Dermatology is a medical speciality concerned with diseases affecting skin and associated structures such as hair, nails, and oral and genital mucous membranes. There is often very little exposure to dermatology within your undergraduate medical curriculum. It is wise to plan your time carefully during your placement to ensure that you gain exposure to the common conditions that you are likely to face in your exams. If you are based in a peripheral hospital, you will spend most of your time in general clinics but larger tertiary centres will also have specialist clinics and some may even have a dermatology inpatient ward for acute cases. The significance of dermatology is that an internal disease process can initially or solely manifest as dermatological signs (e.g. autoimmune disorders). Stigma and psychological stress are also important issues to consider.
• Abscess: localized accumulation of pus in a cavity >1 cm.
• Atrophy: thinning of the epidermis and/or dermis.
• Bulla: raised, clear fluid-filled lesion >0.5 cm in diameter.
• Crust: dried exudate containing sebum, blood, bacteria, and debris.
• Erosion: partial epidermal loss, heals without scarring.
• Erythema: blanching reddening of the skin due to local vasodilatation.
• Fissure: a linear crack in the epidermis.
• Lichenification: thickening of the epidermis with exaggerated skin markings due to repeated scratching or rubbing.
• Macule: a flat area of altered skin colour.
• Nodule: solid, raised lesion >0.5 cm in diameter.
• Papule: solid, raised lesion <0.5 cm in diameter.
• Patch: larger flat area of altered colour.
• Petechiae: pinhead-sized areas of purpura.
• Plaque: palpable, raised lesion >0.5cm in diameter.
• Purpura: (non-blanching) due to extravasation of blood into skin, ~2 mm in diameter.
• Pustule: raised lesion containing pus <0.5 cm in diameter.
• Scales: superficial flakes (stratum corneum).
• Telangiectasia: easily visible, blanching superficial blood vessels.
• Ulcer: break in the skin due to loss of the dermis and epidermis, heals with scarring.
• Vesicle: raised, clear fluid-filled lesion <0.5 cm in diameter.
Top tips on useful dermatology image banks
To practice your diagnostic skills in dermatology look at the following resources:
• DermNet Nz (
www.dermnetnz.org)
• Dermatology Image Bank ( www.library.med.utah.edu/kw/derm)
• DermWeb Photo Atlases ( www.dermweb.com/photo_atlas).
The following dermatological conditions are easily seen in any general dermatology clinic.
Rare but you should be aware of this as it often comes up in written exams where you may be given a photo and a brief clinical history.
There are also usually dedicated clinics for patients referred by their GP for suspected skin cancers under the 2-week referral pathway. These clinics are an excellent opportunity for you to see skin lesions at differing stages of progression.
• Ankle–brachial pressure index (ABPI): e.g. for leg ulcers.
• Minor procedures: punch biopsies, excisions, curette and cauterization, cryotherapy.
• Taking a skin swab: from lesions such as vesicles, pustules, ulcers, and mucus membranes for microbial culture/viral PCR detection.
• Taking a skin scraping: using a scalpel/glass slide from scaly lesions in suspected fungal infection and scabies.
• Suturing: practise in the clinical skills lab; there are also useful videos online demonstrating this skill.
Fig. 10.1 Dermatological descriptors. Reproduced with permission from Richard A. Watts et al, Oxford Textbook of Rheumatology 4e, 2013, Oxford University Press.
Fig. 10.2 Skin cancers. Reproduced from the U.S. National Library of Medicine (NLM). Images are in the public domain.
Look out for unique features in the history and descriptions of the lesion which will allow you to diagnose the condition. Treatment often involves variations on a stepwise escalation, beginning with topical steroids eventually 
systemic immunosuppression.
This is a chronic inflammatory skin condition following a relapsing and remitting course. See Fig. 10.3.
Fig. 10.3 Eczema. Reproduced with permission from Warrell, D., Cox, T., Firth, J., Oxford Textbook of Medicine, 2010, Oxford University Press.
The commonest form is the atopic type, which predisposes individuals to other atopic conditions such as asthma, hay fever, and rhinitis and an inherited genetic defect in skin barrier function (loss-of-function variants of the protein filaggrin). Although atopic eczema can affect people of all ages, it primarily affects children and usually resolves during teenage years.
Include infections, allergens (e.g. chemicals, food, dust, and pet fur), sweating, heat, and stress.
Eczema commonly presents as itchy, erythematous dry scaly patches affecting the face and extensor aspects of limbs in infants, and the flexor aspects in children and adults. Acute lesions are erythematous, vesicular, and exudative. Excoriations and lichenification may be seen due to chronic scratching/rubbing.
