DERMATOLOGY LOs

Describing a Primary Skin Lesion

Primary Lesions Secondary Lesions
Flat, non-palpable • Scale – white layer or bran-like change
• Macule – flat <5mm freckles, moles, malignant melanoma • Crust – dried exudate blood/plasma
• Patch – flat >5mm café au lait • Excoriation – scratch marks
Raised, solid mass • Lichenification – thickening of skin with increased skin
• Papule – raised <5mm marking as a result of repeated excoriations
• Domed: acne • Burrows – scabies, cutaneous larva migrans
• Umbilicated: molluscum
• Plaque - raised, flat topped > 5mm psoriatic plaque Vascular Lesions
• Nodule – dome shaped >5mm warts, sebaceous cyst, lipoma • Telangiectasia – superficial blood vessels
• Wheal – dermal oedema • Spider naevus – single arteriole in skin
Raised, fluid mass • Petechiae – micro-haemorrhage 1-2mm
• Pustule – pus filled papules acne vulgaris, pustular psoriasis • Purpura – non blanching red/purple/brown
• Vesicle – clear filled small papules <5mm chicken pox, herpes • Ecchymosis – a “bruise”
• Blister – fluid below epidermis >5mm • Erythema – redness due to local vasodilation
• Bullae – large blisters >1cm epidermolysis bullosa • Haemorrhagic – red, filled with blood
Loss of Skin
• Erosion – partial epidermal loss Colour Change
• Ulcer – full thickness skin loss • Hypopigmentation – reduced pigmentation
• Atrophy – loss of tissue • Hyperpigmentation – increased pigmentation
• Fissure – fine linear crack • Depigmentation – complete loss of pigmentation
History
Basic demographic details Other skin conditions
• Age , sex, race and country of origin, place of residence • Personal history
• Family history
Duration
• How long have they had Past medical history
• Over what period of time have changes occurred • Previous episodes

Associated symptoms Drugs

• Itching, burning, soreness, pain, weeping, oozing, blisters
or odour Social history
• Site of onset and details of spread • Employment (outside/inside)
• Holidays
Fluctuation or persistence
• e.g. an occupational dermatitis will get better on holiday Psychological history
• How is it affecting them?
Provoking or aggravating factors
• Infective/drug triggers can precede the eruption by Systems enquiry
several weeks
• Response or lack of response to previous treatment
• What the patient been using and what effect its had
Examination
A full skin examination is considered best practice Diagnostic greed
• You don’t need all the features of an illness to make the
Inspection diagnosis
• Note general appearance of patient
• Distribution, symmetry and colour of rash Common things are common
• Look closely at the skin to assess morphology of the rash
Beware of the “great mimickers”
Palpation • HIV
• Nails, scalp and oral mucosa may provide additional clues • Syphilis
• Is there genital involvement?

Diagnostic Tools
• Woods light – UV light, fungal infections fluoresce
• Dermatoscope –
Eczema and Dermatitis
Pathology
• Raised TH2 immune response (IgE, eosinophils, TNFa) Clinical Presentation Examination
• Very itchy • Dry, red, scaly skin
• Atopic: filaggrin gene a/w asthma and rhinitis • Sleep disturbance • Weeping/crusting if infected
• Seborrhoeic dermatitis: a/w yeast overgrowth • Rubbing/scratching  lichenification
• Herpeticum: with HSV infection
• Usually symmetrical distribution
• Often on flexor surfaces except infants
Endogenous Exogenous
Atopic = widespread, babies to young adults • Photosensitive = sun-exposed areas Management:
Seborrhoeic = salmon-pink patches that flake, • Allergic contact dermatitis = usually • Emollient: regular soap substitute
sclap, creases (a/w HIV and Parkinsons) hands or face • Topical steroids
Venous = elderly legs, xerotic (dry), atrophie nickel allergy  wrist strap, belt buckle site,
earrings
blanch, ulcers latex allergy  hands
Asteatotic = elderly, red, flakey patches, winter PPD (hair dye)  face
Discoid: round lesions, often infected Chromate (cement)  hands
Vesicular (pomphylox): palmoplantar skin • Irritant contact dermatitis = hands,
hyperkeratosis, fissuring
Pomphylox Atopic

Seborrhoeic (child) Seborrhoeic (adult) Discoid Contact dermatitis Asteatotic Varicose/Gravitational

Lichen Planus Management:
• Topical steroids
• Tacrolimus
Aetiology
• Acute / chronic inflammatory dermatosis • Ciclosporin
• More common in women • Oral steroids
• T cell mediated autoimmune inflammatory condition
• Retinoids (acretin)
History • PUVA
• Family history in 10% - possible genetic link
• Possible association with hepatitis C
• May be drug-induced (antimalarial, quinine, thiazides)

