Skin lesions; history and examination
Date
Topic
Speaker
Thursday 29 September 2011
0900-1000
Introduction to Dermatology
Dr M Goodfield
Thursday 6 October 2011
0900-1000
Eczema
Dr S Shanmugam
1000-1045
Psoriasis
Dr S Zaghloul
COMFORT BREAK
1115-1215
Skin Cancer
Dr S Zaghloul
LUNCH
Thursday 13 October 2011
1330-1430
Dermatology & Systemic Disease
Dr M Goodfield
1430-1530
Acne & Rosacea
Dr S Zaghloul
1530-1600
Urticaria
Dr S Zaghloul
0900-1000
Infections & Infestations
Dr S Zaghloul
1000-1100
Quiz
COMFORT BREAK
1130-1230
Revision Lecture
Dr S Shanmugam
Skin lesions; history and examination
Skin lesions; history and examination
Terminology:
Lesion = general term for an area of disease, usually small
Eruption (rash) = more widespread involvement, normally composed of several lesions, which may be the primary
pathology (papulaes, vesicles or pustules) or due to secondary factors such as scratching or infection (crusting,
lichenification or ulceration)
Skin lesions; history and examination
Skin lesions; history and examination
History:
PC:
 When, where and how the problem started
 What the initial lesions looked like and how they evolved or extended
 Symptoms such as itching must be recorded along with exacerbating/relieving factors.
PMH:
 Previous skin disease or atopic symptoms (hay fever, asthma, childhood eczema)
 Internal medical disorders may manifest as skin lesions so are important
 Drugs may cause an eruption
DH:
 Cosmetics and moisturising creams can also cause dermatitis.
SH: can cause or influence a complaint
 Occupation: can induce contact dermatitis; suspect if lesion improves when on holiday
 Travel: exposes skin to subtropical infections and sunlight (including sunbeds)
FH:
 Tuberous scleross is genetically inherited
 Psoriasis and atopic eczema have a strong hereditary component
 If another family member has a similar presentation, suspect infection or infestation.
Examination:
Examine whole skin, especially in atypical or widespread eruptions; pt may also think some lesions are not important
or be unaware of their existence.
 Note distribution and colour of lesions
o Localised (tumour);
o Widespread (rash); is the eruption symmetrical, and if so, peripheral or central.
o Flexure aspects involved? (atopic eczema)
o Extensor aspects involved? (psoriasis)
o Is it limited to sun-exposed areas?
o Is it linear?
o Dermatomal pattern (herpes zoster = shingles)
o Regional pattern (axilla, groin) = specific conditions usually (eg guttate psoriasis and tinea versicolor
tend to occur on trunk; lichen planus around the wrists; contact dermatitis on face and hands)
 Examine morphology of individual lesions; their size, shape, border changes and spatial relationship.
Palpation reveals consistency, depth and texture of lesions.
Configuration of lesions
Configuration
Condition
Linear
Psoriasis, lichen striatus, linear epidermal naevus, lichen planus, morphoea
Grouped
Dermatitis herpetiformis, insect bites, herpes simplex
Annular
Tinea corporis (ringworm), mycosis fungoides, urticaria, granuloma annulare, annular
erythemas
Koebner phenomenon
Lichen planus, psoriasis, viral warts, molluscum contagiosum, sarcoidosis
Koebner phenomenon = lesions appear in an area of trauma that is often linear (eg a scratch)


Assess nails, hair and mucus membranes and general examination (eg for lymphadenopathy common in skin
malignancy); examine pedal pulses in pts with leg ulcers
Utilise special technique:
o microscopy of scrapings treated with potassium hydroxide soln: can fonfirm presence of fungal
hyphae
o Wood’s (UV) light: will cause hair and to a lesser extent skin to fluorescesin certain fungal infections;
may also be used to show up vitiligo or hypopigmented macules in TB
o Surgical biopsy: ccan excise lesions as a treatment or use to confirm a diagnosis
o Photography: to record lesions
o Patch testing and skin pricks for type 1 hypersensitivity
Skin lesions; history and examination
Potential Treatments:
1. Topical Therapy: direct delivery so reduced side-effects/toxicity; consists of a vehicle (base) which contains
active ingredient
a. Lotion: liquid vehicle (aqueous or alcohol-based); cool the skin and used for inflamed/exudative
conditions
b. Cream: semi-solid emulsion of oil in water; contains emulsifier for stability and preservatives to
prevent microorganism overgrowth; high water content means it is easy to apply, evaporates and is
non-greasy
c. Gel: transparent semi-solid non-greasy emulsion
d. Ointment: semi-solid grease or oil; no preservative needed; active ingredient suspended (not
dissolved); best for skin conditions eg eczema as rehydrate and occlude skin; difficult to wash off so
often not accepted by pts.
e. Paste: ointment base with high proportion of powder producing stiff consistency; good for applying
to well-defined surfaces eg psoriatic plaques
f. Emollients: help dry skin conditions eg eczema and ichthyosis by re-establishing a lipid layer and
enhancing rehydration of the epidermis. Common are: emulsifying ointment, aqueous cream,
Unguentum M, Diprobase, Hydromol, E45 Ultrabase.
2. Systemic Therapy:
a. For more serious infections and conditions
Skin lesions; history and examination
Skin lesions; history and examination
Eruptions:
Psoriasis, eczema, lichenoid eruptions, papulosquamous eruptions, erythroderma, photodermatology
Infections:
Bacterial (staph and strep), viral (warts, HSV, HIV), fungal, tropical, infestations
Disorders of specific skin structures:
Sebaceous and sweat glands (acne, rosacea), disorders of hair, disorders of nails, leg ulcers, pigmentation
Allergy and autoimmunity:
Urticaria, angioedema, blistering disorders, connective tissue disease, vasculitis and reactive erythemas
Skin tumours:
Benign tumours, naevi, malignant melanoma, malignant epidermal tumours
Skin lesions; history and examination
Eczema/ ‘dermatitis’
Definition
Non-infective, inflammatory condition; ‘boil over’; acute eruption with blistering
Classified according to cause, site or morphology; inconsistent classification: may have exogenous/ endogenous or
acute/chronic (though in clinical practise often no classified and just labelled ‘eczema’)
Acute eczema: epidermal oedema (spongiosis) with separation of keratinocytes leads to formation of epidermal
vesicles. Dermal vessels are dilated and inflammatory cells invade dermis and epidermis.
Chronic eczema: thickening of prickle cell/spinosum layer (acanthosis) and stratum corneum (hyperkeratosis) with
retention of nuclei by some corneocytes (parakeratosis). Rete ridges are lengthened, dermal vessels dilated, and
inflammatory mononuclear cells infiltrate the skin.
Contact dermatitis:
Definition
Epidemiology
Aetiopathogenesis
Pathology
Clinical presentation
Differential diagnosis
Complications
Management
Dermatitis precipitated by an exogenous agent, often a chemical
Common in the home amongst women and young children, and industry
Irritants (water, abrasives: frictional irritancy, chemicals, solvents and detergents) more
often than allergens (allergic contact dermatitis = type 4 hypersensitivity)
If strong irritant = necrosis of epidermal cells within hours; but more often effect is
chronic; more common in those with a Hx of ectopic eczema
Any part of body, hands and face most common; nickel is most common contact allergy so
watch out for watch buckles and cheap earings
Endogenous eczema, latex contact urticaria, psoriasis, fungal infection, contact dermatitis
in face may resemble angiodema or erysipelas
Identify the causative allergen, possibly using patch testing.
Avoidance measures: exclude allergen from pt’s life either by PPE/industrial hygiene and
adequate washing/drying facilities. Barrier creams seldom successful.
Topical steroids may help but are secondary to avoidance measures
Common allergens/irritants: nickel (jewellery), rubber chemicals (tyres, boots, belts, condoms, gloves), fragrance,
chromate, cobolt, preservatives, paraphenylenediamine; medicaments and cosmetics
Skin lesions; history and examination
Atopic eczema:
Definition
Epidemiology
Aetiopathogenesis
Pathology
Clinical presentation
Differential diagnosis
Investigations
Complications
Management
Chronic pruritic inflammation of the epidermis and dermis; often fx of asthma, allergic
rhinitis (hayfever), conjunctivitis or atopic eczema
Incidence ~15% infants; starts within 6 months of life and in 1 year 60% have developed it;
2/3 have Fx of atopy; remission by 15yo in 75% cases
Atopy = high levels of circulating IgE (commonly to inhalant allergens eg dust mite); Th2
response dominates
Varies depending on age:
Infants: most common; itchy vesicular exudative eczema on face and hands (often
secondary to infection): ?uncontrollable scratching
Childhood: after 18months, pattern changes to involvement of antecubital and popliteal
fossae, neck, wrists and ankles. Neck often shows erythema and infraorbital folds.
