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Robert A. Norman - Atlas of Geriatric Dermatology

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Book:
Atlas of Geriatric Dermatology
Author:
Robert A Norman / Edward M Young Jr
Publisher:
Springer
Genre:
Books / Home and family
Year:
2013
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Atlas of Geriatric Dermatology: summary, description and annotation

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This is a comprehensive, practical, densely illustrated diagnostic and therapeutic guide for all geriatric dermatology providers. The book comprises 50 chapters and over 600 color photographs on topics ranging from common conditions such as basal cell carcinoma, rosacea, and seborrheic dermatitis to unusual conditions such as angiosarcoma, dermatofibrosarcoma protuberans, and porphyria cutanea tarda.

Sections include:

- Inflammatory conditions (including contact dermatitis, alopecia, erythema multiforme, pemphigus, bullous pemphigoid, porphyria, pruritus, psoriasis, rosacea, seborrhea, urticaria, xerosis, and more)

- Infections (fungus, herpes simplex and zoster, scabies, lice, and warts)

- Skin signs in systemic disease (skin tags, cutaneous metastases, xanthomas)

- Regional dermatoses (intertrigo, leg ulcers, pressure sores)

- Benign tumors (chondrodermatitis, cysts, ganglion, fibrous papule, seborrheic keratoses, lentigines, and benign vascular lesions)

- Pre-malignant and malignant tumors (actinic keratoses, angiosarcoma, basal cell carcinoma, dermatofibroma and dermatofibrosarcoma protuberans, intraepidermal neoplasia, Kaposis sarcoma, keratoacanthoma, lentigo maligna, cutaneous lymphoma, Mycosis fiungoides, melanoma, nevi and moles, and squamous cell carcinoma)

Robert A. Norman: author's other books

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Part 1
Introduction to Geriatric Dermatology

Robert A. Norman and Edward M. Young, Jr Atlas of Geriatric Dermatology 2013 10.1007/978-1-4471-4579-0_1 Springer-Verlag London 2014

1. Geriatric Dermatology: Overview

Robert A. Norman 1 and Edward M. Young Jr 2

(1)

Dermatology Healthcare, Tampa, FL, USA

(2)

Tarzana, CA, USA

Abstract

With the graying of America, geriatric dermatology is a rapidly growing field. Many skin problems present differently in the elderly, require alterations in standard therapy, or both. In addition, banal-appearing skin rashes in the elderly may signal underlying systemic disease, especially cancer.

The purpose of this chapter is to alert dermatologists, internists, primary care physicians, and all other caregivers to some commonly encountered dermatologic complaints that may portend potentially life-threatening diseases in the elderly. A summary of the biology, histology, and physiology of aging skin provides useful background information for the chapters that follow.

Aging can be defined as a progressive loss of homeostasis that results in decreased organ function []. Intrinsic or chronologic aging refers to changes on sun-protected skin. Extrinsic aging, photoaging, and dermatoheliosis refer to changes on sun-exposed skin. These changes differ quantitatively and qualitatively from those of intrinsic aging.

Two major theories of aging exist []. The genetic program theory is an irreversible, orderly process, whereas the stochastic theory implicates wear and tear by random environmental assaults, particularly free oxygen radicals. These free radicals damage enzymes, DNA, and structural proteins. Both genetic and stochastic processes contribute to aging, depending on the replicative ability of the cell.

Skin changes of premature aging [] include atrophy, loss of fat, wrinkling, alopecia (hair loss), canities (graying hair), nail dystrophy, defective pigmentation, poikiloderma (triad of atrophy, hyperpigmentation and hypopigmentation, and telangiectasia), sclerosis (hardening), and ulceration. Many genetic syndromes have features of premature skin aging, most notably progeria (Hutchinson-Gilford syndrome), xeroderma pigmentosum, and cutis laxa.

Solar elastotic syndromes [] describe changes seen in chronically photodamaged skin, They are not part of intrinsic aging per se, but are nevertheless commonly seen in elderly patients. The most common conditions include Favre-Racouchot syndrome (nodular elastosis with cysts and comedones), cutis rhomboidalis nuchae, actinic cheilitis and actinic keratoses, and poikiloderma of Civatte.

