Pharmacological Management of Rheumatoid Arthritis: Difference between revisions
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=== PATHOPHYSIOLOGY OF RHEUMATOID ARTHRITIS === | === PATHOPHYSIOLOGY OF RHEUMATOID ARTHRITIS === | ||
'''OVERVIEW''' Rheumatoid arthritis (RA) is a chronic, autoimmune disease marked by systemic inflammation of both articular (i.e. joints) and extra-articular areas (e.g. cardiopulmonary systems). RA is a progressive disease, in which the onset can occur at any age, but peaks around 30 to 60 years old. Females are three times as likely to be diagnosed with RA compared to males, and children can also be affected, as seen in juvenile idiopathic arthritis | '''OVERVIEW''' Rheumatoid arthritis (RA) is a chronic, autoimmune disease marked by systemic inflammation of both articular (i.e. joints) and extra-articular areas (e.g. cardiopulmonary systems). RA is a progressive disease, in which the onset can occur at any age, but peaks around 30 to 60 years old. Females are three times as likely to be diagnosed with RA compared to males, and children can also be affected, as seen in juvenile idiopathic arthritis.<ref name=":0">Goodman CC, Fuller KS. Rheumatoid Arthritis. In: Pathology: Implications for the Physical Therapist. 4th ed. St. Louis, MO: Elsevier; 2015:1317-1328.</ref> In total, about 1-2% of people in the United States have RA, with 80% of them testing positive for rheumatoid factors: autoantibodies produced by the immune system that are responsible for the autoimmune component of the disease.<ref>Bukhari M, Lunt M, Harrison BJ, Scott DG, Symmons DP, Silman AJ. Rheumatoid factor is the major predictor of increasing severity of radiographic erosions in rheumatoid arthritis: results from the Norfolk Arthritis Register Study, a large inception cohort. Arthritis & Rheumatology. 2002;46(4):906-912. doi:0.1002/art.10167.</ref><ref>Harris ED. Rheumatoid arthritis: pathophysiology and implications for therapy. N Engl J Med. 1990;322(18):1277-1289.</ref> | ||
'''MECHANISM OF ACTION''' RA is marked by periods of exacerbation and remission. During the exacerbation period, it is theorized that certain cells, such as cytokines and tumor-necrosis-factor-alpha (TNF-⍺), cause the inflammatory and destructive process that occurs in the disease. In joint capsules, these inflammatory factors are found in the pannus, an abnormal layer of granulation tissue, and prevents the synovium from providing the necessary nutrients and lubrication to the joint. As the pannus proliferates, the space within the joint diminishes, consequently leading to the disintegration of the collagen, cartilage, and other surrounding tissues found here. Synovial hyperplasia occurs, causing local swelling and joint pain | '''MECHANISM OF ACTION''' RA is marked by periods of exacerbation and remission. During the exacerbation period, it is theorized that certain cells, such as cytokines and tumor-necrosis-factor-alpha (TNF-⍺), cause the inflammatory and destructive process that occurs in the disease. In joint capsules, these inflammatory factors are found in the pannus, an abnormal layer of granulation tissue, and prevents the synovium from providing the necessary nutrients and lubrication to the joint. As the pannus proliferates, the space within the joint diminishes, consequently leading to the disintegration of the collagen, cartilage, and other surrounding tissues found here. Synovial hyperplasia occurs, causing local swelling and joint pain.<ref name=":0" /> These synovial changes result in irreversible bone and joint deformity, instability, and fusion, which will further affect proper functioning of the body.<ref>Elliot JM, Grainger AJ, Grigorian MA, Szechinksi JW, Harry KG. Rheumatoid arthritis: a guide to imaging studies. J Muscoskel Med. 1999;16(9):507-514.</ref> Extra-articular systems are similarly affected due to the inflammatory components coursing through the circulation.<ref name=":0" /> | ||
'''SIGNS AND SYMPTOMS''' RA begins insidiously; it starts with cartilage degradation, then moves to ligamentous laxity, followed by synovial expansion and erosion. The joints of the hand are affected early on but any joint can be affected, including the knee and temporomandibular joint. Morning stiffness is an iconic symptom of RA, along with fatigue, diffuse musculoskeletal pain, and even depression | '''SIGNS AND SYMPTOMS''' RA begins insidiously; it starts with cartilage degradation, then moves to ligamentous laxity, followed by synovial expansion and erosion. The joints of the hand are affected early on but any joint can be affected, including the knee and temporomandibular joint. Morning stiffness is an iconic symptom of RA, along with fatigue, diffuse musculoskeletal pain, and even depression.<ref name=":0" /> As the disease progresses, joint deformities and subluxation can occur, particularly in the cervical spine (Kim, 2005). Extra-articular signs include vasculitis, anemia, myelopathy, nodulosis, scleritis, and many others (Davis & Matteson, 2012). | ||
