Rheumatoid Arthritis (RA) and Guillain-Barre Syndrome (GBS)

Inflammation is a protecting effect associated with vascular tissue in response to different stimuli such as irritants and pathogens. In addition, other causes of inflammation can include physical incidents and immune reactions on body cells and tissues. Therefore, inflammatory reactions serve to get rid of the stimuli and begin the procedure of curing on damaged skin cells, tissues, and organs (Ferrero-Miliani et al. , 2007, p. 227). Conversely, these inflammatory reactions can be persistent or severe. This essay reveals the etiology, pathogenesis, analysis, professional medical manifestations, prognosis, and the treating ARTHRITIS RHEUMATOID (RA) and Guillain-Barre Syndrome (GBS).

Rheumatoid Joint disease (RA)

Scenario:

45 years of age woman started with severe pain in her hands and feet. She pointed out that she could not shake her wrists whilst she was doing PE with her students in the gym. About 2 month later, when she was working in her yard, the pain became even more pronounced. She was digging the backyard for make a way way. The garden working was difficult to do because every day her foot damage and the power in her hands was so reduced that even lifting a large boiling container in the personnel kitchen was difficult. At night times she put her hands under her pillow to try to decrease the pain so that she could sleep.

Chronic immune inflammatory reactions may appear on synovial cells in response to the synovitis, synovial skin cells, and the gathered synovial substance in the joints. This type of autoimmunity causes Rheumatoid arthritis (Majithia & Geraci, 2007). The symptoms of RA are not only limited by the articular parts however they can also disperse to other parts of your body. Therefore, RA influences the joints, epidermis, lungs, kidneys, arteries, center, and other systemic cells. Furthermore, the disorder causes destruction of the ankylosis and cartilage lining the joints. In addition, it triggers nodular lesions on the skin and diverse inflammatory reactions on different systemic tissues (Majithia & Geraci, 2007, p. 937). The professional medical medical diagnosis of RA will involve physical study of symptoms, blood testing, x-ray radiographic imaging, and other differential diagnoses, that are targeted at distinguishing the symptoms of RA from other disorders.

Moreover, the pathogenesis of RA includes proliferation and fibrosis of skin cells; the damage of cartilage and bones; and pannus development. These changes are caused by the activities of proteolytic enzymes, cytokines, and prostanoids in the synovial region (Majithia & Geraci, 2007, p. 937). Here, swelling is mediated by Tumor Necrosis Factor-alpha and Interleukin-1 (IL-1), which will be the most notable pro-inflammatory cytokines in the disease procedure for RA. The two cytokines improve the production of other inflammatory elements such as nitric oxide (NO) and prostaglandin E2 (PGE2).

However, IL-1 has shown prominence in the pathogenesis of RA. Primary IL-1 release stimulates osteoblasts, synoviocytes, and chondrocytes. The skin cells take part in the inflammatory reactions, bone devastation, and pannus creation. Furthermore, the inflammatory reactions elevate the secretion of IL-1 relative to the improvement of the disease. Furthermore, IL-1 stimulates the movement of neutrophils in to the synovial region; the creation and differentiation of lymphocytes; and lastly the activation of macrophages. Additional IL-1 production causes severe erosion of bone and cartilage, produces pain, and impairs cells repair (Majithia & Geraci, 2007).

Lastly, Rheumatoid arthritis can be cured using medications such as analgesics, steroids, and disease-modifying antirheumatic drugs (DMARDs). In addition, non-pharmacological remedies such as physical therapy and nutritional remedy can halt the development of the condition. Conversely, the prognosis of RA shows mixed symptoms in several patients such as disabilities, poor prognostic factors, and sometimes fatality (Majithia & Geraci, 2007, p. 939).

Guillain-Barre Syndrome (GBS)

Scenario:

A 33 yrs. old man have a burning, sensitive, irritated sensation under his skin that spread throughout his arms and chest muscles over few months in the beginning of 2010. He observed his sense of balance was lost. Then over a weeks more symptoms shown themselves. His hands began to tremble and tremor, his ears commenced humming, tickly in his left feet and the muscle spasms appeared, and muscle strength getting weak and pain grew in his thighs. His conversation became jumbled and his remaining pupil dilated.

Acute infections of the peripheral stressed system can cause an autoimmune response in response to the pathogens and the host tissues. These immune responses are directed at pathogens such as bacterias and the influenza disease but instead they assault the gangliosides of the nerve cells (Hughes et al. , 1999). This is the basis of GBS, which brings about inflammatory demyelination of the nerves and multiple neuropathies. Therefore, GBS is seen as a impaired sense of position, paralysis, lack of fever, areflexia, and symmetrical weaknesses that get started with the thighs and propagate to top of the limbs and finally to the facial skin. Conversely, analyses of the cerebrospinal smooth and electrodiagnostics provide important insights in to the medical diagnosis of GBS. Furthermore, observable paralysis and areflexia can be utilized as the immediate indicators of GBS. However, additional differential diagnoses are important to tell apart the symptoms of GBS with other disorders such as the Engine Neuron Disease (Hughes et al. , 1999, p. 74).

The pathogenesis of GBS is associated with immune responses targeted at an acute an infection. However, the pathogens involved in the illness contain epitopes resembling some the different parts of the peripheral nervous system. Therefore, the immune system reaction episodes the nerve components creating acute infection on the myelin sheath or the axon (Hughes et al. , 1999). Furthermore, the inflammatory reactions cause severe demyelination in the nodes of Ranvier and nerve roots. These inflammatory reactions are mediated by both cellular and humoral immune system components such as activated T-lymphocytes, which invade the demyelinated parts and attract macrophages that eliminate the nerve membranes. Additional demyelination is thus, mediated by the macrophages and components of the complement system.

Lastly, the treatment of GBS includes providing supportive care for patients with paralyzed diaphragms and intravenous shots of immunoglobulin for steady patients. In addition, supervision of plasmapheresis is recommended. Conversely, aside from isolated circumstances of prolonged areflexia, the prognosis of GBS demonstrates most patients begin recovering at the forth week after the onset plus they can be completely healed after a couple of months or twelve months.

Conclusion

The essay presents a detailed debate on two inflammatory conditions, that happen to be caused by immune responses that aim for cells, tissues, and organs in the body. Therefore, the article examines the etiology, clinical manifestations, diagnosis, pathogenesis, treatment, and the prognosis of Rheumatoid arthritis and Guillain-Barre Syndrome (GBS). In the discussions above, it can be deduced that swelling is a serious complication, which occurs in the complete body or within a specific tissue and triggers acute or chronic symptoms. However, most inflammatory conditions are treatable and preventable.

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