Common Sites
• Skin = forearms, wrists, legs, scalp
• Mucous membranes
• Nails

• Mucosal
• Linear
• Annular
• Pigmented
• Follicular
• Bullous
• Atrophic

Classic Lesion Linear LP Pigmented LP Mucosal LP Cutaneous

• Itchy
• Violaceous (lilac) flat-topped papules
• Symmetrical distribution

Associated Features
• Nail changes and hair loss
• Wickham’s striae = lacy white streaks on oral mucosa and skin lesions
• Koebner phenomenon = lesions occurring along scratch/trauma marks
Annular LP Bullous LP Koebner Classic cutaneous
Acne Vulgaris
Disease of the pilosebaceous unit
Pathology Examination
Androgen-induced seborrhoea (excess grease) Always examine the chest and back of a patient with face acne Comedone (blackhead)
• Sebum is produced by the pilosebaceous glands • Greasy skin (seborrhoea)
• The more sebum the greater degree of acne • Non-inflamed lesions ie comedones - blackheads and
• Increased response of the sebaceous glands to normal whiteheads
levels of plasma androgens • Inflamed lesions - papules, pustules and nodules
• Scarring, which may be due to:
Comedone formation (blackheads, whiteheads) • Loss of tissue, the so-called atrophic or ice pick
• Abnormal proliferation of ductal keratinocytes scar
• Controlled, in part, by androgens • Increased fibrous tissue, the so-called
hypertrophic or keloid scar Papule-pustule
Colonisation of the pilosebaceous duct • Pigmentation, which can be a problem especially in dark
• With Propionibacterium acnes (P. acnes) skin
• Seborrhoea and comedone formation alter ductal micro
environment, which results in colonisation of the duct Treatment: take at least 3 month to show effect
• Is a later stage in acne development (esp inflam lesions) Mild:
• topical retinoid – reduce inflammation
Production of inflammation • topical antibiotic – anti-inflammatory and antibacterial
• Biological changes occurring in the duct as a result of • Benzoyl peroxides 5% - antibacterial Nodule
comedone formation and P. acnes colonisation of the Moderate:
duct • As above plus
• Patients cellular (especially lymphocytes) response • Oral antibiotic (doxycycline) for 6 month
within the dermis, which responds to pro-inflammatory • Oral contraceptive pill
cytokines spreading from the duct to the dermis Severe:
• vit A derivative (isotretinoin aka roaccutain) for 4
months – reduces sebum production
• Teratogenic, dry mucous membranes, hair loss
“Ice-pick” scars
Rosacea
Chronic relapsing disease of the facial skin characterised by recurrent episodes of facial flushing
Aetiology
• Patients may reveal history of flushing back to teens
• Usually presents between 30 - 50
• Women more likely to get rosacea (men get rhinophyma)
Aggravating factors​
• Flushing eg sunlight, caffeine, alcohol, spicy food, alcohol
• Drugs that cause vasodilatation
• Topical steroids
Clinical Presentation
• Inflammatory: persistent erythema, papules, pustules
• Vascular: intermittent telangiectasia, erythema (flushing)
sparing peri-oral and peri-orbital skin
• Eyes: gritty, conjunctivitis, blepharitis, episcleritis,
chalazion
Examination
• Skin not greasy (unlike acne) maybe dry
• Telangectasia mostly over forehead and cheeks
• Sebaceous glands are prominent
• Rhinophyma – thickening of nasal skin
Management:
• Advice – avoid precipitating factors, reassure benign condition
• Conservative: sunscreen 15 UVA and UVB, emolients
Medical:
• Oral tetracyclines (Doxycycline and Lymecycline) first line
• Topical metronidazole is also used
• Do NOT use steroids – these aggravate it
• Vascular rosacea does NOT respond to antibiotics
Other:
• Vit A analogue (Isotretinoin) only by dermatology
• Laser treatment – to reduce telangiectasia
• Rhinophyma - dermabrasion, shaving
Referral: persistent symptoms that are causing psychological or social
distress or papulopustular rosacea that has not responded to 12 weeks
of oral plus topical treatment or diagnostic uncertainty
Psoriasis
Chronic relapsing inflammatory dermatosis Examination
Inspection
Pathology • Extensor surfaces: elbows, knees, shins, sacrum
• Triggers: infection, trauma, drugs, alcohol, stress • Well demarcated plaque with silvery scale
• Genetic: HLA-Cw6, B13 and B17 • Nails: pits, onchylosis and oil spots
• T cell driven (CD8 and CD40) • Köebner phenomenon: rash at recent sites of trauma
• Increased keratinocyte turnover due to shortened cell cycle • Arthritis: joint swelling and redness
• Type 1 = onset <40 years
• Type 2 = onset 50-60 years Palpation
• Plaques feel rough
Types: • Auspitz sign: pinpoint bleeding with scale removal
• Vulgaris = chronic plaque (90%)
• Guttate = many small lesions, post-strep pharyngitis/tonsillitis (children) Management:
• Flexural = in folds i.e. armpits, behind knees • Topical: emollient, vitD3 analogue (calitriol)
• Erythrodermic = widespread over back, dermatological emergency • Phototherapy = PUVA + UVB burning, skin cancer
• Generalized pustular = medical emergency • Acitretin = vitamin A (retinoid) teratogenic, dry lips
• Palmoplantar pustulosis = pustules on palms and soles • Methotrexate = folic acid antagonist marrow suppression, liver damage
• Cyclosporine = immunosuppressant HTN, renal damage, skin cancer
Clinical Presentation • Biologics (anti-TNFa infliximab or anti-IL12 ustekinumab) immunosup
• red well demarcated symmetrical plaques
• covered in silvery scale
• extensor aspects of elbows and knees, scalp, sacrum
• nails in 50%: pitting, onycholysis, oil spots, dystrophy
• arthritis in 15%: seronegative, can precede skin disease
Comorbidities
• uveitis/iritis/episcleritis
• inflammatory bowel disease
• metabolic syndrome (DM, hyperlipidaemia, hypertension, higher BMI, MI)
• psychosocial disturbance: depression, anxiety, impact on quality of life
• cardiovascular disease
 · An itchy (pruritic) eruption can be caused by an inflammatory condition (e.g. eczema), infection (e.g. varicel a), infestation (e.g. scabieIstc)h,yaelreuprgt oicn
· An itchy (prurit c) eruption can be caused by an inflammatory condit on (e.g. eczema), infection (e.g. varicel a), infestation (e.g. scabies), al ergic
reaction (e.g. some cases of uItrcthicyaerirau)ptorioann unknown cause, pos ibly autoimmune (e.g. lichen planus). It c h y e r u p tio n
reaction (e.g. some cases of urticaria) or an unknown cause, pos ibly autoimmune (e.g. lichen planus).
· An itchy (prurit c) eruption can be caused by an inflammatory condit on (e.g. eczema), infection (e.g. varicel a), infestation (e.g. scabies), al ergic
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al ergens, ir itants)
Common sites - Variable (e.g. flexor aspects in - Sides of fingers, finger webs, - No specific tendency - Forearms, wrists, and legs
children and adults with atopic wrists, elbows, ankles, fe t, - Always examine the oral
Der matology:

