DERM Flashcards
Eruption
= rash
Lesion
= any small area of skin disease
Macule
= Flat (non-palpable) area of colour change <0.5cm
Patch
Flat (non-palpable) area of colour change >0.5cm
Papule
Raised (palpable) lesion <0.5cm (usually dome shaped)
Nodule
Raised (palpable) lesion >0.5cm (usually dome shaped)
Cyst
Fluctuant papule/nodule containing fluid/pus/keratin
Plaque
Palpable, flat-topped lesion
Vesicle
Fluid-filled lesion/papule <0.5cm
Bulla
Fluid-filled lesion/papule >0.5cm
Pustule
Pus-filled lesion
Wheal/weal
Smooth, skin-coloured superficial swelling lasting <24 hours
Often surrounded by erythema
Erosion
Partial break in skin: loss of epidermis only
Ulcer
Complete break in skin: dermis included
Fissure
Small, slit-like break in skin
Excoriation
Erosion or ulcer due to scratching
Lichenification
Thickening of skin and increased markings due to chronic scratching/rubbing
Scale
Visible white loosening of outermost layer of skin
Crust
Golden deposit on skin due to dried plasma
What is psoriasis?
= chronic, relapsing inflammatory skin disorder (involving increased skin turnover and epidermal thickening).
Who does psoriasis affect mostly?
- Bi-peak onset – early 20s and 50s
- Affects 2% of population
- M = F
What other conditions is psoriasis linked with?
- Inflammatory – IBD, uveitis, coeliac, arthritis
- Obesity
- CVD
Psoriasis - presentation
Red, scaly plaques on EXTENSOR surfaces and scalp
- Causes pain, itching, bleeding
- Significant psychological impact
Psoriatic Arthritis (in 10%)
Psoriasis - Risk Factors
Genetics – FHx or HLA-CW6 gene
Environmental
- Strep throat infection
- Medications – BBs, antimalarials, lithium
- Stress, alcohol, smoking, trauma, sunlight
Psoriasis - principles of management
Depends on the severity and impact on the patient.
=> PASI
=> Dermatology Life Quality Index
Education – avoid lifestyle triggers (e.g. smoking, alcohol, stress)
Manage CV risk factors
1st line = topical
2nd line = phototherapy
3rd line = systemic Tx
Last line = biologics
Topical treatments for Psoriasis
- Emollients (e.g. E45)
- Corticosteroids +/- VitD analogues
- Keratolytics (e.g. 5% salicylic acid) for thick plaques
- Coal tar products for scalp
Phototherapy for Psoriasis
Requires 2o care referral
Exposure to UV light = immunosuppression to decrease symptoms from skin inflammation
2-3x per week for 15-30 episodes.
Base starting dose on skin type and gradually increase time of exposure.
UVB or PUVA
UVB vs PUVA phototherapy
Narrow band UVB = superficial (1st line, can be used if pregnant)
PUVA (UVA + Psoralen tablets) = deeper (not used if pregnant)
Side effects of phototherapy
Of UV – erythema/pruritis, cold sores, photoaging, SKIN CANCER
Of tablets – nausea, headaches
Dermatological indications for phototherapy
- Acne
- Psoriasis
- Vitiligo
- Lichen planus
Counselling for the patient before receiving phototherapy
- Only very short exposure (seconds to minutes)
- Dose carefully calculated for skin type
- Goggles to protect eyes and genitalia covered
Systemic Treatments for Psoriasis (and their side effects / monitoring)
Methotrexate
=> Teratogenic, hepatotoxic, BM suppression, GI upset/nausea
=> Monitor LFTs, FBC
Acitretin
=> Teratogenic, hepatotoxic, increases lipids, dry skin/hair thinning
=> Monitor LFTs, lipids
Ciclosporin
=> Nephrotoxic, increases BP, tingling peripheries
=> Monitor BP and U&Es
Topical steroid choices
MILD 1% hydrocortisone
=> any age, anywhere
MODERATE Eumovate (clobetasone) => any age, caution on face
POTENT Betnovate (betamethasone) => adults only, not used on face/genitals
V. POTENT Dermovate (clobetasol)
=> adults only, not used on face/genitals
Side effects of topical steroids
- Skin thinning
- Can trigger acne/rosacea
- Withdrawal can cause erythroderma
What is the most common type of leg ulcers?
