Chapter 3. Skin, hair and nails

Chapter



3



Skin, hair and nails



Structure of the epidermis, dermis

and hypodermis

horny

layer



granular

layer



spinous

layer

(prickle cells)



basement

membrane



hair



basal layer

(germinal

keratinocytes)

exfoliation

14 days

30 days

superficial

vascular plexus

arrector pili

muscle

reticular

dermis



deep

vascular

plexus



sebaceous

gland



hair follicle

hypodermis

capillaries



Fig. 3.1 Section through full thickness of skin showing the structure

of the epidermis, dermis and hypodermis.



disorders such as wrinkles and a loose skin syndrome

(cutis laxa) occur.

Hypodermis

The dermis rests on the hypodermis, which is the

subcutaneous layer of fat and loose connective tissue.

This layer serves both as a fat store and an insulating

layer.

SKIN APPENDAGES

Sebaceous glands

Skin sebaceous glands can function throughout life,

although activity is latent between birth and puberty.

These glands are partly responsible for the production of

vernix caseosa which covers and waterproofs the fetus

during the latter stages of gestation. The glands become

particularly active during puberty. The secretion is

holocrine (i.e. caused by complete degeneration of the

acinar cells) and is stimulated by androgens and opposed

by oestrogens. Sebaceous glands are absent from the

palms and soles and are concentrated on the face, scalp,

58



midline of the back and the perineum. Sebum contains

triglyceride, scalene and wax esters and functions to

waterproof and lubricate the skin, as well as inhibiting

the growth of skin flora and fungi. Skin disorders such as

acne vulgaris and rosacea occur in areas where sebaceous

glands concentrate.

Apocrine and eccrine glands

The apocrine glands are concentrated in the axillae,

areolae, nipples, anogenital regions, eyelids and external

ears. These glands become functionally active at puberty

and are responsible for an odourless secretion which is

acted on by skin flora, causing characteristic body odour

to develop. The eccrine sweat glands are widely distributed

and are extremely important in heat regulation and fluid

balance. Whereas the eccrine cells secrete an isotonic

fluid, the duct cells modify the fluid to render it hypotonic.

Secretion and its modification are under cholinergic and

hormonal control. Sweating in response to temperature

change is under hypothalamic control.

HAIR

In most mammals, hair is important in the control of

temperature. In humans, however, hair is mainly

important as a tactile organ which also has a sensual

function, important in both sexual attraction and

stimulation. Hair covers all of the body except the palms,

soles, prepuce and glans and inner surface of the labia

minora. During gestation the fetus is covered by a fine

coat of lanugo hair which is lost shortly before birth,

except for the scalp, eyebrows and lashes. Hair may be

vellus, which is short, fine and unpigmented, or terminal

hair, which is thicker and pigmented. Puberty is

characterised by the development of coarse, pigmented

hair in a pubic, axillary and facial distribution.

Hair is formed by specialised epidermal cells that

invaginate deep into the dermal layer. Hair develops

from the base of the hair follicle where the papilla, a

network of capillaries, supports the nutrition and growth

of the hair. Hair growth is cyclical: the active growth

phase is termed anagen; involution of the hair, catagen;

and the resting phase, telogen.

The hair shaft consists of a cuticle, cortex and medulla.

The arrectores pilorum muscles anchor in the papillary

dermis and insert into the perifollicular tissue (Fig. 3.1).

Contraction of these muscles causes goose pimples (cutis

anserina) to occur. Hair colour is determined by the

density of melanosomes within the cortex of the hair

shaft; none is present in white hair, whereas grey hair has

a reduced number. Red hair has different melanosomes

to black hair, both chemically and structurally.

THE NAIL

Nail is a specialised skin appendage derived from an

epidermal tuck that invaginates into the dermis. The

highly keratinised epithelium is strong but flexible and



Chapter



Symptoms of skin disease



Structure of nail

nail bed

nail plate



posterior

nail fold



eponychium

body of nail

nail matrix



3



or domestic toxins or chemicals. Ask whether waterproof

gloves are worn when washing dishes or dusting and

cleaning the home. Question the patient about recent

exposure to medicines, especially antibiotics which often

cause skin rashes. Cosmetics are an important cause of

skin sensitisation so enquire about the use of new soaps,

deodorants and toiletries. Ask about hobbies (e.g.

gardening, model building and photographic developing),

foreign travel and insect bites. Ascertain whether or not

the skin complaint is seasonal.



nail root

Questions to ask



nail plate



Skin history

paronychium

lunule

cuticle



eponychium



Fig. 3.2 Structure of nail.



provides a sharpened surface for fine manipulation,

clawing, scraping or scratching.