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Der matology:
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Lesion - Dry, erythematous patches - Linear burrows (may be - Pink wheals (transient) - Violaceous (li ac) flat-topped
Der matology:
- Acute eczema is tortuous) or rubbery nodules - May be round, annular, or papules
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erythematous, vesicular and polycyclic - Symmetrical distribution

Der matology:

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exudative
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Associated - Secondary bacterial or viral - Secondary eczema and - May be as ociated with - Nail changes and hair los

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mon Important Problems – Itchy eruption

Skin Infections
Viral Warts
• Human Papilloma Virus (HPV)
• HPV is associated with cervical cancer
• Transplant patients can develop multiple viral
warts  predispose to SSC
Fish Tank Granuloma
• Mycobacterium marinum
• Occurs in people who clean fish tanks
• Ix: skin biopsy + culture = shows granuloma +
bacteria
Impetigo
• Staph. aureus or Strep. pyogenes
• Golden crusting
Erysipelas (superficial cellulitis)
• Streptococcus pyogenes
• Has well demarcated edge
• IV abx: benzylpenicillin and erythromycin
Necrotising Fasciitis (deep cellulitis)
• Streptococcus
Exanthems
• Acute inflammatory rashes generally with
childhood infections
• Usually widespread and symmetrical
• Often systemic symptoms (fever and malaise)
• Chicken pox, measles, rubella, parvovirus
(slapped cheek)
Fungal infections
• Annular lesions
• Ix: skin scraping for microscopy (take from
edge of lesion)
Pityriasis Versicolor
• Malassezia furfur fungus
• Brown scaly macules on torso
• Don’t tan – mottled appearance after sun
exposure (looks like vitiligo)
• Ketoconazole shampoo
Secondary Syphilis
• Erythematous papules on palms and soles
• Ix: bloods = treponemal antibodies
Tropical Diseases:
• Rickettsia = transmitted by tic bite
• Lyme disease = due to Borrelia transmitted by
tic bits – after trip to New Forest
Impetigo
Superficial bacterial infection

Pathology
• Superficial bacterial skin infection
• Cause: Staphylococcus aureus or Streptococcus pyogenes
• Really contagious
• Primary infection or a complication of an existing skin condition such as eczema,
scabies or insect bites
• Common in children, particularly during warm weather

Clinical Features:
• Golden crusty lesions
• Tends to be on face, flexures and limbs not covered by clothing

Management
• Local: topical fusidic acid
• Extensive: oral flucloxacillin

Children should be excluded from school until the lesions are crusted and healed or
48 hours after starting antibiotics
Measles
Viral infection caused by mobillivirus

Pathology Management:
• Single stranded RNA from the paromyovirus family • Supportive: paracetamol, ibuprofen, fluids
• Highly contagious by airborne droplets • Stay at home to limit spread of disease
• Incubation for 10-12 days (range 7-18 days) • Vulnerable contacts need post-exposure prophylaxis
• Vaccination within 72 hours
Clinical Presentation • Human Normal Immunoglobulin to immunosuppressed
• Prodrome: 2-4 days of fever, cough, coryza, conjunctivitis
• Rash: starts on face/neck, spreads to trunk and limbs Notifiable disease  need to contact public health
over 3-4d
Complications:
Examination • Bronchopneumonia
• Koplik spots • Encephalitis
• Rash: flat red • Subacute sclerosing panencephalitis
Fungal Infections
• Tinea pedis = foot, known athlete’s foot Candida
Monilia
• Tinea cruris = groin, jock itch • satellite lesions i.e. outside the nappy
• Tinea capitis = head, ringworm of the scalp
• Tinea corporis = body, ringworm
• Tinea unguium = toe or finger nails, onychomycosis