Avoid known exacerbating factors, use of frequent emollients, soap substitutes, antihistamines, and topical steroids for flares. Topical immunomodulators (e.g. tacrolimus, pimecrolimus) can also be used as steroid-sparing agents. Severe cases may require oral steroids or immunosuppressants such as azathioprine or ciclosporin. Phototherapy (commonly narrow band UVB) can also be used to treat severe cases. Secondary bacterial infection is common resulting in crusted, weepy lesions requiring treatment with antibiotics (e.g. flucloxacillin).
This is a chronic inflammatory skin disease due to hyperproliferation of keratinocytes in the epidermis and infiltration of inflammatory cells. It affects 2% of the population.
There is a genetic component to the disease, although often an environmental precipitating factor exists (e.g. trauma–known as Koebner’s phenomenon, infection, or alcohol).
You are most likely to see chronic symmetrical plaques like well-demarcated, erythematous, scaly, silvery white plaques on the extensor surfaces (knees, elbows, and lower back) and scalp. Gentle removal of scales causes capillary bleeding known as the Auspitz sign. Half of patients have associated nail changes (e.g. pitting, onycholysis) and up to 10% suffer from associated psoriatic arthropathy (see Fig. 10.4).
Fig. 10.4 Psoriasis (Koebner phenomenon). Reproduced with permission from Burge, S. Matin, R., and Wallis, D., Oxford Handbook of Medical Dermatology 2e, 2016, Oxford University Press.
For mild/localized diseases, topical therapies include vitamin D analogues, topical corticosteroids, coal tar preparations, dithranol, topical retinoids, keratolytics, and scalp preparations. Extensive disease may require phototherapy such as narrow band UVB or PUVA (psoralen and UVA). Systemic immunosuppressive treatments (e.g. methotrexate, mycophenolate mofetil) can also be used for severe psoriasis, or in patients with joint involvement also.
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Other forms of psoriasis include guttate (widespread, small plaques typically in a young patient after a streptococcal throat infection), seborrhoeic (overlap of seborrhoeic dermatitis and psoriasis, affecting scalp, face, ears, and chest), flexural (smooth, well-defined patches in body folds), palmoplantar (psoriasis affecting the palms and soles), pustular (generalized or localized to palms and soles), nail psoriasis (onycholysis, pitting, ridging, and discolouration), and erythrodermic.
This is an inflammatory disease of the pilosebaceous follicle which commonly affects teenagers across the face, chest, and upper back.
Caused by a combination of factors including hormones (due to androgen), 
sebum production, bacterial colonization by Propionibacterium acnes, and inflammation. Mild acne includes non-inflammatory lesions such as open and closed comedones (blackheads and whiteheads). More severe acne is associated with inflammatory lesions including papules, pustules, nodules, and cysts which scarring.
Topical treatments for mild acne includes benzoyl peroxide and topical antibiotics (due to antimicrobial properties), and topical retinoids (comedolytic and anti-inflammatory properties).
Oral therapies should be considered for moderate to severe acne such as oral antibiotics, oral contraceptive pill in females (antiandrogens), and oral retinoids (isotretinoin). Isotretinoin should be considered in patients not responding to normal treatments and where scarring is involved.
This is an autoimmune, blistering skin disease usually affecting the older population. It can be localized or widespread, and crops of tense, fluid-filled, itchy blisters occur as a result of antibodies directed against components of the basement membrane (hemidesmosomes, important structural proteins between the epidermis and dermis). Some cases may be preceded by a non-specific, red, itchy rash for weeks/months prior to the blistering. (See Fig. 10.5.)
Fig. 10.5 Bullous pemphigoid. Reproduced with permission from Ramrakha, P., Moore, K., San, A., Oxford Handbook of Acute Medicine 3e, 2010, Oxford University Press.
Is usually confirmed by skin biopsy from a blister and surrounding normal skin.
If only mild and localized disease, very potent topical corticosteroids can be used to the lesions. Otherwise, most patients require immunosuppressive treatment, beginning with oral steroids or if these fail, tetracyclines (e.g. doxycycline, due to its antiinflammatory properties), azathioprine, and methotrexate.
Although this is an uncommon cause of painful skin ulceration, pyoderma gangrenosum often comes up in written exams where you may have a clinical image to look at.
Ulceration can occur at any site, often after minor trauma, but usually affects the lower legs and in those >50 years of age. (See Fig. 10.6.)
