Clinical Dermatology E-Book

Richard B. Weller

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 1019

Veröffentlichungsjahr: 2014

Beschreibung

The best-selling text has been completely revised and revitalised in this fifth edition, with the authors once again encouraging general practitioners, medical students, general physicians and early stage dermatology specialist trainees and interns to relish the unique challenge of diagnosing and treating skin conditions.

Clinical Dermatology, 5th edition contains over 400 high quality pictures and diagrams combined with colourful phrases to illustrate and entertain as it teaches. The book has established a reputation as a ‘way of learning’ and as an accessible guide to the subject for the aspiring specialist. Readers are guided through the maze that too often lies between the presenting skin complaint and its final diagnosis and treatment. The authors have skilfully crafted an easily read text with enough detail to clarify the subject, but not enough to obscure it.

This fifth edition contains new chapters on non-invasive physical treatment and dermoscopy, and new material on cosmetic dermatology, surgical dermatology, the skin and the psyche, and dermatoses of non-Caucasian skin. The text throughout the book has been updated in line with developments in the science and practice of dermatology.

“... brilliantly succeeds in enticing you to look further. The writing is clear, and the joint British-American authorship avoids any parochial views.” From a review of a previous edition in BMJ

“...a very well-presented book...an excellent aid for teaching. I recommend this book highly to individuals and departments.” From a review of a previous edition in J Derm Treatment

“… provides a good overview of the structure and function of the skin as well as a good foundation for learning dermatology…well organized and includes a chapter dedicated to skin signs of systemic disease which is not covered in the other dermatology primers.” From a review of a previous edition in JAMA

Leseprobe

For my mother Alison and for Julie, Hiwot and Girma; Foz, Jack and Isabella; Daniel and Samuel.

Clinical Dermatology

Richard B.Weller MD, FRCP (Edin)

Senior Lecturer Department of Dermatology University of Edinburgh Edinburgh, UK

Hamish J.A. Hunter BSc (Hons), MBChB, MRCP (UK) (Derm)

Clinical Research Fellow in Dermatology University of Manchester Manchester, UK

Margaret W. Mann MD, FAAD

Assistant Professor of Dermatology Director of Aesthetic Dermatology Associate Director of Dermatologic Surgery University Hospitals / CaseWestern School of Medicine Cleveland, OH, USA

FIFTH EDITION

This edition first published 2015 © 2015 by John Wiley & Sons Ltd.

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Library of Congress Cataloging-in-Publication Data

Weller, Richard P. J. B., author.     Clinical dermatology / Richard B. Weller, Hamish J.A. Hunter, Margaret W. Mann. – Fifth edition.         p. ; cm.     Preceded by Clinical dermatology / Richard P.J.B. Weller … [et al.]. 4th ed. 2008.     Includes bibliographical references and index.     ISBN 978-0-470-65952-6 (pbk.)     I. Hunter, Hamish J.A., author.    II. Mann, Margaret W., author.    III. Title.     [DNLM: 1. Skin Diseases–diagnosis.    2. Skin Diseases–therapy.    WR 140]     RL71     616.5–dc23

2014032478

A catalogue record for this book is available from the British Library.

Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books.

Contents

Preface to the Fifth Edition

Acknowledgements

Introduction

Dermatology on the internet

Further reading

1 Skin Disease in Perspective

The many roles of the skin

The prevalence and cost of skin disorders

The impact of skin disorders

Further reading

2 The Function and Structure of the Skin

Epidermis

Dermo-epidermal junction

Dermis

The skin immune system

Types of immune reactions in the skin

Further reading

3 Diagnosis of Skin Disorders

History

Examination

Terminology of lesions (Figure 3.2)

Special tools and techniques

Assessment

Side-room and office tests

Laboratory tests

Conclusions

Further reading

4 Disorders of Keratinization

The ichthyoses

Common ichthyoses

Autosomal recessive congenital ichthyoses

Keratinopathic ichthyoses

Other ichthyosiform disorders

Other disorders of keratinization

Further reading

5 Psoriasis

Cause and pathogenesis

Precipitating factors

Histology (Figure 5.2)

Complications

Differential diagnosis

Investigations

Treatment

Further reading

6 Other Papulosquamous Disorders

Pityriasis rosea

Lichen planus

Pityriasis rubra pilaris

Parapsoriasis and premycotic eruption

Pityriasis lichenoides

Other papulosquamous diseases

Erythroderma/exfoliative dermatitis

Further reading

7 Eczema and Dermatitis

Terminology

Pathogenesis

Histology

Clinical appearance

Complications

Differential diagnosis

Investigations

Common patterns of eczema

Further reading

8 Reactive Erythemas and Vasculitis

Urticaria (hives, ‘nettle-rash’)

Physical urticarias

Hereditary angioedema

Erythema multiforme

Erythema nodosum

Acute febrile neutophilic dermatosis (Sweet's syndrome)

Vasculitis

Further reading

9 Bullous Diseases

Bullous disorders of immunological origin

Hailey–Hailey disease

Other causes of subcorneal and intraepidermal blistering

Subepidermal immunobullous disorders

Other causes of subepidermal blisters

Bullous erythema multiforme

Epidermolysis bullosa (also known as the mechanobullous disorders)

Further reading

10 Connective Tissue Disorders

Lupus erythematosus

Systemic sclerosis

Other connective tissue diseases

Further reading

11 Disorders of Blood Vessels and Lymphatics

Disorders involving small blood vessels

Arterial disease

Venous disease

Disorders of the lymphatics

Further reading

12 Sebaceous and Sweat Gland Disorders

Sebaceous glands

Sweat glands

Further reading

13 Regional Dermatology

The hair

The nails

The mouth and genitals

Further reading

14 Racial Skin Differences

Skin types

Racial differences in structure and function

Racially dependent variations in skin conditions

Naevus and melanoma

Keratodermas

Infections

Hair and scalp

Keloids

Cultural practices

Further reading

15 The Skin at Different Ages

Fetal skin

Infancy (the first year of life)

Childhood

Adolescence

Young adults

Pregnancy

Middle age

Old age

Further reading

16 Infections

Bacterial infections

Streptococcal infections

Meningococcal infection

Spirochaetal infections

Other infections

Mycobacterial infections

Other mycobacterial infections

Viral infections

Fungal infections

Further reading

17 Infestations

Arthropods

Parasitic worms

Further reading

18 Skin Reactions to Light

Beneficial effects of sunlight

Sunburn

Phototoxicity

Photoallergy

Chronic actinic dermatitis (actinic reticuloid)

