Integrated clinical assessment

Skin comprises an inner dermis of collagen and elastic tissue lying on subcutaneous fat, and an outer, continuously replenishing epidermis extending from a basal layer of cells with scattered melanocytes to a top layer of protective keratinocytes. These continuously degenerate and slough off to be replaced by cells from beneath. The epidermal–dermal junction is demarcated by a basement membrane. Skin disease can originate in any of these structures and skin, the only visible organ, can be a window to the world of systemic disease, for example: diabetes mellitus (necrobiosis lipoidica, infections); sarcoidosis (erythema nodosum, lupus pernio); inflammatory bowel disease (erythema nodosum); internal malignancy (dermatomyositis, paraneoplastic pemphigus); porphyria cutanea tarda, Graves’ disease (pretibial myxoedema, thyroid acropachy, palmar erythema); Cushing’s syndrome (thin skin, striae, bruising); Addison’s disease (hyperpigmentation).

Table 5.1

Terminology for skin lesions

Term	Description
Macule	Flat area of discoloration ranging from pale (loss of melanin) to brown or black (increased melanin); many macules are red, indicating vascular dilatation or an inflammatory process
Patch	Large macule
Papule	Raised lesion > 1 cm in diameter
Nodule	Raised lesion < 1 cm in diameter
Plaque	Raised lesion with a flattened top, or plateau
Vesicle	Fluid-filled lesion or ‘blister’ < 0.5 cm in diameter
Bulla	Larger blister
Pustule	Vesicle filled with neutrophils (not necessarily infection)
Telangiectasia	Dilated, superficial blood vessels (capillaries, post-capillary venules) – idiopathic or associated with cold outdoor exposure, pulmonary hypertension, scleroderma, systemic lupus erythematosus, rosacea, lupus pernio or necrobiosis lipoidica diabeticorum
Discoid	Flat and disc-like lesion (term sometimes overlapping with nummular or coin-like lesions)
Annular	Ring shaped
Reticular	‘Net-like’ lesions, e.g. erythema ab igne (Granny’s tartan) and livedo reticularis (physiological or associated with sepsis, connective tissue disease or malignancy)
Atrophy	Loss of tissue – loss of dermis or subcutaneous fat usually leaves a depression in the skin; loss of epidermis causes wrinkling and a translucent, hypopigmented appearance
Lichenification	Characteristic skin thickening (resembling lichen on rocks or trees) often produced by chronic inflammation or rubbing
Erosion	Area of lost epidermis that generally heals without scarring
Excoriation	Linear erosions often produced by scratching
Ulcer	Area of skin loss involving the dermis
Fissures	Slit through whole thickness of skin

Summary

A summary of the skin examination sequence is given in the Summary box.

Summary box – skin examination sequence

Look at the distribution of the rash, e.g. bilateral, symmetrical, photosensitive areas

Be able to describe lesions (Table 5.1); the morphology may be diagnostic, e.g. psoriasis; if not diagnostic, comment on differential diagnoses

Look for relevant non-cutaneous signs, e.g. psoriatic arthropathy.

Cases

Case 5.1 Psoriasis

Candidate information

Role

You are a doctor in the medical outpatient clinic.

Scenario

Re: Mrs Jacquie Green, aged 33 years

This young woman is in the outpatient clinic for follow-up of recent lobar pneumonia and mentions that she has had a problematic rash for months on her knees and elbows.

Your task is to assess the problem by means of a focused history and focused examination. You should then advise the patient of your probable diagnosis and plan, and address any questions or concerns raised by the patient.

You have 10 minutes. The examiners wil l alert you when 6 minutes have elapsed, stop you at 8 minutes, and in the remaining 2 minutes ask you to report your findings, the diagnosis or differential diagnosis, and a management plan.

Patient information

You are a 33-year-old woman in the outpatient clinic for follow-up of recent pneumonia. You have had a recurring rash, predominantly on your knees, elbows and hands but also around your scalp, for some years, but worse in the last few months since being unwell with asthma. It does not cause you particular problems but it is scaly, and worse in times of stress and relieved by sunlight. It also seems to flare up whenever you stop courses of steroid for asthma. It is rather irritating and you would be happy if there were some treatment available. You tried some coal tar treatment once and it was incredibly messy.

