(children, young adults, genetics, black skin). No
improvement with time. Can continue to enlarge.
Overgrowth of dense fibrous tissue. HLA
associated. No hair follicles or sweat glands on scar.
Overgrows margins of original wound. Starts red,
becomes pale or brown. Options for Tx: occlusive
dressings, intralesional corticosteroid injections,
compressive dressings, cryosurgery, radiation,
Lumpy within the confines of the wound.
Elevated, rarely painful, regresses
Acute Wounds - burns
degree – extend to
epidermis of upper dermal
layer only. Very painful, dead
skin can peal.
degree – skin = black, brown, yellow, red or
white. Burn reaches subcut fat. Pain minimal –
nerve endings almost all destroyed. No blistering,
but hard, inelastic eschar
degree – extends to
deeper dermal layers, can
blister, more moderate pain
(damage to nerve endings.)
Fourth degree – the most serious. Reaches
underlying fascia, can affect bone and
tendons.no oedema, lots of eschar. Pain
• Venous Ulcers – indicate severe venous
insufficiency. (valve incompetence, increased
hydrostatic pressure and capillary permeability,
increased pericapillary fibrin deposition.) 80% of
leg ulcers. Think about RFs. Haemosiderin,
telangectasia, atrophie blanche, eczema,
Atrophie blanche with
• Frequently seen in diabetes, decreased
sensation, loss of autonomic function,
anhidrosis, loss of intrinsic muscle function.
Ulcers typically wet and deep. Often on
pressure points and surrounded by callous. Tx:
off-load weight, MDT, patient compliance,
• Usually below ankle. Look for signs of
decreased blood flow – cooler, hair
loss, thin and shiny skin, dependant
rubor, thick nails, reduced or absent
pulses. Ulcers are typically small,
distal with steep “cliff edge” and a dry
bottom. Pain at night when leg
elevated. Patient can have
intermittent claudication. Tx: restore
blood flow! Stop smoking! Control RFs
(eg hypertension), NO compression.
Mixed arterial and venous ulcer
Benign Dermal Tumours
Dermatofibroma (commoner in
females, can be a reaction to
Pyogenic granuloma Chondrodermatitis
Low Grade Malignant Tumours
Bowen’s Disease (intraepidermal carcinoma,
squamous carcinoma in situ). Can look like infection
to start with.
Keratocanthoma – benign techincally? but
can look like squamous carcinoma, so biopsy!
Papular lesion with central umbilicated
Lentigo Maligna (Hutchinson’s melanotic freckle).
Light brown with development of darker areas.
Can turn into cancer later in life. Flat (macular) and
when invades dermal layer, becomes lentigo
Malignant Skin Tumours
• 1) Basal Cell Carcinoma – commonest. Rarely spreads.
Most are painless, history of sun exposure. Biopsy! Proliferation of atypical basal
cells. Often clefts between tumour and dermis. Slow growing. Rolled-in edge,
telangectasia, or nodular, or pigmented, pearly appearance.
• 2) Squamous Cell Carcinoma
Malignant tumour of epithelial keratinocytes – skin and mucous membranes. Sun
exposure = major RF. Persists and grows. Can be solitary, keratotic or eroded,
papular or nodular. Can arise from actinic keratoses. Lymph spread. Old men.
How long have you had it? Has it changed?
Over what period of time? Larger?
Changed in colour or shape? Has it
Incidence = 10/100k/year (increasing 7%
each year) F:M = 2:1 (equal in hot
countries). Commonest sites = lower leg in
women, back in men. Pre-existing naevus
RFs: Previous Hx, FHx, Red hair, blue
eyes, multiple melanocytic naevi,
Is it worrying? Breslow thickness (depth)
and Clarks level (where it is in dermis in
relation to other structures).
Prevention: SLIP, SLAP, SLOP! Report
Skin Manefestations of
Systemic Diseases and Drug
• 1) Henoch-Schonlein Purpura
necrotising vasculitis of small vessels. Children. Palpable
purpuric rash, arthritis, haematuria, bowel angina and
ischaemia. Post strep throat inf = most common.
• 2) Polyarteritis Nodosa
rare, autoimmune, necrotising vasculitis of medium vessels.