Polymorphic light eruption

Actinic prurigo

Solar urticaria

Actinic keratoses

Actinic cheilitis

Lupus erythematosus

Carcinomas

Exacerbated diseases

Porphyria cutanea tarda

Cutaneous ageing

Further reading

19 Disorders of Pigmentation

Normal skin colour

Abnormal skin colours

Further reading

20 Skin Tumours

Prevention

Tumours of the epidermis and its appendages

Tumours of the dermis

Further reading

21 The Skin in Systemic Disease

The skin and internal malignancy

The skin and diabetes mellitus

The skin in sarcoidosis

The skin in liver disease

The skin in renal disease

Graft versus host disease

Malabsorption and malnutrition

The porphyrias

Metabolic disorders

Generalized pruritus

Pyoderma gangrenosum

Further reading

22 Cosmetic Dermatology

Ageing of the skin

Cosmeceuticals

Dermal fillers

Skin resurfacing

Further reading

23 The Skin and the Psyche

Reactions to skin disease

Dermatological delusional disease

Psychological side effects of dermatological therapy

Dermatoses precipitated or perpetuated by psychosocial stress

Further reading

24 Other Genetic Disorders

Non-Mendelian genetics

Red hair

The neurofibromatoses

Tuberous sclerosis

Xeroderma pigmentosum

Incontinentia pigmenti

Ehlers–Danlos syndrome

Pseudoxanthoma elasticum

Further reading

25 Drug Eruptions

Mechanisms

Presentation

Course

Differential diagnosis

Treatment

Further reading

26 Medical Treatment

Therapeutic options

Topical treatment

Systemic therapy

Further reading

27 Physical Forms of Treatment

Surgery

Skin biopsy

Excision

Cryotherapy

Curettage

Electrosurgery

Microscopically controlled excision (Mohs' micrographic surgery)

Flaps and grafts

Radiotherapy

Phototherapy

Photodynamic therapy

Laser therapy

Further reading

28 Dermoscopy

Dermoscopic evaluation

Further reading

Formulary 1 Topical Treatments

Formulary 2 Systemic Medication

Index

End User License Agreement

List of Tables

Chapter 1

Table 1.1

Table 1.2

Table 1.3

Table 1.4

Chapter 2

Table 2.1

Table 2.2

Table 2.3

Table 2.4

Table 2.5

Chapter 3

Table 3.1

Table 3.2

Table 3.3

Chapter 5

Table 5.1

Table 5.2

Chapter 6

Table 6.1

Table 6.2

Table 6.3

Table 6.4

Chapter 7

Table 7.1

Table 7.2

Table 7.3

Table 7.4

Table 7.5

Table 7.6

Table 7.7

Table 7.8

Chapter 8

Table 8.1

Table 8.2

Table 8.3

Table 8.4

Table 8.5

Table 8.6

Table 8.7

Chapter 9

Table 9.1

Table 9.2

Chapter 10

Table 10.1

Table 10.2

Table 10.3

Table 10.4

Table 10.5

Table 10.6

Table 10.7

Table 10.8

Chapter 11

Table 11.1

Table 11.2

Table 11.3

Table 11.4

Table 11.5

Table 11.6

Table 11.7

Table 11.8

Chapter 12

Table 12.1

Table 12.2

Chapter 13

Table 13.1

Table 13.2

Table 13.3

Table 13.4

Table 13.5

Table 13.6

Table 13.7

Chapter 14

Table 14.1

Chapter 15

Table 15.1

Table 15.2

Chapter 16

Table 16.1

Table 16.2

Chapter 17

Table 17.1

Chapter 18

Table 18.1

Table 18.2

Table 18.3

Table 18.4

Table 18.5

Chapter 19

Table 19.1

Table 19.2

Table 19.3

Chapter 20

Table 20.1

Table 20.2

Table 20.3

Table 20.4

Table 20.5

Table 20.6

Chapter 21

Table 21.1

Table 21.2

Chapter 22

Table 22.1

Table 22.2

Table 22.3

Table 22.4

Chapter 23

Table 23.1

Table 23.2

Chapter 24

Table 24.1

Chapter 25

Table 25.1

Table 25.2

Chapter 26

Table 26.1

Table 26.2

Table 26.3

Table 26.4

Chapter 27

Table 27.1

Table 27.2

Table 27.3

Chapter 28

Table 28.1

Table 28.2

Table 28.3

Table 28.4

List of Illustrations

Introduction

Describe the primary lesion. What is your diagnosis? Turn over the page to find the answer.

A raspberry! ‘See and then reason and compare and control, but see first.’ (W. Osler)

Chapter 1

Figure 1.1

Internal and external factors causing skin diseases.

Figure 1.2

The age-dependent prevalence of some skin conditions.

Figure 1.3

Skin problems in the United Kingdom and how they are dealt with in 1 year. Patients in the United States usually refer themselves to dermatologists. (Adapted from Schofield

et al

. (2009) Skin conditions in the UK: a healthcare needs assessment. Metro Commercial Printing Ltd, Watford.)

Figure 1.4

The ‘iceberg’ of psoriasis in the United Kingdom during a single year.

Figure 1.5

The five D's of dermatological disease.

Figure 1.6

(a) This patient has a port-wine stain. (b) Her life is transformed by her clever use of modern camouflage cosmetics, which take her less than a minute to apply.

Chapter 2

Figure 2.1

Three-dimensional diagram of the skin, including a hair follicle.

Figure 2.2

Changes during keratinization.

Figure 2.3

The cell cycle.

Figure 2.4

Layers of the epidermis. (a) Light microscopy and (b) electron micrograph.

Figure 2.5

Melanocyte, Langerhans cell and Merkel cell.

Figure 2.6

Melanocyte (electron micrograph), with melanosomes (inset).

Figure 2.7

Adenosine triphosphase-positive Langerhans cells in an epidermal sheet. The network provides a reticulo-epithelial trap for contact allergens.

Figure 2.8

Langerhans cell (electron micrograph), with characteristic granule (inset).

Figure 2.9

Structure and molecular composition of the dermo-epidermal junction.

Figure 2.10

Blood vessels of the skin (carmine stain).

Figure 2.11

The keratinocyte and wound healing. The injured keratinocyte turns on wound healing responses. When a keratinocyte is injured (1), it releases interleukin-1 (IL-1) (2). IL-1 activates endothelial cells causing them to express selectins that slow down lymphocytes passing over them. Once lymphocytes stop on the endothelial cells lining the vessels, IL-1 acts as a chemotactic factor to draw lymphocytes into the epidermis (4). At the same time, IL-1 activates keratinocytes by binding to their IL-1 receptors. Activated keratinocytes produce other cytokines (3). Among these is tumour necrosis factor α (TNF-α) which additionally activates keratinocytes and keeps them in an activated state (5). Activation of keratinocytes causes them to proliferate, migrate and secrete additional cytokines. GM-CSF, granulocyte–macrophage colony-stimulating factor; TGF, transforming growth factor.

Figure 2.12

T-lymphocyte activation by (a) antigen and (b) superantigen. When antigen has been processed it is presented on the surface of the Langerhans cell in association with major histocompatibility complex (MHC) Class II. The complex formation that takes place between the antigen, MHC Class II and T-cell receptor (TCR) provides signal 1, which is enhanced by the coupling of CD4 with the MHC molecule. A second signal for T-cell activation is provided by the interaction between the co-stimulatory molecules CD28 (T cell) and B7 (Langerhans cell). CD2/LFA-3 and LFA-1/ICAM-1 adhesion augment the response to signals 1 and 2. Superantigen interacts with the TCR Vβ and MHC Class II without processing, binding outside the normal antigen binding site. Activated T cells secrete many cytokines, including IL-1, IL-8 and γ-interferon, which promote inflammation (Figure 2.13).

Figure 2.13

Characteristics of Th1, Th2 and Th17 responses.

Figure 2.14

Urticaria: an immediate (type I) hypersensitivity reaction.

