Epidermis

This layer consists of a modified stratified squamous epithelium and arises from basal, germinal columnar keratinocytes that evolve as they migrate towards the surface through a prickle cell layer (where the cells acquire a polyhedral shape) and a granular cell layer (where the nucleated cells acquire keratohyalin granules) and eventually form the superficial keratinised layer (horny layer of the stratum corneum) where the cells lose their nuclei and form a tough superficial barrier (Fig. 3.1). The migratory cycle from the basal to horny layer takes approximately 30 days, with the cornified cells shedding from the surface some 14 days later. Abnormalities of this transit time may lead to certain skin diseases such as psoriasis, in which the migration rate is greatly accelerated. Epidermal cells are linked by structures known as desmosomes. The epidermis rests on a thin basement membrane and is anchored to the dermis by hemidesmosomes and other anchor proteins such as laminin, basement membrane proteoglycan and type IV collagen. These and other proteins are of importance in the pathogenesis of diseases occurring at the epidermal–dermal junction (e.g. bullous pemphigoid and epidermolysis bullosa).

Fig. 3.1 Section through full thickness of skin showing the structure of the epidermis, dermis and hypodermis.

Melanocytes develop among the basal cells. These cells are derived from neural crest cells and synthesise melanin pigment which is transferred to keratinocytes through dendritic processes. Melanin is responsible for skin and hair pigmentation. The pigment protects the skin from the potentially harmful effects of ultraviolet irradiation. Skin colour is determined by the total number, size and distribution of melanin granules, not the number of melanocytes. Hereditary failure to synthesise melanin results in albinism.

Dermis

This layer provides the supporting framework on which the epidermis rests and consists of a fibrous matrix of collagen and elastin set in a ground substance of glycosaminoglycans, hyaluronic acid and chondroitin sulphate (Fig. 3.1). The skin appendages are set in the dermis. Nerves, blood vessels, fibroblasts and various inflammatory cells also populate this layer. The dermis is divided into two layers: the papillary dermis apposes the undulating dermal–epidermal junction, whereas the reticular dermis lies beneath, forming the bulk of collagen, elastic fibres and ground substance. Dermal fibroblasts synthesise and secrete the dermal collagen subtypes (I and III) and elastin. If there is disruption of dermal elastin, disorders such as wrinkles and a loose skin syndrome (cutis laxa) occur.

Hypodermis

The dermis rests on the hypodermis, which is the subcutaneous layer of fat and loose connective tissue. This layer serves both as a fat store and an insulating layer.

Sebaceous glands

Skin sebaceous glands can function throughout life, although activity is latent between birth and puberty. These glands are partly responsible for the production of vernix caseosa which covers and waterproofs the fetus during the latter stages of gestation. The glands become particularly active during puberty. The secretion is holocrine (i.e. caused by complete degeneration of the acinar cells) and is stimulated by androgens and opposed by oestrogens. Sebaceous glands are absent from the palms and soles and are concentrated on the face, scalp, midline of the back and the perineum. Sebum contains triglyceride, scalene and wax esters and functions to waterproof and lubricate the skin, as well as inhibiting the growth of skin flora and fungi. Skin disorders such as acne vulgaris and rosacea occur in areas where sebaceous glands concentrate.

Apocrine and eccrine glands

The apocrine glands are concentrated in the axillae, areolae, nipples, anogenital regions, eyelids and external ears. These glands become functionally active at puberty and are responsible for an odourless secretion which is acted on by skin flora, causing characteristic body odour to develop. The eccrine sweat glands are widely distributed and are extremely important in heat regulation and fluid balance. Whereas the eccrine cells secrete an isotonic fluid, the duct cells modify the fluid to render it hypotonic. Secretion and its modification are under cholinergic and hormonal control. Sweating in response to temperature change is under hypothalamic control.

Inspection and palpation

Scan the skin, looking for skin lesions and noting both position and symmetry. Remember to expose hidden areas like the axillae, inner thighs and buttock with its natal cleft. Many skin lesions can be diagnosed by their appearance and localisation. Unlike any other organ system, the examination relies almost entirely on careful inspection and meticulous use of descriptive terminology.

Measurement of the length and breadth of skin lesions is useful, especially when monitoring progression or regression. A broad beam torch or electric light helps to define the outline of the border of a skin lesion; a thin beam is helpful if you wish to check whether or not a lesion transilluminates. A fluid-filled but not solid lesion emits a red glow when the torch light shines through it. A Wood’s lamp helps to distinguish a fluorescing lesion; by shining the lamp at a suspect lesion, it may be possible to show the characteristic blue-green fluorescence of fungal infections.

Skin colour

Skin colour varies between individuals and races and is usually even and symmetrical in distribution. Normal variations occur in freckling and sun-exposed areas. During pregnancy, there may be darkening of the skin overlying the cheek bones (melasma) and the areolae surrounding the nipple (chloasma).

Abnormal skin colour

Generalised changes in skin colour occur in jaundice, iron overload, endocrine disorders and albinism. The yellow tinge of jaundice is best observed in good daylight, appearing initially as yellowing of the sclerae and then as a yellow discoloration on the trunk, arms and legs. Jaundice is less apparent in unconjugated as opposed to conjugated hyperbilirubinaemia. In longstanding, deep obstructive jaundice, the skin may turn a deep yellow-green. Remember that people eating large quantities of carrots or other forms of vitamin A may develop yellow skin pigmentation (carotenaemia) and that the absence of scleral discoloration distinguishes this syndrome from jaundice.

