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Arthritis is a joint disorder that involves inflammation of one or more joints. There are currently over 100 different types of arthritis (Felson, 2005). Osteoarthritis, also known as degenerative joint disease, is the most common form of arthritis and is caused by age, trauma to a joint, or infection in the joint. Other common forms of arthritis include rheumatoid arthritis and psoriatic arthritis, which are autoimmune diseases. Arthritis can lead to constant pain and life style changes. This detrimental disease is chronic in nature and no cure has yet to be found. This paper will discuss arthritis and the physical examination used to diagnosis arthritis, chief complaints associated with arthritis, types of arthritis, effects on the immune system, and treatments.
According to Felson (2005) approximately 33% of those within the United States are affected by musculoskeletal signs or symptoms of arthritis. This includes swelling, pain, or limitation of movement. According to Ling & Rudolph (2006) arthritis affects over 20 million people in the United States. It is often diagnosed in the elderly but can affect all age groups. The disease is debilitating and can result in job loss, disability, and impairments. Due to the high prevalence rates across the United States many patients seek treatment from their primary care physician, rheumatologist, or require hospitalization due to the severity of the disease. Felson $124.8 billion US dollars were spent in 1996 to treat musculoskeletal diseases (Felson, 2005). This number will continue to increase as individuals with this disease continue to live longer.
Types of arthritis
Osteoarthritis is the most common form of arthritis. It is more common in the elderly. It often affects joints that typically include the hips, knees, feet, hands, and back. Osteoarthritis can be a direct result from an injury, or wear and tear of the body. The erosion of cartilage causes the two bones to rub together causing bone spurs, resulting in inflammation in the joint. Ling & Rudolph (2006) state that matrix metalloproteinase (MMPs) and proinflammatory cytokines are released by synovial cells to these destructive forces, but are unsuccessful in treating the area affected. This can lead to severe pain, which can limit one's capabilities.
Rheumatoid arthritis is an autoimmune disorder, where the immune system attacks healthy body tissue. This eventually affects other parts of the body, including vital organs. Damage within the joint lining and cartilage leads to erosion of two connecting bones, which causes inflammation. It is most common in hands, elbows, knees, and wrists. The disease is symmetrical, affecting both sides of the body. If it is not treated it can result in deformities in the affected joint. The etiology is unknown and consists of periods of remission and exacerbation (Turkiewicz & Moreland, 2006). It has been demonstrated that there is a genetic marker linked (HLA- DR4), which increases the likelihood of developing rheumatoid arthritis. Individuals that smoke and also have the genetic marker are at a higher risk for developing rheumatoid arthritis. There is both an inflammatory and autoimmune deficiency in rheumatoid arthritis. This chronic disorder causes joint pain, swelling, stiffness, which typically occurs in the morning, and fatigue (Turkiewicz & Moreland, 2006).
Medical professionals are required to perform a medical examination in order to diagnosis and treat arthritis as there is no cure. To diagnosis arthritis, doctors perform a physical evaluation based on the patient's symptoms and order blood tests. Physicians look for signs of swelling, redness, fluid around the joints, soreness, tenderness, pain, and limited range of motion in the affected area. They also ask about fatigue, at what time the pain is most prevalent, how long it lasts, and how severe the pain is. Beardmore, Wener, & Schur (2006) explain blood analysis would look for a rheumatoid factor, antinuclear antibodies, complete blood count, erythrocyte sedimentation rate, c-reactive protein, and creatinine levels. These levels need to be reviewed by a doctor to determine whether they are within normal limits.
Pain, swelling, weakness, fatigue, stiffness, limitation of movement, and emotional instability are symptoms associated with arthritis (Ziminski & Nichols, 2006). "Analysis of these symptoms helps the examiner to consider the rheumatic complaint as articular vs. non-articular, inflammatory vs. non-inflammatory or mechanical, symmetric vs. asymmetric, peripheral vs. central, articular (in the joints) only vs. articular plus extra-articular (outside the joints), systematic rheumatic disease vs. non-rheumatic disease causing musculoskeletal symptoms, or another process" (Ziminski & Nichols, 2006, p 26). These symptoms need to be examined in more depth by the medical profession.