Lichenification, excoriations and dry skin are common and palmar markings may be
increased. Scratching/rubbing cause most clinical signs and big problem at night.
Adults: most common is hand dermatitis in someone with a past history of atopic eczema
Infantile flexural eczema may develop into atopic variety; ?scabies;
Prick tests to inhalant allergens are often positive
Total serum IgE levels raised in 80% cases
Tests are rarely needed for diagnosis
Bacterial infection: secondary infection by Staph A causes exacerbation
Viral infection: increased susceptibility to infection with molluscum contagiosum
Eczema herpeticum: propensity to develop widespread lesions with herpes simplex
Cataracts: infrequent but can occur in young adults with severe atopic eczema
Growth retardation in children: unknown cause
Ichthyosis vulgaris is more common in pts with atopic eczema
Explain the disorder and good prognosis
Avoid tight clothing and excessive heat and pets
Emollients: moisturise dry skin and reduce pruritis
Topical steroids: 1% hydrociortisone
Other forms of eczema: suborrhoeic dermatitis
Definition
Chronic, scaly inflammatory eruption usually affecting the scalp and face
Aetiopathogenesis
Sebum production is normal but eruption often occurs in sebaceous gland areas of face,
scalp and chest; overgrowth of commensal Pityrosporum ovale involved; this condition is
severe in pts with HIV
Clinical presentation
Four patterns:
1. Scalp and facial involvement: excessive dandruff; itchy erythematous eruption
affecting sides of nose, scalp, margin, eyebrows and ears; common in young males
2. Petaloid: dry scaly eczema over the presternal area
3. Pitysporum folliculitis: an erythematous follicular eruption with papules or pustules
over the back
4. Flexural: involvement of the axillae, groins and sub-mammary areas, often colonised
by C. albicans; seen in elderly commonly
Management
Scalp lesions: medicated shampoo
Facial, truncal, flexural involvement: an imidazole or antimicrobial (?+steroid)
Other forms of eczema: discoid (nummular) eczema
Definition
Eczema of unknown aetiology characterised by coin-shaped lesions on the limbs
Epidemiology
Middle-aged or elderly men commonly
Clinical presentation
Coin-shaped lesions are often symmetrical and itchy; eczema may be identified as chronis,
vesicular and lichenified; secondary bacterial infection common
Differential diagnosis
Tinea corporis and contact dermatitis
Management
Topical steroid (?+antimicrobial)
Skin lesions; history and examination
Other forms of eczema: venous (stasis) eczema
Definition
Eczema affecting lower legs and is associated with underlying venous disease
Epidemiology
Middle-aged or elderly women
Aetiopathogenesis
Incompetence of the deep perforating veins increases hydrostatic pressure in the dermal
capillaries
Clinical presentation
Leashes of venules and haemosiderin pigmentation around the ankles are early signs.
Eczema develops, sometimes with fibrosis of dermis and subcutaneous tissue
(lipodermatosclerosis) and ulceration.
Management
Emollient with ?topical steroid; venous disease treated accordingly
Other forms of eczema: hand dermatitis
Epidemiology
Young adults in warm weather
Aetiopathogenesis
Children: mostly due to atopic eczema
Adults: previous atopy? with exposure to irritants
Clinical presentation
Often presents as chronic eczema but may appear as a vesicular eruption known as
pompholyx; vesicles may be seen with atopic eczema or contact dermatitis but there is
usually no associated disorder in pompholyx.
Management
Acute pompholyx requires draingage of large blisters and application of wet dressings;
potent steroid lotions/creams
Other forms of eczema: asteatotic eczema
Definition
Dry eczema with fissuring and cracking in the skin, often affecting limbs in elderly
Aetiopathogenesis
Overwashing of pts in institutions, a dry winter climate, hypothyroidism and use of
diuretics can produce eczema in elderly atrophic skin
Clinical presentation
Skin of limbs and trunk is dry, ertythematous and itchy, showing a fine crazy-paving style
of fissuring
Management
Emollients are usually sufficient
Skin lesions; history and examination
Psoriasis
Definition
Epidemiology
Aetiopathogenesis
Pathology
Chronic, non-infectious inflammatory dermatosis characterised by erythematous plaques
topped by silvery scales
Affects 1.5-3% Europe and N America population; men=women; onset at any age, even in
elderly but peaks of onset 2nd-3rd and 6th decades; unusual in children <8yo
Genetics: 35% have fx; twin studies = 73% concordance; trigger = environmental
Epidermal kinetics: epidermal cell proliferation = increased 20x; turnover time reduced
from 28days to 4days
Precipitating factors: Koebner phenomenon (trauma eg scratch or scar) may trigger
damaged skin; infection: streptococcal sore throat may precipitate guttae psoriasis;
drugs: β-blockers, lithium and antimalarials; sunlight: 10% aggravates it but usually makes
it better; stress aggravates it
Thickened epidermis with keratinocytes retaining nuclei. There is no granular layer and
keratin accumulates at the stratum corneum. Rete ridges are elongated and polymorphs
infiltrate up into the stratum corneum where they form micro abscesses. Capillaries are
dilated in papillary dermis. Lymphocytes infiltrate early on and may initiate many of the
changes seen.
Skin lesions; history and examination
Clinical presentation
Differential diagnosis
Complications
Management
Varies from trivial to life-threatening
Plaque (classic): well-defined disc-shaped plaque involving elbows, knees, scalp hair
margin or sacrum; plaques are red and covered in white waxy scales which if detached
may leave bleeding points; vary in size and may be pruritic
Guttae: acute symmetrical eruption of ‘drop like’ lesions usually on the trunks and limbs;
mostly in adolescents and follows streptococcal infection
Flexural: affects axillae, sub-mammary areas and natal cleft; plaques are smooth and
often glazed; common in elderly
Localised:
 Palmoplantar pustulosis: yellow-brown coloured steril plaques on plams or soles;
middle-aged women, smokers
 Acrodermatitis of Hallopeau: uncommon indolent form affecting digits and nails
 Scalp involvement: appears like dandruff but is generally demarcated and more thickly
scaled
 Napkin psoriasis: well-defined psoriasiform eruption in nappy area
Generalised pustular: rare but serious; sheets of small, sterile yellowish pustules develop
on an erythematous background and may rapidly spread. Acute onset too. Pt is unwell –
fever, malaise, hospital admission.
Nail involvement: affects nails in 50% cases and associated with psoriatic arthropathy;
thimble pitting commonest; then onycholysis; subungal hyperkeratosis affects toe nails
mainly (build up of keratin beneath distal nail edge)
Plaque (classic): psoriasiform drug eruption (β-blockers)
Palmoplantarform psoriasis: Reiter’s disease
Scalp psoriasis: seborrhoeic dermatitis
Flexural: candidiasis of the flexures
Nail involvement: fungal infection of the nails
Psoriatic arthropathy: psoriatic joint disease occurs in 5% of psoriasis pts. 4 forms:
Distal arthritis: commonest; swelling of terminal IPJ of hands and feet sometimes with a
flexion deformity; sausage-like swelling of digits may result
Rheumatoid-like arthritis: mimics RA with a polyarthropathy but less symmetrical and RF
test –ve.
Mutilans arthritis: ass with severe psoriasis; erosions develop in small bones of hands and
feet; progressive deformity
Ankylosing spondylitis: often ve for HLA-B27
Non-infectious nature and long-term therapy to be explained to pt
Topical:
Vit D analogues (inhibit cell prolif and stim keratinocyte differentiation); clean and good
compliance = 1st line
Topical corticosteroids: clean, non-irritant and easy to use; side effects
Coal tar preparations: inhibit DNA synthesis; smells and messy
Dithranol: anti-mitotic effect; irritant to normal skin; stains everything a purply colour
Keratolytics: scalp psoriasis
Systemic: if psoriasis unresponsive,life-threatening or inhibiting pt to work
Methotrexate, retinoids, cyclosporin
Skin lesions; history and examination
Skin lesions; history and examination
Acne vulgaris (spots)
Definition
Epidemiology
Aetiopathogenesis
Clinical presentation
Chronic inflammation of the pilosebaceous units, producing comedones, papules,
pustules, cysts and scars
Almost every adolescent, 12-25yo; men=women; peak age = 18yo; 3/10 teenagers have
acne bad enoughto warrant treating to prevent scarring
Increased sebum excretion, pilosebaceous duct hyperkeratosis, colonisation of the duct
with Propionibacterium acnes, release of inflammatory mediators
Comedones: due to blocked pores that sebum would normally pass
 Open (black heads): dilated pores with black plugs of melanin-containing keratin,
oxidized oil and dead skin cells; nb the black of black-heads is due to skin pigment not
dirt
 Closed (whiteheads): small, cream/skin-coloured/slightly red dome shaped papules
raised bumps on skin surface).
They appear and can evolve into inflammatory papules, pustules (same as papules but
have a central pocket of pus) or cysts (v destructive).
