Skin disorders

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  • Harrison's Internal Medicine Chapter 52. Approach to the Patient with a Skin Disorder APPROACH TO THE PATIENT WITH A SKIN DISORDER: INTRODUCTION The challenge of examining the skin lies in distinguishing normal from abnormal, significant findings from trivial ones, and in integrating pertinent signs and symptoms into an appropriate differential diagnosis. The fact that the largest organ in the body is visible is both an advantage and a disadvantage to those who examine it.

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  • Figure 52-5 Meningococcemia. An example of fulminant meningococcemia with extensive angular purpuric patches. (Courtesy of Stephen E. Gellis, MD; with permission.) Figure 52-4 Necrotizing vasculitis. Palpable purpuric papules on the lower legs are seen in this patient with cutaneous small vessel vasculitis. (Courtesy of Robert Swerlick, MD; with permission.)[newpage] APPROACH TO THE PATIENT: SKIN DISORDER In examining the skin it is usually advisable to assess the patient before taking an extensive history.

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  • Allergic contact dermatitis (ACD). A. An example of ACD in its acute phase, with sharply demarcated, weeping, eczematous plaques in a perioral distribution. B. ACD in its chronic phase demonstrating an erythematous, lichenified, weeping plaque on skin chronically exposed to nickel in a metal snap. (B, Courtesy of Robert Swerlick, MD; with permission.) As in other branches of medicine, a complete history should be obtained to emphasize the following features: 1. Evolution of lesions a. Site of onset b. Manner in which the eruption progressed or spread c. Duration d.

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  • Table 52-2 Description of Secondary Skin Lesions Lichenification: A distinctive thickening of the skin that is characterized by accentuated skin-fold markings. Scale: Excessive accumulation of stratum corneum. Crust: Dried exudate of body fluids that may be either yellow (i.e., serous crust) or red (i.e., hemorrhagic crust). Erosion: Loss of epidermis without an associated loss of dermis. Ulcer: Loss of epidermis and at least a portion of the underlying dermis. Excoriation: Linear, angular erosions that may be covered by crust and are caused by scratching.

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  • A–D. The distribution of some common dermatologic diseases and lesions Figure 52-7 Psoriasis. This papulosquamous skin disease is characterized by small and large erythematous papules and plaques with overlying adherent silvery scale.

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  • Dermatitis herpetiformis. This disorder typically displays pruritic, grouped papulovesicles on elbows, knees, buttocks, and posterior scalp. Vesicles are often excoriated due to associated pruritus. The shape of lesions is also an important feature. Flat, round, erythematous papules and plaques are common in many cutaneous diseases. However, targetshaped lesions that consist in part of erythematous plaques are specific for erythema multiforme (Fig. 52-9). In the same way, the arrangement of individual lesions is important.

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  • Malassezia are common lipiddependent fungi that grow on the sebaceous areas of human skin. Malassezia can cause and exacebate several skin diseases: Tinea versicolor, pitirosporum folliculitis and seborrheic dermatitis. Malassezia also have been associated with subsets of psoriasis and atopic dermatitis, especially those affecting the scalp.

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  • Tzanck Smear A Tzanck smear is a cytologic technique most often used in the diagnosis of herpesvirus infections [herpes simplex virus (HSV) or varicella zoster virus (VZV)] (see Figs. 173-1 and 173-3). An early vesicle, not a pustule or crusted lesion, is unroofed, and the base of the lesion is scraped gently with a scalpel blade. The material is placed on a glass slide, air-dried, and stained with Giemsa or Wright's stain. Multinucleated epithelial giant cells suggest the presence of HSV or VZV; culture or immunofluorescence testing must be performed to identify the specific virus.

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  • Table 52-4 Selected Common Dermatologic Conditions Dia gnosis mmon Co ual Us is Diagnos mmon Co al Usu Distributi on Morpholo gy Distributio Morpholog n y Ac ne vulgaris e, back Fac upper en closed Op Seborrh Tru nk, face Bro wn plaques with adherent, greasy and eic keratosis comedone s, erythemat ous papules, pustules, cysts scale; "stuck on" appearance Ros acea Blu sh area of thema, cheeks, nose, forehead, chin Ery Folliculi tisImpetigo hair- Any cular Folli telangiecta ses, papules, pustules bearing pustulesPap areaAnywh ules, ere vesicles, pustules, often...

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  • Tuyển tập các báo cáo nghiên cứu về hóa học được đăng trên tạp chí sinh học đề tài : New insights into HIV-1-primary skin disorders

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  • Harrison's Internal Medicine Chapter 54. Skin Manifestations of Internal Disease Skin Manifestations of Internal Disease: Introduction It is now a generally accepted concept in medicine that the skin can show signs of internal disease. Therefore, in textbooks of medicine one finds a chapter describing in detail the major systemic disorders that can be identified by cutaneous signs. The underlying assumption of such a chapter is that the clinician has been able to identify the disorder in the patient and needs only to read about it in the textbook.