Focused history and examination

Initial history

• Ask about duration of symptoms. Psoriasis is a chronic condition that waxes and wanes.

• Ask about precipitating and relieving factors. Psoriasis is often worse in stress and flares up after stopping steroids, and improves with relaxation and sunlight.

• Ask about the distribution. Chronic plaque psoriasis is usually symmetrical, affecting extensor surfaces.

• Ask about the lesions themselves.

Initial examination

• Be aware of the commonest type of psoriasis – chronic plaque psoriasis, and of psoriasis variants (Table 5.2). Looks at the skin lesions and at the hands and nails.

Table 5.2

Psoriasis variants

Chronic plaque psoriasis

There are numerous symmetrically distributed plaques (Fig. 5.1) most prominent on extensor surfaces (elbows, knees), the scalp and hairline and behind the ears, the lower back (sacrum), the shin and the umbilicus. Plaques may range in size from a few millimetres to a large area of the limbs or trunk. These are sharply marginated and pink / red with silvery-white scaling surfaces (sometimes said to resemble limpets).

Seventy-five per cent of people with psoriasis have onset before 40 years; 80–90% of people with psoriasis have chronic plaque psoriasis. The predominance of erythema or scaling can vary from patient to patient. Scratching of scales may result in a waxy appearance, although lesions are not usually itchy. Lifting larger scales (do not do this) may result in capillary bleeding (Auspitz sign). Occasionally, instead of scaling, the surfaces of plaques are covered by hard, thickened firmly adherent keratin. Köbner’s phenomenon, in which lesions often appear at sites of minor trauma (e.g. surgical wound, trivial scratch, abrasion, burn), is a helpful diagnostic feature, and sometimes the first sign of psoriasis. Other causes of Köbner’s phenomenon include lichen planus, pemphigoid and certain viruses, but it does not occur in dermatitis.

Hands and nails

There may be nail pitting and onycholysis and arthropathy of the hands.

Further assessment

• Ask about joint symptoms. Psoriatic arthropathy affects up to 10% of patients with psoriasis and may precede or follow skin disease by months or even years. There are, in theory, five types, although overlap is common (Table 5.3). If there is arthropathy, consider the tendency for HLA B27 spondyloarthropathies to overlap, common features being sacroiliac discomfort and enthesopathies such as plantar fasciitis.

Table 5.3

Psoriatic arthropathy

Type	Features
Asymmetrical distal interphalangeal joint arthropathy	Relatively uncommon but the form most strongly associated with psoriasis; affected digits often show nail changes such as pitting
Rheumatoid-like hands	The commonest type; seronegative
Asymmetrical large-joint mono- or oligoarthropathy	Large joint pain or swelling
Spondyloarthropathy and sacroiliitis	Low back pain
Arthritis mutilans	Very uncommon, severely destructive type

• Explore concerns.

Feedback to patient

This looks like psoriasis, a very common skin condition that tends to be scaly and patchy like this. It tends to wax and wane, although some people do find that it improves with sunlight and worsens with stress or if they have been unwell. I think that your general practitioner could provide some simple creams to help settle it down in the first instance. Coal tar can be effective but many people these days opt for newer creams for exactly the reasons you mention. I’d be happy to answer any further questions or concerns that you may have.

Feedback to examiners

Summarise the key history and examination findings

This lady has numerous symmetrically distributed plaques, most prominent on extensor surfaces (elbows, knees), the scalp and hairline. These are sharply margined and pink / red with silvery white scaling surfaces.

Provide a diagnosis or differential diagnosis with supporting evidence

These are features of chronic plaque psoriasis.