Figure 2.15

Bullous pemphigoid: a humoral cytotoxic (type II) reaction against a basement membrane zone antigen.

Figure 2.16

Immune complex-mediated vasculitis (type III reaction).

Figure 2.17

Induction phase of allergic contact dermatitis (type IV) reaction.

Figure 2.18

Elicitation phase of allergic contact dermatitis (type IV) reaction.

Chapter 3

Figure 3.1

The typical distribution of some common skin conditions.

Figure 3.2

Terminology of skin lesions.

Figure 3.3

Surface contours of papules.

Figure 3.4

Configuration of lesions.

Figure 3.5

Dermatoscopic appearance of a malignant melanoma.

Figure 3.6

Preparing a skin scraping for microscopy by adding potassium hydroxide (KOH) from a pipette.

Figure 3.7

Fungal hyphae in a KOH preparation. The polygonal shadows in the background are horny layer cells.

Figure 3.8

Patch testing equipment. Syringes contain commercially prepared antigens, to be applied in aluminium cups.

Figure 3.9

A strong positive reaction to a rubber additive.

Figure 3.10

Prick testing: many positive results in an atopic individual.

Figure 3.11

Incision biopsy. This should include adjacent normal skin.

Figure 3.12

Steps in taking a punch biopsy.

Figure 3.13

Direct immunofluorescence detects antibodies in a patient's skin. Here immunoglobulin G (IgG) antibodies are detected by staining with a fluorescent dye attached to antihuman IgG.

Figure 3.14

Indirect immunofluorescence detects antibodies in a patient's serum. There are two steps. (1) Antibodies in this serum are made to bind to antigens in a section of normal skin. (2) Antibody raised against human immunoglobulin, conjugated with a fluorescent dye can then be used to stain these bound antibodies (as in the direct immunofluorescence test).

Chapter 4

Figure 4.1

Ichthyosis: large rather dark scales suggest recessive X-linked ichthyosis.

Figure 4.2

The typical yellow–brown greasy papules of Darier's disease.

Figure 4.3

Extensive Darier's disease, in this case made worse by sun exposure.

Figure 4.4

The nail in Darier's disease. One or more longitudinal pale or pink stripes run over the lunule to the free margin where they end in a triangular nick.

Figure 4.5

Tylosis.

Figure 4.6

Keratoderma climactericum – thickly keratotic skin, especially around the heels. Painful fissures are a problem.

Chapter 5

Figure 5.1

The Köbner phenomenon seen after a recent thoracotomy operation.

Figure 5.2

Histology of psoriasis (right) compared with normal skin (left).

Figure 5.3

Psoriasis: extensive plaque psoriasis.

Figure 5.4

Psoriasis favours the extensor aspects of the knees and elbows.

Figure 5.5

Guttate psoriasis.

Figure 5.6

Untreated severe and extensive scalp psoriasis.

Figure 5.7

Thimble-like pitting of nails with onycholysis.

Figure 5.8

Onycholysis.

Figure 5.9

Sharply defined glistening erythematous patches of flexural psoriasis.

Figure 5.10

Pustular psoriasis of the sole.

Figure 5.11

A closer view of pustules on the sole.

Figure 5.12

An irritant napkin rash now turning into napkin psoriasis.

Figure 5.13

Erythrodermic psoriasis.

Figure 5.14

Fixed flexion deformity of distal interphalangeal joints following arthropathy.

Figure 5.15

Rheumatoid-like changes associated with severe psoriasis of hands.

Figure 5.16

Unstable psoriasis following long-term use of a potent topical steroid.

Figure 5.17

Ultraviolet radiation therapy.

Figure 5.18

Therapeutic targets of biological treatments.

Chapter 6

Figure 6.1

The herald plaque of pityriasis rosea is usually on the trunk and is larger than the other lesions. Its annular configuration is shown well here.

Figure 6.2

An extensive pityriasis rosea showing a ‘fir tree’ distribution on the back.

Figure 6.3

Shiny flat-topped papules of lichen planus. Note the Wickham's striae.

Figure 6.4

Lichen planus: classic white lacy network lying on the buccal mucosa.

Figure 6.5

Lichen planus: striking Köbner effect on the forearm.

Figure 6.6

The thickened purplish lesions characteristic of hypertrophic lichen planus on the shins.

Figure 6.7

Histology of lichen planus.

Figure 6.8

Pityriasis rubra pilaris. Note the red plugged follicles, seen even in the ‘spared’ areas.

Figure 6.9

A bizarre eruption: its persistence and variable colour suggested a prelymphomatous eruption. Biopsy confirmed this.

Chapter 7

Figure 7.1

The sequence of histological events in eczema.

Figure 7.2

Acute vesicular contact eczema of the hand.

Figure 7.3

Vesicular and crusted contact eczema of the face (cosmetic allergy).

Figure 7.4

Lichenification of the wrists – note also the increased skin markings on the palms (atopic palms).

Figure 7.5

Stretch marks following the use of too potent topical steroids to the groin.

Figure 7.6

Licking the lips as a nervous habit has caused this characteristic pattern of dry fissured irritant eczema.

Figure 7.7

Typical chronic hand eczema – irritants have played a part here.

Figure 7.8

Contact eczema caused by allergy to nickel in a jean stud.

Figure 7.9

Dry fissured eczema of the fingertips caused by handling garlic.

Figure 7.10

Assembly workers in an electronic factory – potential victims of industrial dermatitis. (Dr P.K. Buxton. Reproduced with permission of Dr P.K. Buxton.)

Figure 7.11

The pattern of atopic eczema varies with age. It may clear at any stage.

Figure 7.12

Atopic eczema in a child: worse around the eyes due to rubbing. (Dr Olivia Schofield. Reproduced with permission of Dr Olivia Schofield.)

Figure 7.13

Chronic excoriated atopic eczema behind the knees.

Figure 7.14

Trivial scratching has led to striking white dermographism.

Figure 7.15

Facial eczema in a young boy worsening recently. Crusting on the cheeks and upper lip points to possible bacterial superinfection. (Dr Olivia Schofield. Reproduced with permission of Dr Olivia Schofield.)

Figure 7.16

Infected facial eczema – herpes simplex was isolated.

Figure 7.17

Protective tubular gauze dressings being applied over a topical steroid ointment.

Figure 7.18

Areas most often affected by seborrhoeic eczema.

Figure 7.19

Dry scaly seborrhoeic eczema of the ear.

Figure 7.20

Active seborrhoeic eczema of the face.

Figure 7.21

Typical presternal patch of seborrhoeic eczema.

Figure 7.22

Infantile seborrhoeic eczema.

Figure 7.23

Vesicular and weeping patch of discoid eczema.

Figure 7.24

Pompholyx vesicles along the side of a finger.

Figure 7.25

Chronic gravitational eczema, perhaps with a superimposed contact dermatitis from a local medication.

Figure 7.26

Asteatotic eczema with network of fine fissures in the stratum corneum.

Figure 7.27

It is often hard to tell palmar lichen simplex from hyperkeratotic fissured eczema, as shown here.

Figure 7.28

The shiny skin and fissures of juvenile plantar dermatosis.

Figure 7.29

Irritant napkin erythema with a hint of sparing of the skin folds.

Chapter 8

Figure 8.1

Ways in which a mast cell can be degranulated and the ensuing reaction.