Venous ulcers - Account for ~70% of ulcers
Pathophysiology of venous ulcers
- Valve incompetence and reflux
- Calf muscle dysfunction
Toxins accumulate => inflammation and necrosis of tissue.
Venous ulcers - risk factors
DVT, varicose veins, age, pregnancy, surgery
Venous ulcers - location
Generally located in the gaiter area (= below the knee and above the ankle)
Venous ulcers - Features
- Large and irregular
- Shallow with sloping edges
- Granulation tissue
Venous ulcers - Leg condition
- Lipodermatosclerosis
- Venous eczema
- Haemosiderin (red/brown colour)
- Atrophie Blanche (smooth, white sclerotic plaques)
- Heavy, aching, pruritis, oedema
GENERAL treatment for all ulcers
- Dressings +/- antibiotics +/- emollients
* Debridement – surgery/dressings/larvae
Specific treatment for venous ulcers
MUST exclude arterial insufficiency before starting compression therapy (ABPI)
Elevation and compression
=> 1st line = 4-layer bandaging
=> Other = stockings
Skin graft / superficial venous surgery
Arterial ulcer - pathophysiology
Atheromatous changes cause compromised blood flow
Results in hypoxia and accumulation of toxins => inflammation and necrosis of tissue.
Arterial ulcer - Risk Factors
Diabetes, HTN, arterial disease, high cholesterol, Raynaud’s disease
Smoking
Trauma
Arterial ulcer - Location
Located on bony prominences (usually lateral malleolus and toes)
Arterial ulcer - Features
- Smaller and round
- “Punched out” borders
- Little granulation tissue and dry
- Very painful
Arterial ulcer - Leg condition
- 6Ps – pain, pulseless, pale, paraesthesia, paralysis, perishingly cold
- Claudication/ischaemic rest pain symptoms
- Cool, hairless, dry, shiny skin
Specific treatment for arterial ulcers
- Manage vascular risk factors – e.g. antiplatelets, stop smoking
- Surgical revascularisation
Neuropathic Ulcers - Pathophysiology
- Peripheral neuropathy => loss of protective sensation and trauma goes unnoticed
- Vascular disease => reduced wound healing
Neuropathic Ulcers - Risk factors
Diabetes,
Trauma,
Prolonged pressure
Neuropathic Ulcers - Location
Located on pressure areas
Neuropathic Ulcers - Features
- Small, round, deep
- “Punched out” borders
- Thick rim
- PAINLESS
Neuropathic Ulcers - Leg condition
- Surrounding callous
- Loss of sensation
- Dry, cracked skin
Specific treatment for neuropathic ulcers
- Optimise glycaemic control
- Treat co-existing arterial disease
- Good foot care
- Offload pressure
What is eczema?
= itchy skin condition, characterised by erythema, dry skin and scaling.
\+/- vesicles and blisters (acute) \+/- fissures and lichenification (chronic)
Atopic Eczema - features
red, dry, scaly skin affecting FLEXURES
How common is atopic eczema?
Affects 20-30% of schoolkids, 5-10% of adults
Onset usually <2 years
Atopic Eczema - causes / risk factors
Genetics – PMHx/FHx of atopies
Environmental – irritants, allergens, illness/infection/stress, cold weather
Atopic Eczema - complications
= susceptible to infection
S. aureus/Strep – weeping pustules/crusting; fever/malaise
HSV (Eczema Herpeticum) – pain, fever, lethargy; clustered blisters and punched-out erosions
Management of Eczema
Patient education - avoiding triggers, how to apply treatments, signs of infection
- First Line = TOPICAL emollients/steroids
- Second Line = TOPICAL Calcineurin Inhibitors
- Third Line = PHOTOTHERAPY / IMMUNOSUPPRESSANTS
- Additional Treatments
=> Systemic ABX / acyclovir (infection)
=> Antihistamines
First line management for eczema
- Avoid irritants/allergens/triggers
- Emollients for dry skin – liberally, as often as needed.