Look for scarring and hyperpigmentation, which occurs when acne heals especially if
nodules were present; atrophic in nature leading to ‘ice-pick’ scars or ‘pock marks’
Appear on face, shoulders, back, upper chest => areas of many sebaceous glands
Whiteheads may seem like they appear
overnight, but they can actually take up to
two months to form before they're visible.
Whiteheads form when the pore is totally
blocked, and the growing matter has
forced the comedo (blockage) to just
beneath the surface of the skin.
If there is a plug of cells in the pore and the
pore opening expands, so that it's not
entirely blocked off, then a blackhead
appears. The portion of the comedo that is
nearest the surface has a concentration of
melanin, giving it its appearance and
appropriate name.
Differential diagnosis
Complications
What makes it worse?
Rosacea, bacterial folliculitis (often more acute than acne)
Embarrassment, shame and lack of confidence, scarring
 The progestogen-only contraceptive pill may make acne worse.
 In women, the hormone changes around the monthly period may cause a flare-up of
spots.
Skin lesions; history and examination

Management
Acne Rosacea
Definition
Epidemiology
Aetiopathogenesis
Thick or greasy make-up may, possibly, make acne worse. However, most make-up
does not affect acne. You can use make-up to cover some mild spots. Noncomedogenic or oil-free products are most helpful for acne-prone skin types.
 Picking and squeezing the spots may cause further inflammation and scarring.
 Sweating heavily or humid conditions may make acne worse. For example, doing
regular hot work in kitchens. The extra sweat possibly contributes to blocking pores.
 Spots may develop under tight clothes. For example, under headbands, tight bra
straps, tight collars, etc. This may be due to increased sweating and friction under
tight clothing.
 Some drugs can make acne worse; phenytoin, steroids and ointments
 Anabolic steroids (which some body-builders take illegally) can make acne worse.
Some myths and wrongly held beliefs about acne
 Acne is not caused by poor hygiene. In fact, excessive washing may make it worse.
 Diet has little or no effect on acne. For example, there is no evidence that chocolate,
sweets, or fatty foods cause acne or make acne worse.
 Stress does not cause acne.
 Acne is not just a simple skin infection. The cause is a complex interaction of changing
hormones, sebum, overgrowth of a normally harmless bacteria, inflammation, etc,
(described above). You cannot 'catch' acne - it is not contagious.
 Acne cannot be cured by drinking lots of water.
 There is no evidence to say that sunbathing or sunbeds will help to clear acne.
 Some people believe that acne cannot be helped by medical treatment. This is not
true. Treatments usually work well if used correctly
Depends on type, extent and psycholigcal distress. OTC remedies tried but no effect.
Treatment = a single drug, combination or oral Abx
1. Mild acne black/whiteheads, pimples; unlikely to scar: single treatment
Benzoyl peroxide cream (2.5, 4, 5, 10%): kill bacteria P. acnes, reduces inflammation and
helps to unplug blocked pores; use 30 mins after washing face; use lowest strength first,
applying od and washing off after several hours over time ↑ time left on face with aim to
apply bd; s/e = irritation, contact allergy, stains clothing, hair and bed linen
Topical retinoid eg (iso)tretinoin, adapalene: prescription only; ↓ number of comedones
and unblocks them, slightly anti-inflamm; s/e = irritant (red skin that settles over time);
spots may get a bit worse before improving; skin may be more sensitive to light so apply
ON and wash in the am; congential abnormalities risk so use contraception
2. Moderate acne: larger spots and inflammation; combined treatment
Benzoyl peroxide combined with topical Abx (consider an oral Abx if acne on the back and
hard to reach to apply cream, or if oral Abx can’t be tolerated)
Antibiotics: tetracycline, oxytetracycline, clindamycin, erthyromycin; kill bacteria but
don’t unblock comedones
Consider a standard combined oral contraceptive in women who require contraception
and acne appears related to menstrual cycle; suppress sebum production; oestrogen-part
of the pill is thought to help; variant of pill is co-cyprindiol (Dianette; oestrogen pluc
cyproterone, an anti-androgen) may be useful if androgen sensitivity is making acne worse
Self-care for pts:
Don’t wash >2x/day; use mild soap or cleanser and lukewarm water; scrubbing or pick
acne is liable to worsen condition (don’t attempt to ‘clean’ blackheads); avoid excessive
make up and cosmetics; use fragrent-free water-based emoillent if dry skin is an issue
Benzoyl peroxidise is available in some OTC meds, but other OTC drugs (antiseptic
washes) lack evidence; use treatment for months! Compliance is an issue. May need to
continue treatment into 20s to avoid acne flair-ups.
Chronic inflammatory facial dermatosis characterised by erythema and pustules
Common in middle-aged (but can occur in young and elderly)
Unknown
Skin lesions; history and examination
Pathology
Clinical presentation
Differential diagnosis
Complications
Management
Vitilgo
Definition
Epidemiology
Pathology
Clinical presentation
Differential diagnosis
Management
Urticaria (hives)
Definition
Epidemiology
Aetiopathogenesis
Pathology
Dilated dermal blood vessels, sebaceous gland hyperplasia and an inflammatory cell
infiltrate seen. Sebum production is normal.
Earliest symptom is flushing. Erythema, telangiectasia, papules, pustules, and sometimes
lymphoedema involve the cheeks, nose, forehead and chin.
Acne. Note that rosacea lacks comedones and appear in elderly unlike acne. Contact
dermatitis, photosensitive eruptions, seborrhoeic dermatitis or lupus erythematosus
involve face but are more acute, scaly or lack pustules.
Rhinophyma-hyperplasia of the sebaceous glands and connective tissue of the nose, and
eye involvement by blepharitis and conjunctivitis
Sunlight and topical steroids exacerbate the condition
Metronidazole gel
Tetracycline or erythromycin.
Plastic surgery is needed for rhinophyma.
An acquired idiopathic disorder showing white scaly macules
~30% of pts have a Fx of the disorder; affects 1% of population, seen in all races;
men=women, onset usually between 10-30yo, may be precipitated by area of injury or
sunburn
Associated with pernicious anaemia, thyroid disease and Addison’s disease (autoimmune)
Sharply defined white macules are often symmetrical; hands, wrists, neck, knees and
areas around orifices (mouth) affected; occasionally it is segmental (down one arm) or
generalised; areas remain static, spread or rarely re-pigment (unknown course)
Post-inflammatory hypopigmentation often associated with other changes
Unsatisfactory; camouflage cosmetics require patience and skill
Common eruption characterisd by transient, usually pruritic, wheals due to acute dermal
oedema from extravascular leakage of plasma
Mediated through immune (allergic) or non-immune mechanisms. Lesions result from
release of histamine from mast cells = vasodilation and increased vascular permeability
IgE mediated (type 1) hypersensitivity: antigen crosslinks IgE on surface of mast cells
Complement activation: can produce dermal oedeam
Direct release of histamine: from mast cells (in non-immune manner); opiods, contrast
media
Blocking of prostaglandin pathway: NSAIDS
A serum histamine-releasing factor: has been suggested in ‘chronic’ urticaria with IgG
found in 60% pts
Dermis is oedematous with dilatation of vessels and mast cell degranulation. Vessel
damage and a lymphocytic infiltrate may be seen with urticaral vasculitis
Skin lesions; history and examination
Clinical presentation
Differential diagnosis
Management
¾ cases fall into 1 or 2.
1. ‘chronic idiopathic’: itchy pink wheals appear as papulaes or plaques anywhere on
skin; typically last for <24hrs, vary in diameter from a few mm to several cm; a fewmany appear/day; condition resolves within a few months usually with no treatments)
2. acute categories: sudden onset; ?due to IgE-mediated reaction; pt often knows
offending allergen: nuts, shellfish, eggs, latex, antibiotics (penicillins), insect bites and
stings,
3. physical urticaria: many causes
o cold: relatively uncommon, affects chilled parts of body eg swimming
(affects whole body)
o sun: solar urticaria; rare, develops on sun-exposed sites
o water: aquagenic; develops on skin exposed to water of any temperature
o demographism: = skin writing (5% people) is whealing due to firm stroking
of the skin
o cholinergic urticaria: = heat bumps; small itchy papules that appear in
response to sweating (due to exercise, heat, emotion, spicy food) and
typically last mins-1hr.
4. hereditary angioedema: rare and ?fatal autosomal dominant condition; present sin
childhood with episodes of angioedema involving the larynx and GIT=> respiratory
obstruction and vomiting and abdo pain; a deficiency of C1 esterase inhibitor allows
complement activation (eg due to trauma) to go unchecked. Attacks are treated with
IV C1 esterase inhibitor. Long term = anabolic steroids inc hepatic synthesis of C1 E.I.