Outline an investigation and management plan

Most psoriasis is mild and responds to topical therapy – emollients, coal tar and pastes, dithranol or vitamin D3 analogues are all suitable first-line therapies for limited chronic plaque psoriasis. About 10–20% of patients have moderate–severe psoriasis as determined by the Psoriasis Activity Severity Index scoring > 10. Most of these will require second-line (phototherapy or systemic) therapy, and around 20% have arthritis. Cognitive behavioural therapy is effective in psoriasis triggered by psychological stress. If these standard therapies [Table 5.4] prove unsuccessful, other immunomodulatory or biological therapies are available [Table 5.5 and Fig. 5.2].

Table 5.4

Standard therapies in psoriasis

Treatment	Comment
Topical therapy
Emollients
Short-contact dithranol	Useful in incremental concentrations as first-line treatment for stable plaques, resulting in prolonged remission; stains plaques and hair and must not be applied for longer than directed, usually 30 minutes
Coal tar ointments and pastes	Easier to apply in hospital; messy but safe and effective for stable plaques but salicylic acid may also be needed to dissolve thick keratin
Vitamin D3 analogues / deltanoids, e.g. calcipotriol, tacalcitol	Useful for mild to moderate stable plaques; remission duration short so treatment is constant; high doses (extensive psoriasis) may cause hypercalcaemia
Other	Corticosteroids are effective but tachyphylaxis (rebound on withdrawal) is a major drawback; retinoids may have some benefit but are teratogenic; topical calcineurin inhibitors (tacrolimus, pimecrolimus) are effective on thin plaques only (face and flexures) but should not be combined with phototherapy
Phototherapy
Ultraviolet B	Useful in widespread plaque or guttate psoriasis
Oral (or topical psoralens), followed by irradiation with long-wave ultraviolet A (PUVA)	Useful in widespread plaque psoriasis
Systemic therapy
Ciclosporin	Rapid acting and highly effective; inhibits calcineurin; side effects are immunosuppression, hypertension and nephrotoxicity
Methotrexate	Widely used in extensive plaque psoriasis, generalised pustular psoriasis, erythrodermic psoriasis and psoriatic arthropathy; side effects are bone marrow suppression and hepatotoxicity
Acitretin	A treatment of choice for psoriasis as monotherapy or in combination with PUVA; teratogenic
Hydroxycarbamide	Less commonly used; causes bone marrow suppression

Table 5.5

Other immunomodulatory or biological therapies in psoriasis

Figure 5.2 Current and proposed immunomodulatory therapies or ‘biologicals’ in psoriasis. HLA, human leucocyte antigen; ICAM, intercellular adhesion molecule; IFN, interferon; IL, interleukin; Th, T-helper; TNF, tumour necrosis factor.

Case 5.2 Dermatitis

Candidate information

Role

You are a doctor on the medical ward.

Scenario

Re: Ms Eleanor Whiting, aged 35 years

This young woman was admitted to your ward yesterday with asthma. She has a chronic skin rash that has worsened.

You have 10 minutes. The examiners will alert you when 6 minutes have elapsed, stop you at 8 minutes, and in the remaining 2 minutes ask you to report your findings, the diagnosis or differential diagnosis, and a management plan.

Patient information

You are a 35-year-old woman admitted to hospital yesterday with worsening asthma. You mention to the admitting doctor that you have had a chronic itchy skin condition on the flexor surface of your arms and legs for many years but that it is worse. You are also concerned that the skin is breaking down much more easily than it used to, especially on the hands, where water and soap and possibly chemicals (you are a hairdresser) and the hot atmosphere appears to be preventing it from ever fully healing. You cannot give up work. You take occasional over-the-counter emollients.

Focused history and examination

Initial history

• Ask about the duration of symptoms.

• Ask about itch.

• Ask about atopic symptoms, e.g. asthma and hayfever.

• Ask about any provoking and relieving factors, notably any occupational or household allergens or irritants.

• Ask whether there is a family history.

• Ask about treatments to date.

Initial examination

• Note the distribution of the rash and its appearances. The skin is red, swollen and blistering or dry, thickened and leathery, with erythema, scaling and evidence of scratching. Both extremes are itchy.

