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Chapter: Medicine Study Notes : Skin

Inflammatory skin lesions

Chronic characterised by rich red, erythematous silvery scaly plaques. May or may not itch

Inflammatory skin lesions




·        Epidemiology:

o   Begins at any age

o   ~2% of the population

·        Chronic characterised by rich red, erythematous silvery scaly plaques.  May or may not itch

·        May be inherited (autosomal dominant with mixed penetrance)

·        Precipitated or aggravated by:

o   Cigarette smoking and alcohol consumption

o   Strep infection

o   Trauma (Koebner phenomenon)

o   Hypocalcaemia

o   Drugs: lithium, beta blockers, Antimalarials, withdrawal of systemic steroids

o   Stress 

·        Characterised by rapid turnover of epidermis.  Normally 28 days, reduced to 4 days ® parakeratosis

·        Histology: epidermal squamous cell hyperplasia, neutrophil accumulation

·        Psoriasis vulgaris:

o   Elbows, knees, scalp 

o   Histology: parakeratosis, acanthosis, focal thinning, oedema of dermal papillae, micro-abscesses in the stratum corneum

·        Pustular psoriasis:

o  Abscess formation within the epidermal layer ® widespread sloughing ® risk of infection/electrolyte imbalance 

o  Generalised (rare and life-threatening) or localised (most commonly palms and soles)

·        Nail involvement: pitting, discoloration, subungual hyperkeratosis and onycholysis (especially lateral)

·        Differential:

o  Bowen‟s disease: usually over leg

o  Superficial BCC

o  Eczema: may show Lichenification or fissures or vesicles

o  Lichen planus

o  Fungal: do a scraping

o  Discoid Lupus: face, leaves scars, has plugs of follicular hyperkeratosis

o  Seborrheic dermatitis

·        Treatment:

o  Mild steroid creams for face and flexures

o  Stronger steroid creams for short periods on trunk and limbs (but rebound flare up)

o  Coal tar creams: messy and smells

o  Dithranol + salicylic acid in white soft paraffin

o  Scalp: steroid of Betnovate strength to shift scale then a maintenance cream

o  UVB treatment 

o  PUVA: Psoralen tablets 2 hours prior to UVA treatment twice a week. Effective but may have to travel

o  If severe: methotrexate, Acitretin, cyclosporin, etc


Bullous Lesions


·        Epidermis sloughs off dermis

·        Intraepidermal: if any of the epidermis is left attached

o  Burns

o  Herpes

o  Pemphigus:

§  40 – 60 years, very fragile blisters skin, and also on oral and nasal mucosa

§  Less common than Phemigoid but more serious (40% mortality)

§  Histology: BM is intact, acantholysis 

§  Pathogenesis: Autoimmune reaction to desmosomes in the epidermis ® infection etc. IgG above the basement membrane. Chicken-wire pattern on immunoflouresence within the epidermis 

§  Types:


·        Pemphigus vulgaris: suprabasal lesions. More serious of the two. Mucosal and scalp involvement, more fragile blisters, looks like burn. Generalised bullous phase ~ 5 months after the onset of oral lesions. Heals without scaring. Patients are ill


·        Pemphigus foliaceous: acanthosis only in the superficial epidermis. Small flaccid blisters, rupture leaving erythematous lesion, heals with crusting and scarring. Face, scalp, chest and back. Oral lesions not common


§  Treatment: High dose steroids

·        Subepidermal:

o  Pemphigoid: 

§  Smaller, localised, sturdy, grape-like blisters, generally rest of skin remains in tact. Ruptured lesions heal rapidly. No oral involvement

§  May have only urticarial lesions with no blisters, or just vesicles, or eczema like appearance

§  Usually self-limiting, chronic relapsing, > 60 years.  Can become generalised

§  Histology: Epidermis lifts in total at the dermo-epidermal junction

§  Pathogenesis: IgG in the BM, linear stain with immunoflouresence

§  Differential: 

·        Diagnosis of bullae difficult. Usually need to refer, and histology (prior to treatment) usually necessary

·        Pemphigus (flaccid bullae with mucosal involvement)

·        Eczema (but not itchy)

·        Russian hog weed et al

·        Treatment: 

o   Systemic steroids: may need 20 – 40 mg per day. Unsuitable for long term use ® problem especially in the elderly 

o   Topical steroids if localised

o   Tetracycline 1 – 2 g per day, especially in elderly

o   Other immunosuppressive treatment (eg methotrexate)


Discoid Lupus Erythematous (DLE)


·        = Mild end of Lupus spectrum and much much more common than SLE. Mild skin rash, normal serum ANAs and ENAs

·        Rash usually on the face, usually crosses the nose, sometimes scalp, ears, nose, arms 

·        Erythematous plagues varying from several mm to several cm. Adherent scale (not flaky like eczema) and pitted surface. Rough feel, doesn‟t itch. May heal with hyperpigmentation or white scar. Scarring alopecia 

·        Alopecia in scalp lesions which is normally permanent

·        More common in Polynesians and Maori, F > M

·        Characteristic histology and direct immunoflouresence (DIF) +ive

·        Differential:

o   Eczema (doesn‟t scar, uncommon to get discoid eczema on face, eczema can be weepy)

o   Solar keratosis or Bowen‟s (but patient usually to young for these)

·        Treatment: 

o   Topical or intralesional steroids: fairly potent ones but be careful on the face. Systemic if widespread

o   Sun protection 

o   Antimalarials (eg hydroxychloroquine.  SE: eye problems ® regular check-ups)

o   Topical Retinoids – also ­ penetration of topical steroids

·        See also Systemic Lupus Erythematosus




·        Localised cutaneous scleroderma, occurs any age but especially 20 - 40

·        Thickened dermis with dense collagen, progressive loss of subcutaneous fat

·        Waxy, ivory coloured skin without hair or sweating

·        Vary in size from 2 – 15 cm with lilac coloured edge

·        Any site, especially the trunk

·        Tend to improve over time (years)

·        Treatment: intralesional steroid

·        See Progressive Systemic Sclerosis (PSS)




·        Slowly progressive amelanotic macules, initially on sun exposed areas.  Usually symmetrical

·        Affected areas prone to sunburn

·        ?Autoimmune

·        Associated with family history and other autoimmune disorders (eg alopecia arearta)

·        In 50% develops before age 20

·        Differential:

o   Tinea versicolor (but hypopigmented, not amelanotic, and scaly)

o   Pityriasis alba (but hypopigmented, not amelanotic, and scaly)

·        Treatment: usually unsatisfactory

o   PUVA or narrow band UVB (may need 2 or 3 treatments a week for a year)

o   Various surgical procedures


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