The primary complaint from those with arthritis is joint pain. The pain is often localized and persistent in the joint area affected. Pain is a result of inflammation that occurs around the joint, muscle strains, damage to the joint from the disease, and wear and tear of the joint. The course and level of pain is critical in determining the type of arthritis. Patients with arthritis also suffer from stiffness. Stiffness is a result of restrictive movement or non-movement. According to Ziminski & Nichols (2006) stiffness levels can vary for those with inflammatory (rheumatoid) vs. non-inflammatory arthritis (osteoarthritis). Those with inflammatory arthritis feel stiffer in the morning, which causes discomfort, but feel better throughout the day. This varies for those with non-inflammatory arthritis. As one awakes with this form of arthritis they feel much better, but as the day goes on their discomfort levels increase due to excessive use of their joints. Another characteristic associated with arthritis is swelling, which is the inflammation of the joint. Those with arthritis develop an abnormal amount of fluid in the joints, which causes swelling and damage. Soft tissues that line and surround the joints produce the excess fluid.
Limitation of movement can cause limited range of motion for those with arthritis. This can lead to impairments in daily functioning (i.e. an inability to walk, dress oneself, shower, toilet, open containers, or work). Such impairments eventually may require the patient to utilize a cane or walker for assistance when ambulating. Physical therapy and occupational therapy are often recommended to help assist those with absent or limited range of motion. Weakness is the loss of or decreased use of muscle strength. The patient may exhibit "clumsiness" behaviors, which could be evident in holding or opening an object or difficulty going up steps. Fatigue causes the patient to feel exhausted and tired. Fatigue can be caused by pain, inactivity, and sleep instability. Fatigue can lead to decreased activity levels, which can cause muscle atrophy and deterioration. Exercise and enhancing one's sleep can aid in treating fatigue. If this is not treated it can lead to depression. Anxiety and depression are common for those suffering from arthritis. Many worry about their current and future physical limitations. Stress management and exercise techniques, which promote physical activity, can benefit the patient. This can help in eliminating the fear associated with arthritis (Ziminski & Nichols, 2006).
The Immune System
The immune system is composed of a network of cells that function from basic to highly complex levels. The immune system is geared at protecting us from our environment and to detect any cell damage. It recognizes and reacts to bacteria, viruses, and fungi, and other pathogens that can affect our body. There are cells within our body that are geared at recognizing these pathogens and eliminating them before they can cause damage. According to Carpenter (2006) there are two different components of the immune system, which include innate and adaptive immunity.
Innate immunity is used to stop the spread and growth of a pathogen. All humans are born with this type of immunity. Natural killer cells and macrophages are found in the synovial membrane, and neutrophils are in the synovial fluid. Neutrophils and microphages are released as a foreign object first enters the body. They are recognized as being the first line of defense against infection. Carpenter (2006) states that they mediate the effects of phagocytosis and the release of granules, which help destroy the foreign pathogen. Natural killer cells recognize abnormal cells and kill cancer cells, infected cells, or damaged cells.
Adaptive immunity is comprised of antibody responses and cell-mediated responses in the synovial membrane. These responses are executed by B and T cells, which are types of lymphocytes. B cells help in creating antibodies, which bind to foreign antigens. These B cells are found in the blood plasma and lymph. They help assist in manufacturing antibodies against antigens. Adaptive immunity also involves natural killer cells, T-lymphocytes, macrophages, and cytokines, where each respond to an antigen. "Macrophage-derived and dendritic-cell-derived transforming growth factor Î² and interleukin-1Î², 6, 21, and 23 provide a milieu that supports Th17 differentiation and suppresses differentiation of regulatory T cells, thus shifting T-cell homeostasis toward inflammation" (McInnes & Schett, 2011, p 2213). Those with rheumatoid arthritis have T cells with inadequate abilities. "This imbalance between Th17 and regulatory T cells may also reflect local TNF-Î±, which blocks the activity of regulatory T cells" (McInnes & Schett, 2011, p 2213). T cells are used to help B cells secrete cytokines. The adaptive immune system's key characteristic is its memory. It can recall each pathogen by its distinct antibody. One's adaptive immunity is developed throughout one's life.
According to Abbas & Lichtman (2006) inflammation is the body's response to invasion or injury. Inflammation can either be chronic or acute. Acute inflammation is a direct response by the innate and adaptive immune system, which is geared at destroying pathogens. According to Carpenter (2006) acute inflammation is associated with cellular infiltrate, but will diminish when the pathogen is eliminated. Carpenter (2006) describes chronic inflammation as a steady infection or tissue damage, consisting of complex infiltrates. These complex infiltrates are made up of lymphocytes and macrophages as opposed to neutrophils, which are consistent with acute inflammation. These lymphocytes and macrophages enter the synovial membrane, which is a thin membrane that lines the joints.
