is absorbed by cartilage. When the joint is used, synovial fluid is squeezed out of the cartilage in the same way that water is squeezed from a sponge. As a result, joint use is required to circulate synovial fluid throughout the joint. (E. Konstantakos, MD, 2016) There are six types of freely moveable joints, each named after its movement and function. Elbows, knees, and fingers are examples of hinge joints that allow movement in only one direction. A ball and socket joint is formed when one bone’s ball-shaped end articulates with another bone’s cup-shaped socket. These are found in the shoulder and hip and allow for a wide range of movement. Pivot joints allow for rotation; an example is shaking your head “no.” Another example is the distal radioulnar joint, which allows palms to move forward and backwards. When the surfaces of both articulating bones are saddle-shaped, saddle joints form. The carpometacarpal joint at the base of the thumb, for example, has a wide range of motion. The interaction of flat surfaces creates a gliding joint. This joint enables limited but complex gliding movement. The wrist, ankle, and vertebral column joints are examples of these joints. Finally, a condyloid joint is formed when one bone’s oval-shaped articular surface fits into the oval-shaped depression of the second articulating bone. Condyle joints include the radiocarpal (wrist) and metacarpophalangeal (knuckles). B. Herlihy (2011)

Pathophysiology Mechanisms

Cartilage damage in RA is caused by at least three different processes. 1) Neutrophils and other cells in the synovial fluid become activated, degrading the articular cartilage’s surface layer. Causes the predominant feature of inflammation in the synovium. 2) Cytokines stimulate the synthesis of proinflammatory compounds, including interleukin-, -6, and -8. Chondrocytes attack cartilage as a result of this. 3) As the synovium digests nearby cartilage, inflammatory modules are released. There is an increase in both types of synoviocytes, as well as immune and inflammatory cells such as macrophages, B- and T-lymphocytes, plasma cells, and dendritic cells. There is an increase in cytokine levels. Cytokines are essential in the maintenance of synovial inflammation. Swelling is caused by leukocyte infiltration, which causes the synovial membrane in RA to thicken hyper plastically as its cells proliferate and enlarge. J. Morovi-Vergles Huether and McCance (2008)


Because the cause of RA is unknown and there appear to be multiple triggers, there is no single intervention or vaccine to prevent the disease. There are, however, ways to reduce the risks, potentially delaying the onset and/or slowing the progression of RA. While some risk factors are unchangeable, there are ways to avoid or reduce the risk of severe joint damage. Age, family history, and gender are risk factors that cannot be changed. However, there are steps that can be taken to reduce the risk of RA, such as eating a healthy diet, limiting sugary drinks or food, avoiding joint injuries, reducing stress, and boosting immune system function. Other interventions include quitting smoking if one is a smoker, losing weight if one is overweight, and boosting one’s immune system. One could also exercise moderately to maintain mobility and strength. Early detection of RA is thought to be critical and is the best way to reduce the risk of severe joint damage. Knowing the signs and symptoms is critical for getting help early in the disease process. Stiffness, swelling, pain, redness, fatigue, malaise, loss of appetite, muscle aches, rheumatoid nodules, shortness of breath, inflammation around the heart, dry, red eyes, and a sore throat are all symptoms.


Although there are few ways to truly prevent RA, there are numerous options for treating this disease. Depending on the severity of the disease, RA can be treated surgically or non-surgically. Rest of the inflamed joint and whole-body rest for several hours daily; use of hot and cold packs; physical therapy; patient education; aggressive, early interventions using disease-modifying antirheumatic drugs (DMARDs) and biologic response modifiers (BRMs); a diet high in calories and vitamins; corticosteroids; and anti-inflammatory drugs are taken orally or injected into the joint are all nonsurgical treatments. Synovitis can be treated with intra-articular injections of a radionuclide. Early in the disease process, surgical synovectomy may be performed to reduce inflammatory effusion and remove the pannus. Surgery, such as arthrodesis, arthroplasty, or total joint replacement, is used to correct deformities caused by rheumatoid nodules or mechanical deficiency in the intermediate or late stages. There is evidence that complete fasting reduces joint pain, swelling, morning stiffness, and other symptoms in people with RA. Huether and McCance (2008) Drugs like DMARDs work to suppress the body’s overactive immune system response while also preventing joint damage and slowing disease progression. The most commonly used DMARD is methotrexate, which is prescribed shortly after a diagnosis to prevent as much joint damage as possible. 2017 (Iliades) Biologic response modifiers (BRMs) are substances that help to stimulate the body’s response to infection and disease. Acetaminophen and Ibuprofen are examples of nonsteroidal anti-inflammatory drugs (NSAIDs).