The nail has three major components: the root, the nail

plate and the free edge (Fig. 3.2). The proximal and lateral

nail folds overlap the edges of the nail and a thin cuticular

fold, the eponychium, overlies the proximal nail plate.

The lunule is the crescent-shaped portion of the proximal

nail formed by the distal end of the nail matrix. The

free margin of the distal nail is continuous along its

undersurface with the hyponychium, a specialised area

of thickened epidermis. The nail plate lies on the highly

vascularised nail bed, which gives the nail its pink

appearance. The paronychium is the soft, loose tissue

surrounding the nail border; it is particularly susceptible

to bacterial or fungal infection infiltrating from a breach

in the eponychium (a paronychia). Fingernails grow

approximately 0.1 mm per day, with more rapid growth

in summer compared with winter.



•

•

•

•

•

•

•

•

•

•

•

•



Was the onset sudden or gradual?

Is the skin itchy or painful?

Is there any associated discharge (blood or pus)?

Where is the problem located?

Have you recently taken any antibiotics or other

drugs?

Have you used any topical medications?

Were there any preceding systemic symptoms (fever,

sore throat, anorexia, vaginal discharge)?

Have you travelled abroad recently?

Were you bitten by insects?

Any possible exposure to industrial or domestic

toxins?

Any possible contact with sexually transmitted

disease or HIV?

Was there close physical contact with others with

skin disorders?



Differential diagnosis

Systemic diseases causing pruritus



• Intrahepatic and extrahepatic biliary obstruction

(cholestasis)

• Diabetes mellitus

• Polycythaemia rubra vera

• Chronic renal failure

• Lymphoma (especially Hodgkin’s disease)



Symptoms of skin disease

The history should evaluate possible precipitating factors

and determine whether the skin problem is localised or

a manifestation of systemic illness.

The skin is readily examined and for this reason the

history often assumes less importance than with other

systems. However, a thorough history may unearth

crucial information to aid diagnosis. Attempt to gain

some insight into the patient’s social conditions, as

overcrowding and close physical contact are important

when considering infectious disorders such as scabies

and impetigo. Enquire in some depth about possible

precipitating factors, especially contact with occupational



Systemic disorders may also present with skin

symptoms. Infectious diseases often present with skin

rashes or lesions. Ask about a recent sore throat, as

streptococcal infection may be accompanied by typical

rash (scarlet fever), painful red nodules on the extensor

surface (erythema nodosum) or guttate psoriasis. In a

cutaneous candidal infection, the patient often complains

of an itchy rash and sore tongue or, in women, a vaginal

discharge. Candida albicans infection often follows a

course of broad-spectrum antibiotics. Skin rashes

developing in sun-exposed areas (in the absence of strong

59



Chapter



3



Skin, hair and nails

sunburn, known as photosensitive rashes) should raise

the possibility of systemic lupus erythematosus, porphyria

or drugs. If the patient complains of skin lesions around

the genitalia, enquire about possible contact with sexually

transmitted disease. AIDS may present with the nodular

lesions characteristic of Kaposi’s sarcoma or thrush

affecting the mucosa or skin. Therefore, it is important to

take a history of risk factors (e.g. male homosexuality,

high-risk heterosexual contact, blood transfusion and

intravenous drug abuse). Skin itching (pruritus) in the

absence of an obvious rash should alert you to an

underlying systemic disorder.

Topical steroids and other topical substances are

commonly prescribed to treat a variety of skin lesions.

Always ask about topical treatment as this may alter the

appearance of a skin lesion, making the diagnosis more

difficult.



Fig. 3.3 Alopecia.