- Topical steroids – for active areas; a “fingertip” portion 1-2x daily.
Second line management for eczema
Topical Calcineurin Inhibitors (e.g. Tacrolimus, Pimecrolimus)
=> Used if mod/severe eczema or if there are CIs to topical steroids
Usually initiated by specialists
Third line management for eczema
Phototherapy + emollients and topical steroids
Immunosuppressants (e.g. ciclosporin, methotrexate, azathioprine)
(Initiated by specialists)
Acne Vulgaris - Pathophysiology
- Hyperkeratinisation of follicle = pore blockage
- Increased sebum production (due to increased androgens at puberty)
- Overgrowth of P. Acnes (a gram +ve commensal)
=> Releases pro-inflammatory mediators
=> Follicles rupture and contents leak into surrounding dermis
Acne Vulgaris - Risk factors
- Male
- Cosmetic/hair products
- Excess washing
- Progesterone-only OCP/steroids
- Hormonal changes / Endocrine disorders
Lesions of Acne
- Non-Inflammatory:
- Closed comedones (whiteheads) – small papules that may burst
- Open comedones (blackheads) – flat or raised with impacted keratin - Inflammatory:
- Papules – burst comedones cause inflammation
- Pustules – papules containing pus
- Nodules – painful swellings lasting weeks-months
Sequelae of acne
- Non-scarring:
- Hyper/hypo-pigmentation
- Eythematous macules - Scarring:
- “ICE-PICK” scars (atrophic) – collagen loss
- “KELOID” scars (hypertrophic) – increased collagen
Management of Acne
Depends on severity, psychological impact, response to previous Tx.
- Topical retinoids/antibacterials/ABX = 1st line for mild/moderate
- Systemic ABX = 2nd line or 1st line for severe
- Oral Isotretinoin (Roaccutane) = severe or Tx resistant subtypes
- Hormonal Tx = Tx resistant females/ cyclical flares/hirsutism
- Tx for Scars
1st line for mild/moderate acne
= topical retinoids/antibacterials/ABX
Retinoids = unblock pores
Antibacterials – e.g. benzyl peroxide
Antibiotics – e.g. erythromycin/clindamycin
What is something to remember with all topical treatments for acne?
All may cause irritation/erythema and photosensitivity.
2nd line for mild/moderate acne
1st line for severe acne
Systemic ABX
=> Lymecycline/doxycycline
Treatment for severe or Tx-resistant acne
= Oral Isotretinoin (Roaccutane)
=> Retinoid, decreases sebum production
Side effects of Roaccutane
- Teratogenic
- Hepatitis – avoid alcohol (check LFTs)
- Photosensitivity and dry skin
- Muscle aches
- Mood changes
- Anaemia and thrombocytopaenia (check FBC)
- Increased TGs and cholesterol (check lipids)
Contraindications for Roaccutane
- Pregnancy
- Liver/renal disease
- Diabetes
- Peanut allergy
When is hormonal Tx used in acne?
= Tx resistant females/ cyclical flares/hirsutism
=> COCP Dianette
What are contraindications for the COCP dianette?
Pregnancy/lactation,
PHx or FHx of VTE
Management of acne - Scar treatments
Microdermabrasion (removes dead skin) – superficial scars
Laser resurfacing – for atrophic scars
Punch biopsy/excision – for ice-pick scars
Intralesional steroids – for keloid scars
Severity of Psoriasis
=> PASI = Psoriasis Area and Severity Index.
Used to measure severity and extend of psoriasis
Non-cutaneous manifestations of Psoriasis
Psoriatic Arthritis (in 10%)
Cardiovascular risk factors and metabolic syndrome
Dermatology Life Quality Index
Used to identify the impact of a skin condition on the patient’s life
Guides treatment / monitor improvement
What is a problem with topical vit D analogues in management of psoriasis?
Skin irritation
Metabolic effects (limit use to 100 g per week)
How is methotrexate taken?
Taken once weekly
Folic acid on the OTHER days.