Middle aged me. Renal failure, CHS, Cardiac
involvement, pulmonary, GI, blood. Subcut nodules.
Livedo Reticularis p-ANCA and ANA negative. Tends to
follow artery lines. Can ulcerate and become necrotic.
Common post HepB
• 3) Wegener’s Granulomatosis
granulomatous vasculitis. URT and LRT, renal involvement,
arthritis, c-ANCA +ve. Saddle-shaped deformity. M>F
Tx: find and treat cause and systemic
dapsone for cutaneous involvement.
• Inflammation of subcut fat causing
painful red nodules on the legs
• Causes: 20% idiopathic, infection
(strep, TB), drugs (OCP), systemic
diseases (IBD, Sarcoidosis)
• Tx: rest, analgesia, treat underlying
• Reaction of dermal vessels
resulting in changes – papular
and vesicobullous eruptions,
• Palms, soles, mucosal
• If severe, “Stevens-Johnson
• Causes: 50% idiopathic. HSV,
Strep, pregnancy, SLE, drugs
• Tx: Treat cause. Symptomatic
care (analgesia, IV fluids if
unable to drink etc)
• Rapidly progressing ulcer,
often with erythematous to
violaceous undermined edge.
Can occur at site of
• Causes: 50% idiopathic.
• Associated with: RA, IBD,
• Tx: Systemic steroids,
• * Subacute cutaneous lupus erythematosus *
Positive autoantibodies, widespread rash, well defined, can get everywhere on body,
photosensitive. Other body systems can be involved – heart (pericarditis), lungs
• * Discoid Lupus Erythematosus *
autoantibodies usually negative (<20% ANA). Only 5% develop SLE. Discoid lesions on
sun-exposed sites. Scarring alopeica.
• Autoantibodies positive: Scl-
70, centromere antibodies.
• F:M = 4:1
• Proximal skin sclerosis and
any 2 of: sclerodactyly,
digital pitting scars, pulp loss
and bi-basal lung fibrosis
• CREST Syndrome has less
internal involvment and a
better prognosis (Calcinosis,
• Localised fibrotic plaques, atrophic changes, self-limiting,
no internal involvment. Localised cutaneous sclerosis.
Indurated plaques with erythematous edge or brown
macules. F:M = 3:1.
• Spectrum of disease
• Polymyositis: high CK, CRP
• Jo-1 Antibodies
• 60% ANA positive
• Photosensitive rash
• Heliotrope (purple) changes
• Red papules on dorsa of
hands and fingers (gottron’s
• If >55yrs, associated with
malignancy – breast, lung,
stomach, uterus, colon
Muscle biopsy: pink
muscle cells being
Manifestations of Malignancy,
Endocrine Conditions, and Drug
Manifestations of Malignancy
Acanthosis Nigricans: typically neck and axillae.
Papillomatous. Associated with GI malignancy.
Pagets Disease of the Nipple: associated with
Breast Ca, suspect if unilateral breast eczema.
Secondary Cutaneous Metastases: various.
Present late, represents poor prognosis. Usually
scalp, trunk, umbilicus.
Erythema Gyratum Repens: associated with
Cutaneous Manifestations of Endocrine
generalised in IDDM
• Almost all drugs can cause rashes. Certain ones more likely to cause a certain
pattern. 2-3% of hospitalised patients. Ask about drugs started in the last 2-3 weeks,
Generalised Fixed Drug
• Type I: IgE mediated. Causes Urticaria, angioedema,
• Type II: cytotoxic leading to haemolysis, purpura.
• Type III: immune comples reaction, resulting in
vasculitis, serum sickness, urticaria
• Type IV: delayed-type reaction with cell-mediated
hypersensitivity resulting in contact dermatitis,
exanthematous reactions, photoallergic reactions.
TEN – Toxic Epidermal Necrolysis
• Erythema-multiforme =>
Steven-Johnsons Syndrome =>
toxic epidermal necrolysis
• Allopurinol, Anticonvulsants,
sulphonamides, penicillins. (can
also be cause by things like
infection! herpies especially.)
• Fever, chills, headache, D&V,
no pruritis. Can get mouth
• Macules => papules, vesicules,
bullae, uritcarial plaques,
• TEN: Muco-cutaneous
detatchement. Burns unit.
• TEN: up to 30% die