Aging research [] has been confounded by four factors: (1) confusing chronologic aging and photoaging; (2) confusing development and senescence; (3) confusing aging with age-associated diseases (e.g. diabetes mellitus); and (4) confusing aging with age associated hormonal changes (e.g. menopause).

The epidemiology of skin disease in the elderly [] can reveal several different patterns: some diseases increase steadily with age, others show a bimodal peak early and late in life, and some decline with age or show a single peak incidence in middle age.

Cellular and Molecular Changes in Aging Skin

Intrinsic or chronologic aging results in decreased mitogenic (replicative) potential or decreased life span of fibroblasts, melanocytes, and keratinocytes []. Decreased responsiveness to growth stimulators and increased responsiveness to growth inhibitors occur. When this responsiveness fails, malignancies develop. Photoaging accentuates these changes and also tilts the balance from cellular differentiation toward proliferation, with obvious implications for photocarcinogenesis.

Intrinsic aging adversely affects nucleic acids and cellular proteins, such as collagen, elastin, fibronectin (an adhesion molecule), intercellular ground substance, membrane composition, and catalase (an antioxidant enzyme that prevents free radical damage). Photoaging is characterized by severe solar elastosis, which results in massive dermal deposits of elastin-like material. This solar elastotic material probably originates from elastin rather than collagen, because it cross-reacts with antielastin antibodies and is susceptible to elastase, but is resistant to collagenase. It is only partially cross-linked by desmosine, however, so it lacks normal physiologic elasticity. These changes predispose the elderly skin to easy tearing, bruising, and wrinkling.

Histologic Changes in Aging Skin

Clinically, aged skin exhibits roughness (dryness, xerosis), laxity, wrinkling, uneven pigmentation, and benign and malignant growths.

Histologically, flattening of the dermal-epidermal junction and effacement of the epidermal rete ridges and interdigitating dermal pegs are the most consistent findings in aged skin []. The stratum corneum and epidermal barriers remain well formed. Cellular heterogeneity (variation in cell size, shape, and staining characteristics) results in a diffuse epidermal dyscrasia (mild actinic keratosis) of photoaged skin. Melanocytes decline by 1020 % each decade, resulting in poor tanning, decreased melanocytic nevi (moles), poor pigment transfer to keratinocytes, and guttate hypomelanosis on the arms and shins. Langerhans cells are intraepidermal macrophages that decrease in density and in immune responsiveness to ultraviolet damage with age.

The dermal-epidermal junction shows reduplication of structural components, a loss of interdigitating basal cell foot processes, and decreased dermatoglyphics (fingerprints and other skin markings). This loss of dermal-epidermal adhesion predisposes to blistering from such diverse causes as cardiac edema, lichen planus, and autoimmune bullous pemphigoid.

The dermis becomes less dense, relatively acellular, and avascular. Loss of functional elastic tissue results in wrinkles, both temporary and permanent. Sun-protected aged skin shows fewer fibroblasts, macrophages, and mast cells. In contrast, photo aged skin has an increased number of inflammatory cells, especially partly degranulated mast cells. This chronic heliodermatitis [] may stimulate fibroblasts to produce solar elastotic material.

The microcirculation and nerves undergo a gradual decline, predisposing to poor thermoregulation and decreased sensation for burning. Erythema ab igne (redness from the fire) occurs from overuse of heating pads and space heaters and is manifest as a reticulate poikiloderma. The eccrine and apocrine sweat glands decline in number and activity, with decreased perspiration, body odor, and thermoregulation. Sebaceous glands paradoxically increase in size despite a decrease in function; this is related to decreased serum androgen levels. Sebaceous hyperplasia, rhinophyma (bulbous, greasy nose), and asteatotic (xerotic or nummular) eczema occur, the last exacerbated by overbathing and inadequate moisturizing. Hair decreases in number, caliber, and pigment density, resulting in male pattern androgenetic alopecia in men and diffuse hair thinning in women. Conversion of fine vellus to coarse terminal hairs occurs on the ears and nose of men and on the upper lip and chin of women, a common cosmetic annoyance. Nails undergo a slow irregular decline in growth, thinning of the nail plate, and longitudinal ridging, softening, splitting, and shaling. Subcutaneous fat atrophies on the cheeks and distal extremities but hypertrophies on the waist of men and thighs of women.

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