What is important to do before starting biologics?
screen for any sign of infection (esp. TB, HIV, Hep B&C)
What is erythroderma?
= a severe and potentially life-threatening inflammation of most of the body’s skin surface
Causes of erythroderma
Psoriasis - withdrawal from steroids
Eczema
Drugs
Cutaneous T cell Lymphoma
Management of erythroderma
Admission to hospital
IV fluid, thermoregulation
Regular emollients
Consider moderate potency topical steroids
Prevent/treat any complications (e.g. infection)
How long do systemic ABX take to show improvement in acne?
Around 3 months
What is required for females to take Roaccutane (oral retinoid) for acne?
requires 2x contraception and monthly urinary pregnancy test
What is rosacea?
Who does it affect?
= a chronic inflammatory skin condition affecting the centre of the face
Can affect ANYONE
=> Peak onset age 30-60
=> more common with fair skin and Celtic/North European descent.
Pathogenesis of rosacea
thought to be multifactorial
=> genetics and environmental factors
Cutaneous features of rosacea
- Transient and persistent facial erythema
- Inflammatory papules and pustules ( but no comedones)
- Telangiectasia
- Rhinophyma
(Occasionally) Facial lymphoedema, burning/pain
neurogenic rosacea
Features of rosacea and also facial tenderness/ burning pain
Morbihan Disease
= chronic and persistent erythematous lymphoedema on the face
Sometimes occurs in rosacea
Telangiectasia in rosacea
Telangiectasia = persistent dilated capillaries/small blood vessels in the skin
In rosacea - present on facial skin, apart from nasal alar region.
Rhinophyma
Nasal skin is thickened and the sebaceous (oil) glands are enlarged.
Due to hyperplasia/fibrosis of the sebaceous glands of the face
More common in M > F
Ophthalmic complications of rosacea
Dryness
Conjunctivitis
Blepharitis – ophthalmology referral
Keratitis – ophthalmology referral
Rosacea - diagnosis
One diagnostic and 2 major criteria are needed for a diagnosis.
DIAGNOSTIC
- Persistent centrofacial erythema, associated with periodic intensification by potential trigger factors
- Phymatous changes
MAJOR (must occur in centrofacial distribution):
- Flushing/transient centrofacial erythema
- Inflammatory papules and pustules
- Telangiectasia
- Ocular rosacea (lid margin telangiectasia, blepharitis, keratitis/conjunctivitis/sclerokeratitis/anterior uveitis).
General management of rosacea
Assess the patient’s psychosocial burden of disease and consider referral for psychological support where necessary.
Lifestyle advice:
- Avoid triggers, oil-based products, exfoliants
- Moisturise frequently
- NEVER apply topical steroid
- Sun protection
Tx for Papulopustular/Inflammatory Rosacea
Topical – metronidazole/ azelaic acid
Oral ABX – e.g. tetracyclines, metronidazole
Isotretinoin
Mx of Erythmatotelangiectatic Rosacea
Treat any inflammatory component first
Topical azelaic acid / metronidazole may also help erythema
Laser can be used for severe telangiectasia
When do drug eruptions usually occur?
Usually 8-21 days post-exposure
BUT can occur with drugs that have been used without issue for years.
Mechanism of Drug Eruptions
- Allergy – e.g. ABX
- Intrinsic Drug Action – e.g. tetracycline and photosensitivity
- Non-specific – e.g. vasculitis
What are some common drugs causing rashes?
- Penicillins, sulphonamides
- Thiazide diuretics
- Gold, Penicillamine
- NSAIDs
- Allopurinol
- Anticonvulsants
General Management of a drug eruption
- STOP DRUG
- Supportive care (burns etc.)
- Wound care
Features of Toxic Erythema
Drug reaction - ~7-10 days post-exposure
- Measle-like Rash
- Symmetrical erythematous macules & papules
- May merge into larger plaques
- +/- malaise, fever, pruritis
Complications of Toxic Erythema
can progress to erythroderma/TEN
Toxic erythema - management
- Stop drug (resolves in a week)
2. Consider emollients and antihistamines
Urticaria - features, causes, complications, Mx
Occurs ~24 hours post-exposure.