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  • It has long been noted anecdotally that affect, psychological state and neurologic state have influences on inflammatory skin diseases. Disorders such as psoriasis, atopic dermatitis, acne and rosacea, among many others, are reported to become exacerbated by stress. Furthermore, it is widely believed that stress alters cutaneous immunity. However, mechanisms responsible for these effects have remained incompletely understood. Scientific evidence for an influence of the nervous system on immune and inflammatory processes in the skin has been developed only relatively recently.

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  • Absence of melanocytes. b Normal number of melanocytes. c Platelet storage defect and restrictive lung disease secondary to deposits of ceroid-like material; one form due to mutations in β subunit of adaptor protein. d Giant lysosomal granules and recurrent infections. The differential diagnosis of localized hypomelanosis includes the following primary cutaneous disorders: idiopathic guttate hypomelanosis, postinflammatory hypopigmentation, tinea (pityriasis) versicolor, vitiligo, chemical leukoderma, nevus depigmentosus (see below), and piebaldism (Table 54-9).

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  • Several metabolic disorders are associated with blister formation, including diabetes mellitus, renal failure, and porphyria. Local hypoxia secondary to decreased cutaneous blood flow can also produce blisters, which explains the presence of bullae over pressure points in comatose patients (coma bullae). In diabetes mellitus, tense bullae with clear viscous fluid arise on normal skin. The lesions can be as large as 6 cm in diameter and are located on the distal extremities. There are several types of porphyria, but the most common form with cutaneous findings is PCT.

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  • Table 54-14 Causes of Urticaria and Angioedema I. Primary cutaneous disorders A. Acute and chronic urticariaa B. Physical urticaria 1. Dermatographism 2. Solar urticariab 3. Cold urticariab 4. Cholinergic urticariab C. Angioedema (hereditary and acquired)b II. Systemic diseases A. Urticarial vasculitis B. Hepatitis B or C infection C. Serum sickness D. Angioedema (hereditary and acquired) a A small minority develop anaphylaxis. b Also systemic. The common physical urticarias include dermographism, solar urticaria, cold urticaria, and cholinergic urticaria.

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  • Papulonodular Skin Lesions (Table 54-15) In the papulonodular diseases, the lesions are elevated above the surface of the skin and may coalesce to form plaques. The location, consistency, and color of the lesions are the keys to their diagnosis; this section is organized on the basis of color. Table 54-15 Papulonodular Skin Lesions According to Color Groups I. White A. Calcinosis cutis II. Skin-colored A. Rheumatoid nodules B. Neurofibromas (von Recklinghausen's disease) C. Angiofibromas (tuberous sclerosis, MEN syndrome, type 1) D. Neuromas (MEN syndrome, type 2b) E.

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  • Palpable purpura are further subdivided into vasculitic and embolic. In the group of vasculitic disorders, cutaneous small-vessel vasculitis, also known as leukocytoclastic vasculitis (LCV), is the one most commonly associated with palpable purpura (Chap. 319). Underlying etiologies include drugs (e.g., antibiotics), infections (e.g., hepatitis C virus), and autoimmune connective tissue diseases. Henoch-Schönlein purpura is a subtype of acute LCV that is seen primarily in children and adolescents following an upper respiratory infection.

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  • Also associated with systemic diseases. b Reviewed in section on Purpura. cReviewed in section on Papulonodular Skin Lesions. d Favors plantar surface of the foot. Note: TEN, toxic epidermal necrolysis. Livedoid vasculopathy (livedoid vasculitis; atrophie blanche) represents a combination of a vasculopathy plus intravascular thrombosis. Purpuric lesions and livedo reticularis are found in association with painful ulcerations of the lower extremities. These ulcers are often slow to heal, but when they do, irregularly shaped white scars are formed.

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  • Harrison's Internal Medicine Chapter 55. Immunologically Mediated Skin Diseases Immunologically Mediated Skin Diseases: Introduction A number of immunologically mediated skin diseases and immunologically mediated systemic disorders with cutaneous manifestations are now recognized as distinct entities with consistent clinical, histologic, and immunopathologic findings. Many of these disorders are due to autoimmune mechanisms.

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  • Neutrophil Abnormalities A defect in the neutrophil life cycle can lead to dysfunction and compromised host defenses. Inflammation is often depressed, and the clinical result is often recurrent with severe bacterial and fungal infections. Aphthous ulcers of mucous membranes (gray ulcers without pus) and gingivitis and periodontal disease suggest a phagocytic cell disorder. Patients with congenital phagocyte defects can have infections within the first few days of life. Skin, ear, upper and lower respiratory tract, and bone infections are common. Sepsis and meningitis are rare.

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