Fig. 10.6 Pyoderma gangrenosum. Reproduced with permission from Burge, S. Matin, R., and Wallis, D., Oxford Handbook of Medical Dermatology 2e, 2016, Oxford University Press.
Half of cases are associated with an underlying internal disease including IBD, RA, haematological disorders, chronic active hepatitis, and vasculitis. The initial lesion may be a small pustule, a raised, red lesion, or a blood blister which subsequently breaks down into a rapidly enlarging, painful ulcer. The edge of the ulcer is characteristically purplish in colour with undermined edges.
This is by stepwise immunosuppression.
This is the commonest skin tumour. Slow growing, locally invasive tumour of the epidermal keratinocytes commonly found on sites such as the head and neck. (See Fig. 10.7.)
Fig. 10.7 Basal cell carcinoma. Reproduced with permission from Thomas, W.E.G. et al, Oxford Textbook of Fundamentals of Surgery, 2016, Oxford University Press.
Include UV exposure, fair skin type (see Table 10.1), increasing age, immunosuppression, previous history of skin cancer, and genetic predisposition.
Different morphological types include nodular, superficial, cystic, morphoeic, and pigmented. The most common type of BCC you are most likely to be tested on in your exams is the nodular subtype. This typically presents as a pale papule or nodule with a pearly, rolled edge and surface telangiectasia. Sometimes these may have an ulcerated centre giving rise to the term ‘rodent ulcer’.
Options include surgical excision or radiotherapy. Low-risk small lesions can be treated with cryotherapy or topical treatment (e.g. imiquimod). BCC do not tend to metastasize but may cause local tissue destruction and invasion.
Unlike BCCs, SSCs have the potential to metastasize. SCCs are tumours arising from squamous cells within the epidermis.
Include those listed previously for BCCs with the addition of chronic inflammation (e.g. leg ulcers, wounds) and pre-existing areas of sun damage (solar/actinic keratoses).
As a scaly (keratotic), ill-defined nodule which may ulcerate (see Fig. 10.8). Lesions are often tender.
Fig. 10.8 Squamous cell carcinoma. Reproduced with permission from Thomas, W.E.G. et al, Oxford Textbook of Fundamentals of Surgery, 2016, Oxford University Press.
Surgical excision is the treatment of choice. Radiotherapy can also be used for large, non-resectable tumours. Bowen’s disease is also known as SSC in situ (SCC confined to the epidermis) which can be treated with cryotherapy and topical treatments (e.g. Efudix®, 5-fluoruracil).
Invasive malignant tumour of the epidermal melanocytes which has the potential to metastasize.
Include excessive UV exposure, fair skin type, episodes of severe sun burn during childhood, multiple moles or atypical moles, and family history or previous history of melanoma.
Melanomas are variable in presentation but the ‘ABCDEs’ rule helps us to assess suspicious lesions. The following features are considered:
• Colour irregularity (two or more colours within the lesion).
• Evolution of lesion (change in size, shape, colour).
• Plus symptoms (itching/bleeding).
The different morphological types of melanoma includes superficial spreading melanoma, nodular, acral lentiginous melanoma (common on the palms, soles, nails beds, no clear relation to UV exposure), lentigo maligna melanoma (common on the face in the elderly population, related to long-term cumulative UV exposure).
Trivia
Sunscreens in the UK are labelled with an ‘SPF’ and UVA star system. ‘SPF’ stands for sun protection factor which indicates the level of burn protection against UVB. This usually varies between SPF 6 and 50. The UVA star system varies from 1 star to 5 stars and indicates the percentage of UVA radiation absorbed by the sunscreen compared to UVB. A sunscreen with an SPF of 30 and a UVA rating of 4 or 5 stars is recommended.
Surgical excision is the definitive treatment but radiotherapy can be used in cases where excision is not appropriate.
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• Low risk = <0.76 mm Breslow thickness.
• Medium risk = 0.76–1.5 mm Breslow thickness.
• High risk = >1.5 mm Breslow thickness.
• Stage 1 (T<2 mm Breslow thickness, N0, M0) = 90% 5-year survival.
• Stage 2 (T>2 mm Breslow thickness, N0, M0) = 80% 5-year survival.
Areas of sun-damaged skin from chronic excessive sun exposure. You will find these on sun-exposed areas (scalp, face, backs of hands, lower legs in women). Commonly seen in elderly patients and usually considered harmless with a small risk of them progressing into SCC.
Clinically these lesions are variable in colour but are usually scaly in appearance and rough to touch. They usually cause no symptoms.
