Friday, May 31, 2019

Treatment for Raynaud Syndrome :: essays research papers

Treatment for Raynauds - 2 -IntroductionRaynaud syndrome is an auto-immune disorder in which teleph angiotensin-converting enzyme line vessels in the digits constrict. It usually strikes females between the ages of eighteen and thirty. Between three to five percent of people are affected. (Harvard, 2003) There is no known campaign or cure. (Segala et al, 2003) Clinical features primarily deal with (but are non limited to) the digits of the fingers. Other digits that may be affected include toes, nose, and ear lobes. Exposure to coolness and excited stress triggers the vasoconstriction of the digits. It was originally described by the Catholic, French physician Maurice Raynaud in 1862. In this condition, the vasospastic response is more frequently induced by exposure to arctic temperatures and is often accompanied by digital color changes. After onset, a tri-color change blanching (white), cyanosis (blue), and reactive hyperemia (red) occurs. Pallor (blanching) shows vasospasm and loss of arterial blood flow, cyanosis shows the deoxygenation of noneffervescent venous blood, and rubor (red) shows reactive hyperemia following return of blood flow. (Bowling, 2003) Theories for the causes of Raynaud syndrome include arterial wall damage, connective tissue disease (CTD), or clamant use of vibrational tools. (Ko, 2002) There are various methods of diagnosing Raydaund syndrome. Cold water emersion is one method. In this method, patients hands are immersed in cold water to observe any clinical features. Another mode of diagnosis looks at medical conditions that are associated with Raynaud syndrome, such as CTD, scleroderma, and lupus. A third proficiency includes physical examination of the ulnar and radial vessels, nail folds in the capillaries, presence of digital inflammation, sclerodactyly (sleroderma, hardening of the skin, of the fingers and toes), or telangiectasia (chronic dilation of groups of capillaries Treatment for Raynauds - 3 -that cause dark red blotches on the skin, usually on the face). Laboratory tests are another consideration of diagnosis. Tests consist of anti-nuclear anti-body (ANA) counts and anti-topoisomerase (an enzyme that reduces super-coiling in DNA by breaking and rejoining one or both strands of DNA). High ANAs and low anti-topoisomerases are found in patients with Raynaud syndrome. (Desai, 2003) Patients with circulating autoantibodies, antinuclear antibodies, and anti-Scl 70 antibodies are at (an) increased risk of underdeveloped a connective tissue disease. Systemic sclerosis is the connective tissue disease most frequently associated with Raynauds phenomenon. (Bowling, 2003) This syndrome is described as primary Raynaud phenomenon (PRP) if is not associated with another disorder and as secondary Raynaud phenomenon (SRP) if it occurs in association with another disorder.

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