Symptoms
• Itching and stinging
• Red scaly rash that is shaped like a ring (annular)
• Cracking, splitting and peeling in the toe web spaces
• Blisters
• Yellow or white discoloration of the nails
• Bald spots on the scalp
Pyogenic Granuloma
Benign skin lesion due to reactive proliferation of capillary blood vessels
Aetiology
• Relatively common
• More common in women and young adults
• Most common sites are head/neck, upper trunk and hands
• Lesions in the oral mucosa are common in pregnancy
Causes
• Trauma – some develop at minor injury sites, e.g. pinprick
• Infection – Staph aureus often present in the lesion
• Hormonal – pregnancy and sometimes oral contraception
• Drug-induced – multiple lesions in patients on oral retinoid (acitretin or
isotretinoin)
Clinical Features
• Initially small red/brown painless spot
• Rapidly grows within days to weeks
• Raised, red/brown lesions which are often spherical in shape
• May bleed profusely or ulcerate
Management
• Curettage and cauterisation – lesion is scraped off with a curette and the
feeding blood vessel cauterised to reduce the chances of re-growth.
• Laser surgery – remove the lesion and burn the base
• Cryotherapy – may be used for small lesions
• Lesions associated with pregnancy often resolve spontaneously post-partum
Skin TB
Invasion of the skin by Mycobacterium tuberculosis
Pathology
• Direct infection of the skin or mucous membranes from an outside source of
mycobacteria results in an initial lesion called the tuberculous chancre
• Chancres are firm shallow ulcers with a granular base
• They appear about 2-4 weeks after mycobacteria enter through broken skin
• The immune response of the patient and the virulence of the mycobacteria
determine the type and severity of cutaneous TB
Investigations
• Histology: caseating epithelioid granulomas that contain acid-fast bacilli.
• Tuberculin skin test (Mantoux or PPD test)
• Interferon gamma release assay blood test
• Sputum culture (it may take a month or longer for results to be reported)
• Chest X-ray and other radiological tests for extrapulmonary infection.
Treatment
• Antitubercular drugs = combination of antibiotics (isoniazid, rifampicin, pyrazinamide
and ethambutol) given over a period of several months and sometimes years.
• Patients with latent TB infection but no active disease may also be treated with
antitubercular drugs to prevent development of active disease.
• Occasionally surgical excision of localised cutaneous TB is recommended.
Types of cutaneous TB
TB verrucosa cutis
• Occurs after direct inoculation of TB into the skin in someone who
has been previously infected with mycobacteria
• Presents as a purplish or brownish-red warty growth
• Lesions most often on the knees, elbows, hands, feet and buttocks
Lupus vulgaris
• Persistent and progressive form of cutaneous TB
• Small sharply defined reddish-brown lesions with a gelatinous
consistency (called apple-jelly nodules)
• Lesions persist for years, leading to disfigurement and skin cancer
Scrofuloderma
• Extension of underlying TB infection of lymph nodes, bone or joints
• Often associated with TB of the lungs
• Firm, painless lesions that eventually ulcerate with a granular base
Miliary TB
• Chronic TB infection that has spread from the primary infection to
other organs and tissues via the bloodstream
• Small (millet-sized) red spots that develop into ulcers and abscesses
• More likely in immunocompromised patients, eg HIV, AIDS, cancer
• The patient is generally sick
• Prognosis is poor (many patients die even if diagnosed and treated)
Tuberculid
• Generalised exanthem
• Usually in good health with no identifiable focus of active TB
• Erythema induratum (Bazin disease) presents as recurring nodules or
lumps on the back of the legs (mostly women) that may ulcerate and
scar. It is a type of nodular vasculitis.
• Papulonecrotic tuberculid results in crops of recurrent crusted skin
papules on knees, elbows, buttocks or lower trunk that heal with
scarring after about 6 weeks.
• Lichen scrofulosorum is an extending eruption of small follicular
papules in young persons with underlying TB.
Naevi Blue naevus
• Colour due to pigment deep in dermis
Benign melanocytic naevi • Appear during childhood or adult life
• Most common benign skin lesion • May be flat or elevated and smooth surface
• Start to appear in puberty • Generally solitary
• Located on head, neck, dorsum of hands/feet
3 stages of development: • Dermoscopy: uniform steel-blue colour
• Junctional – melanocyte proliferation in base epidermis
• Compound – both in epidermis and dermis
• Intradermal – melanocytes in dermis, variable appearance
Halo naevus
• Usually seen in young adults

Congenital melanocytic naevus

• Present at birth
• Develop  get hairy and thicker
Dermatofibroma
A common overgrowth of the fibrous tissue situated in the dermis

Aetiology Clinical Features

• More common in women • Firm rubbery lump under the surface of the skin
• Usually only one • Less than 1 cm across
• Multiple = immunosuppression (SLE, HIV, cancer) • Lie within the skin (so move with it)
• Usually on lower legs or upper arms • Dimple when they are pinched
• Colour pink to brown
Causes
• Minor injury e.g. prick from a thorn or an insect bite Treatment
• Observation – some go away spontaneously
Symptoms • Reassurance – benign
• Itch • Steroid injection – can reduce the size (aesthetics)
• Pain ± bleeding with contact • Cryotherapy
• Surgical excision
Localised Scleroderma
Autoimmune condition of excess collagen production
Aetiology
• Usually women aged 25 - 55 years
Symptoms
• Thick, dry, hard and shiny skin
• Red/purple patches of skin on abdomen, chest or back
• Patches gradually develop a lighter or whitish center
• Loss of hair and sweat glands over time

Pathology Treatment
• Excess collagen production • Reassure - usually goes away without treatment
• Tightening and fibrosis of skin • Vitamin D cream (calcipotriene) – soften skin patches
• Corticosteroid cream – reduce inflammation
Plaque = localised patches • UV light therapy
• Smooth and shiny • Immunosuppressant (methotrexate)
• Usually on the trunk
• Painless Complications
• Scarring
Linear = affected skin in a line • Skin discoloration
• Usually along an arm or leg
• Shiny, miscoloured or scarred
• Skin feels tight and uncomfortable
• Can cause abnormal limb growth due to restriction