Clinical Importance

As new therapies emerge, one study demonstrates the efficacy of treatment for RA patients. Treatment efficacy on radiography for joint damage. Finckh et al. conducted a meta-analysis of 12 studies to demonstrate the long-term impact of early treatment on bone radiographic progression in RA. The pooled estimate of effects revealed a 33% reduction in radiographic progression in patients treated with DMARDs before 2 years of disease duration compared to those treated later. The advantages last for up to 5 years. Prednisolone added to DMARD therapy at the start of the initial treatment slows the progression of radiographic damage. This was demonstrated in a study by Svensson et al. in patients with active RA for at least a year. Patients who received prednisolone 7.5 mg daily for two years had fewer newly eroded joints than those who did not. (Radiation progression was 25.9% and 39.3%, respectively). In two years, the corresponding remission rates were 55.5% and 32.8%. Korpela et al. compared the effect of a combination of three DMARDs on radiographic erosions in early RA to a single DMARD. The median Larsen sore in combination therapy was significantly lower after 5 years than in single therapy (11 vs. 24). In a similar study, Harfstrom et al. found that the remission rate after two years was significantly higher in the prednisolone group compared to the non-prednisolone group (55% vs. 30%) and that the prednisolone group had a higher probability of being in remission during the longitudinal analysis. The changes in bone density did not differ between the two groups after 4 years. In a systematic review, glucocorticoids given in addition to standard therapy significantly reduced the rate of progressive erosions in rheumatoid arthritis. B. Heidari (2011)


Heidari, B. (2011). Rheumatoid Arthritis: Early diagnosis and treatment outcomes. Retrieved November 29, 2017, from

Herlihy, B. (2011). The human body in health and illness. Maryland Heights, MO: Elsevier.

Huether, S.E., & McCance, K.L. (2008). Understanding pathophysiology. (4th ed.) St. Louis MO: Mosby/Elsevier.

Iliades, C. (2017, September 25). 10 Ways to Fight Chronic RA Pain. Retrieved November 2, 2017, from management/chronic-pain/ Konstantakos, E., MD. (2016, May 13). What Is a Synovial Joint? Retrieved November 15, 2017, from anatomy/what-synovial-joint

Martini, F., & Bartholomew, E. F. (2017). Essentials of anatomy & physiology. (7th ed.) Hoboken, NJ: Pearson Education, Inc.

Morović-Vergles, J. (n.d.). [Pathophysiology of rheumatoid arthritis]. Retrieved November 15, 2017, from


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1. Explain the pathophysiology of autoimmune disease in relation to the destruction of the synovial joints, capsule, and membrane to Rheumatoid arthritis.

Understanding the pathophysiology of rheumatoid arthritis

Understanding the pathophysiology of rheumatoid arthritis

2. Compare and contrast signs and symptoms of OA ( osteoarthritis) to RA (Rheumatoid arthritis).

3. Describe the difference between Heberden’s nodes vs Bouchard’s nodes.

4. What is Gouty arthritis and how does it differ from OA ( osteoarthritis)?



Include TWO references from professional peer-reviewed scholarly journals in APA format. MUST USE databases such as CINAHL, Academic Search Complete, or Social Sciences

All writing and references must follow the current American Psychological Association (VERY IMPORTANT YOU MUST USE APA – PEER REVIEW ARTICLES 5 YEARS OR NEWER)


Minimum of 2 PAGES.




Whitney, D. G., & Peterson, M. D. (2019). US national and state-level prevalence of mental health disorders and disparities of mental health care use in children. JAMA Pediatrics, 173(4), 389-391.

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