Figure 8.2

Typical small transient wheals of cholinergic urticaria – in this case triggered by exercise.

Figure 8.3

Dermographism: a frenzy of scratching by an already dermographic individual led to this dramatic appearance.

Figure 8.4

A classic wheal.

Figure 8.5

Severe and acute urticaria caused by penicillin allergy.

Figure 8.6

Angioedema of the upper lip.

Figure 8.7

A massive urticarial reaction to a wasp sting.

Figure 8.8

Erythema multiforme: bullous and target lesions occurring in a favourite site.

Figure 8.9

Erythema multiforme major. The eyelids were also severely involved.

Figure 8.10

Erythema nodosum: large painful dusky plaques on the shins. Always investigate this important reaction pattern (see text).

Figure 8.11

Pathogenesis of vasculitis.

Figure 8.12

The three P's of cutaneous small vessel vasculitis.

Figure 8.13

The palpable purpuric lesions of cutaneous small vessel vasculitis.

Figure 8.14

Urticarial vasculitis: a combination of urticaria and bruising.

Figure 8.15

Clinical features of polyarteritis nodosa.

Chapter 9

Figure 9.1

The differential diagnosis of bullous diseases based on the histological location of the blister.

Figure 9.2

Pemphigus vulgaris: widespread erosions that have followed blisters.

Figure 9.3

Painful sloughy mouth ulcers in pemphigus vulgaris.

Figure 9.4

Pemphigus vegetans in the axilla, some intact blisters can be seen.

Figure 9.5

Immunofluorescence (red) in bullous diseases.

Figure 9.6

Numerous large tense blisters in an elderly person suggest pemphigoid.

Figure 9.7

Indirect immunofluorescence using serum from a patient with pemphigoid, showing basement zone immunofluorescence.

Figure 9.8

Long-standing mucous membrane pemphigoid. Adhesions are now forming between the upper and lower eyelids.

Figure 9.9

The typical small tense grouped itchy blisters of dermatitis herpetiformis.

Figure 9.10

The itchy blisters of dermatitis herpetiformis favour the points of the elbows and knees, where they are quickly destroyed by scratching.

Figure 9.11

The burn-like appearance of toxic epidermal necrolysis.

Figure 9.12

Levels of blister formation in epidermolysis bullosa at the dermo-epidermal junction.

Figure 9.13

Junctional epidermolysis bullosa: minor trauma has caused large blisters and erosions which will heal slowly or not at all.

Figure 9.14

Recessive dystrophic epidermolysis bullosa: note large blood-filled blister. Scarring has led to fixed deformity of the fingers and loss of nails.

Chapter 10

Figure 10.1

In systemic lupus erythematosus (SLE) (left) the eruption is often just an erythema, sometimes transient, but occupying most of the ‘butterfly’ area with sparing of the nasolabial fold. In discoid LE (right) the fixed scaling and scarring plaques may occur in the butterfly area (dotted line), but can occur outside it too.

Figure 10.2

Erythema in the butterfly area, suggestive of SLE.

Figure 10.3

Red scaly fixed plaques of discoid lupus erythematosus (LE). This degree of scaling is not uncommon in the active stage. Follicular plugging is seen on the nose.

Figure 10.4

Discoid LE of the scalp leading to permanent hair loss. Note the marked follicular plugging.

Figure 10.5

The histology of discoid LE.

Figure 10.6

Acute dermatomyositis: oedematous purple face with erythema on presternal area. Severe progressive muscle weakness, but no underlying tumour was found.

Figure 10.7

Erythema and telangiectasia of the nail folds are important clues to systemic connective tissue disorders. This patient has dermatomyositis. Note Gottron's papules over the knuckles.

Figure 10.8

Systemic sclerosis: radial furrowing around the mouth.

Figure 10.9

Mat-like telangiectasia seen in a patient with systemic sclerosis.

Figure 10.10

Signs of systemic sclerosis.

Figure 10.11

Loss of fingertip pulp, and extrusion of chalky material.

Figure 10.12

Morphoea. Pale indurated plaques on the arm, showing a purplish rim.

Figure 10.13

Morphoea (en coup de sabre type) on the forehead. In a young child this can lead to facial hemiatrophy.

Figure 10.14

Lichen sclerosus. Follicular hyperkeratosis differentiates this from morphoea.

Chapter 11

Figure 11.1

The typical purplish swellings of chilblains.

Figure 11.2

Erythema ab igne: this patient persisted in sitting too close to an open fire and burned herself.

Figure 11.3

The metabolism of ethanol.

Figure 11.4

Digital gangrene. In this case caused by frostbite.

Figure 11.5

A deep pressure sore on the buttock.

Figure 11.6

The direction of blood flow in normal leg veins.

Figure 11.7

Factors causing venous leg ulceration.

Figure 11.8

Irregular areas of whitish scarring and dilated capillary loops – the changes of atrophic blanche.

Figure 11.9

Large venous ulcer overlying the medial malleolus.

Figure 11.10

Chronic ulcer failing to respond to treatment. Biopsy, taken from rolled edge, excluded malignant change.

Figure 11.11

Large, shallow and recalcitrant ulcer complicating rheumatoid arthritis.

Figure 11.12

This ulcer on the foot was not caused by venous insufficiency but cryoglobulins were detected.

Figure 11.13

Clean healing ulcer. Weekly dressing would be suitable.

Figure 11.14

Infected ulcer with sloughing. Tendon visible at bottom of figure. Hospital admission and frequent dressings needed to save leg.

Figure 11.15

Typical purpura, which is not abolished by pressure.

Figure 11.16

This gingery colour is typical of haemosiderin rather than melanin. It is caused by capillary fragility.

Chapter 12

Figure 12.1

Factors causing acne.

Figure 12.2

The seborrhoea, comedones and scattered inflammatory papules of teenage acne.

Figure 12.3

Prominent and inflamed cysts are the main features here.

Figure 12.4

Conglobate acne with inflammatory nodules, pustulocystic lesions and depressed scars.

Figure 12.5

Late-onset acne in a woman. Often localized to the chin.

Figure 12.6

Papulopustular lesions in an odd distribution. The patient played the violin (‘fiddler's neck’).

Figure 12.7

A group of open comedones (blackheads) following the use of a greasy cosmetic.

Figure 12.8

Steroid-induced acne in a seriously ill patient.

Figure 12.9

A successful systemic treatment of acne – the picture tells its own story.

Figure 12.10

Acne scarring: worth treating a test area with a resurfacing laser.

Figure 12.11

Typical rosacea with papules and pustules on a background of erythema. Note the patient also has a patch of scaly seborrhoeic eczema on his brow.

Figure 12.12

Marked rhinophyma.

Figure 12.13

A peri-oral dermatitis following withdrawal of the potent topical steroid that had been wrongly used to treat seborrhoeic eczema.

Figure 12.14

The result of the prolonged use of potent topical steroids for rosacea. Note the extreme telangiectasia.

Figure 12.15

Severe palmar hyperhidrosis demanding treatment.

Chapter 13

Figure 13.1

Anatomy of the hair follicle.

Figure 13.2

The hair cycle.

Figure 13.3

An average scalp.

Figure 13.4

The characteristic uninflamed patches of alopecia areata.