Options include cryotherapy, creams (e.g. diclofenac, fluorouracil, or imiquimod), surgery, and photodynamic therapy (using certain wavelengths of light to treat specific areas of damaged skin which have been treated with a photosensitizing cream beforehand).
Cutaneous manifestations of systemic and localized autoimmune disease are not only common but may also be the first presentation of an undiagnosed condition. Some of the common conditions you may encounter in clinic include vitiligo (loss of pigmentation), Henoch–Schönlein purpura (HSP; acute immunoglobulin (Ig)-A-mediated cutaneous vasculitis), scleroderma (e.g. CREST syndrome), and lupus.
Herpes simplex (cold sores) presents with localized blistering and is often recurrent (after triggering its latent state). Triggers include trauma, upper respiratory tract infection (URTI), hormonal imbalance, and stress. Type 1 is usually associated with facial eruptions whereas type 2 results in anogenital herpes. Infectivity lasts for 1–2 weeks. Persistence should also be investigated in high-risk patients (e.g. immunodeficiency). Viral swabs from fresh vesicles can be cultured or PCR used to confirm diagnosis. Antivirals (e.g. aciclovir) may be required to treat severe eruptions.
These form a spectrum of presentations. Urticaria presents as itchy wheals affecting any part of the body. Angio-oedema occurs due to oedema of the deeper structures of the skin (dermis and subcutaneous tissues).
Whilst urticaria is normally uncomplicated, angio-oedema can be life-threatening if swelling of the tongue and lips leads to airway obstruction. Both urticaria and angio-oedema can progress to anaphylaxis which presents with hypotension, bronchospasm, facial oedema, and laryngeal oedema.
Include food, medications, and insect bites.
Antihistamines and corticosteroids can be given, while (IM) adrenaline (epinephrine) is used in cases of anaphylaxis.
You are unlikely to see either of these two very serious conditions, and these patients are often managed in HDU or ITU due to the high risk of multisystem organ failure and death (10% and >30% respectively). SJS is characterized by mucocutaneous necrosis of at least two mucosal sites.
Skin detachment is usually <10% of total body surface area. Drugs or combinations of infections or drugs are the main associations. SJS may have features overlapping with TEN including a prodromal illness (fever, cough, malaise). TEN is usually drug induced and patients are acutely unwell with extensive skin and mucosal necrosis accompanied by systemic toxicity. (See Fig. 10.9.)
Fig. 10.9 Stevens–Johnson syndrome and toxic epidermal necrolysis. Reproduced with permission from Haddad, P., Dursun, S., Deakin, B., Adverse Syndromes and Psychiatric Drugs: A clinical guide, 2004, Oxford University Press.
With features of meningitis such as headache, fever, neck stiffness, along with septicaemia including hypotension, fever, myalgia, and a rash. Rash is typically a non-blanching purpuric rash on the trunk and extremities, which may be preceded by a blanching maculopapular rash. The rash can rapidly progress to ecchymoses, haemorrhagic bullae, and tissue necrosis. (See Fig. 10.10.)
Fig. 10.10 Acute meningococcaemia. Reproduced with permission from Warrell, D., Cox, T., Firth, J., Oxford Textbook of Medicine, 2010, Oxford University Press.
Early recognition is important as acute meningococcaemia can lead to septicaemic shock, disseminated intravascular coagulation (DIC), multiorgan failure, and death.
Suspected cases should be given IV antibiotics (e.g. benzylpenicillin). A LP and CT head should be performed (if signs of confusion, low GCS score, or raised intracranial pressure) but should not delay the first dose of antibiotics. Family members and close contacts should be given prophylactic antibiotics (e.g. rifampicin).
Disproportionate limb pain following an injury should immediately bring to mind a compartment syndrome (see 
pp. 762–763). However, disproportionate pain without any history of an injury and in the context of skin lesions in a systemically unwell patient, should bring necrotizing fasciitis to mind. Skin changes include erythema, blisters, and necrotic skin with crepitus on palpation (subcutaneous emphysema). (See Fig. 10.11.) This may all start with an aggressive cellulitis necrotizing cellulitis and so on.
Fig. 10.11 Necrotizing fasciitis. Reproduced from Late diagnosed necrotizing fasciitis as a cause of multiorgan dysfunction syndrome: A case report. Cases Journal 2008, 1:125. doi:10.1186/1757-1626-1-125. Licensed under the Creative Commons Attribution 2.0 Generic license.
Plain radiography and CT may show soft tissue gas but its absence should not exclude a possible diagnosis.