Linear Plaque
Seborrheic Keratosis
Benign warty spot that appears during adult life as a common sign of skin ageing. Some people
have hundreds of them
Aeitology
• Extremely common – over 90% of adults over the age of 60 years have one or more
• Occur in males and females of all races
• Typically beginning to erupt in the 30s or 40s
Causes
• Sunburn
• Dermatitis
• Skin friction
• Stable and clonal mutations or activation of FRFR3, PIK3CA, RAS, AKT1 and EGFR genes are
found in seborrhoeic keratoses.
• Seborrhoeic keratosis can arise from solar lentigo (FRFR3 mutation)
• Epidermal growth factor receptor inhibitors (used to treat cancer) often result in an increase
in verrucal (warty) keratoses.
Clinical features
• have a 'stuck-on' appearance
• Any area of skin, covered or uncovered (not palms and soles)
• Highly variable appearance.
• Flat or raised papule or plaque
• 1 mm to several cm in diameter
• Colour: skin, yellow, brown to black
• Smooth, waxy or warty surface
• Solitary or grouped in certain areas, e.g. scalp, under breasts, over spine or in the groin
• Keratotic plugs may be seen on the surface
Management
• Reassurance
• Removal: curettage, cryosurgery and shave biopsy
Actinic (Solar) Keratosis
Sun-induced scaly or hyperkeratotic lesion, which has the potential to become malignant

• Occur on sun exposed sites – bald scalp, tips of ears, back of hands
• Risk factors: fair skin, outdoor occupation, sunny climes and increasing incidence
with age
• A flat lesion with white, rough surface scale
• Feels like sandpaper, can appear as scaly, rough patches on a red background
• Can be thick and warty and tender on palpation – ‘like a pin prick’
Management:
• Sun protection – hats, sunscreens and simple moisturisers
• Cryotherapy (liquid nitrogen), 5-Fluorouracil cream (Efudix), Imiquimod (Aldara),
Curettage (scrape) and Cautery, excision (useful for large AKs), and photodynamic
therapy.
 Blistering Skin Conditions
Subepidermal Blisters
Hemidesmosomes: adhesion of dermis and epidermis, contains proteins include: keratins,
collagens, laminins, integrins

Blistering Disorders – Pemphigus vulgaris

Dermatology: Handbook for medical students & junior doctors

Autoimmune Pemphigus vulgaris Genetic

• Type 7 collagen = bullous SLE Description
• Type 17 collagen = junctional epidermolysis
● A blistering skin disorder which usually affects the middle-aged

• Type 17 collagen = bullous pemphigoid Cause bullosa (“hypoplastic” hemidesmosome and

● Autoantibodies against antigens within the epidermis causing an

widespread erosions/blistering)
intra-epidermal split in the skin

Blistering Disorders
Presentation ● Flaccid, easily ruptured blisters forming erosions and crusts

Topical and oral corticosteroids

Dermatology: Handbook for medical students & junior doctors
Gene therapy Protein therapy

Blistering Disorders – Pemphigus vulgaris

● Lesions are often painful Dermatology: Handbook for medical students & junior doctors

● Usually affects the mucosal areas (can precede skin involvement)

emphigoid Steroid sparing agents (Azathioprine) Dermatology: Handbook for medical students & junior doctors
Management Cell therapy Drug therapy
● General measures – wound dressings where required, monitor for
Blistering Disorders
Pemphigus vulgaris signs of infection, good oral care (if oral mucosa is involved)
on ● A blistering skin disorder which usually affects the elderly
● Oral therapies – high-dose oral steroids, immunosuppressive
Intraepidermal Blister
● Autoantibodies against antigens between the epidermis and

Descriptionsplit in the skin● A blistering skin disorder which usually affects theagents
dermis causing a sub-epidermal · In general, blistering skin disorders can be divided into: immunobullous diseases
(e.g. methotrexate, azathioprine, cyclophosphamide,
middle-aged
tion Desmosome cell-cell junctions maintain intercellular adhesions within epidermis by
● Tense, fluid-filled blisters
Causeon an erythematous ●
base mycophenolate
Autoantibodies against antigens within the epidermis causing an mofetil, and other) (e.g. bullous pemphigoid, pemphigus vulgaris), blistering skin infections (e.g. herpes
● Lesions are often itchy simplex) and other (e.g. porphyria cutanea tarda).
binding to keratin filaments in neighbouring cells
● May be preceded byPresentation
intra-epidermal split in the skin
a non-specific itchy rash ● Flaccid, easily ruptured blisters forming erosions and crusts · The fragility of blisters depends on the level of split within the skin – an intra-

Blisters break easily and present clinically as flaccid blisters or erosions

● Usually affects the trunk and limbs (mucosal involvement less

common)
● Lesions are often painful epidermal split (a split within the epidermis) causes blisters to rupture easily;

● Usually affects the mucosal areas (can precede skin involvement) whereas a sub-epidermal split (a split between the epidermis and dermis) causes
ment ● General measures – wound dressings where required, monitor
Management ● General measures – wound dressings where required, monitor for blisters to be less fragile.

