Pharmacology
The drug that is chosen for this paper is Rituxan (Rituximab), which is prescribed for the treatment of non-Hodgkin's lymphoma; Rheumatoid arthritis; and chronic lymphocytic leukemia (Rituxan.com). This is a drug that comes with stern warnings of dangerous reactions, including serious infections, heart problems, kidney problems, stomach and serious bowel problems, and some side effects "can lead to death" (Rituxan.com).
Clinical Pharmacology
Under the heading "prescribing directions," the drug company offers "Clinical Pharmacology" -- "Mechanism of Action," "Pharmacodyamics," and Pharmacokinetics"
Pharmacodyamics
In patients suffering with Non-Hodgkin's Lymphoma (NHL), tests revealed that when NHL patients were administered Rituxan there was a depletion of "tissue-based B cells." The first study (using 166 patients) showed that "circulating CD 19-positive B cells were depleted" in the first three weeks of the test. And the depletion of B cells continued for 6 to 9 months after the treatment. As to B-cell recovery, 83% of the 166 patients began to experience recovery of B-cells at about 6 months after treatment, and "median B-cell levels" were normal a year after treatment with Rituxan.
Fourteen percent of patients treated with Rituxan had IgM and/or IgG serum levels "below the normal range" from 5 to 11 months after...
Rheumatoid Arthritis What is happening to the synovium in Arletha's knees and probably her hands as well? In all likelihood, the synovium is inflamed and is not doing its job. The synovium is meant to secret liquid that keeps the joint lubricated. If it's not present or is not doing its job at high efficiency any more, then the joints in the hands and knees will start to become damaged and broken
As well as several reports relating diseases and mood, mental status has also been reported to affect immuno-regulatory systems. Chronic depression or chronic stress conditions lead to immuno-suppressive status and imbalance in corticotrophin-releasing hormone, which induces cancer and hyperthyroidism. It has been reported that depressive states induce suppression of mitogenic reaction in lymphocytes, decreases the number and activity of natural killer cells and decreases the production of interferon." Sadamoto,
Rheumatoid arthritis is a widespread autoimmune disease that is linked to progressive disability, socioeconomic costs, systemic complications, and even early death. In addition to having an unknown cause, the disease also has a guarded prognosis. In the past few years, there have been several attempts to understand the pathogenesis of the disease, which have resulted in the creation of new therapeutics with enhanced outcomes (McInnes & Schett, 2011, p.2205). As
Though this work focuses specifically on the risk factors of atherosclerosis for RA patients and how to better identify them prior to clinical presentation of atherosclerosis the work is also insightful in that it builds a case for the connection between RA clinical presentations and atherosclerosis, in general. To move forward from this progressive idea is the fact that research has indicated that there is an even greater connection
Rheumatoid Arthritis: Risks/Benefits of Latest Treatments Rheumatoid arthritis (RA) is a form of arthritis characterized by swelling and tenderness which recent studies have revealed that approximately 1% of grownups suffer from. A common symptom of this disease is symmetric polyarticular inflammation of the synovium, typically of the small joints of the hands (MCP and PIP), wrists and feet. This swelling causes discomfort and difficulty of movement and could result into gradual
h2 { color: blue; } Introduction Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by inflammation and progressive destruction of the joints. Understanding its pathophysiology is crucial for developing effective treatment strategies. Immune Dysregulation: RA is mediated by an aberrant immune response involving the activation of T cells and B cells. Dysregulated T cells secrete pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-?)
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