The infection can spread rapidly through the deep fascia causing secondary tissue necrosis, and is associated with 75% mortality. Half of patients may be postoperative (e.g. abdominal surgery), have a history of poorly controlled diabetes, or malignancy.
Requires extensive surgical debridement (see ‘Debridement and reconstruction’, pp. 742–743).
Are carried out under local anaesthetic (revise the maximum doses for lidocaine, bupivacaine, levobupivacaine, etc.) which can be safely administered and also sites where adrenaline (epinephrine) should be avoided (end-arterial supply as in digits and penis). Lesions are usually removed with a margin of normal skin (depending on the type of lesion). Incisions are usually elliptical and orientated in the same direction as relaxed skin tension lines for cosmesis and reducing wound tension.
Diameter varies from 3 to 8 mm. Usually used to take a small sample of skin under local anaesthetic from an area (e.g. rash).
Using liquid nitrogen to freeze localized skin superficial destruction of the epidermis. Used to treat benign lesions such as viral warts, seborrhoeic keratoses, molluscum contagiosum, actinic keratosis, and low-risk tumours (superficial BCC and Bowen’s disease).
A curette is a sharp instrument used to scrape off skin lesions under local anaesthetic. The wound surface is then cauterized with an electrosurgical unit (diathermy) which stops bleeding and also destroys a thin layer of the epidermis (therefore useful if used to treat low-risk skin cancers). Commonly used to remove benign lesions such as seborrhoeic warts, molluscum contagiosum, viral warts, and low-risk tumours.
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Different areas of the body require different suture thicknesses and time periods for their removal (see Table 10.1).
Table 10.1 Sutures
| Site | Suture | Removal of sutures |
| Face | 4.0/5.0 Ethilon® | 5–7 days |
| Legs and back | 3.0 Ethilon® | 10–14 days |
| Elsewhere | 4.0 Ethilon® | 7–10 days |
Subcuticular sutures can be used in addition to interrupted surface stitches to maintain and add extra support to the wound. Useful in areas normally under tension (e.g. posterior trunk/scapula) where there is a risk of wound dehiscence. Vicryl® is commonly used and absorption is usually complete by 3 months. Methods of achieving haemostasis include applying firm pressure, chemical haemostasis (Driclor®, silver nitrate), sutures, cautery, and ligation (tie off) of vessels.
It is important to learn how to take a basic dermatological history. The following are important aspects to consider when taking a history from a patient with a skin-related problem. Eczema and psoriasis are the most likely conditions you will be tested on.
• Presenting complaint: nature, site, and duration.
• History of presenting compliant: initial appearance, changes in appearance, symptoms such as itching and pain, aggravating and relieving factors, previous and current treatments and their effects, and potential triggers including travel, illness, stress, use of new products. History of sun burn, use of sun beds, and skin type are important for skin lesions such as moles.
• Past medical history: in particular, history of atopy (i.e. asthma, hay fever, and rhinitis), is important in eczema. History of skin cancer/atypical moles if a patient is presenting with a suspected skin tumour.
• Family history: of atopy, skin cancers, or skin disease.
• Drug history: enquire about any over-the-counter medications, as well as recent systemic and topical treatments.
• Social history: smoking, alcohol, pets, occupation (plus occupational exposure to substances if relevant), and impact on quality of life. It is important to explore patients’ concerns and expectations especially in conditions such as psoriasis where the physical appearance of the condition is associated with significant psychological distress.
Practise performing a basic dermatological examination and also describing skin lesions. You are most likely to get a patient or clinical photos of a patient with chronic eczema or chronic plaque psoriasis to describe and then discuss the treatment options.
• General inspection: site/number of lesions and distribution of lesions.
• Describe individual lesions: size, shape, colour, associated secondary change, morphology, and margins. For pigmented lesions, assess according to the ‘ABCD’ system.
• Palpate: surface, consistency, mobility, and tenderness.
• Complete systems examination: this includes scalp, hair, mucous membranes, and nails as well as a general systems examination.
• Eczema: in an adult, you will generally see lichenified, dry, scaly patches of skin over flexor aspects. Practise describing the typical lesions seen in eczema including the distribution.
• Psoriasis: in contrast to eczema, chronic plaque psoriasis is normally seen in a symmetrical distribution over the extensor aspects of the body and scalp. Plaques are well demarcated, pink/red, with an overlying silvery scale in an asymmetrical distribution. Look for koebnerization (psoriasis at sites of scarring). Also check for nail changes—pitting/onycholysis.