Symptoms of hair disease

HAIR THINNING

Balding (alopecia) worries patients and you will often be

asked to assess scalp hair loss. Male pattern baldness

is common; the patient will note the slow onset of hair

loss with the hairline receding from the frontal and

temporal scalp and crown. Ask about a family history of

baldness as male alopecia is an expression of autosomal

dominance and may begin early in life. After the

menopause, many women note thinning of the hair

(Fig. 3.3); this is often associated with growth of facial

hair.



Questions to ask

Hair history



• Was the hair loss sudden or gradual?

• Does the loss occur only on the scalp or is the body

hair involved as well?

• Is the baldness localised or general, symmetrical or

asymmetrical?

• Is there a family history of baldness (especially in

men)?

• What drugs have you taken recently?

• Any recent illnesses, stress or trauma?

• Are there other systemic symptoms (e.g. symptoms

of hypothyroidism)?



Hair loss may also be a feature of disease and the

characteristics of the alopecia may be helpful. Patients

complaining of localised alopecia (alopecia areata) (Fig.

3.4) may have an autoimmune disease (e.g. Hashimoto’s

thyroiditis with myxoedema). Patients with stress or

anxiety neurosis may nervously pluck hair from the scalp,

60



Fig. 3.4 Alopecia areata characterised by localised patches of hair

loss.



causing a local area of thinning or baldness. Severe illness

and malnutrition, as well as sudden psychological shock,

may be associated with hair loss, which usually recovers

once the stress has been resolved.

ABNORMAL HAIR GROWTH

Remember to warn patients undergoing cytotoxic

treatment for cancer that they can expect generalised hair

loss. Failure to develop axillary and pubic hair at the

expected time of puberty should alert you to the possibility

of pituitary or gonadal dysfunction.

Abnormal facial hair growth (hirsutism) is a distressing

symptom in women. It is important to recognise that

a certain degree of facial hair growth occurs naturally

in postpubertal women. There are racial differences:

physiological hirsutism is least apparent in Japanese and

Chinese women and most apparent in women of

Mediterranean, Middle Eastern, Indian and Negroid

extraction. The unexpected occurrence of hirsutism,

especially if accompanied by other symptoms and signs

of virilism, should alert you to the possibility of a hormonal

imbalance.



Chapter



Examination of the skin, hair and nails

Questions to ask

Hirsutism



• Is there a family history of hirsutism?

• Are your menstrual periods normal or absent

(or scanty)?

• Is there a history of primary or secondary infertility?

• Do you experience visual disturbances or headaches

(pituitary disease)?

• What medications do you take (e.g. phenytoin,

anabolic steroids, progestogens)?



Differential diagnosis

Hirsutism



• Racial variation in hair distribution

• Hormonal imbalance

– polycystic ovaries

– ovarian failure or menopause

– virilising adrenal tumours

• Drugs

– phenytoin

– progestogens

– anabolic steroids

– ciclosporin



Symptoms of nail disease

Whereas examination of the nails may be very revealing,

nail-related symptoms are usually nonspecific. Patients

may relate symptoms suggestive of bacterial infection

along the nail edge; these include intense pain, swelling

and often a purulent discharge. Complaints of brittleness,

splitting or cracking provide little diagnostic information.

Ask specifically about skin disease that may affect the

nail, such as psoriasis, severe eczema, lichen planus or a

susceptibility to fungal skin infection.



Examination of the skin, hair and nails

EXAMINING THE SKIN

When examining the skin, there is a tendency to focus

on the local area noticed by the patient. Nonetheless, you

should consider the skin as an organ in its own right and,

like any other examination, the whole organ should be

examined to gain maximum information. The patient

should be stripped to the underwear, covered with a

gown or blanket and the examination area should be well

lit (preferably natural daylight or fluorescent light).

Inspection and palpation

Scan the skin, looking for skin lesions and noting both

position and symmetry. Remember to expose hidden



3



areas like the axillae, inner thighs and buttock with

its natal cleft. Many skin lesions can be diagnosed by

their appearance and localisation. Unlike any other

organ system, the examination relies almost entirely on

careful inspection and meticulous use of descriptive

terminology.

Measurement of the length and breadth of skin lesions

is useful, especially when monitoring progression or

regression. A broad beam torch or electric light helps to

define the outline of the border of a skin lesion; a thin

beam is helpful if you wish to check whether or not a

lesion transilluminates. A fluid-filled but not solid lesion

emits a red glow when the torch light shines through it.