Dermatitis and eczema are interchangeable terms. The term ‘eczema’ means skin ‘boiling over’. There are many types of dermatitis and the clinical appearance can fall anywhere between the two extremes. Pathologically, there is breakdown in the skin’s horny barrier and there may be oedema high in the dermis. Any blisters tend to have a honeycomb, multiloculated core, not typical of other blistering diseases such as pemphigus.

Further assessment

• Features of the history that should be further explored are atopy, occupation and exposure to irritants.

• Explore concerns.

Dermatitis may have endogenous or exogenous causes, the latter generally contact dermatitis and photosensitivity (Table 5.6). Bilateral dermatitis is more likely to have an endogenous cause and unilateral dermatitis an exogenous cause (but contact dermatitis commonly affects both hands if dipped in chemical irritants). It is worth remembering that the differential diagnoses of acute ‘dermatitis’ include infectious skin conditions such as scabies (intensely itchy and worse after hot showers or baths and at night; burrows of the scabies mite Sarcoptes scabei may be seen) and Tinea pedis in foot dermatitis, often unilateral, dry, scaly and interdigitate.

Table 5.6

Types of dermatitis

IgE, immunoglobulin E; Th2, T helper type 2.

Figure 5.3 Seborrhoeic dermatitis.

Dermatitis can be severe and even life threatening, especially with secondary infection. Apparent dermatitis occasionally represents a more sinister aetiology. An eruption resembling flexural atopic dermatitis is occasionally the result of agammaglobulinaemia, coeliac disease or mycosis fungoides.

Feedback to patient

This looks like eczema, also known as dermatitis, a very common condition that affects the areas in which you have it and gives rise to exactly this sort of dry and itchy skin. There are many causes or types. A common type, known as atopic dermatitis, occurs in people with hayfever or asthma. However, I suspect that you also have a type known as irritant contact dermatitis from the water and exposure to substances at work. I would be confident that some stronger creams or ointments could be used in the first instance to settle this down, and then we could ask your general practitioner to prescribe something a little less strong regularly to keep it settled down. I’d be happy to answer any further questions or concerns that you may have.

Chemical and allergen avoidance is the mainstay of prevention but not always practical. Patients should certainly avoid identified allergens (e.g. vacuuming, damp dusting) but improvement may take many months (e.g. after changing bedding). Emollients and emollient bathing promote skin hydration. Ointments and creams differ in their grease–water ratio. The epidermis can absorb both greasy and aqueous preparations. Generally, the greasy ointments are best for dry, scaling skin and watery creams for crusted weeping lesions. Pastes may be used for sustained action or occlusion. Topical corticosteroids (Box 5.1) are the main treatment for inflammation and pruritus. Less potent drugs should be used on the eyelids, face and flexural surfaces because of the risk of cataracts, skin atopy and telangiectasia. More potent treatment is allowable for these areas for a few days before stepping down to less potent maintenance treatment.

Box 5.1 Potency of some typical corticosteroids

Mild

• Hydrocortisone

• Fucidic acid and hydrocortisone (Fucidin H)

Moderate

• Clobetasone butyrate (Eumovate)

Potent

• Hydrocortisone butyrate (Locoid)

• Betamethasone valerate (Betnovate)

• Fucidic acid and betamethasone (Fucibet)

• Mometosone furoate (Elocon)

Very potent

• Clobetasol proprionate (Dermovate)

• Clobetasol proprionate, neomycin and nystatin (Dermovate NN)

Topical / systemic antibiotics and antihistamines may be needed. Topical immunomodulators – tacrolimus and pimecrolimus – are very effective for intermittent use in mild to moderate atopic dermatitis, but should be applied thinly and only when needed to limit neoplastic risk. They do not cause skin atrophy and there is minimal absorption. They may be used on the face. Severe, refractory atopic dermatitis might need systemic corticosteroids; ciclosporin, azathioprine or mycophenolate mofetil are sometimes needed.

You have 10 minutes. The examiners will alert you when 6 minutes have elapsed, stop you at 8 minutes, and in the remaining 2 minutes ask you to report your findings, the diagnosis or differential diagnosis, and a management plan.

• Ask about any provoking and relieving factors.

• Ask about atopic symptoms, e.g. asthma and hayfever.