Figure 13.5

Exclamation-mark hairs: pathognomonic of alopecia areata.

Figure 13.6

An exclamation-mark hair.

Figure 13.7

Regrowth within a patch of alopecia areata after a triamcinolone injection.

Figure 13.8

A trial of diphencyprone to one side of the scalp caused some regrowth.

Figure 13.9

Variations on male-pattern baldness.

Figure 13.10

Androgenetic alopecia beginning in the frontal area.

Figure 13.11

Traction alopecia. The rollers she thought would help to disguise her thin hair actually made it worse.

Figure 13.12

Diffuse hair loss causing much anxiety.

Figure 13.13

The cone-shaped incisors of hypohidrotic ectodermal dysplasia.

Figure 13.14

Moderate hirsutism caused by polycystic ovaries.

Figure 13.15

Hypertrichosis in a young man of Mediterranean extraction.

Figure 13.16

An approach to hirsutism. CT, computed tomography; FSH, follicle stimulating hormone; LH, luteinizing hormone.

Figure 13.17

A typical Becker's naevus with marked localized hypertrichosis within a patch of hyperpigmentation.

Figure 13.18

The nail and nail bed.

Figure 13.19

Gross splinter haemorrhages caused by trauma.

Figure 13.20

A subungual haematoma of the big toe. Although there was no history of trauma we were happy to watch this grow out over 6 months as the appearance was sudden, the colour was right and the nail folds showed no pigment.

Figure 13.21

Onychogryphosis.

Figure 13.22

Nail plate abnormalities.

Figure 13.23

In this case severe clubbing was accompanied by hypertrophic pulmonary osteoarthropathy.

Figure 13.24

Clubbing.

Figure 13.25

Other nail changes.

Figure 13.26

The curved slow-growing greenish-yellow nails of the yellow nail syndrome.

Figure 13.27

Large tortuous capillary loops of the proximal nail fold signal the presence of a connective tissue disorder.

Figure 13.28

Paronychia with secondary nail ridging.

Figure 13.29

Myxoid cyst creating a groove in the nail.

Figure 13.30

Black hairy tongue.

Figure 13.31

Geographic tongue.

Figure 13.32

Aphthous ulcer of the labial mucosa.

Figure 13.33

Fordyce spots are ectopic sebaceous glands.

Figure 13.34

Venous lake.

Figure 13.35

Squamous cell carcinoma in a heavy smoker.

Figure 13.36

White lace-like appearance of vulval lichen planus.

Figure 13.37

Lichen sclerosus of the foreskin, carrying the risk of causing phimosis.

Chapter 14

Figure 14.1

Post-inflammatory hyperpigmentation. Inflammation often stimulates pigment cells to produce excessive melanin, so that previously inflamed areas are marked long afterwards with dark patches.

Figure 14.2

Vitiligo. Note the complete loss of pigment and the mirror-like symmetry.

Figure 14.3

Dermatosis papulosa nigra. These small facial seborrhoeic keratoses commonly occur on the faces of Africans. Removing them may leave unsatisfactory white scars.

Figure 14.4

Vitiligo. If just on the hands, it may have been set off by depigmenting chemicals.

Figure 14.5

Vitiligo. The pigmented macules in the porcelain-white patches are areas where pigment cells have migrated to the skin surface from hair follicles. Phototherapy regimens work by encouraging this.

Figure 14.6

Subungual melanoma. The tumour is in the proximal nail fold and has caused a longitudinal band of pigment and a groove in the nail plate. Note the pigmentation of the proximal nail fold (positive Hutchinson's sign).

Figure 14.7

Tinea capitis. This is the seborrhoeic form where inflammation is slight and hair loss and scaling prevail. Culture scale and short hairs for fungus.

Figure 14.8

Pseudofolliculitis barbae (shaving bumps). These are caused by ingrown hairs.

Figure 14.9

Traction alopecia. The tight braids have caused hair loss.

Figure 14.10

Keloids. These arose after ears were pierced for jewelry.

Figure 14.11

Post-surgical keloid. Small keloids even developed where the skin was pierced by sutures used to close the excision site.

Chapter 15

Figure 15.1

Mongolian spot.

Figure 15.2

Lichen sclerosus.

Figure 15.3

Adolescent striae.

Figure 15.4

Polymorphic eruption of pregnancy with stretch marks. Widespread urticated papules.

Figure 15.5

Cosmetic changes of skin ageing.

Chapter 16

Figure 16.1

Pitted keratolysis of the heel.

Figure 16.2

Impetigo on an uncommon site showing erosions, crusting and rupture blisters.

Figure 16.3

Chronic furunculosis.

Figure 16.4

Staphylococcal scalded skin syndrome.

Figure 16.5

Erysipelas – note sharp spreading edge, here demarcated with a ballpoint pen.

Figure 16.6

The stages of syphilis.

Figure 16.7

A tick bite was followed by erythema migrans.

Figure 16.8

A plaque with the brownish tinge characteristic of lupus vulgaris. Diascopy was positive.

Figure 16.9

The spectrum of leprosy: tuberculoid to lepromatous.

Figure 16.10

Tuberculoid leprosy: subtle depigmentation with a palpable erythematous rim at the upper edge.

Figure 16.11

The ‘leonine’ facies of lepromatous leprosy.

Figure 16.12

Tuberculoid and lepromatous leprosy.

Figure 16.13

Type 1 reversal reaction. The posterior auricular nerve is grossly swollen.

Figure 16.14

Dead tropical fish picked out of the tank by the patient shown in Figure 16.15.

Figure 16.15

The sporotrichoid spread of an atypical mycobacterial infection.

Figure 16.16

Leishmaniasis acquired in the Middle East.

Figure 16.17

Viral warts – variations on the theme.

Figure 16.18

Typical common warts on the fingers.

Figure 16.19

Multiple hand warts in a fishmonger.

Figure 16.20

Solitary plantar wart on the heel. (Dr E.C. Benton. Reproduced with permission of Dr E.C. Benton.)

Figure 16.21

Group of warts under the forefoot pared to show mosaic pattern.

Figure 16.22

Plane warts resolving with inflammation.

Figure 16.23

Multiple penile warts in an immunosuppressed patient.

Figure 16.24

Spontaneous resolution of a group of plantar warts. The blackness is caused by capillary thrombosis.

Figure 16.25

A wart treated with cryotherapy: area includes a small frozen halo of normal surrounding skin.

Figure 16.26

Multiple scars following the injudicious surgical treatment of warts.

Figure 16.27

Zoster–varicella relationships.

Figure 16.28

Herpes zoster of the left ophthalmic division of the trigeminal nerve. No nasociliary involvement (see text); this is reassuring.

Figure 16.29

The grouped vesicles of herpes simplex, here provoked by sunlight. Those in the lower group are beginning to crust.

Figure 16.30

An umbilicus surrounded by umbilicated papules of molluscum contagiosum.

Figure 16.31

The pseudopustular nodule of orf.

Figure 16.32

Disseminated Kaposi's sarcoma in AIDS.

Figure 16.33

Kaposi's sarcoma in AIDS.

Figure 16.34

Kaposi's sarcoma of hard palate, anterior fauces and uvula in AIDS.

Figure 16.35

Seborrhoeic dermatitis (otitis externa) and seborrhoeic folliculitis in HIV disease.