A Wood’s lamp helps to distinguish a fluorescing lesion;

by shining the lamp at a suspect lesion, it may be possible

to show the characteristic blue-green fluorescence of

fungal infections.

Skin colour

Skin colour varies between individuals and races and is

usually even and symmetrical in distribution. Normal

variations occur in freckling and sun-exposed areas.

During pregnancy, there may be darkening of the skin

overlying the cheek bones (melasma) and the areolae

surrounding the nipple (chloasma).

Abnormal skin colour

Generalised changes in skin colour occur in jaundice,

iron overload, endocrine disorders and albinism. The

yellow tinge of jaundice is best observed in good daylight,

appearing initially as yellowing of the sclerae and then as

a yellow discoloration on the trunk, arms and legs.

Jaundice is less apparent in unconjugated as opposed to

conjugated hyperbilirubinaemia. In longstanding, deep

obstructive jaundice, the skin may turn a deep yellowgreen. Remember that people eating large quantities of

carrots or other forms of vitamin A may develop yellow

skin pigmentation (carotenaemia) and that the absence

of scleral discoloration distinguishes this syndrome from

jaundice.

Iron overload (haemosiderosis and haemochromatosis)

causes the skin to turn a slate-grey colour. The astute

observer may recognise this metabolic disease by the

characteristic skin pigmentation. Addison’s disease

(autoimmune adrenal destruction) is characterised by

darkening of the skin, occurring first in the skin creases

of the palms and soles, scars and other skin creases. The

mucosa of the mouth and gums also becomes pigmented.

Striking pigmentation also arises after bilateral

adrenalectomy for adrenal hyperplasia: this syndrome

(Nelson’s syndrome) is caused by unopposed pituitary

overstimulation. In hypopituitarism, the skin is soft, pale

and wrinkled.

Albinism is an autosomal recessive disorder caused by

failure of melanocytes to produce melanin. The skin and

hair are white and the eyes are pink because of a lack

of pigmentation of the iris, and there may also be

nystagmus.

61



Chapter



3



Skin, hair and nails



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



Fig. 3.8 Typical appearance of petechial haemorrhage in a patient

with thrombocytopenia.



hand.



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



Fig. 3.9 Telangiectasia on the tongue.



Telangiectasia refers to fine blanching vascular lesions

caused by superficial capillary dilatation (Fig. 3.9).

Localised skin lesions



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



Common localised abnormalities of skin pigmentation

include vitiligo (Fig. 3.5), café-au-lait spots (Figs 3.6, 3.7),

pityriasis versicolor and idiopathic guttate hypomelanosis.

Erythema of the skin is caused by capillary dilatation;

when pressure is applied the red lesion blanches and

reforms. When examining a patient, you may notice an

erythematous flush in the necklace area which is caused

by anxiety. Purpura is the term used for red-purplish

lesions of the skin caused by seepage of blood from skin

blood vessels. Unlike erythema, these lesions do not

blanch with pressure. If the lesions are small (<5 mm)

they are called petechiae (Fig. 3.8), whereas larger lesions

are purpura. Traumatic bruises are called ecchymoses.

62



Careful descriptions of size, shape, colour, texture and

position of lesions are helpful in skin diagnosis. Try

to ascertain a primary and secondary description of

the skin lesion. To establish the primary nature of the

skin lesion decide whether the lesion is flat, nodular or

fluid-filled. Flat circumscribed changes in colour are

termed macules if less than 1 cm or patches if more than

1 cm. If the lesion is raised and can be palpated, assess

whether the mass is a papule, plaque, nodule, tumour

or wheal. If a circumscribed elevated lesion is fluctuant

and fluid-filled, describe whether it is a vesicle, bulla or

pustule (Fig. 3.10). If possible, describe the arrangement

of the lesions; that is, whether linear, annular (ringshaped) or clustered. In shingles (herpes zoster), the

rash occurs in the distribution of one or more skin

dermatomes.

Add to the primary description any secondary

characteristics such as superficial erosions, ulceration,

crusting, scaling, fissuring, lichenification, atrophy,

excoriation, scarring, necrosis or keloid formation.

