By Robert A. Norman
The manifestations of dermatologic affliction within the geriatric inhabitants are frequently subtly diversified to these within the more youthful age teams and there's a have to produce a pragmatic and medical reference for dermatology fellows and citizens, geriatricians and comparable clinicians to spot dermatoses and their differential prognosis particular to the getting older inhabitants. prognosis of getting older epidermis illnesses will give you the clinician with a visible encyclopedia of geriatric dermatoses that may be used on rounds or in a reference setting. It additionally presents a dependent evaluate of the differential prognosis of the lesions illustrated in the publication, in order to make this a important reference source for all physicians facing older dermis.
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Additional info for Diagnosis Aging Skin Diseases
It has also been observed two-dimensionally that fibroblasts had greater surface area contact with collagen fibrils than old skin . Solar elastosis, also known as dermal elastosis (the accumulation of elastotic material in the dermis) is the histological feature specific to photoaging. The elastotic material includes changes in elastin (the principal component of the elastic fibers), and extracellular-matrix components normally present in the skin. In photo-damaged skin, there is a disturbance of the organization of these structures and their function.
29. Lipschitz D. Medical and functional consequences of anemia in the elderly. J. Am. Geriatr. Soc. 2004; 51: S10–S13. 30. Dharmarajan TS, Adiga GU, Norkus EP. B12 deficiency: recognizing subtle symptoms in older adults. Geriatrics 2003; 58: 30–8. 31. Etter L, Myers SA. Pruritus in systemic disease: mechanisms and management. Dermatol. Clin. 2002; 20: 459–72. 32. Elgart ML. Skin infections and infestations in geriatric patients. Clin. Geriatr. Med. 2002; 18: 89–101. 33. Adam JE. Skin cancer: a review.
The remaining forms are asymptomatic, usually found during routine examination [5, 23]. Although of unknown etiology, the current tendency is to consider lichen planus as an autoimmune disease, mediated by cells and unlocked by alteration in the antigens of the basal layer of the epidermis in genetically predisposed patients [23, 24]. The lymphocytic infiltrate and the amplified production of cytokines result in an increased expression of the intercellular-1 adhesion molecule (ICAM-1) and antigens of the histocompatibility complex, mainly of class II (MHC-II), by the keratinocytes .
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