Chapter 24 Skin
COMMON CLINICAL PROBLEMS FROM SKIN DISEASE
Pathological basis of dermatological signs
Clinical sign | Pathological basis |
---|---|
Scaling | Parakeratosis |
Erythema | Dilatation of skin vessels |
Blisters | Separation of layers of the epidermis or epidermis from dermis |
Bruising | Leakage of blood into dermis |
Pigmentation | |
Plaques | Increase in epidermal and dermal thickness with cells |
Macules | |
Papules | |
Nodules | |
Rashes restricted to exposed areas | |
Nail abnormalities |
NORMAL STRUCTURE AND FUNCTION
The two major layers of the skin—the superficial epidermis and deeper dermis—are derived from different embryonic components and retain a radically different morphology (Fig. 24.1). The epidermis is highly cellular, avascular, lacks nerves, sits on a basement membrane and shows marked vertical stratification (Fig. 24.2). It produces a complex mixture of proteins collectively termed keratin. A series of specialised adnexa extend from the epidermis into the dermis. The density of these adnexa varies from site to site on the body, as does the thickness of the epidermis and the structure of the keratin layer. This site-to-site variation means that the histological interpretation of diagnostic biopsies has to take into account the area of the body from which the biopsy was taken; what may constitute severe hyperkeratosis (excess keratin) on the forehead may be normal for the sole of the foot.
The dermis is relatively acellular and is recognisably divided into two zones: the upper zone comprises extensions of the dermis (dermal papillae) between the downward projecting rete ridges (‘pegs’) of the epidermis and is called the papillary dermis; beneath this zone is the reticular dermis. Both regions of the dermis contain blood and lymph vessels as well as nerves. The intervening connective tissue consists of the characteristic dermal proteins collagen and elastin, together with various glycosaminoglycans. These proteins and complex carbohydrates are secreted by the principal cells of the dermis, the fibroblasts. Although the proteins of the dermis appear to be arranged in a haphazard fashion when viewed in standard histological preparations, they are in fact arranged in specific patterns that are characteristic of different sites in the body; these patterns are the Langer’s lines. The significance of this knowledge is that if incisions are made in the skin along the long axis of the dermal collagen fibres then little permanent scarring will occur. If, however, incisions are made across the fibres and disrupt them, then in the effort to repair the damage scarring is bound to result. A considerable part of the surgeon’s skill relies on knowing the characteristic orientation of these fibres and in making incisions that generate the minimum risk of permanent scars. Scattered within the dermis and often clustered about blood vessels are the mast cells. The nerves of the dermis approach close to the epidermis and often end in specialised sensory structures such as Pacinian corpuscles. Similarly, the dermal blood vessels run close to the underside of the epidermis, although they are organised into two recognisable structures—the superficial and deep vascular plexuses.
Skin as a barrier
The other way in which the barrier is often breached is at the weak points where there are natural holes in the barrier, such as the sweat glands and hair ducts, and organisms may use these portals of entry.
Failure of the barrier (eczema and immersion)
Eczema/dermatitis
The word eczema comes from the Greek meaning to ‘bubble up’; this meaning conveys well the clinical development of the lesions. The word dermatitis is often used in an interchangeable manner, in particular when referring to the histopathological changes. The skin becomes reddened (erythematous) and tiny vesicles may develop (pompholyx); the surface develops scales, and cracking and bleeding can cause great discomfort (Fig. 24.3). The skin becomes tender and secondary infection may occur. The clinical pattern is very varied and there are several different types of eczema. Sometimes the variation is due to the cause of the eczema, such as contact with a toxic or allergenic material; sometimes the site of the lesion or the age of the patient is sufficient to make the disease a clinical entity. For example, chromate hypersensitivity causes eczema in cement workers and discoid/atopic eczema occurs in atopic individuals. Seborrhoeic eczema has a tendency to involve the scalp, face, axillae and groins. Whatever the cause, the underlying pathological processes are recognisably similar and can be seen as a stereotyped reaction pattern to a variety of different stimuli.
The earliest histological change in eczema is swelling within the epidermis (Fig. 24.4). This swelling is due to separation of the keratinocytes by fluid accumulating between them and this appearance is known as spongiosis. Later, there may be hyperkeratosis (an increase in the thickness of the stratum corneum) and parakeratosis (retention of nuclei in the stratum corneum), which give rise to the clinical scales. Various degrees of inflammation also give rise to the classical inflammatory signs and symptoms (Ch. 10). In severe cases the intercellular oedema can then join up to form foci of fluid within the epidermis, recognised clinically as blisters or vesicles (pompholyx) (Fig. 24.5).