Carpenter (2006) states that fluid and cells move to the extravascular spaces because of changes in the endothelial cells lining the vessel walls. As this occurs symptoms of inflammation become evident. They consist of redness, pain, and swelling in the affected area. "The inflammatory response is a complex process initiated by a variety of foreign insults (microbes, altered cells, and foreign particles) and involving a variety of cells and soluble inflammatory mediators" (Carpenter, 2006, p 17). Inflammatory cells respond to invasion or injury by sending out mediators due to endothelial activation. These mediators and inflammatory cells attempt to return the tissue to its normal state as quickly as possible by sending adhesion molecules. One mediator often used is cytokines. Mikuls (2005) explains that cytokines, which are small proteins produced by macrophages and lymphocytes, help in controlling inflammation. Other mediators such as prostaglandins and leukotrienes, developed from phospholipids, help eliminate inflammation. These mediators provide "chemotaxis, smooth-muscle constriction, and vasoactive properties" (Carpenter, 2006, p 18). This helps in controlling inflammation. "Arachidonic acids a precursor in the generation of prostaglandins and leukotrienes that is predominately generated from membrane phospholipids by phospholipase A2 enzymes. Arachidonic acide can then proceed by the cyclooxygenase pathway to form prostaglandins and thromboxanes or via the lipoxygenase pathway to yield leukotrienes" (Carpenter, 2006, p 18).
This is not always obtainable. If the inflammatory response is sluggish and prolonged, it can lead to severe tissue damage. Those suffering from rheumatoid arthritis have lymphocytes that react to proteins they believe are harmful. The reaction causes a release of cytokines, which are chemical messengers that trigger more inflammation and destruction. Cytokines accumulate as they respond to inflammation in the synovium. According to McInnes & Schett (2011) the patterns of cytokines change over time. A cytokine profile can develop in those suffering from rheumatoid arthritis. It consists of interleukin-4, 13, and 15, 52. "TNF-Î± plays a fundamental role through activation of cytokine and chemokine expression, expression of endothelial-cell adhesion molecules, protection of synovial fibroblasts, promotion of angiogenesis, suppression of regulatory T cells, and induction of pain" (McInnes & Schett, 2011, p 2212). The main target of inflammation in rheumatoid arthritis is the synovium. The inflammation spreads to other areas in the body, ultimately causing joint damage, inflammation, chronic pain, fatigue, and loss of function. It can lead to joint destruction, organ damage and disability.
Abbas & Lichtman (2006) describe autoimmunity as the immune systems reaction towards self-antigens, resulting in pathological changes. White blood cells are used to fight against pathogens that enter the body. Autoantibodies develop, which results in T-cells reacting towards self-antigens. Instead of attacking viruses or bacteria these defensive cells attack healthy cells within the body. The immune system has difficulty in recognizing healthy tissues and antigens. This causes tissue, muscle, joint, blood vessels, and kidney damage. The autoimmune system may result in destruction of one or multiple body tissues, changes in organ functioning, and abnormal growth of an organ. The proteins are attacked, which lead to pain and inflammation. After time it causes deformities in the connective tissues and joints. Patients with rheumatoid arthritis have autoimmune deficiencies.
At this point it is unclear why autoimmunity occurs. "One explanation is that individuals who develop autoimmune disease have a defect in central or peripheral tolerance mechanisms, allowing self-reactive cells to emerge" (Carpenter, 2006, p 18). Molecular mimicry is another model that has been formulated to describe autoimmunity. Rose (2001) believes that self-reactive T-cells are stimulated by microbial antigens. These T-cells mimic self-molecules, which are then suspected as being foreign and are attacked. It can resemble flu-like symptoms, including fever, fatigue, and weakness. Carpenter (2006) states that not one specific theory explains the autoimmune system. It is rather a combination of environmental factors and a genetic predisposition, which increases the likelihood of an autoimmune disorder.
Each form of treatment needs to be individualized for the patient. Some forms may be effective while others may not. The effectiveness of the treatment should be based on the patient's improvement of pain and functioning.
Psychoeducation, psychosocial interventions, exercise, and dieting, are forms of nonpharmacological treatments. Fitzcharles, Lussier, & Shir (2010) state that psychoeducation is utilized to help provide information about the disorder, eliminate fear associated with the disorder, and provide self-management strategies, which help their quality of life. Psychosocial interventions are used to help those diagnosed with arthritis develop coping strategies to compensate for their illness. Therapy can assist in relinquishing depression and anxiety, which are often associated with arthritis. Exercise is critical as it can counteract stiffness within the body. It also strengthens muscles and increases range of motion. Fitzcharles, Lussier, & Shir (2010) explain that being overweight can affect weight bearing joints and soft tissue. Dieting is used to reduce pain and tension on these weight beating joints and soft tissue.