Pemphigus vulgaris = antibodies to desmoglein 3

for signs of infection
signs of infection, good oral care (if oral mucosa is involved)
● Topical therapies for localised disease - topical steroids
· The common causes of blisters are impetigo (see below ), insect bites, herpes simplex
infection (see page 34), herpes zoster infection (see page 36), acute contact
Pemphigus Foliaceous = antibodies to desmoglein 1● Oral therapies – high-dose oral steroids, immunosuppressive
● Oral therapies for widespread disease – oral steroids, combination
agents (e.g. methotrexate, azathioprine, cyclophosphamide,
of oral tetracycline and nicotinamide, immunosuppressive agents
dermatitis, pompholyx (vesicular eczema of the hands and feet, see below) and

Bullous impetigo = S.aureus toxins cleave desmoglein 1

mycophenolate
(e.g. azathioprine, mycophenolate mofetil, methotrexate, and mofetil, and other) burns.
· Bullous pemphigoid (see page 53) and pemphigus vulgaris (see page 54) are
Staphylococcal scalded skin syndrome = Staphylococcal toxins cleave desmoglein 1
other)
uncommon conditions due to immune reaction within the skin.
Pemphigus vulgaris

Pemphigus vulgaris Pemphigus vulgaris affecting the oral mucosa

Bullous im petigo in a new tattoo Pom pholyx
Bullous pemphigoid

54 British Association of Dermatologists

Pre-Malignant
Various dermatological growths that are at an increased risk of developing into skin cancer
Lentigo Maligna (LM)
Precancerous lesion with intraepithelial proliferation of
dysplastic melanocytes
• Etiology: exposure to UV light
• Lesion: darkly pigmented macule, irregular borders and
varying size (usually 1 mm–2 cm), grow gradually,
developing color irregularities and "island-like" speckling
• Common sites: areas exposed to sun (e.g., face, neck)
• Treatment: surgical excision with a safety margin
• Complications: may transform into lentigo maligna
melanoma
Leukoplakia
Hyperkeratosis of the epithelium and mucous membranes
• Etiology: tobacco smoking, alcohol consumption
• Lesion: persistent white plaques that usually cannot be
scraped off
• Common site: oral cavity
• Treatment: smoking cessation, cryotherapy, laser
ablation, surgical excision
• Complications: may develop into squamous cell
carcinoma
Bowen's disease
Squamous cell carcinoma in situ of the skin
• Etiology: exposure to sun, HPV 16 and 18, arsenic
exposure
• Lesion: single, irregularly shaped and sharply defined
borders, erythematous, scaly
• Common site: skin that is exposed to sun
• Prognosis: may progress to invasive SCC, but if treated
the prognosis is excellent
• Treatment: 5-Flourouracil, imiquimod, or photodynamic
therapy, surgical excision with a margin
Erythroplasia of Queyrat (= Bowen's of the glans penis)
Squamous cell carcinoma in situ of the penile mucosa
• Etiology: chronic irritation or infection, lack of
circumcision, HPV 16 and 8
• Lesion: single or multiple sharply demarcated,
nonhealing lesions that may ulcerate and bleed easily
• Common site: preputium, glans penis
• Prognosis: may progress to invasive SCC, but if treated
the prognosis is excellent
• Treatment: 5-FU, imiquimod, or photodynamic therapy,
surgical excision with a margin
 increasing age, male sex, immunosuppression, previous history of
skin cancer, and genetic predisposition

Malignancy: Basal Cell Carcinoma Presentation ● Various morphological types including nodular (most common),

superficial (plaque-like), cystic, morphoeic (sclerosing), keratotic

“shiny pearly nodule with rolled edge, surface telangiectasia
and pigmented with translucent appearance”
● Nodular basal cell carcinoma is a small, skin-coloured papule or

• Slow-growing, locally invasive malignant tumour of the epidermal nodule withManagement: 2 week
surface telangiectasia, wait
and a pearly rolled edge; the
keratinocytes – metastasis is rare lesion may have a necrotic or ulcerated centre (rodent ulcer)
• Most common skin cancer in fair skinned people (up to 30% of Caucasians) High risk tumours
● Most common over the head and neck
• Can be multiple and associated with a higher risk of other skin cancers (SCC • Mohs surgery – excision of the lesion and tissue
Management ● Surgical excision - treatment of choice as it allows histological
and malignant melanoma) borders are progressively excised until free of tumour
• Development of BCC is complex (genetic factors and ultraviolet irradiation)examination of the tumour and margins
Lower surgery
● Mohs micrographic risk tumours
(i.e. excision of the lesion and tissue
• Subtypes: nodular, superficial (plaque-ike), cystic, morphoeic (infiltrative),
borders are• progressively
Excision,excised
curettage & cautery
until specimens are – useful for small &
pigmented superficial tumours but avoid in disease of lower legs
microscopically free of tumour) - for high risk, recurrent tumours
• Nodular = shiny pearly nodule with rolled edge, surface telangiectasia • Topical therapy (imiquimod) – useful for small nodular
with translucent appearance ● Radiotherapy -&when surgery is not
superficial appropriate
disease
• Stretching the skin around the tumour can accentuate these features ● Other e.g. •cryotherapy,
Radiotherapy
curettage and– frail ortopical
cautery, elderly
photodynamic therapy, and topical treatment (e.g. imiquimod
Risk factors: skin type 1 (fair, red hair, blue/green eyes) frec kling, family cream) - forFollow up
small and low-risk lesions
history, immunosuppression, childhood sunburn, arsenic exposure, Gorlin’s • Incompletely excised at deep margins are managed as
Complications ● Local tissue invasion and destruction
syndrome high-risk
Prognosis ● Depends on • tumour
Incomplete lateral
size, site, type, growthmargins on low risk site are treated
pattern/histological
High risk tumours: subtype, failureless aggressively
of previous treatment/recurrence, and
• Eyes, nose, lips, nasolabial folds, ears • Low risk tumours – may not require routine follow up
immunosuppression
• Tumours >= 2 cm diameter
• Infiltrative, ill-defined, perineural invasion, basisquamous
• Recurrent or incompletely excised
 Malignancy: Squamous Cell Carcinoma
“warty tumours on a fleshy base”
• A locally invasive malignant tumour of the epidermal
keratinocytes or its appendages, which has the potential to
metastasise - esp on high risk sites
• Well-differentiated: papule or nodules with surface scale
• Poorly differentiated: lose the ability to produce keratin, so
may appear as ulcerated nodules
Risk factors: sun exposure, actinic keratoses, immunosuppression,
chronic inflammation, ulceration, HPV 5 and 8
High Risk Tumours
• Sun-exposed sites: lip, ear, scalp, eyelids
• Non-sun-exposed sites: sacrum, perineum, sole of foot, or site
of chronic injury & radiation
• >2cm in diameter and > 4mm depth
• Poor differentiation, perineural invasion, extending into deep
dermis subcutaneous fat
• Patient immunosuppressed, recurrence or incomplete excision
Keratoacanthoma
• Rapidly growing, keratin plug falls out and resolves leaving depressed scar
• Associated with sun exposed sites, late middle age
• May appear similar to early SCC, therefore, treated in same way
Management: 2 week wait
High risk tumours
• Surgical excision
• Radiotherapy- useful for areas of tissue conservation. Can be
used as an adjunct or patients not able to tolerate surgery
• MOHS – consider in recurrence and where margins may be
difficult to achieve or are indistinct
Low risk tumours
• Surgical excision – treatment of choice
• Curettage & Cautery – shallow tumours and in situ disease
• Cryotherapy – can be useful for small, shallow, and in situ disease
• Radiotherapy – frail and elderly not able to tolerate surgery
Follow up
• Check scar for reoccurrence
• Low risk tumours – 3 months & discharge if no recurrence
• High risk tumours – minimum 2 years at 3 monthly intervals
• Patients on immunosuppression – 5 year follow up
• *Discuss all cases in MDT*
Malignancy: Melanoma
• Melanoma – asym pigmented lesion