Palpation is used to decide whether a lesion is flat,

raised or tender. Compression may be helpful (e.g.

demonstration of the characteristic arteriolar dilatation of

spider naevi occurring in decompensated liver disease)

(Fig. 3.11). Use the back of your hand to assess



Chapter



Examination of the skin, hair and nails



3



Primary localised lesions

macule



patch

<1cm



vesicle



papule



wheal



nodule



bulla



>1cm



plaque



Fig. 3.10 Primary localised skin lesions.



Fig. 3.11 Spider naevi in hepatocellular disease.



temperature. Inflamed lesions (e.g. cellulitis) are hotter

than surrounding tissue, whereas skin overlying a lipoma

(subcutaneous fat tumours) is cooler than adjacent tissue.

Skin turgor may be used as a measure of moderate to

severe hydration. Pinch a small area of skin between



index finger and thumb. Hold firmly for a few seconds

and then release. Healthy, well-hydrated skin immediately

springs back into its resting position. In significant

dehydration or when skin elastic tissue is lost (e.g.

ageing), the skin behaves like putty and only slowly

reshapes to its resting position. Skin oedema can be

demonstrated by pressing your thumb or fingers into the

skin, maintaining the pressure for a short while and then

releasing. Your thumb or finger impression will remain

indented in the skin if there is excessive fluid (‘pitting’

oedema).

Although most disorders can be diagnosed from their

appearance, special techniques such as microscopy of

skin biopsies or skin scrapings, immunofluorescent

staining and culture of specimens may be required to

confirm diagnosis.

Common skin lesions

Skin lesions are often readily recognisable and you should

be able to distinguish some common conditions.

63



Chapter



3



Skin, hair and nails



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



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



Acne vulgaris

This common disorder of the pilosebaceous unit occurs

at puberty. Plugging of the duct, increased sebum

production, bacterial growth and hormonal changes all

predispose to the condition. Acne presents with greasy

skin, blackheads (comedones), papules, pustules and

scars (Fig. 3.12). The lesions are common and vary in

severity and most teenagers recognise the problem before

visiting the doctor. The disorder affects the face, chest

and back. Acne usually subsides in the third decade.

Rosacea

This facial rash usually presents in the fourth decade,

although in women it may present after the menopause.

Papules and pustules erupt on the forehead, cheeks,

bridge of the nose and the chin. The erythematous

background highlights the rash (Figs 3.13, 3.14).

Comedones do not occur, distinguishing the condition

clinically from facial acne. Occasionally, the rash may

be localised to the nose. Eye involvement is characterised

by grittiness, conjunctivitis and even corneal ulceration.

There appears to be vasomotor instability and patients

flush readily in response to stimuli such as hot drinks,

alcohol and spicy foods. If this disorder is treated with

potent topical corticoids there may be a temporary

response, but a marked relapse occurs on cessation of

treatment. It is important to check carefully whether or

not steroids have been applied and to dissuade your

patient from using this treatment (like acne vulgaris,

antibiotics are the treatment of choice).

Drug reactions

Drugs are probably the most common cause of acute skin

disease and your history must include a complete history

of all drugs the patient may have been exposed to over

the preceding month. Antibiotics such as ampicillin,

penicillin and sulphonamides commonly cause drug

rashes. It may be difficult to distinguish between a drug

reaction and the manifestations of the disease under

treatment. In addition, drug reaction may closely mimic

skin diseases. Diagnosis may be further confused in

64



Fig. 3.14 Rosacea: lesions occur on the nose, cheeks and chin.



patients taking more than one drug, because it may be

difficult to decide which the offending agent is. Also,

remember that drugs may cause secondary skin eruptions:

broad-spectrum antibiotics may encourage the growth of

candida, which, in turn, can present as a ‘drug-related’

skin rash. Drug reactions may occur within minutes or

hours of taking the medication but there may also be

delays of up to 2 weeks for the reaction to manifest. This

may even follow the discontinuation of the drug (well

known with ampicillin). It is important to recognise

different expressions of drug sensitivity.