Iron overload (haemosiderosis and haemochromatosis) causes the skin to turn a slate-grey colour. The astute observer may recognise this metabolic disease by the characteristic skin pigmentation. Addison’s disease (autoimmune adrenal destruction) is characterised by darkening of the skin, occurring first in the skin creases of the palms and soles, scars and other skin creases. The mucosa of the mouth and gums also becomes pigmented. Striking pigmentation also arises after bilateral adrenalectomy for adrenal hyperplasia: this syndrome (Nelson’s syndrome) is caused by unopposed pituitary overstimulation. In hypopituitarism, the skin is soft, pale and wrinkled.

Albinism is an autosomal recessive disorder caused by failure of melanocytes to produce melanin. The skin and hair are white and the eyes are pink because of a lack of pigmentation of the iris, and there may also be nystagmus.

Common localised abnormalities of skin pigmentation include vitiligo (Fig. 3.5), café-au-lait spots (Figs 3.6, 3.7), pityriasis versicolor and idiopathic guttate hypomelanosis. Erythema of the skin is caused by capillary dilatation; when pressure is applied the red lesion blanches and reforms. When examining a patient, you may notice an erythematous flush in the necklace area which is caused by anxiety. Purpura is the term used for red-purplish lesions of the skin caused by seepage of blood from skin blood vessels. Unlike erythema, these lesions do not blanch with pressure. If the lesions are small (<5  mm) they are called petechiae (Fig. 3.8), whereas larger lesions are purpura. Traumatic bruises are called ecchymoses. Telangiectasia refers to fine blanching vascular lesions caused by superficial capillary dilatation (Fig. 3.9).

Fig. 3.5 Depigmented skin (vitiligo): white discoloration of brown hand.

Fig. 3.6 Café-au-lait patches with neurofibromas.

Fig. 3.7 Café-au-lait patches in neurofibromatosis.

Fig. 3.8 Typical appearance of petechial haemorrhage in a patient with thrombocytopenia.

Fig. 3.9 Telangiectasia on the tongue.

Localised skin lesions

Careful descriptions of size, shape, colour, texture and position of lesions are helpful in skin diagnosis. Try to ascertain a primary and secondary description of the skin lesion. To establish the primary nature of the skin lesion decide whether the lesion is flat, nodular or fluid-filled. Flat circumscribed changes in colour are termed macules if less than 1  cm or patches if more than 1  cm. If the lesion is raised and can be palpated, assess whether the mass is a papule, plaque, nodule, tumour or wheal. If a circumscribed elevated lesion is fluctuant and fluid-filled, describe whether it is a vesicle, bulla or pustule (Fig. 3.10). If possible, describe the arrangement of the lesions; that is, whether linear, annular (ring-shaped) or clustered. In shingles (herpes zoster), the rash occurs in the distribution of one or more skin dermatomes.

Fig. 3.10 Primary localised skin lesions.

Add to the primary description any secondary characteristics such as superficial erosions, ulceration, crusting, scaling, fissuring, lichenification, atrophy, excoriation, scarring, necrosis or keloid formation.

Palpation is used to decide whether a lesion is flat, raised or tender. Compression may be helpful (e.g. demonstration of the characteristic arteriolar dilatation of spider naevi occurring in decompensated liver disease) (Fig. 3.11). Use the back of your hand to assess temperature. Inflamed lesions (e.g. cellulitis) are hotter than surrounding tissue, whereas skin overlying a lipoma (subcutaneous fat tumours) is cooler than adjacent tissue. Skin turgor may be used as a measure of moderate to severe hydration. Pinch a small area of skin between index finger and thumb. Hold firmly for a few seconds and then release. Healthy, well-hydrated skin immediately springs back into its resting position. In significant dehydration or when skin elastic tissue is lost (e.g. ageing), the skin behaves like putty and only slowly reshapes to its resting position. Skin oedema can be demonstrated by pressing your thumb or fingers into the skin, maintaining the pressure for a short while and then releasing. Your thumb or finger impression will remain indented in the skin if there is excessive fluid (‘pitting’ oedema).

Fig. 3.11 Spider naevi in hepatocellular disease.

Although most disorders can be diagnosed from their appearance, special techniques such as microscopy of skin biopsies or skin scrapings, immunofluorescent staining and culture of specimens may be required to confirm diagnosis.

Common skin lesions

Skin lesions are often readily recognisable and you should be able to distinguish some common conditions.

Acne vulgaris

This common disorder of the pilosebaceous unit occurs at puberty. Plugging of the duct, increased sebum production, bacterial growth and hormonal changes all predispose to the condition. Acne presents with greasy skin, blackheads (comedones), papules, pustules and scars (Fig. 3.12). The lesions are common and vary in severity and most teenagers recognise the problem before visiting the doctor. The disorder affects the face, chest and back. Acne usually subsides in the third decade.

Fig. 3.12 Papules, pustules and scarring in acne vulgaris.

Rosacea

This facial rash usually presents in the fourth decade, although in women it may present after the menopause. Papules and pustules erupt on the forehead, cheeks, bridge of the nose and the chin. The erythematous background highlights the rash (Figs 3.13, 3.14). Comedones do not occur, distinguishing the condition clinically from facial acne. Occasionally, the rash may be localised to the nose. Eye involvement is characterised by grittiness, conjunctivitis and even corneal ulceration. There appears to be vasomotor instability and patients flush readily in response to stimuli such as hot drinks, alcohol and spicy foods. If this disorder is treated with potent topical corticoids there may be a temporary response, but a marked relapse occurs on cessation of treatment. It is important to check carefully whether or not steroids have been applied and to dissuade your patient from using this treatment (like acne vulgaris, antibiotics are the treatment of choice).

Fig. 3.13 Rosacea: papules and pustules occur on the face.

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