5. urticarial vasculitis: acute onset with widespread lesions that persist for >24hrs and
fade leaving purpura
Angiodema signifies a larger area of skin involving the dermis and subcutis; pemphigoid
and dermatitis herpetiformis occasionally present with urticarial eruptions; toxic
erythema and erythema multiforma may be urticarial at first, but when lesions exist for
>48hrs, urticaria can be excluded; facial erysipelas sometimes resembles angioedema but
has a sharper margin and the pt is unwell with a fever
Eliminate any underlying cause (NSAIDS, swimming)
Antihistamines (H1 blocker): reduce wheal size and itch eg fexofenadine (less sedative) or
cetirizine
Corticosteroids: for severe acute urticaria or angioedema, not for chronic urticaria
Adrenaline: IM injection if airway obstruction
Diet: only if routine measures ineffective; avoid foods with salicylates and azo dyes
(preservatives)
Skin lesions; history and examination
Normal skin flora = harmless bacteria, yeasts and mites. Bacteria usually Staph epidermidis, micrococci,
corynebacteria (diptheroids) and propionibacteria.
Infections


Staphylococcal:
o Primary: impetigo, ecthyma, folliculitis
o Secondary: superinfection of eczema, psoriasis or leg ulcers
Streptococcal:
o Primary: erysipelas or cellulitis, impetigo, ecthyma, necrotising fasciitis
o Secondary: infections of dermatoses or leg ulcers
Bacterial infections: Staphyloccocal
20% of people intermittently carry Staph A in the nose, axilla or perineum. Staph can infect the skin secondary to
eczema or psoriasis too.
Impetigo
Definition
Epidemiology
Aetiopathogenesis
Pathology
Clinical presentation
Differential diagnosis
Complications
Management
Superficial skin infection due to either stapyloccocal or streptococcal infection.
Relatively uncommon in the UK due to improved social conditions. Mainly occurs in
children.
Atopic eczema, scabies, herpes simplex and lice infestation may all become impetiginized.
Thin-walled easily ruptured vesicles, often on the face, which leaves a yellow crusted
exudates. Lesions spread rapidly and are contagious. A bullous form with blisters 1-2cm in
diameter may be seen in all ages and present oon the face and extremities.
Herpes simplex or fungal infection
If impetigo is caused by Strep pyogenes then glomerulonephritis may occur. Treat with
oral phenoxymethylpenicillin (penicillin V).
Removal of crusts with saline soaks and the application of a topical antibiotic (mupirocin,
fusidic acid, neomycin). Systemic fluoxacilin or erythromycin if widespread infection.
impetigo
ecthyma
Ecthyma
Definition
Epidemiology
Aetiopathogenesis
Clinical presentation
Management
Circumscribed, ulcerated and crusted infected lesions that heal with scarring.
An insect bite or neglected minor injury may become infected with staphylococci or
streptococci
Mostly on the legs and may be
seen in drug addicts or debilitated pts.
Treatment with systemic or local antibiotics.
Folliculitis and related conditions
Definition
Infection of the hair follicles; an acute pustular infection of multiple hair follicles (a
furuncle/boil is an acute abscess formation in adjacent hair follicles; a carbuncle is a deep
abscess formed in a group of follicles giving a painful suppurative mass).
Epidemiology
Obesity, DM and occlusion from clothing are RF.
Skin lesions; history and examination
Aetiopathogenesis
Pathology
Clinical presentation
Differential diagnosis
Complications
Management
Folliculitis
Follicular pustules are seen in hair-bearing places – legs or face (beard area in men =
sycosis barbae). Staph A is usually responsible (prolonged AB treatment for acne may
cause a Gram –ve folliculitis eg by pseudomonas). Furuncles present as tender red
pustules which suppurate and heal with scarring, and often occur on the face, neck, scalp,
axillae and perineum. Large carbuncles may cause systemic upset.
Pityrosporum folliculitis is a separate condition caused by commensal yeast.
Infrequent – thrombosis in the cavernous sinus ass with facial infection.
Swabs from the lesion and carrier site are taken for bacterial culture (nose, axillae and
groin). AB administered for local and systemic infections. Carbuncles often require surgical
drainage. General improved hygiene will help – baths in antiseptics and chlorhexidine.
SSSS
Staphyloccocal Scalded Skin Syndrome (SSSS)
Definition
An acute toxic illness with shedding of sheets of skin and infection with phage type 71
staphylococci.
Epidemiology
Infants usually
Aetiopathogenesis
Staphylococci release an exotoxin which causes the epidermis to split.
Pathology
SSSS may follow impetigo.
Clinical presentation
Large epidermal sheets, resembling a scald (red and look sore!), shed leaving a denuded
erythematous area.
Differential diagnosis
In adults, toxic epidermal necrolysis is a related condition. This is a drug-induced eruption
(eg NSAIDs, anticonvulsants, AB and allopurinol), life-threatening disorder. The split is
intra-epidermal; may be a severe form of erythema mulitforme. Results in fluid and
electrolyte imblanaces.
Complications
Good prognosis!
Management
Systemic fluoxacilin or erythromycin
Bacterial infections: Streptococcal
Strep pyogenes (principal skin pathogen) is usually found in the throat and may persist after an infection. It is
sometimes carried in the nose and can contaminate and colonise damaged skin.
Erysipelas
Definition
Epidemiology
Aetiopathogenesis
Pathology
Clinical presentation
Differential diagnosis
Complications
An acute infection of the dermis by Strep pyogenes.
Skin lesions may follow fever, malaise and ‘flu-like’ symptoms.
Strep gain entry to the skin via a fissure eg behind the ear.
Well-demarcated erythema, oedema and tenderness (painful, red swelling). Usually
affects the face (?bilateral), or lower leg. Lesion may blister.
Angioedema or allergic contact dermatitis if lesion occurs on the skin, but it is
distinguished by tenderness and systemic upset.
Recurrent infections in the same place may cause lymphatic damage and =>
Skin lesions; history and examination
Management
lymphoedema. A fatal streptococcal septicaemia may also occur. Guttate psoriasis and
acute glomerulonephritis may follow a streptococcal infection.
Good prognosis if prompt treatment. Topical therapy inappropriate and penicillin should
be prescribed. If severe, parenteral benzylpenicillin at first for a couple of days, then oral
penicillin V for 7-14 days. Recurrent erysipelas (2 or more infections in the same place)
requires prophylactic penicillin V, and good hygiene at entry sites.
Erysipelas
Necrotising fasciitis
Necrotising Fasciitis
Definition
Epidemiology
Aetiopathogenesis
Pathology
Clinical presentation
Differential diagnosis
Complications
Management
Acute and serious infection.
Occurs in otherwise healthy pts after a minor trauma.
Ill-defined erythema, often on the leg, with associated high fever, rapidly becomes
necrotic.
Early surgical debridement and systemic AB are essential.
Diseases due to commensal overgrowth:
Pitted keratolysis
Definition
Epidemiology
Aetiopathogenesis
Overgrowth of micrococci, which digest keratin
Pathology
Clinical presentation
Occurs with occluding footwear and sweaty feet. This causes malodorous pitted erosions
and depressed discoloured areas
Differential diagnosis
Complications
Management
Better hygiene, topical neomycin or aqueous potassium permanganate or aqueous
formaldehyde often help.
Pitted keratolysis
Erythrasma
Skin lesions; history and examination
Erythrasma
Definition
Epidemiology
Aetiopathogenesis
Pathology
Clinical presentation
Differential diagnosis
Complications
Management
Trichomycosis axillaris
Definition
Epidemiology
Aetiopathogenesis
Pathology
Clinical presentation
Differential diagnosis
Complications
Management
A dry, reddy-brown, slightly scaly and usually asymptomatic eruption that affects the body
folds (axillae and groin). It fluoresces coral-pink in Wood’s light due to the production of
porphyrins by the corynebacteria.
Imidazole creams, topical fusidic acid or oral erthyromycin help.
Overgrowths of corynebacteria
Yellow concretions on axillary hair
Topical antimicrobials
Trichomycosis axillaris
Other bacterial infections:
Cellulitis
Definition
Infection of the subcutaneous tissues
Epidemiology
Aetiopathogenesis
Often due to streptococci, but is deeper and more painful than erysipelas. Often gains
access through fissures between the toes or via a leg ulcer
Pathology
Clinical presentation
Swelling, redness and local pain with systemic upset and fever. Often affects the leg
Differential diagnosis
Complications
Lymphangitis is common and lymphatic damage may result.
Management
Lupus vulgaris, anthrax, lyme disease,
Skin lesions; history and examination
Viral infections:
Viruses do not exist on the skin as commensals.