Medications are often prescribed to help eliminate pain in arthritic patients. Some of these medications include non-opioid analgesics, NSAIDs, opioids, and adjuvant medications. At this point there is no single best medication that can be offered to those with arthritis. Medications should be based on the patient's presenting symptomology and their severity. Ling and Rudolph (2006) recognize that medications need to be appropriately managed because of the high likelihood of co-morbid diagnoses. In order to control a patient's pain level it is critical to understand the biological mechanisms of action of pain. Arthritic patients can suffer from either chronic or acute pan. Pain is located in the joints and tissues affected with arthritis. According to Kalat (2009) these pain sensitive cells within the spinal cord are relayed to ventral posterior nucleus of the thalamus and then the somatosensory cortex. He describes that as pain travels from the periphery to the spinal cord it switches tracts, where it ascends contralaterally in the spine before it reaches the brain. An individual suffering from arthritis in their hands may use a pencil to write. Kalat (2009) explains that this is a form of touch pain and causes the signal to be sent up the ipsilateral side of the spine where it reaches the medulla. Here it crosses contra-laterally. "Painful stimuli also activates a pathway through the reticular formation of the medulla and then to several of the central nuclei of the thalamus, the amygdala, hippocampus, prefrontal cortex, and cingulate cortex" (Kalat, 2009, p 204). Each of these areas affects one's emotional response to the painful stimuli. Pain triggers glutamate to moderate pain. Stronger pain will cause a release of both glutamate and Substance P, neurotransmitters, to be released in the spinal cord. This will result in pain.
Rosenstein (1999) states that topical medications are effective in treating those with osteoarthritis and rheumatoid arthritis. He states that capsaicin can be applied to individuals' hands 2-4 times per day. This will result in heat or a burning sensation. Axons send pain information, typically at a slower than usual rate, to the brain where it is processed rapidly. These pain axons within the spinal cord release Substance P and glutamate. The Substance P is released quicker than it can be re-synthesized. This hinders the ability for the pain receptor to send its message. It results in a longer period of decreased pain.
Acetaminophen, a non-opioid analgesic, can be taken as a means to subdue moderate and mild pain. According to Towheed et al. (2006) taking over 1 gram 4 times daily of acetaminophen can lead to hepatotoxicity. Fitzcharles, Lussier, & Shir (2010) demonstrate that acetaminophen inhibits cyclooxygenase (COX-2) and is used as an anti-inflammatory. According to Hinz, Cheremina, & Brune (2008) acetaminophen sends a message to the TRPA1- receptors, located in the spinal cord, and suppresses transduction in the dorsal horn. Pain is then eased. It is also involved in inhibiting the nitric oxide pathway, which releases Substance P. Ottani, Leone, Sandrini, Ferrari, & Bertolini (2006) explain that acetaminophen also blocks cannabinoid receptors with synthetic antagonists. It showed decreased levels of pain and diminished inflammation. Cannabinoid receptors decreases pain on the peripheral portion of the body.
Opioids are also prescribed by doctors to alleviate arthritic pain. Some of these medications include methadone, fentanyl, oxycodone, morphine, and hydrocodone. Opioids are often prescribed to those with moderate to severe pain. However, these medications are highly addictive. Kalat (2009) states that opioid receptors block the release of Substance P in the spine and periaqueductal gray area, located in the midbrain. Opioid receptors are found in the ascending and descending portions of the brain. Endorphins, a neurotransmitter which mimics morphine, is released to decrease pain. This concept led to evolution of Gate Theory by Melzack & Walls (1965). Gate theory proposes that areas in the spinal cord receive messages from pain receptors, input from touch receptors, and also from axons descending from the brain to reduce the sensation of pain.
Nonsteroidal anti-inflammatory drugs.
Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most common medication prescribed to those with arthritis. It is used to treat both pain and inflammation. This medication is effective in treating acute pain but needs to be given in higher dosages and for a longer period of time to treat and reduce inflammation. If given for chronic pain one may develop a tolerance for this form of medication. Carpenter (2006) states that this drug is effective as it impedes the cyclooxygenase (COX-2) pathway to form prostaglandins and thromboxanes. It is similar to acetaminophen, but has greater effectiveness in reducing inflammatory pain. Common NSAIDs include ibuprofen and naproxen.
Arthritis currently affects 20 million Americans, and continues to grow. Although medical professionals have been able to treat arthritic pain with pharmacological and non-pharmacological medications, it does not alleviate the disabilities and deformities associated with the disorder. It is critical that additional research be conducted to help develop a cure for arthritis, and to end this horrific disease.