• A - asymmetrical
• B – border irregular
• C – colour multiple / different to others
•D-
•E-

Treatment:
• 2 week wait referral Lentigo maligna = type of melanoma in situ

• Wide local excision

 Non-Scarring Alopecia
Hair Telogen effluvium
• Follows significant physiological upset in prev 4-12wk
• In history ask about significant history (e.g. new meds)
Two types of hair: Alopecia areata
• Vellus – fine and fair (arms, legs) • Autoimmune condition
• Terminal – coarse and dark (eyebrows, groin) • “salt-and-pepper” pattern of growth (pale hair not affected)
• “exclamation mark” hair
Hair Cycle: • Can cause nail dystrophy
1) Anagen = growth phase • Ophiasis pattern = posterior scalp
2) Catagen = abrupt stop of growth phase • Totallis pattern = complete scalp loss
3) Telogen = rest phase  shedding • Universalis = complete body hair loss
Eczema: itch  stratch (trauma)  hair loss
Too Much Hair Trichotillomania: self-inflicted hair pulling, impulsive disorder
Hirsutism = excess terminal hair on female in male pattern
• Too long anagen phase  matures to more coarse hair Scarring Alopecia
• Cause: PCOS, idiopathic, ovarian/adrenal tumours Discoid lupus erythematosus (DLE)
• Ix: free testosterone • Itchy, scale
• Inflammation destroys follicles and pigment
Too Little Hair “plugged follicular appearance”
Female pattern loss = hair thinning behind margin Lichen plano-pilaris
• Pre-menopausal • Perifollicular redness
Androgenetic loss = bitemporal recession with thinning • Minimal scale
• Post-menopausal Folliculitis decalvans
Male pattern loss = • Perifollicular redness
• Androgens • “Crust” due to Staph. aureus
• “Tufting” where one follicle has multiple hairs
Treatments Fungal infection
• Finasteride – blocks conversion of testosterone  • Intense, inflammatory reaction
dihydrotestosterone by inhibiting 5a-reductase • Destroys follicles
Psycho-Cutaneous Disease
Primary psychiatric diseases presenting as skin disease: Primary dermatological disease which presents with psycho-
social morbidity:
Delusional parasitosis
• Monosymptomatic hypochondriacal psychosis Disorders of affect, depsression, anxiety and assessment of suicide
• Primary psychotic = delusion but no underlying psycopathology risk
• Secondary functional = underlying psychiatric disorder
• Secondary organic = underlying organic disease (drug abuse, Self esteem issues and body image problems
hypothyroid etc)
• Management: citalopram, emollients, abx, topical steroids

Body dysmorphic disorder

• Fixed perceived body defect in physical appearance
• Management: CBT, citalopram

Dermatitis artefacta
• Skin lesions solely produced/inflicted by patient themselves
• Patient claim they don’t know how they happened
• Linear tears, gauges, bruises, excoriations
• Management: CBT, identify cause

Neurotic excoriation

OCD spectrum disorders

 Topical Steroids
Therapeutics • Acute; use strong steroid for short course; 2-3 days
• Chronic; use lowest appropriate potency and apply thinly
Emollients to affected skin; 7-10 days
• No ideal emollients • If not improving increase to more potent steroid
• Patient preference is most important
• Vary from greasy to non-greasy
• Ointments have less preservatives
• Some have antimicrobials

Immunomodulators (Calcineurin inhibitors)