Viral warts (warts = verrucae)
Definition
Common and benign cutaneous tumours due to infections of epidermal cells with human
papilloma virus (HPV)
Epidemiology
Aetiopathogenesis
>70 subtypes of DNA HPV identified; infects by direct inoculation – caught by touch,
sexual contact, swimming baths;
Common hand warts: type 2
Plantar warts: types 1 and 4
Genital warts: types 6, 11, 16 and 18 – these cause cytological dysplasia of the cervix and
may be precancerous
Pathology
Epidermis is thickened and hyperkeratotic. Keratinocytes are vacuolated due to being
infected with the wart virus.
Clinical presentation
Common warts: dome-shaped papules or nodules with a papilloferous surface; usually
multiple; commonly on hands or feet in children (may also affect face and genitals); their
surface interrupts skin lines
Plane warts: smooth-topped papules, often slightly brown in colour, common on face and
dorsal aspect of hands; usually multiple and resist treatment; resolve spontaneously after
becoming inflamed; ?display Koebner phenomenon
Plantar warts: children and adolescents; soles of feet; pressure causes them to grow into
the dermis; painful and covered with a callus, which when removed reveals dark
punctuate spots = thrombosed capillaries; mosaic warts = multiple individual warts
Genital warts: in males, affects the penis, and in homosexuals, the perianal area. In
females, the vulva, perineum and vagina may be involved. Warts may be small or coalesce
into cauliflower-like projection (‘condylomata acuminata’). Perianal and female genital
warts require proctoscopy and colposcopy are needed to treat any rectal and cervical
warts respectively due to risk of neoplastic change. Examin sexual partners too.
Differential diagnosis
Corns on the sole or hand, molluscum contagiosum, if viral warts are under finger or
tonails consider amelanotic malignant melanoma, ,periungal fibroma (of tuberous
sclerosis) and bony subungal exotosis,
Complications
HPV 16 and 18 carry risk of malignant change
Management
30-50% common warts disappear spontaneously within 6 months; hand and foot warts
should be pared with a scalpel or using a pumice stone. This removes keratotic skin and
allows easier treatment.
Molluscum contagiosum
Plantar warts
Viral warts on hand
Mulluscum contagiosum
Definition
Discrete, pearly pink umbilicated papules caused by the DNA pox virus.
Epidemiology
Children and young adults
Aetiopathogenesis
Spread is by contact, sexual transmission or use of bath towels
Pathology
Skin lesions; history and examination
Clinical presentation
Differential diagnosis
Complications
Management
Orf
Definition
Epidemiology
Aetiopathogenesis
Pathology
Clinical presentation
Differential diagnosis
Complications
Management
Dome-shaped papule a few mm in diameter with a punctum in the middle, if squeezed
releases cheesy material; lesions are usually multiple and grouped, common on face, neck
and trunk. Will persist for months untreated.
Removal by forceps, curettage under LA aor cryotherapy. Squeeze them after bathing!
Solitary, rapidly growing papule on the hand due to orf pox virus
Orf pox virus is endemic in sheep causing pustular eruption around the muzzle area;
humans affected = shepherds, vets, farmer’s wife who has bottle-fed the lambs
Solitary red papule on a finger after an incubation period of ~6days. Grows to ~1cm
evolving into a painful purple pustule often with a necrotic umbilicated area
Erythema multiforma and lymphangitis
Sponataneous resolution in 2-4wks. Secondary infection requires Abx.
Herpes Simplex (coldsores)
Definition
Common, acute self-limiting vesicular eruption due to infection of Herpes virus. Recurrent
Epidemiology
Aetiopathogenesis
Highly contagious and spread by direct contact with infected individuals. Virus penetrates
the epidermis or mucous membrane epithelium and replicates in epithelial cells. Remains
latent when non-replicating in dorsal root ganglion fibres. Can reactivate and invade the
skin and cause recrudescent lesions.
Pathology
Two types: though not entirely distinct
Type 1: facial or non-genital
Type 2: genital
Clinical presentation
Type 1: primary infection usually occurs in childhood and is subclinical. Vesicles on the ;ips
and mucous membranes quickly erode and are painful; accompanied by fever, malaise
and local lymphadenopathy lasting ~2wks
Attacks may be precipitated by resp infection (hence ‘cold’ sore), sunlight or trauma.
Herpetic whitlow: painful vesicle or pustule found on a finger
Types 2: seen after sexual contact in young adults who develop vulvovaginitis, penile or
perianal lesions; culture +ve genital herpes simplex in pregnant women indicates c-section
as it can be fatal to neonates if infected.
Recurrence is a hallmark, occurring in a similar place each time. Rarely re-appears as a
zosteriform dermatomal distribution. Preceeded by tingling/burning sensation with crusts
forming within 48hrs.
Differential diagnosis
Impetigo
Complications
Infrequent but serious
1. Secondary bacterial infections: due to Staph A
2. Eczema herpeticum: potentially fatal if pts have atopic eczema or Darier’s disease
3. Disseminated herpes simplex: widespread vesicles in newborn or immunosuppressed
4. Chronic herpes simplex: atypical and chronic lesions seen in HIV +ve pts
5. Herpes encephalitis: not always accompanied by skin lesions
6. Carcinoma of the cervix: more common in women with type 2 viurs
7. Erythema multiforme: herpes is most common cause of recurrent erythema
multiforme
Management
Mild forms = no treatment necessary. Zovirax (acyclovir) applied 5x/day for 5days reduces
length of attack and viral shedding, and be applied at the ‘tingly’ stage. More severe forms
require oral acyclovir 200mg 5x/day for 5days. IV acyclovir in immunosupressed and
infants with eczema herpeticum. In those with genital herpes, oral famcyclovir may help,
and barrier methods should be advised, and sex avoided during symptomatic episodes.
Skin lesions; history and examination
Varicella Zoster (chickenpox)
Definition
Epidemiology
Usually occurs in childhood (Indian subcontinent = affects adults!)
Aetiopathogenesis
Virus enters through upper resp tract; rarely occurring twice in people; infectious spread
is from fresh skin lesions via direct contact or airborne transmission; period of infectivity is
2 days prior to appearance of the rash until all the skin lesions are at the crusting stage;
virus then remains latent in the dorsal root and cranial nerve ganglia
Pathology
Fever, rash, dry cough/ sore throat
Clinical presentation
14-21 days after exposure to VZV: fever, hearache, malaise, eruption (macules to papules
to pustule) in a matter of hours; lesions occur on the face, scalp and trunk, and
?extremities; fever subsides as soon as new lesions cease to appear; pustules crust and
heal w/o scarring
Differential diagnosis
Complications
Scratching causes scarring; pneumonia (begins 1-6 days after skin eruption) – more
common in adults and smokers; bacterial superinfection of skin lesions in 1/10 cases; CNS
involvement in 1/1000 cases presenting as acute truncal cerebellar ataxia and encephalitis
At risk: neonates, elderly, pregnant women (risk of intrauterine infection with structural
damage to fetus; maternal infection within 20wks = varicella embyopathy is 1-2%),
immunocompromised (susceptible to disseminated infection with multiorgan
involvement), people on steroids
Management
Symptomatic relief:
For fever: paracetamol and ibuprofen (liquid forms eg Calpol); if room is warm then
clothes can be removed; plenty of fluids to prevent dehydration; do not cold sponge a
child with a fever as this closes off capillaries and actually retains heat; use a fan but not
directly at the pt;
For itchiness: calamine lotion, ?antihistamines if child >1yo to help child sleep and ↓ itch;
keep fingernails short to reduce scratching
Stay away from school for ~5 days until rash crusted over, and from high-risk groups
There is a vaccine for chickenpox but this is only used in UK for certain groups (used
routinely in USA)
No treatment required in healthy children and infection results in lifelong immunity (USA
give acyclovir for health economic reasons)
Immunocompromised offered protection afterwards with zoster immune immunoglobulin
(ZIG)
If >16yo, give acyclovir within 72hrs of onset
Prophylactic ZIG recommended for women in pregnancy exposed to VZV and if
chickenpox develops, the acyclovir given; if a women has chickenpox at term then baby
should be protected with ZIG if delivery occurs within 7 days of onset of mother’s rash
Tell pt to come and see you if any of these develop:
 Breathing problems.
 Weakness.
 Drowsiness.
 Convulsions.
 Pains or headaches which become worse despite paracetamol or ibuprofen.
 Being unable to take fluids, due to a severe rash in the mouth.
 A severe rash, or a rash which bruises or bleeds into the skin (haemorrhagic rash).
 Becoming generally more and more unwell.
Herpes Zoster (shingles)
Definition
Acute self-limiting vesicular eruption in dermatomal distribution due to
infection/reactivation of varicella zoster virus.
Epidemiology
Nearly always occurs in those who have previously had chicken pox (varicella). 2/3 >50yo
Skin lesions; history and examination
Aetiopathogenesis
Pathology
Clinical presentation
Differential diagnosis
Complications
Management
Varicella lies dormant in sensory root ganglion of spinal cord, reactivates, replicates and
moves along the nerve to the skin producing pain and cutaneous lesions of shingles.