CLINICAL ASPECTS OF SKIN DISEASES
Incidence of skin diseases
Skin diseases, like all diseases, vary in their distribution according to a wide range of factors (Table 24.1), but they also vary markedly in the experience of particular doctors. A hospital dermatologist running a pigmented skin lesion clinic will see many melanomas in a year, depending on the population make-up of the catchment area and its size, whereas a general practitioner in the same area may expect to see only one every 2 years. A dermatologist will see only the difficult cases of acne and pityriasis rosea but a general practitioner will see many more straightforward ones. With these reservations in mind, skin diseases can be categorised according to their frequency:
Table 24.1 Incidence of skin diseases
Variable | Associations |
---|---|
Age | |
Sex | |
Anatomical site | |
Geography | |
Exposure | Basal cell carcinoma and squamous cell carcinoma common on sun-exposed sites |
Race | Basal cell carcinoma and squamous cell carcinoma and melanoma rare in blacks (protected by pigmentation) |
DISORDERS INVOLVING INFLAMMATORY and HAEMOPOIETIC CELLS
Many of the characteristics of inflammation (Ch. 10) were first observed and studied in the skin. The various phases and types of inflammation are characterised by a particular spectrum of cells that mediate the inflammatory response. Because the types of cell in a particular lesion are there in response to the initiating factor, a careful analysis of the composition of a particular lesion will significantly narrow down the differential diagnosis. Thus, cuffing of vessels by plasma cells would strongly suggest syphilis and the presence of granulomas with caseous centres would suggest tuberculosis.
Polymorph infiltrates
Some diseases, such as Sweet’s disease and pyoderma gangrenosum (skin lesions that may occur in association with various internal diseases such as chronic inflammatory bowel diseases; Ch. 15), show massive infiltration by polymorph neutrophils in the dermis.
In some cases, polymorphs are attracted by the deposition of auto-antibodies (Ch. 9) and in these cases the resulting damage often causes blistering. Antibodies to the basement membrane on which the epidermis sits and to proteins in the papillary dermis cause pemphigoid and dermatitis herpetiformis respectively (see below). The presence of one type of polymorph rather than another suggests different aetiological processes and dermatitis herpetiformis can sometimes be distinguished from bullous pemphigoid by the relative excess of neutrophil polymorphs in the former and eosinophil polymorphs in the latter. Eosinophil polymorphs are a frequent reflection of allergic diseases (such as eczema) and parasitic infestation.
Lymphocytic infiltrates
Any chronic inflammation of the skin will eventually come to be dominated by lymphocytes, but there are many skin conditions that are primarily due to lymphocyte accumulation and whose distinctive clinical character is due to the disposition and behaviour of these cells. The lymphocytes present in inflammation are usually of T-cell type and most commonly of CD4/helper phenotype.
Cutaneous lymphomas
Secondary deposits of systemic lymphomas and primary lymphomas may occur within the skin. Both are relatively rare. Any of the lymphomas and leukaemias that occur systemically (Ch. 22) can give secondary deposits in the skin, but usually only in advanced cases. The primary lymphomas include mycosis fungoides which is a T-cell lymphoma and which, as it develops, can spill over into the blood to give an associated T-cell leukaemia, called the Sézary syndrome.
Occasionally, skin lymphomas also result from B-cell lymphocytes.
INFECTIONS
The clinical appearance depends on:
There are two routes by which infection may arrive in the skin:
In practice, most infections arise via the latter route.
Another possible mechanism whereby infections can cause skin lesions is where the organism infects some other part of the body but produces a skin rash in which it is impossible to identify any organisms; this mechanism, for example, occurs in acute rheumatic fever and is similar to the effects on the heart also seen in this condition (Ch. 13). Staphylococcus can produce a toxin and give rise to a blistering disorder called the staphylococcal scalded skin syndrome.
Viral infections
Other herpes viruses are responsible for cold sores (HSV1) and for genital herpes (HSV2). The great problem with these kinds of herpetic infections is that they are infections for life.
Protozoal infections
Leishmaniasis is an infection caused by Leishmania tropica which is transmitted by sandflies. The organisms have developed a mechanism for subverting the body’s defences and can be found living in abundance within the host macrophages.
NON-INFECTIOUS INFLAMMATORY DISEASES
Urticaria
Histologically, the collagen bundles of the dermis are separated by the oedema and a sparse infiltrate of polymorphs, often including eosinophils and an increased numbers of mast cells. The most important mediator of this process is histamine but other substances such as kinins and various circulating globulins, mainly IgE, play a role (Ch. 10). Agents causing urticaria include:
Lupus erythematosus
Clinicopathological features
Clinically, LE is a multisystem disease which may present with symptoms associated with almost any organ; in practice, skin and renal (Ch. 21) involvement are among the commonest. In many cases the skin appears to be the only organ involved and the disease is then called discoid LE. The systemic variant may or may not involve the skin. However, the fact that the lesions in discoid and systemic cases are often indistinguishable, and the occurrence of serological abnormalities in systemic and some discoid cases, suggest that the relationship is close.
The skin lesions are initially erythematous, scaly and indurated and slowly progress to atrophic scarred patches, often with hyperpigmented edges in the older lesions. They are often symmetrical on the face in a butterfly distribution over the nose and cheeks, and on the scalp may be associated with a scarring alopecia. These features are explained by the histology, which shows a dilatation of superficial vessels with a dense accumulation of lymphocytes around them, leading to the observed erythema. The infiltrate also involves the dermo-epidermal interface and damages the melanocytes. The melanocytes lose their melanin to dermal macrophages in which the pigment accumulates, accounting for the hyperpigmentation in older lesions. The persistent junctional inflammation results in damage to hair follicles, with the formation of follicular plugs (tin-tacks) and eventually atrophy of hair follicles and the epidermis itself.
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