• Ask about treatments.

Initial examination

• There are well-demarcated, polygonal, raised plaques on the flexor surfaces, especially the wrists and ankles (Fig. 5.4). Their flat tops are shiny with a violaceous colour, interrupted by milky white streaks – Wickham’s striae. They are very likely to be intensely itchy. There may be Köbner’s phenomenon. Lesions usually resolve over a period of months to leave brownish macules.

Figure 5.4 Lichen planus.

Lichenification is a feature of many skin diseases such as eczema and itchy drug eruptions. The shiny, purplish flat tops of lichen planus, and their distribution, usually aid diagnosis.

Further assessment

• Look at the oral mucosa and nails. There may be white, ‘net-like’ lesions on the buccal mucosa (Fig. 5.5) or tongue (Fig. 5.6), often with ulceration. Atrophy and longitudinal grooves may affect the nail plates; sometimes nails disappear altogether.

Figure 5.5 Lichen planus of buccal mucosa.

Figure 5.6 Lichen planus of tongue.

• Explore any concerns.

Feedback to patient

I think this is probably a condition called lichen planus. It is usually quite harmless but very itchy and sometimes associated with eczema. It should all settle down very well with some mild steroid cream. I’d be happy to answer any questions you may have.

Lichen planus is not life threatening, but white oral lesions may not be lichen planus; differential diagnoses include candidiasis and leucoplakia (hyperkeratotic lesions associated with Epstein–Barr virus), both more common in human immunodeficiency virus infection.

Outline an investigation and management plan

Lesions usually resolve over a period of months to leave brownish macules. The cause is uncertain, with no family history and no definite association with stress. The epidermis is thickened, with increased keratin (the white streaks imply a thickened granular layer and the basal layer is infiltrated with T lymphocytes in a band pattern). Moderately potent topical (occasionally systemic) steroids are effective for this condition, which appears to have an immune basis. Lichen planus is self-limiting but tends to relapse and remit over months or even years.

You have 10 minutes. The examiners will alert you when 6 minutes have elapsed, stop you at 8 minutes, and in the remaining 2 minutes ask you to report your findings, the diagnosis or differential diagnosis, and a management plan.

Patient information

You are a 74-year-old man in hospital for investigation of altered bowel habit. You mention to the doctor that you have a rather severe blistering rash on your thighs and trunk that has developed in the past fortnight, with tense, itchy lesions of varying sizes. You do not have any oral lesions. You are, however, keen to get home very soon as you wife has Alzheimer’s disease, although family are looking after her.

Focused history and examination

Initial history

• Ask about the duration of symptoms.

• Ask about symptoms, e.g. pain, itch, weeping, crusting or bleeding.

• Ask about distribution.

• Ask about any provoking and relieving factors.

• Ask about treatments.

Initial examination

• Be aware of pemphigus and pemphigoid as important chronic widely distributed blistering diseases.

Bullous pemphigoid

There are tense blisters of variable size (much more variable than pemphigus, from a few millimetres to a few centimetres, but large, tense blisters up to 3 cm in diameter are typical) on the flexor surfaces spreading to the trunk (Fig. 5.7) on an erythematous base. Blisters may be broken because of excoriation. Early disease may appear as a pruritic, urticarial rash. Oral lesions are less frequent than in pemphigus, occurring in around one-third of patients and seldom a presenting feature. The anus, vagina and oesophagus are occasionally involved.

Figure 5.7 (A–D) Pemphigoid.

Pemphigus

There is a bullous eruption (in a middle-aged / older patient) comprising flaccid, fragile, thin-walled blisters on the trunk 1–2 cm in diameter (Fig. 5.8). Many have burst, leaving red, exuding, tender patches (even rubbing of normal skin can cause sloughing of the epidermis – Nikolsky’s sign). Oral erosions (Fig. 5.9) are common and painful and may precede the rash. Pemphigus foliaceous is characterised by superficial blisters that affect only the skin. Pemphigus vulgaris is characterised by mucosal involvement and subsequent skin involvement with blisters and erosions.