Figure 16.36

Hairy leucoplakia on the side of the tongue.

Figure 16.37

The typical vesicles of hand, foot and mouth disease.

Figure 16.38

Tinea pedis. Scaly area spreading to the sole from the toe webs.

Figure 16.39

Powdery scaling, most obvious in the skin creases, caused by a

Trychophyton rubrum

infection.

Figure 16.40

Chronic tinea of the big toe nail. Starting distally, the thickness and discoloration are spreading proximally.

Figure 16.41

A very gross example of tinea of the groin. The

T. rubrum

infection has spread on to the abdomen and thighs, aided by the use of topical steroids.

Figure 16.42

Animal ringworm of the beard area showing boggy inamed swellings (kerion).

Figure 16.43

Animal ringworm of a child's scalp: not truly a kerion as flat and non-pustular.

Figure 16.44

Tinea incognito. Topical steroid applications have thinned the skin and altered much of the morphology. A recognizable active spreading edge is still visible.

Figure 16.45

Factors predisposing to the different types of candidiasis.

Figure 16.46

Sites susceptible to

Candida

infection.

Figure 16.47

Candidal angular stomatitis associated with severe candidiasis of the tongue.

Figure 16.48

Pink circinate areas with only a little scaling. Consider Reiter's syndrome or candidiasis.

Figure 16.49

Pityriasis versicolor: fawn areas stand out against the untanned background.

Figure 16.50

This patient's holiday was spoilt by versicolor ruining her expensive tan.

Chapter 17

Figure 17.1

This woman had acquired a head louse infection from her grandchild.

Figure 17.2

Pediculosis pubis. Numerous eggs (nits) can be seen on the plucked pubic hairs.

Figure 17.3

Florid insect bites on the leg. Note the tendency of the lesions to lie in lines and groups.

Figure 17.4

The adult female acarus (scabies mite).

Figure 17.5

Typical burrows seen on the side of the thumb.

Figure 17.6

The characteristic plantar lesions of scabies in infancy.

Figure 17.7

Common sites of burrows in scabies.

Figure 17.8

Unmistakable rubbery nodules on the penis, diagnostic of scabies.

Figure 17.9

Scabies with bacterial superinfection.

Figure 17.10

The treatment of scabies.

Figure 17.11

Larva migrans – a red serpiginous line on the instep.

Chapter 18

Figure 18.1

Skin disorders and the wavelengths that cause them.

Figure 18.2

The balance between the benefits and drawbacks of sun exposure.

Figure 18.3

Peeling after acute sunburn. This doctor's son should have known better.

Figure 18.4

Extreme photosensitivity of a patient taking griseofulvin. Note sparing of the area covered by the watch strap and ring.

Figure 18.5

Cow parsley contains psoralens and is a common cause of photodermatitis.

Figure 18.6

Severe bullous eruption in areas in contact with giant hogweed (contains psoralens) and then exposed to sunlight (phytophotodermatitis).

Figure 18.7

Features distinguishing airborne allergy from photosensitivity.

Figure 18.8

Polymorphic light eruption: eczematous plaques on the face of a sad freckly boy. Persists throughout the summer but fades in the winter.

Figure 18.9

Thin skin on the back of the hand. The whitish areas are stellate pseudoscars, the skin having never been broken. The pseudoscars follow the dispersion of senile (Batemen's) purpura.

Figure 18.10

Solar elastosis is a sign of photoageing.

Chapter 19

Figure 19.1

The control of melanogenesis. Melanocortin 1 receptor (MC1R) activity is both constitutive and rate limiting when promoting melanogenesis, via cyclic adenosine monophosphate (cAMP) production and tyrosinase stimulation. The MC1R is activated by ligands such as α-melanocyte-stimulating hormone (α-MSH) and other pituitary peptides. In the absence of such ligands or the MC1R itself (knockout animals), and with loss-of-function mutations of the MC1R, phaeomelanin is produced. The precise mechanism by which ultraviolet radiation stimulates melanogenesis remains uncertain.

Figure 19.2

The mechanisms involved in some types of hypopigmentation.

Figure 19.3

Oculocutaneous albinism. An albino baby born to a normally pigmented African family (autosomal recessive inheritance).

Figure 19.4

Striking patchy vitiligo on the knees.

Figure 19.5

Vitiligo: patchy repigmentation is caused by the migration of melanocytes from the depths of the hair follicles.

Figure 19.6

Pityriasis alba.

Figure 19.7

The mechanisms of some types of hyperpigmentation.

Figure 19.8

Histology of a freckle and a lentigo.

Figure 19.9

Melanotic macule of the lip: slow to evolve and benign, as suggested by its even colour and sharp margin.

Figure 19.10

Senile lentigines on the back of an elderly hand (

liver spots

). Note accompanying atrophy.

Figure 19.11

A simple lentigo showing a sharp edge and an even distribution of pigment.

Figure 19.12

Profuse lentigines on and around the lips in the Peutz–Jeghers syndrome.

Figure 19.13

Chloasma worsened by sun exposure.

Figure 19.14

A drop of psoralen-containing perfume on the chest photosensitized this pendant-shaped area. It became pigmented after exposure to the sun.

Chapter 20

Figure 20.1

This family lived in the tropics. No prizes for guessing which of them avoided the sun.

Figure 20.2

An eye-catching and effective way of teaching the public how to look at their moles. A pamphlet produced by the Cancer Research Campaign in the United Kingdom.

Figure 20.3

These Scottish schoolchildren attending an Australian school were surprised to find that wide-brimmed sun protective hats were a compulsory part of the school uniform. These are fashionable after several clever campaigns, and the ‘no hat, no play’ rule has become an accepted way of life.

Figure 20.4

Typical multiple seborrhoeic warts on the shoulder. Each individual lesion might look worryingly like a malignant melanoma but, in the numbers seen here, the lesions must be benign.

Figure 20.5

Numerous unsightly seborrhoeic warts of the face.

Figure 20.6

Dermatosis papulosa nigra.

Figure 20.7

Histology of a seborrhoeic keratosis.

Figure 20.8

Numerous axillary skin tags.

Figure 20.9

Linear warty epidermal naevus.

Figure 20.10

Types of acquired melanocytic naevi.

Figure 20.11

Congenital melanocytic naevus.

Figure 20.12

A large hairy congenital melanocytic naevus. (Dr Auf Qaba, St John's Hospital, Livingstone. Reproduced with permission of Dr Auf Qaba.)

Figure 20.13

Junctional melanocytic naevus.

Figure 20.14

Compound melanocytic naevus. No recent change.

Figure 20.15

Intradermal melanocytic naevus with numerous shaved hairs.

Figure 20.16

Spitz naevus.

Figure 20.17

The blue ink matches the blue naevus.

Figure 20.18

Atypical moles in a 12-year-old girl. Note the malignant melanoma lying between the scapulae.

Figure 20.19

Halo naevus.

Figure 20.20

Malignant melanoma developing within a congenital melanocytic naevus.

Figure 20.21

Sebaceous naevus of the scalp.

Figure 20.22

Milia.

Figure 20.23

Chondrodermatitis nodularis helicis. The inflammation of the underlying cartilage is painful enough to wake up patients repeatedly at night.

Figure 20.24

Typical rough-surfaced actinic keratoses on the scalp.

