3. Wound Healing
Keloid scars:
(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,
laser.
Hypertrophic Scars:
Lumpy within the confines of the wound.
Elevated, rarely painful, regresses
spontaneously.
4. Acute Wounds - burns
1st
degree – extend to
epidermis of upper dermal
layer only. Very painful, dead
skin can peal.
3rd
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
2nd
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
minimal.
6. Venous Ulcers
• 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,
lipodermatosclerosis, ulceration
Atrophie blanche with
haemosiderin deposition
telangectasia
7. Neuropathic Ulcers
• 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,
glucose control.
8. Arterial Ulcers
• 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
12. Benign Dermal Tumours
Dermatofibroma (commoner in
females, can be a reaction to
trauma
Campbell de
Morgan spots
(cherry angiomas)
Haemangioma
Pyogenic granuloma Chondrodermatitis
nodularis
Intradermal Naevus
13. 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
keratinous core.
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
maligna melanoma.
14. 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.
16. 4) Malignant
Melanoma
Questions:
How long have you had it? Has it changed?
Over what period of time? Larger?
Changed in colour or shape? Has it
become itchy?
Facts:
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
in 30%.
RFs: Previous Hx, FHx, Red hair, blue
eyes, multiple melanocytic naevi,
congential naevus.
Is it worrying? Breslow thickness (depth)
and Clarks level (where it is in dermis in
relation to other structures).
Prevention: SLIP, SLAP, SLOP! Report
changes early.
24. • * 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
(pneumonitis), CNS.
• * Discoid Lupus Erythematosus *
autoantibodies usually negative (<20% ANA). Only 5% develop SLE. Discoid lesions on
sun-exposed sites. Scarring alopeica.
25. Systemic Sclerosis
• 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,
Raynauds, Oesophageal
stricture, sclerodactyly,
telangectasia)
calcinosis
26. Morphea
• 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.
27. Dermatomyositis
• Spectrum of disease
• Polymyositis: high CK, CRP
• Jo-1 Antibodies
• 60% ANA positive
• Photosensitive rash
• Heliotrope (purple) changes
on face
• Red papules on dorsa of
hands and fingers (gottron’s
papules)
• If >55yrs, associated with
malignancy – breast, lung,
stomach, uterus, colon
Heliotrope rash
Gottron’s
papules
Muscle biopsy: pink
muscle cells being
attacked by
inflammatory cells
29. 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
Lung Ca.
30. Cutaneous Manifestations of Endocrine
Disease
HYPERPIGMENTATIO
N: Addisons,
pregnancy, Cushings
VITILIGO: Addisons,
organ specific
autoimmunes, DM,
thyroid disease
HIRSUITISM:
Cushings, PCOS
GRANULOMA
ANNULARE:
generalised in IDDM
NECROBIOSIS
LIPIODICA: IDDM
PRETIBIAL
MYXOEDEMA:
Grave’s Disease
31. Drug Eruptions
• 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,
inc. OTCs.
Erythema
Mobilliform: eg.
amoxicillin
Fixed Drug
Eruption: eg.
Streptomycin,
cephs.
Generalised Fixed Drug
Eruption: eg.
Anticonvulsants, aspirin,
NSAIDS, phenobarbs,
doxycycline, metronidazole
etc etc.
32. Hypersensitivty Reactions:
• Type I: IgE mediated. Causes Urticaria, angioedema,
anaphylaxis
• 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.
33. TEN – Toxic Epidermal Necrolysis
• Erythema-multiforme =>
Steven-Johnsons Syndrome =>
toxic epidermal necrolysis
• Allopurinol, Anticonvulsants,
aspirin, isoniazid,
sulphonamides, penicillins. (can
also be cause by things like
infection! herpies especially.)
• Fever, chills, headache, D&V,
no pruritis. Can get mouth
involvment/GU involvment.
• Macules => papules, vesicules,
bullae, uritcarial plaques,
erythema.
• TEN: Muco-cutaneous
detatchement. Burns unit.
• TEN: up to 30% die