'''TYPES OF DRUG THERAPY''' There are two primary sub classifications of drugs used in the treatment of RA; drugs that provide disease modifying therapy (DMARDs) and drugs for symptomatic treatment. DMARDs are medications taken regularly for longer periods of time independent of acute symptoms. DMARDs consist of Traditional DMARDs (DMARDs) and Biological DMARDs (bDMARDs). Symptomatic therapy is used to relieve acute pain and inflammation associated with the disease process. Non-steroidal anti-inflammatory drugs (NSAIDs), acetaminophen, and corticosteroids are the primary drugs of choice for symptomatic therapy (Singh et al., 2015). | '''TYPES OF DRUG THERAPY''' There are two primary sub classifications of drugs used in the treatment of RA; drugs that provide disease modifying therapy (DMARDs) and drugs for symptomatic treatment. DMARDs are medications taken regularly for longer periods of time independent of acute symptoms. DMARDs consist of Traditional DMARDs (DMARDs) and Biological DMARDs (bDMARDs). Symptomatic therapy is used to relieve acute pain and inflammation associated with the disease process. Non-steroidal anti-inflammatory drugs (NSAIDs), acetaminophen, and corticosteroids are the primary drugs of choice for symptomatic therapy (Singh et al., 2015). | ||
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=== REFERENCES === | === REFERENCES === | ||
<references /> | |||
Revision as of 04:08, 30 November 2018
PATHOPHYSIOLOGY OF RHEUMATOID ARTHRITIS[edit | edit source]
OVERVIEW Rheumatoid arthritis (RA) is a chronic, autoimmune disease marked by systemic inflammation of both articular (i.e. joints) and extra-articular areas (e.g. cardiopulmonary systems). RA is a progressive disease, in which the onset can occur at any age, but peaks around 30 to 60 years old. Females are three times as likely to be diagnosed with RA compared to males, and children can also be affected, as seen in juvenile idiopathic arthritis.[1] In total, about 1-2% of people in the United States have RA, with 80% of them testing positive for rheumatoid factors: autoantibodies produced by the immune system that are responsible for the autoimmune component of the disease.[2][3]
MECHANISM OF ACTION RA is marked by periods of exacerbation and remission. During the exacerbation period, it is theorized that certain cells, such as cytokines and tumor-necrosis-factor-alpha (TNF-⍺), cause the inflammatory and destructive process that occurs in the disease. In joint capsules, these inflammatory factors are found in the pannus, an abnormal layer of granulation tissue, and prevents the synovium from providing the necessary nutrients and lubrication to the joint. As the pannus proliferates, the space within the joint diminishes, consequently leading to the disintegration of the collagen, cartilage, and other surrounding tissues found here. Synovial hyperplasia occurs, causing local swelling and joint pain.[1] These synovial changes result in irreversible bone and joint deformity, instability, and fusion, which will further affect proper functioning of the body.[4] Extra-articular systems are similarly affected due to the inflammatory components coursing through the circulation.[1]
SIGNS AND SYMPTOMS RA begins insidiously; it starts with cartilage degradation, then moves to ligamentous laxity, followed by synovial expansion and erosion. The joints of the hand are affected early on but any joint can be affected, including the knee and temporomandibular joint. Morning stiffness is an iconic symptom of RA, along with fatigue, diffuse musculoskeletal pain, and even depression.[1] As the disease progresses, joint deformities and subluxation can occur, particularly in the cervical spine (Kim, 2005). Extra-articular signs include vasculitis, anemia, myelopathy, nodulosis, scleritis, and many others (Davis & Matteson, 2012).
TYPES OF DRUG THERAPY There are two primary sub classifications of drugs used in the treatment of RA; drugs that provide disease modifying therapy (DMARDs) and drugs for symptomatic treatment. DMARDs are medications taken regularly for longer periods of time independent of acute symptoms. DMARDs consist of Traditional DMARDs (DMARDs) and Biological DMARDs (bDMARDs). Symptomatic therapy is used to relieve acute pain and inflammation associated with the disease process. Non-steroidal anti-inflammatory drugs (NSAIDs), acetaminophen, and corticosteroids are the primary drugs of choice for symptomatic therapy (Singh et al., 2015).
DRUG CLASSES[edit | edit source]
SUMMARY[edit | edit source]
REFERENCES[edit | edit source]
- ↑ 1.0 1.1 1.2 1.3 Goodman CC, Fuller KS. Rheumatoid Arthritis. In: Pathology: Implications for the Physical Therapist. 4th ed. St. Louis, MO: Elsevier; 2015:1317-1328.
- ↑ Bukhari M, Lunt M, Harrison BJ, Scott DG, Symmons DP, Silman AJ. Rheumatoid factor is the major predictor of increasing severity of radiographic erosions in rheumatoid arthritis: results from the Norfolk Arthritis Register Study, a large inception cohort. Arthritis & Rheumatology. 2002;46(4):906-912. doi:0.1002/art.10167.
- ↑ Harris ED. Rheumatoid arthritis: pathophysiology and implications for therapy. N Engl J Med. 1990;322(18):1277-1289.
- ↑ Elliot JM, Grainger AJ, Grigorian MA, Szechinksi JW, Harry KG. Rheumatoid arthritis: a guide to imaging studies. J Muscoskel Med. 1999;16(9):507-514.