Same as for herpes simplex.
Pain, tenderness or parasthesia (tingling/ burning) in a dermatome a few days before
eruption of the vesicles. Erythema and grouped vesicles follow. Vesicles become pustular
and separate in 2-3wks leaving a scar. Normally unilateral and sensory (dermatomal).
Thoracic dermatomes affected in 50% cases; ophthalmic division of trigeminal nerve
involved in elderly. Contacts with no previous exposure may develop chickenpox.
Lymphadenopathy usual.
Prodromal pain may mimic cardiac or pleural pain, or acute abdo emergency
1. Recurrence in 5% of cases.
2. Secondary bacterial infection
3. Ophthalmic disease: corneal ulcers and scarring
4. Motor palsy: rarely, virus may spread from dorsal (sensory) horn to ventral (motor)
horn. Cranial nerve palsies or paralysis of diaphragm or other muscle groups
5. Disseminated herpes zoster: immunosuppressed pts may develop haemorrhagic
involvement which spread and becomes necrotic or gangrenous.
6. Post-herpetic neuralgia: infrequent in pts <40yo but is found in 1/3 of those >60yo;
pain usually subsides within 12 months; most common complication
Mild: symptomatic treatment; rest, analgesia, bland drying preparations such as calamine
lotions. Abx may be needed if infection too.
Severe: if seen within 48hrs onset, acyclovir 800mg 5x/day for 1wk promotes resolution
and ↓ posthepetic neuralgiaand oral prednisolone for 14days ↓ postherpetic neuralgia
(not if pt is immunosuppressed).
Viral warts
Definition
Epidemiology
Aetiopathogenesis
Pathology
Clinical presentation
Differential diagnosis
Complications
Management
Fungal infections:
Dermatophyte infections:
Definition
Epidemiology
Aetiopathogenesis
Pathology
Clinical presentation
Differential diagnosis
Complications
Management
Yeast Infections (Candida albicans)
Definition
Epidemiology
Aetiopathogenesis
Pathology
Clinical presentation
Differential diagnosis
Skin lesions; history and examination
Complications
Management
Infestations:
Harbouring of insect or worm parasites in or on the body. Worms are infrequent unless in tropical areas.
Insect bite
Definition
Cutaneous reaction following the bite of an insect is pharmacological, irritant or allergic
response to the foreign material.
Clinical presentation
Vary from itchy wheals through papulae or large bullae (blisters). Insect bites are usually
grouped or track up a limb
Lice (pediculosis)
Definition
Epidemiology
Aetiopathogenesis
Pathology
Clinical presentation
Differential diagnosis
Complications
Management
Flat, wingless, blookd-sucking insects. Eggs = nits and are laid on hair or clothing.
Two types:
1. Head louse
2. Body louse (pubic louse is a variant)
 Head lice are commonest in school children and spread by head-to-head contact.
 Body louse usually found on vagrants in unhygienic conditions, spread by infested
bedding/clothing
 Pubic louse is spread by sexual contact and found in young adults = ‘crabs’
Lice cause intense scratching (excoriation), which may lead to secondary infection.
Body lice may result in chronic infestation and lichenification and pigmentation following
excoriation.
Body louse = scabies, chronic eczema
Head louse = impetigo, eczema
Pubic louse = scabies, eczema
Head lice = malathion or carbaryl lotion applied to the scalp for 12hrs and washed out and
repeated for 7 days. Permethrin is an alternative.
Body lice = treat clothing with tumble-drying, laundering or dry-cleaning. Malathion or
phenothrin lotions may be applied to the skin. Sexual partners should be treated too.
Scabies (mite = Sarcoptes scabei)
Epidemiology
Spread by physical transfer including sexual contact
Aetiopathogenesis
Fertilised female burrows through the stratum corneum at 2mm/day, laying 2-3 eggs/day.
The eggs hatch after 3 days into larvae which form shallow pockets in the stratum
corneum where they moult and mature within 2 weeks. The mites mate in the pockets;
male dies and females continues the cycle.
Pathology
After 4-6wks, hypersensitivity reaction forms and intense itching develops. About 12 mites
are present at the itching stage.
Clinical presentation
Irregular, tortuous and scaly burrow measure upto 1cm long. Commonest on fingers,
wrists, ankles, nipples and on the genetalia. Itching induces excoriations.
Often accompanied by an ill-defined eczematous urticated popular hypersensitivity
reaction on the trunk.
Differential diagnosis
Lichen planus, dermatitis herpetiformis, popular uritcaria and eczema may be considered
because they’re itchy, but only scabies burrows.
Complications
Secondary infection
Management
Untreated, it becomes chronic. Malathion and permethrin are common
Lymphatic disorders:
Lymphoedema
Lymphoedema is oedema, often in a limb, due to inadequate lymphatic drainage.
 Primary = the result of a congenital developmental defect; presents in adolescence and may follow infection.
Skin lesions; history and examination
 Secondary = recurrent infection (lymphangitis); blockage (filariasis, tumour), destruction (surgery, radiotherapy)
In chronic lymphoedema, the oedema is non-pitting and the overlying spidermis is hyperkeratotic.
Lymphoedematous limb is at risk iof infection, esp erysipelas, and long-term penicillin V recommended.
Lymphangitis
Lymphangitis is an infection of lymphatic vessels usually die to streptococci that presents as a tender, red line
extending proximally up a limb, usually from a focus of infection. Hospital admission appropriate.
Blistering diseases:
Blistering often seen with skin disease eg acute contact dermatitis, herpes simplex, herpes zoster, bullous impetigo,
insect bites, burns, friction, cold injury.
The type of blister depends on the level of cleavage; subcorneal/intraepidermal blisters rupture easily, subepidermal
don’t.
Primary bullous disorders:
Pemphigus (vulgaris)= superficial
Definition
Uncommon, severe, potentially fatal autoimmune blistering disorder of the skin and
mucous membranes. Associated with other autoimmune disease (myasthenia gravis)
Epidemiology
Middle-aged or young adults
Aetiopathogenesis
90% pts have circulating IgG autoAB which bind desmoglein, a desmosomal cadherin
involved in epidermal intracellular adhesion.
Pathology
Cause loss of adhesion and intraepidermal split.
Clinical presentation
Oral erosions signal the onset of pemphigus vulgaris in 50% pts, preceding blistering by
some months. Flaccid superficial blisters develop over the face, back, chest and flexures.
Blisters may not be obvious and just be crusted erosions. Trunk > limbs
Differential diagnosis
Apthous ulcers or Behcet’s disease can cause oral erosions of pemphigus. If widespread
bulla may be epidermolysis bullosa. Diagnosis relies on histoligical examination of bulla
and immunofluorescence.
Complications
Untreated, blistering is progressive.
Management
Systemic steroids and immunosuppressive agents required. Prednisolone 100-300mg daily
until blistering is controlled. Treatment continued for years normally, though remission
occasionally occurs. Used to be a ¾ mortality rate, but now much lower.
(Bullous) Pemphigoid = deep
Definition
Chronic blistering eruption
Epidemiology
Fairly common in elderly
Aetiopathogenesis
Linear IgG autoAB to bullous pemphigoid Ag in the hemidesmosomes at the basement
membrane bind complement which induce and inflammation and protease release,
leading to subepidermal bulla formation. IgG and C3 are detected by direct
immunofluroscence.
Pathology
Clinical presentation
Tense large blisters arise on red or normal-looking skin often on limbs > trunk and
flexures. Oral lesions only occur in 10% cases. An urticarial eruption may precede the
onset of blistering.
Differential diagnosis
Pemphigus, dermatitis herpetiformis, linear IgA disease. Immunofluorescence and
histology confirm diagnosis.
Management
Responds to lower doses necessary for pemphigus; 30-60mg daily oral prednisolone.
Dermatitis herpetiformis
Definition
Uncommon symmetrical eruption of itchy blisters on extensor surfaces
Epidemiology
30-40s; 2x M>F
Aetiopathogenesis
Finding of granular IgA at the dermal papillae on immunofluorescence and by the
response of the skin lesions (and jejuna villus atrophy seen in 75% pts = seen in celiac
disease!) to a gluten-free diet. Cause of eruptions is unclear.
Skin lesions; history and examination
Pathology
Clinical presentation
Differential diagnosis
Complications
Management
Linear IgA disease
Definition
Differential diagnosis
Management
Groups of small, intensely itchy vesicles on the knees, elbows and buttocks. Excoriations
present. Change in bowels is uncommon despite atrophy of villi. Immunofluorescence
shows subepidermal bulla
Scabies, eczema and linear IgA disease.
Gluten-free diet, but Dapsone (50-200mg) is often given to control the eruptions until the
diet kicks in.
Rare, heterogenous conditions of blisters and urticarial lesions on the back or extensor
surfaces.