Differential diagnosis

Skin lesions associated with drug sensitivity



•

•

•

•

•

•

•

•

•



Toxic erythema

Exfoliative dermatitis

Urticaria

Angioneurotic oedema

Erythema nodosum

Erythema multiforme

Fixed drug reaction

Photosensitive drug reactions

Pemphigus



Chapter



Examination of the skin, hair and nails

Toxic erythema



3



Questions to ask



Profuse eruptions affect most of the body. Red macules

appear and overlap and coalesce to give the appearance

of diffuse erythema (Fig. 3.15). The erythematous skin

desquamates as it heals. This condition is most often

caused by ampicillin but also by sulphonamides (including

co-trimoxazole), phenobarbital and infections.



Exfoliative dermatitis



• Is there any loss of hair or nails?

• Have you ever had psoriasis or eczema?

• What drugs have you taken recently (barbiturates,

sulphonamides, phenylbutazone, streptomycin)?

• Do you have a fever?



Exfoliative dermatitis

Also known as erythroderma, this form of dermatitis

is characterised by diffuse erythema and desquamation

of the epithelium. If severe, the patient may lose both

heat and fluids. Many drugs are implicated, although

barbiturates, sulphonamides, streptomycin and gold are

especially predominant.



Urticaria

This presents with intense itching and localised swellings

of the skin that may occur anywhere on the body.

Typically, wheals occur that are red at the margins with

paler centres (Fig. 3.16). The characteristic feature of the

rash is its tendency to disappear within a few hours.

Angio-oedema usually occurs in association with urticaria

and is characterised by swelling of the face and hands.

Erythema nodosum



Fig. 3.15 Toxic erythema.



Fig. 3.16 Urticaria: lesions vary in size and

shape.



Symmetrical in distribution, the acute crops of painful,

tender, raised red nodules usually affect the extensor

surfaces, especially the shins but also the thighs and

upper arms (Figs 3.17, 3.18). Over 7–10 days, the lesions

change colour from bright red through shades of purple

to a yellowish area of discoloration. Erythema nodosum

is caused by vasculitis, may be recurrent, and is

most commonly associated with sulphonamides, oral

contraceptives and barbiturates.



Fig. 3.17 Erythema nodosum: painful,

smooth red nodules on the lower leg.



Fig. 3.18 Erythema nodosum: the nodules

are raised and tender.

65



Chapter



3



Skin, hair and nails

Differential diagnosis

Erythema nodosum



Infections



•

•

•

•

•



Streptococcal infections

Tuberculosis

Leprosy

Syphilis

Deep fungal diseases



Drugs



• Sulphonamides

• Barbiturates

• Oral contraceptives

Systemic diseases



• Sarcoidosis

• Inflammatory bowel disease



Fig. 3.19 Erythema multiforme: the lesions are widespread on this

patient.



Erythema multiforme

This is characterised by symmetrical, round (annular)

lesions occurring especially on the hands and feet but

which may extend more proximally (Figs 3.19, 3.20).

Central blistering may occur, giving the appearance of

‘target’ lesions. In severe forms, bullae may appear. This

skin disease occurs with drugs, vaccination and, frequently,

with a herpes simplex infection.

Stevens–Johnson syndrome

This is a severe blistering form of erythema multiforme

with blistering and ulceration affecting the mucous

membranes of the mouth and often affecting the eyes

and nasal and genital mucosa (Fig. 3.21).

Fixed drug eruption



Fig. 3.20 Erythema multiforme.



This presents with one or more red blotches that

may become swollen and even bullous. The rash always

recurs in the same anatomical site: usually the mouth,

a limb or genital area. The rash fades, leaving an

area of skin discoloration (Fig. 3.22). Associated

with many drugs but especially phenolphthalein

(common in laxatives), sulphonamides, tetracycline and

barbiturates.

Photosensitive drug rashes

This rash occurs in sun-exposed areas (face, necklace

region and extensor surfaces of limbs). It may appear

as erythema, oedema, blistering or an eczematous

rash.



66



Fig. 3.21 Stevens–Johnson syndrome: ulceration is present on the

lips and in the mouth.



Chapter



Examination of the skin, hair and nails



Fig. 3.22 Fixed drug eruption, with hyperpigmentation of the



3



Fig. 3.23 Eczema: note the vesicle formation.



breasts.