• Tacrolimus (Protopic)
• Pimecrolimus (Elidel)
• Main benefit they don’t cause skin atrophy
• Consider when you want to reduce/ avoid steroid e.g.
• Eczema of eyelids / periorbital skin
• Reg use of steroids on face
• Elderly patients using steroid reg on legs
Emergencies: Erythroderma
Inflammatory process involving >90% skin
Mortality 3-4%

“Skin failure”: fluid loss, infections, heat loss

Caused by: eczema, psoriasis, drugs, lymphoma

Investigations:
• History
• Associated signs (nail pitting, pustulation)
• CTCL (chronic T cell lymphoma) histology

Management: admit
• Fluid balance
• Warmth
• Nutrition
• Monitor and treat infection
Emergencies: Staphylococcal Scalded Skin Syn
Staphylococcal toxins cleave desmosome (intraepidermal) desmoglein 1

Outbreaks can occur in neonatal units as the immune system and kidneys
(toxin excreted by kidneys) are not fully developed.

Rare in adults, but can affect those who have kidney failure and immune
deficiency, those on immune suppressant drugs or chemotherapy

Clinical features
• Blistering rash which joins
• Superficial epidermal loss (skin peels leaving areas of raw skin)
• Dehydration

Management:
• Supportive
• IV antibiotics (flucloxacillin)
Emergencies: Steven’s Johnson Syndrome /
Toxic Epidermal Necrolysis
These are drug reactions: symptoms often start within a few days of the drug being
commenced although it can take a little longer with anticonvulsants
Allopurinol, Antibiotics, Anticonvulsants, Analgesics (NSAIDS)
Symptoms: fever, malaise, myalgia and arthralgia
Clinical features
• Painful erythema
SJS
• Erosions that quickly progresses to areas of confluent erythema
• Sheet-like skin loss
• Mucosal involvement includes the eyes, lips/mouth
Full thickness epidermal loss
SJS = disease involves less than 10% of the total body surface area
TEN = disease involves more than 30% of the body surface area
Management: admission.
• Stop causative drug
• Supportive: fluid balance, warmth TEN
• Dressing: silicon coating mesh, “exudry” suit
Emergencies: Angioedema
Dramatic urticaria involving deeper tissue

Causes: drugs (NSAIDS, ACEIs), C1 esterase deficiency

Clinical features
• Oedema
• Tongue and laryngeal involvement = life threatening

Management:
• ABCDE
• Antihistamine ± systemic steroid
• Epipen if allergic cause
 Presentation ● Discrete tender nodules which may become confluent

● Lesions continue to appear for 1-2 weeks and leave bruise-lik

Emergencies: Erythema Nodosum

discolouration as they resolve
● Lesions do not ulcerate and resolve without atrophy or scarr

● The shins are the most common site

Hypersensitivity response to a variety of stimuli e.g.:

• NO – idiopathic
• Drugs – penicillin, sulphonamides
• Oral contraceptive, pregnancy
• Sarcoidosis, TB
• Ulcerative colitis, Crohn's disease, Behçet's disease
• Microbiology – streptococcus, mycoplasma, EBV, UTRI
Clinical features
• Discrete tender nodules which may become confluent
• Lesions continue to appear for 1-2 weeks and leave bruise-like
discolouration as they resolve
• Lesions do not ulcerate and resolve without atrophy or scarring
• Shins most common site
Management:
• Antibiotics if infectious cause
• Stop any drug causes
• Symptomatic: bed-rest, leg elevation, and NSAIDs Erythem a nodosum
Emergencies: Cellulitis
Deep skin infection, typically on lower leg
Group A Streptococcus most common, but Staphylococcus also

Portal of entry site e.g. between toes

Clinical Features:
• Preceding illness

Management:
• Admit if: peri-orbital, rapidly progressive, major comorbidities,
moderate-severe pain that appears out of context to clinical findings
(suggests necrotising fasciitis)
• IV antibiotics: benzylpenicillin / flucloxacillin

Complications:
• Necrotising facciitis
 Description ● Widespread eruption - serious complication of atopic eczema or

less commonly other skin conditions

Cause ● Herpes simplex virus

Emergencies: Eczema herpeticum Presentation ● Extensive crusted papules, blisters and erosions

● Systemically unwell with fever and malaise

Management ● Antivirals (e.g. aciclovir)

​Widespread eruption – serious complication of atopic eczema ● Antibiotics for bacterial secondary infection

Complications ● Herpes hepatitis, encephalitis, disseminated intravascular

Cause: Herpes simplex virus coagulation (DIC) and rarely, death

Clinical features
• Extensive crusted papules, blisters and erosions
• Systemically unwell with fever and malaise

Management:
• Admit
• High dose antivirals (e.g. aciclovir)
• Antibiotics for secondary bacterial infection

Complications:
• Herpes hepatitis
Eczem a herpeticum
• Encephalitis
• Disseminated intravascular coagulation (DIC)
Emergencies: Cutaneous Drug Eruption
Minor exanthem: antibiotics, anticonvulsants

Acute generalized exanthematous pustulosis (AGEP): antibiotics, Ca channel blockers, antimalarials

Urticaria / angioedema: antibiotics, NSAIDs, contrast media, ACE inhibitors

Vasculitis: antibiotics, NSAIDs, thiazides, furosemide

SJS / TEN: sulphonamides, anticonvulsants, NSAIDs

Skin necrosis: anticoagulants (warfarin)

Keep an open mind, though, as any drug can cause any reaction. Look at their history, recent drugs started etc