Dermatitis herpetiformis or pemphioid.
Dapsone
Connective tissue disorders:
Lupus
Definition
Epidemiology
Aetiopathogenesis
Pathology
Clinical presentation
Differential diagnosis
Complications
Management
Systemic sclerosis
Definition
Epidemiology
Aetiopathogenesis
Pathology
Clinical presentation
Differential diagnosis
Complications
Management
Sscleroderma
Definition
Epidemiology
Aetiopathogenesis
Pathology
Clinical presentation
Differential diagnosis
Complications
Management
Cutaneous systemic disease
Definition
Epidemiology
Aetiopathogenesis
Pathology
Skin lesions; history and examination
Clinical presentation
Differential diagnosis
Complications
Management
Skin cancer
Benign Epidermal Tumours
Seborrhoeic wart/keratosis (basal cell papilloma)
Definition
A proliferation of basal keratinocytes causing hyperkeratotic epidermis, thickened by
basal cell proliferation with keratin cysts
Epidemiology
Affects elderly or middle-aged
Aetiopathogenesis
Unknown cause; seborrhoea is not a feature
Pathology
Clinical presentation
Often multiple on face or trunk, round/oval in shape, start as small papules (lightly
pigmented or yellow) and warty nodules (dark) 1-6cm in diameter; have a ‘stuck on’
appearance with keratin plugs and well-defined edges
Differential diagnosis
May resemble actinic keratosis, melanocytic naevus, pigmented BCC or malignant
melanoma
Complications
Management
Liquid nitrogen cryotherapy; curettage or shave biopsy
Skin Tags
Definition
Epidemiology
Aetiopathogenesis
Pathology
Clinical presentation
Differential diagnosis
Complications
Management
Epidermal Cyst
Definition
Epidemiology
Aetiopathogenesis
Pathology
Clinical presentation
Differential diagnosis
Complications
Management
Milium (pl = milia)
Definition
Epidemiology
Aetiopathogenesis
Pathology
Clinical presentation
Differential diagnosis
Complications
Management
Pedunculated benign fibroepithelial polyps, a few mm in length
Common, mainly seen in elderly or middle aged
Unknown, but often found in obese people
Found in neck, axillae, groin and eyelids
Occasionally confused with seborrhoeic warts or small melanocytic naevi
Usually for cosmetic reasons, snipping the stalk with scissors or using cryotherapy
Keratin-filled and derived from epidermis
Usually seen on the scalp, face or trunk; firm, skin-coloured, mobile and normally 1-3cm in
diameter
Sometimes misleadingly called sebaceous cysts
Bacterial infection
Excision
Often seen in children but can occur in any age
Mostly seen on face (around eyelids and upper cheeks) as small, round keratin cysts (12mm in diameter)
Can normally be extracted using a sterile needle
Skin lesions; history and examination
Benign Dermal Tumours
Dermatofibroma (histiocytoma)
Definition
Dermal nodules
Epidemiology
Commonly women, young adults, lower legs
Aetiopathogenesis
?represent reaction pattern to insect bites or other trauma, though often not the case
Pathology
Histologically, there is proliferation of fibroblasts, with dermal fibrosis and ?epidermal
hyperplasia
Clinical presentation
Usually asymptomatic, firm dermal nodules 5-20mm in diameter and may be pigmented.
They enlarge slowly if at all
Differential diagnosis
Melanocytic naevus or malignant melanoma
Complications
Management
Excision if symptomatic or ?diagnosis
Pyogenic Granuloma
Definition
Epidemiology
Aetiopathogenesis
Pathology
Clinical presentation
Differential diagnosis
Complications
Management
Keloid
Definition
Epidemiology
Aetiopathogenesis
Pathology
Clinical presentation
Differential diagnosis
Complications
Management
A rapidly developing, bright-red or blood-crusted nodule; it is neither pyogenic nor
granulomatous but actually an acquired haemangioma!
Young adults and children
Usually develops at the site of trauma (a prick from a thorn); may be on a lip, face, foot
Bright red, sometimes pedunculated, nodule which bleeds easily. It enlarges rapidly over
2-3wks
Malignant melanoma – need to exclude so send a sample after excision
May reoccur after excision
Curettage and cautery or excision needed
An excessive proliferation of connective tissue in response to skin trauma
More common in black Africans, 20-40yo
Protuberant and firm small nodules or plaques, mainly on upper back, chest and ear lobes,
Differs from a hypertrophic scar as it extends beyond the the limit of the original injury
Injection of a steroid into the keloid
Campbell-de-morgan spot (cherry angioma)
Definition
Benign capillary proliferations, commonly seen as bright red papules on the trunk in
elderly and middle-aged pts.
Epidemiology
Aetiopathogenesis
Pathology
Clinical presentation
Differential diagnosis
Complications
Management
Lipoma
Definition
Epidemiology
Aetiopathogenesis
Pathology
Clinical presentation
Benign tumours of fat
Soft masses in the subcutaneous; often multiple on trunk, neck and upper extremities;
Skin lesions; history and examination
?painful
Differential diagnosis
Complications
Management
Removal is rarely needed
Chondrodermatitis nodularis
Definition
Epidemiology
Elderly
Aetiopathogenesis
Inflammation in the cartilage that may be a response to degenerative changes in the
dermis
Pathology
Clinical presentation
A small, painful nodule on the upper rim of the helix of the pinna
Differential diagnosis
BCC
Complications
Management
Excision is curative
Summary of benign tumours
Lesion
Epidermal
Viral wart
Actinic keratosis
Seborrhoeic wart
Milia
Epidermal cyst
Skin tag
Dermal
Dermatofibroma
Melanocytic naevus
Cherry angioma
Pyogenic granuloma
Keloid
Lipoma
Chrondrodermatitis nodularis
Age of onset
Features
Childhood
Old
Old/middle
Childhood
After childhood
Middle/old
Usually hands and feet
Sun-exposed areas
Keratosis, often on trunk or face
White cysts, often on face
Mostly on face or scalp
Neck, axillae, groin
Young adult, F>M
Teens, young adult
Old/middle
Child/young adult
20-40yo
Any
Old/middle
Nodule, often on leg
Brown macule or papule
Small red papule on trunk
Red nodule, often on finger
Chest and neck, black Africans
Soft tumour on trunk or limbs
Nodule on pinna M>F
Melanocytic Naevi = moles
The most common type are those containing collections of benign melanocytic naevus cells, though others are
found.
Definition
A benign proliferation of one or more of the normal constituent cells of the skin.
Epidemiology
May present at birth (congenital = 1%) or develop during childhood and adolescence; peak
# during puberty; may be provoked by pregnancy or sun-exposure
Aetiopathogenesis
Naevus cells in melanocytic naevi are thought to be derived from melanocytes migrating
to the epidermis from the neural crest during embryonic development. Reson for
development of naevi is unknown; ?inherited trait in families.
Pathology
Position of the naevus cells in dermis = type of naevus
 Junctional = clusters of naevus cells at dermo-epidermal junction
 Compound = found in both areas
 Intradermal = nests of naevus cells in dermis alone
Naevus cells produce melanin (hence brown/black colour). If pigment is deep in dermis,
an optical effect can give the lesion a blue colour = blue naevus!
Clinical presentation of Congenital = usually <1cm in size, vary in colour from light brown to black, often more
naevi
protuberant and hairy, may be disfiguring (rare bathing trunk naevus) and carry a 5% risk
of developing into a malignant melanoma
Junctional = flat macules, vary in size from 2-10mm and colour from light to dark brown,
Skin lesions; history and examination
Differential diagnosis
Complications
Management
Epidermal Naevi
Definition
Epidemiology
Aetiopathogenesis
Pathology
Clinical presentation
Differential diagnosis
Complications
Management
usually round or oval shaped, common on palms, soles and genetalia
Intradermal = dome-shaped papule or nodule that may be skin-coloured or pigmented,
common on face or neck
Compound = usually <10mm in diametersmooth surface and vary in pigmentation; larger
lesions may appear ‘warty’ or cerebriform appearance, occur anywhere on skin
Spitz = firm, reddish brown nodule rounded nodule on the face of a child, rapid growth
initially
Blue = steely-blue colour, solitary, common on extremities – hands and feet especially
Halo/Sutton’s = seen on trunk of children or adolescent and represent the destruction by
the body’s IS of naevus cells in a naevus. A white halo of depigmentation surrounds the
pre-existing naevus that then involutes - ?reason; RF = vitiligo
Becker’s = rare, males, adolescents, unilateral lesion on upper back or chest,
hyperpigmented at first, later becomes hairy.