Figure 20.25

Cutaneous horn with a bulbous fleshy base.

Figure 20.26

Early basal cell carcinoma with rolled opalescent edge and central crusting.

Figure 20.27

Basal cell carcinoma with marked telangiectasia and ulceration.

Figure 20.28

Cicatricial basal cell carcinoma.

Figure 20.29

Persistent scaly plaque – the whipcord edge gives away the diagnosis of a superficial basal cell carcinoma.

Figure 20.30

A pigmented tumour on the temple. The opalescent rim points to the diagnosis of a basal cell carcinoma.

Figure 20.31

A grossly neglected basal cell carcinoma already invading underlying bone.

Figure 20.32

Histology of nodular basal cell carcinoma.

Figure 20.33

Squamous cell carcinoma. Not a venous ulcer – too high up the leg, too raised and no signs of venous insufficiency.

Figure 20.34

The histology of a squamous cell carcinoma.

Figure 20.35

Intraepidermal carcinoma: a slowly expanding warty plaque. Note the reniform projections and notches so suggestive of an

in situ

malignancy.

Figure 20.36

Keratoacanthoma with its epidermal shoulders and central plug of keratin.

Figure 20.37

Histology of keratoacanthoma.

Figure 20.38

Radial intraepidermal growth phase of melanoma (1 and 2) precedes vertical and invasive dermal growth phase (3).

Figure 20.39

This elderly patient, her friends and family doctor, had ignored for too long the slowly spreading macule of a lentigo maligna: now she has a frankly invasive melanoma within it (the darker area).

Figure 20.40

Superficial spreading melanoma of the jawline. Small, and still curable at this stage.

Figure 20.41

This shows the hallmarks of a malignant melanoma with its asymmetry, irregular borders and variations in colour. The pink amelanotic nodule signifies deep dermal invasion.

Figure 20.42

A nodular malignant melanoma: just beginning to ulcerate.

Figure 20.43

An amelanotic malignant melanoma on the heel of an elderly person. Always obtain histology even if you think it is just a pyogenic granuloma or an atypical wart.

Figure 20.44

Histology of the different types of melanoma.

Figure 20.45

Schematic representation of Breslow's and Clark's methods of microstaging malignant melanoma.

Figure 20.46

Talon noir.

Figure 20.47

Such a wide excision and unsightly graft is no longer acceptable for a thin good-prognosis melanoma. Note the many atypical moles.

Figure 20.48

Be alert to the possibility of Paget's disease if a red plaque affects only one nipple, and alters its normal architecture.

Figure 20.49

Lifelong capillary malformation of the cheek showing no tendency to resolve. Note port-wine appearance of the upper pole, contrasting with the nodular elements elsewhere.

Figure 20.50

Port-wine stain of the right cheek. No neurological problems in this patient.

Figure 20.51

Classic strawberry naevus, occurred and enlarged rapidly shortly after birth. (Dr M.J. Tidman, The Royal Infirmary of Edinburgh, Edinburgh, UK. Reproduced with permission of Dr M.J. Tidman.)

Figure 20.52

The same strawberry naevus as shown in Figure 20.51, showing the whitening of the surface which is a sign of spontaneous remission. (Dr M.J. Tidman, The Royal Infirmary of Edinburgh, Edinburgh, UK. Reproduced with permission of Dr M.J. Tidman.)

Figure 20.53

Campbell de Morgan spots (cherry angiomas) of the chest.

Figure 20.54

Pyogenic granuloma of the palm: soggy after elastoplast dressing and bleeding easily.

Figure 20.55

A 0.5-cm diameter dermatofibroma. Typically, these lesions feel larger than they look. Its depressed surface became more obvious when the surrounding skin was pinched.

Figure 20.56

Multiple lipomas.

Figure 20.57

Juvenile type of mastocytosis.

Figure 20.58

Poikiloderma vasculare atrophicans may be a precursor of the tumour stage of cutaneous T-cell lymphoma.

Figure 20.59

An ulcerated tumour of mycosis fungoides against a background of plaques.

Figure 20.60

Immunopathology showed that these nodules were caused by a B-cell lymphoma. (Dr E.C. Benton. Reproduced with permission of Dr E.C. Benton.)

Figure 20.61

Several scalp metastases arising from a breast carcinoma.

Chapter 21

Figure 21.1

Acanthosis nigricans – in this case caused by obesity.

Figure 21.2

Acute febrile neutrophilic dermatosis (Sweet's syndrome).

Figure 21.3

Necrobiosis lipoidica: shiny yellowish patch with marked telangiectasia.

Figure 21.4

Granuloma annulare.

Figure 21.5

Diabetic cheiropathy – the prayer sign. Poor finger apposition in the diabetic hand (on the left) compared with the normal one (on the right).

Figure 21.6

Sarcoidosis: plum-coloured plaques on the cheek.

Figure 21.7

Solitary spider naevus showing the central feeding vessel. No underlying liver disease in this case.

Figure 21.8

Porphyria cutanea tarda.

Figure 21.9

Blisters, milia and erosions on the side of a finger.

Figure 21.10

Porphyria cutanea tarda. Coral-red fluorescence of urine under Wood's light denoting excessive uroporphyrins (chloroform extraction).

Figure 21.11

Xanthelasma: flat yellow lesions on the eyelids, often with normal blood lipids.

Figure 21.12

Tuberous xanthoma on the points of the elbows – a mixture of nodules and papules.

Figure 21.13

Plane xanthoma with yellow palmar creases.

Figure 21.14

An example of the butterfly sign. This lady could not reach her upper back but could scratch her skin everywhere else. In other patients, the spared area is shaped more like a butterfly.

Figure 21.15

Pyoderma gangrenosum: a plum-coloured lesion with a typical cribriform appearance.

Figure 21.16

Another manifestation of Crohn's disease: grossly oedematous vulva with interconnecting sinuses. Biopsy at the site arrowed showed a granulomatous histology.

Figure 21.17

This long-standing ulcer was pyoderma gangrenosum secondary to the patient's rheumatoid arthritis. (Dr G.W. Beveridge. Reproduced with permission of Dr G.W. Beveridge.)

Chapter 22

Figure 22.1

Before (a) and after (b) photographs of the effect of botulinum toxin injections on glabella and horizontal forehead frown lines. “X” marks typical injection sites to reduce glabella and forehead rhytids.

Figure 22.2

Before (a) and after (b) photographs showing reduction in nasolabial folds following injection of a hyaluronic acid filler.

Figure 22.3

Before (a), seven days (b), and six months (c) after a 25% TCA peel. Once the post-treatment crusting has settled, there is a reduction in peri-oral wrinkles and signs of epidermal photoaging.

Chapter 23

Figure 23.1

Mind–skin interactions.

Figure 23.2

Delusional infestation – the sequence of events.

Figure 23.3

Obvious dermatitis artefacta: back your own judgement against the patient's here.

Figure 23.4

A lighted cigarette was responsible for this appearance.

Figure 23.5

Dermatitis artefacta: denials of self-trauma did not convince us that this was caused by any other skin disease.

Figure 23.6

Unusually extensive neurotic excoriations.

Figure 23.7

The excoriated nodules of prurigo nodularis.