Differential diagnosis

Photosensitive skin reactions



Drugs



•

•

•

•

•



Tetracyclines

Sulphonamides

Phenothiazines

Psoralens

Hydroxychloroquinones



Systemic disorders



•

•

•

•



Pellagra (nicotinic acid deficiency)

Systemic lupus erythematosus

Porphyria cutanea tarda

Erythema multiforme



Fig. 3.24 Acute eczema: red exudative eruption which is painful.



Eczema

This common skin abnormality is caused by a number

of different mechanisms and the disease may be acute,

subacute or chronic, all of which may coexist. Itching is

a major symptom. Acute eczema is characterised by

oedema, vesicle formation (Fig. 3.23), exudation (weeping)

(Fig. 3.24) and crusting. In chronic eczema there are

dry, scaly, hyperkeratotic patches and thickening and

fissuring of the skin (Fig. 3.25). The appearance of

eczema is often modified because the patient scratches,

causing secondary changes such as excoriation and

secondary infection. The boundaries of an area of

chronic eczema are less well defined than psoriasis and

this may be a helpful sign in the differential diagnosis

(Fig. 3.26).

Discoid (nummular) eczema Unlike other forms of

eczema, this subtype has a well-defined, coin-shaped (L.

nummularius = of money) outline and may be confused

with psoriasis. However, nummular eczema tends to

occur on the back of the fingers and hands. It also weeps



Fig. 3.25 Chronic eczema: the skin is dry and scaly.



and does not have the characteristic scales typical of

psoriasis.

Atopic eczema This usually presents in infancy, although

it does occasionally present for the first time in adulthood.

There is normally a family history of eczema or some

other atopic disorder (e.g. asthma, hay fever, urticaria).

The rash is symmetrical, usually starting on the face



67



Chapter



3



Skin, hair and nails



Fig. 3.28 Seborrhoeic dermatitis in an infant.

Fig. 3.26 Typical appearance of eczematous lesion. Note that the

boundary is less distinct than plaques of psoriasis.



Fig. 3.29 Seborrhoeic dermatitis occurs most commonly on the

Fig. 3.27 Contact dermatitis caused by shampoo.



and migrating to the trunk and limbs (where it tends

to affect the flexures of the elbows, knees, wrists and

ankles).

Contact dermatitis This variant of eczema is caused

by an exogenous irritant (Fig. 3.27). The lesion may

be a primary irritant phenomenon, occurring almost

predictably when skin contact is made with a concentrated

toxic agent, or an allergic contact dermatitis which only

occurs in patients who generate a delayed (type IV)

immune response to a substance in contact with the skin.

The distribution of the eczema may provide an important

clue to the nature of the topical irritant. Individuals

who regularly immerse their hands in water containing

detergents or other sensitising substances will present

with the rash restricted to the hands. Jewellery may

cause an allergic contact dermatitis; nickel is an

important sensitising agent. Rubber, dyes, cosmetics

and industrial chemicals are common allergens implicated

in this immune-mediated form of eczema. Plants

such as primulas and chrysanthemums have also been

implicated.

Seborrhoeic dermatitis This is an eczematous condition

occurring in infants (Fig. 3.28), adolescents and young

adults. There is erythema and scaling with a symmetrical

rash (Fig. 3.29). Secondary infection may occur, altering

68



face.



the appearance of the primary lesion. The scalp is most

commonly involved and the condition is distinguished

from dandruff by the associated erythema of the skin due

to inflammation. Other regions involved include the

central areas of the face, eyelid margins, nasolabial folds,

cheeks, eyebrows and forehead. Involvement of the

outer ear occurs (otitis externa). The vulva may also be

affected.

Pompholyx Pompholyx is another variant of eczema

affecting the hands and feet (Figs 3.30, 3.31). This variant

is characterised by the eruption of itchy vesicles, especially

on the lateral margins of the fingers and toes, as well as

the palms and soles.

Varicose eczema This subtype occurs in patients with

longstanding varicose veins. The eczematous patches

affect the lower leg and may or may not be associated

with other skin disorders caused by varicose veins; for

example, venous ulcers that occur in the region of the

medial malleolus, pigmentation and oedema.

Psoriasis

The lesions are well-defined, slightly raised and

erythematous. In the chronic phase, silvery scales cover

the surface. The lesions vary in size from small (guttate)