Dysplastic = irregularity in outline or pigmentation
Freckle: tan-coloured macules on sun-exposed areas
Lentigine: usually multiple, onset in later life
Seborrhoeic wart: stuck-on appearance, warty lesions, may show keratin plugs
Haemangioma: vascular but may show pigmentation
Dermatofibroma: on legs, elevated nodule, firm and pigmented
Pigmented BCC: often on face, pearly edge, increase in size, ulcerate, other photodamage
Malignant melanoma: variable colour and outline, increase in size, itchy, inflamed
Increasing public awareness has meant that normal moles present at the clinic. But
excision occurs if there is:
Concern about malignancy: increase in size, itchiness
An increased risk of malignant change: large congenital naevus
Cosmetic reasons: especially if on face or neck
Repeated inflammation: bacterial folliculitis, often in hairy naevi
Recurrent trauma: naevi on theback that scratch on bra straps
All excised naevi should be sent to histology.
Present at birth or early childhood
Warty, pigmented and frequently linear, a few cm long but may involve the length of the
limb or side of the trunk
Variant on the scalp, naevus sebaceous, carries a risk of malignancy
Excision but recurrence is common
Connective tissue Naevi eg cobblestone naevus (shagreen patch) seen in tuberous sclerosis
Definition
Epidemiology
Rare
Aetiopathogenesis
Pathology
Course collagen bundles in the dermis on histology
Clinical presentation
Smooth, skin-coloured papules or plaques and may be multiple.
Differential diagnosis
Complications
Management
Malignant Skin Tumours Summary
Cell Origin
Keratinocyte
Premalignant Condition
Actinic keratosis
Malignant Tumour
Basal cell carcinoma
Skin lesions; history and examination
Intraepidermal carcinoma Squamous cell carcinoma
Melanocyte
?dysplastic naevus
Malignant melanoma
Fibroblast
Dermatofibrosarcoma
Lymphocyte
Lymphoma
Endothelium
Kaposi’s sarcoma
Non-cutaneous
Secondary
Dermal malignancies very rare; majority are epidermal.
Malignant Melanoma
Definition
Epidemiology
Aetiopathogenesis
Pathology
Clinical presentation
Differential diagnosis
Complications
Management
Malignant tumour of melanocytes usually arising in the epidermis. Most lethal of skin
tumours
Increasing incidence (rises by 7% yearly and doubles every decade) due to increasing sun
exposure (holidays etc) – now 1/10,000; upto 5% have a Fx; F 2x > M; common site on
males is the back, and females are the legs. Incidence is proportional to geographical
lattitude
Not known but repeated, short, intensive exposure to UV radiation may be involved; RF =
dysplastic naevi with Fx (=100-400x inc), >100 melanocytic naevi, congenital naevus
>1.5cm diameter, previous malignant melanoma, red hair/blue eyes =1.5x risk
Any of the following changes in a naevus or pigmented lesion may suggest a malignant
melanoma:
Size: recent increase
Shape: irregular in outline
Colour: variation, lighter or darker
Inflammation: may be at the edge
Crusting: some ooze or bleed
Itching: commonly
Four main clinic-pathological variants are described:
Superficial spreading malignant melanoma: 20-60yo; 50% of all British cases, F>M,
commonest on lower leg, tumour is macular, variable pigmentation often with regression
Lentigo malignant melanoma: >60yo; develops in a long-standing lentigo maligna, 15% of
UK cases, arises in sun-damaged areas (face of an elderly person who has had an outdoor
job)
Nodular malignant melanoma: 20-60yo; 25% of UK pts, M>F, commonest on trunk,
pigmented, grows rapidly and ulcerates
Acral lentigous malignant melanoma: 10% of UK pts, affects the palms, soles and nail
beds, often late diagnosis and poor prognosis
Benign melanocytic naevus; seborrhoeic wart; haemangioma; dermatofibroma;
pigmented BCC; benign lentigo
Recurrence:
 Local
 Lymphatic – regional lymph nodes of in transit in the draining lymph nodes
 Blood-borne to distant sites
Staging: malignant melanomas usually progress through two stages – horizontal (within
the epidermis and may evolve into vertical) and vertical. Metastases are uncommon in
tumours restricted to the epidermis
Prognosis: relates to tumour depth (Breslow thickness = distance between granular cell
layer to the deepest identifiable melanoma cell); 5-year survival rates =
<1mm: 95-100%
1-2mm: 80-96%
2.1-4mm: 60-75%
>4mm: 50%
Surgical excision: tumours of a thickness of <1mm require a 1cm clearance margin; >1mm
require 1-2cm clearance margin; skin grafts may be necessary to close the gap
Malignant Epidermal Tumours
Skin lesions; history and examination
Basal Cell Carcinoma = ‘rodent ulcer’
Definition
Commonest form of skin cancer and seen typically on the face in elderly or middle-aged pt
Epidemiology
Commonest in Caucasians with fair hair who live near the equator; M>F; >40yo (earlier if
in Australia)
Aetiopathogenesis
Malignant transformation of basal cells may be induced by:
 Prolonged UV radiation exposure (acute sunburn)
 Arsenic ingestion (in ‘tonics’)
 X-rays
 Chronic scarring (burns and vaccination scars)
 Genetic predicposition (basal cell naevus syndrome)
Pathology
Arise from basal keratinocytes of the epidermis, are locally invasive but very rarely
metastasize; histologically = uniform basophilic cells in well-defined islands that invade
the dermis from the epidermis as buds, lobules or strands. Invades but almost never
metastasizes
Clinical presentation
Occur on light-exposed areas: nose, inner canthus of the eyelids, temple. The grow slowly
but relentlessly, locally invasive, destroy cartilage, bone and soft tissues. A lesion is often
present for >2years before pt seeks advice. Four main types of BCC:
Nodular: commonest; starts as a small, skin-coloured papule that shows fine
telangiectasia and a glistening pearly edge. Central necrosis occurs leaving a small ulcer
with a crust. Normally <1cm.
Cystic: these become tense and show cystic spaces on histology
Multicentric: superficial, often multiple, several cm in diameter, sometimes seen on the
trunk, have a rim-like edge and are lightly pigmented normally
Morphoeic: most common on the face; shows a white or yellow morphoea-like plaque
that may be centrally depressed.
Differential diagnosis
Depends on type, pigmentation and location of BCC:
Nodular/ Cystic: intradermal naevus, molluscum contagiosum, keratoacanthoma, SCC,
sebaceous hyperplasia (a benign proliferation of sebaceous glands)
Multicentric: discoid eczema, psoriatic plaque, intraepidermal carcinoma
Morphoeic: morphoea
Pigmented: malignant melanoma, seborrhoeic wart, compound naevus
Complications
Recurrence rate of 5% at 5 years
Management
Depends on size, site, type and pt’s age. Complete excision is best. If not possible, then
incisional biopsy (to confirm diagnosis) and radiotherapy.
Squamous Cell Carcinoma
Definition
Epidemiology
Occurs mainly in pts >55yo, M 3x> F;
Aetiopathogenesis
SCC is derived from moderately or well-differentiated keratinocytes
 Chronic actinic damage due to sun-exposure over a lifetime
 x-rays; radiant heat from fires etc
 chronic ulceration and scarring (burns or lupus vulgaris)
 smoking pipes or cigars (relevant for lip lesions)
 industrial carcinogens (coal tars, oils)
 human papilloma (wart) virus and immunosuprresion: transplant pts
 genetic: albinos, xeroderma pigmentosa
Pathology
The malignant keratinocytes still produce keratin so destroy the dermo-epidermal
junction and invade the dermis in an irregular manner
Clinical presentation
Two main types:
Keratosis-dervied: Sun-exposed areas: face, neck, forearm, hand; tumour may start within
an actinic keratosis(a small, rough, raised area found on skin that has been exposed to the
sun over a long period of time)as a small papule that, if left, progresses to ulcerate and
form a crust. This type doesn’t metastasize commonly.
Nodular-type of SCC: dome-shaped, sun-damaged skin, more aggressive ulcers develop in
Skin lesions; history and examination
Differential diagnosis
Complications
Management
scars and chronic scarring sites. Metastases more often.
Keratocanthoma, actinic keratosis, BCC, intyraepidermal carcinoma, amelanotic malignant
melanoma, seborrhoeic keratosis – excisional biopsy required to confirm
May metastasize in >10% cases
Surgical excision; skin grafts may be necessary; biopsy of suspicious lymph nodes.
Premalignant Epidermal disorders
Bowen’s disease (intraepidermal carcinoma)
Definition
Epidemiology
Typically occurs on the lower leg of elderly women; lesions are solitary or multiple
Aetiopathogenesis
Pathology
Transformation into SCC is infrequent; epidermis is thickened and keratinocytes are
atypical but not invasive
Clinical presentation
Pink or lightly pigmented scaly plaques upto several cm in size.
Differential diagnosis
Discoid eczema, psoriasis or superficial BCC
Complications
Management
Cryotherapy, curettage, excision, topical 5-fluorouracil
Southampton hospital – plastic surgeon
Jim brady
sarahloewenberg@gmail.com