Chapter 24

Figure 24.1

Neurofibromatosis: one large but benign neurofibroma has ulcerated over the sacrum. Several café au lait patches are visible.

Figure 24.2

Freckling of the axilla and a café au lait patch – both markers of neurofibromatosis.

Figure 24.3

Lisch nodules: best seen with a slit-lamp.

Figure 24.4

Tuberous sclerosis. Adenoma sebaceum, understandably, was referred to the acne clinic.

Figure 24.5

The peri-ungual fibromas of tuberous sclerosis are found in adult patients.

Figure 24.6

Computed tomography scan of a patient with tuberous sclerosis. Modern imaging techniques can sometimes show cortical tubers (white) even when the skin changes are minimal.

Figure 24.7

Xeroderma pigmentosum: obvious freckling on neck. Scars on nose mark the spots where tumours have been removed.

Figure 24.8

The ‘plucked chicken’ appearance of pseudoxanthoma in the antecubital fossa.

Chapter 25

Figure 25.1

Gross striae caused by systemic steroids.

Figure 25.2

Symmetrical erythematous maculopapular rash as a result of ampicillin.

Figure 25.3

Gingival hyperplasia caused by long-term phenytoin treatment.

Figure 25.4

Toxic erythema with urticarial features.

Figure 25.5

The cause, clinical features and treatment of anaphylaxis.

Figure 25.6

Fixed drug eruption – an unusually severe bullous reaction.

Figure 25.7

Acute generalized exanthematous pustulosis precipitated by amoxicillin.

Figure 25.8

Note sparing of skin creases and area shielded by spectacle frames in this patient with photorelated hyperpigmentation from a phenothiazine drug.

Chapter 26

Figure 26.1

Stretch marks behind the knee caused by the topical corticosteroid treatment of atopic eczema.

Figure 26.2

Often attributed to Cushing's disease or to local corticosteroid therapy, but stretch marks across the back are common in normal fast-growing teenagers.

Figure 26.3

The derivation of vehicles.

Figure 26.4

The minimum amount of a cream required in 1 week by an adult applying it twice daily.

Figure 26.5

A fingertip measures about 0.5 g ointment.

Chapter 27

Figure 27.1

An example of a biopsy tray setup with clean gloves.

Figure 27.2

Typical excision tray. Hibiclens is positioned at the top left corner (for prepping the skin), followed by sterile gauze and sterile towel (for draping the surgical area). Surgical instruments include forceps, blade and blade holder, suture scissors and undermining scissors, skin hook, needle driver, haemostat and electrocautery.

Figure 27.3

Skin wrinkle figures are helpful in deciding the direction of wounds following skin surgery. Those performing dermatological surgery should have ready access to them.

Figure 27.4

Suspicious pigmented lesions should be removed with a 2-mm margin marked out in advance.

Figure 27.5

Steps for surgical excision of a melanoma in situ. (a) An fusiform shape is marked with 5-mm margins. (b) Incision is carried perpendicular to the skin down to the subcutaneous fat. (c) The tissue specimen is carefully removed with the help of a fine-toothed forceps. (d) Undermining is carried out with a skin hook to minimize trauma to the epidermis. (e) The dermis is closed with absorbable sutures. (f) The epidermis is reapproximated with subcuticular sutures. (g) Steristrips are placed. (h) Pressure dressing is left in place for 24–48 hours.

Figure 27.6

Liquid nitrogen can be applied through a spray, or with a cotton wool bud direct from a vacuum flask (centre).

Figure 27.7

Two freeze–thaw cycles with liquid nitrogen cleared this actinic keratosis. (Dr R. Dawber, The Churchill Hospital, Oxford, UK. Reproduced with permission of Dr R. Dawber.)

Figure 27.8

Curettage beats excision if a seborrhoeic wart has to be removed. Stretching the skin helps to hold the lesion steady.

Figure 27.9

Types of electrosurgery.

Figure 27.10

An example of Mohs' micrographic surgery for an ill-defined basal cell carcinoma on the forehead near the eyebrow. (a) Initial lesion measured 10 × 8 mm. (b) After four stages of Mohs', the lesion measured 25 × 16 mm. (c) Mohs map showing presence of tumor in red in stage 1–3 with final clearance on stage 4. (d) Reconstruction of the defect with an advancement flap and a skin graft centrally. (e) Final outcome at 6 months.

Figure 27.11

(a) A 90-year-old, unfit for surgery, did well with radiotherapy for this massive basal carcinoma. (b) The reaction was healing well after a few weeks.

Figure 27.12

Radiodermatitis with scarring, telangiectasia and hyperkeratosis.

Figure 27.13

A basal cell carcinoma: (a) showing, by fluorescence (b), selective uptake of 5-aminolaevulinic acid (ALA). (The Photobiology Unit, Ninewells Hospital, Dundee, UK.)

Figure 27.14

Photodynamic therapy of the face with blue light after 2 hours of incubation with ALA. Appropriate safety goggles should be worn by the patient and staff during treatment.

Figure 27.15

(a) Hyperkeratotic Bowen's disease on a finger; (b) treated successfully with photodynamic therapy. This would have been an awkward site for surgery. (The Photobiology Unit, Ninewells Hospital, Dundee, UK.)

Figure 27.16

An example of a port-wine stain treated with a pulsed-dye laser with resultant purpura: (a) prior to treatment; (b) immediately posttreatment; (c) 1 month posttreatment with improvement in the treated area.

Figure 27.17

Many vascular lesions can be treated with the pulsed-dye laser, including angiokeratoma circumscriptum: (a) pretreatment; (b) after four treatments with significant improvement in the area; (c) after six treatments with near resolution.

Figure 27.18

Leucoplakia caused by chronic actinic damage – most suitable for laser resurfacing treatment.

Figure 27.19

Rhinophyma treated with Erb:YAG ablative resurfacing laser: (a) preoperative; (b) partial re-epithelization at 1 week; (c) complete healing at 3 weeks.

Chapter 28

Figure 28.1

Hand-held dermascopes.

Figure 28.2

Physician examining a pigmented lesion using a contact immersion system (a) and cross-polarized light which does not require direct contact (b).

Figure 28.3

Two-step dermoscopic evaluation. BCC, basal cell carcinoma.

Figure 28.4

Typical dermascopic appearance of non-melanocytic lesions. Figures courtesy of Dr. Kelly Nelson, Department of Dermatology, Vanderbilt University, Nashville, Tennessee, USA.

Figure 28.5

(a) Melanoma with asymmetry of colour and structure as well as irregular pigment network. There are pseudopods irregularly distributed at one edge of the lesion (black arrows), blue–black structureless area (white arrow) as well as areas of thin and thickened reticular lines. Blue–white veil can be seen at the centre of the lesion (circle). (b) Another example of a melanoma with asymmetry of multiple colours and structure. There are areas of irregular thickened hyperpigmented lines in a reticular pattern at the periphery. Centrally there is a structureless area of regression with scar-like depigmentation. (c) While this lesion is clinically subtle for a melanoma, it has concerning features on dermoscopic examination including multiple colours, asymmetry of structure and multiple peripheral brown and black dots. This lesion was biopsied and histopathology confirmed the diagnosis of melanoma. Figures courtesy of Dr. Kelly Nelson, Department of Dermatology, Vanderbilt University, Nashville, Tennessee, USA.

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