Features:
- Wheals = raised, pale red, itchy plaques.
Causes:
- Drugs (salicylates, ACEIs)
- Infection
- Sun, exercise, stress
Complications = angioedema
Management = antihistamines
What is SJS/TEN?
= type 4 hypersensitivity reaction
Variants of severe skin reaction, with SJS being the less severe.
Who is affected by SJS/TEN?
Anyone on medication can develop SJS/TEN unpredictably.
It is more common in those with HIV
Features of SJS/TEN?
Usually a prodromal illness before the rash resembling an URTI or flu-like illness.
Abrupt onset of a tender/painful red skin rash
=> Starting on the trunk and extending rapidly over hours to days onto the face and limbs.
=> Symmetrical red macules and central blistering
=> 2+ mucosal sites involved (especially the mouth)
=> Severe eye involvement
Dermal necrolysis in TEN
How is severity/mortality measured in SJS/TEN?
= SCORTEN
One point is scored for each of the seven criteria present at the time of admission
- > 40 years
- Urea >10 mmol/L
- HCO3- <20 mmol/L
- HR >120
- Glucose >14mmol/L
- > 10% surface area
- Presence of malignancy
SJS / TEN - complications
POTENTIALLY FATAL
- Sepsis
- Dehydration
- Electrolyte imbalance
- ARDS
- Shock and multiple organ failure
SJS / TEN - Management
- STOP DRUG
2. ICU support (fluids, NG tube, analgesia)
Acanthrosis Nigricans
= Velvety, thickened, hyperpigmented skin
Affects skin folds (axilla, groin, neck)
Associations:
- Obesity, T2DM, Cushing’s, Addison’s, PCOS
- GI tract cancers
Pyoderma Gangrenosum - features
= auto-inflammatory chronic, recurrent ulceration.
Sudden onset:
- May start as a small pustule, red bump, or blood-blister, often misinterpreted as an insect bite.
- Very painful, ulcerated nodules
- Purple/blue border
- +/- fever and systemic illness
Pyoderma Gangrenosum - associations and differentials
ASSOCIATIONS
=> UC, Crohn’s, diverticulitis, vessel inflammation (Behcet’s)
=> Active hepatitis
=> Haematological malignancy
DIFFERENTIALS
Arterial/venous ulceration
Pyoderma Gangrenosum - Mx
= topical/PO steroids
What is dermatomyositis?
= rare, acquired muscle disease + RASH
Features of dermatomyositis
Violaceous rash on photoexposed areas
Helitrope rash on eyelids
Gottron’s papules on knuckles
Dermatomyositis - associations
MALIGNANCY (breast, cervix, ovaries, lungs, pancreas, GIT)
Autoimmune conditions
Drugs
Acquired Ichthyosis
= Fish-scale skin (dry)
Associations:
- Hodgkin’s Lymphoma (and other malignancies)
- Drugs – e.g. allopurinol
Erythema Multiforme
= inflammation of blood vessels
Red, “bulls-eye” lesions (usually on hands)
Associations:
- HSV infection (may follow cold sores)
- Drugs (penicillin, sulphonamides, allopurinol, phenytoin)
Erythema Nodosum - features
= inflammation of s.c. fat.
Bilateral red, tender subcutaneous nodules (3-20cm in diameter)
=> Usually lower legs
+/- fever, malaise, arthralgia
Erythema Nodosum - Associations
Associations:
- Infection – strep, TB
- Inflammatory disease – sarcoid, IBD, Behcet’s
- Drugs – sulphonamides, OCP
Dermatitis Herpetiformis
Chronic, recurrent pruritic rash.
=> Symmetrical
=> On extensor surfaces
Associations:
- Coeliac Disease
Cutaneous Vasculitis - features
= inflammation of skin blood vessels.
On legs/ankles/feet
Non-blanching, erythematous, purpuric rash
\+/- pain, itching, burning \+/- fever, arthralgia
Cutaneous Vasculitis - investigations
Hx and examination
Skin biopsy
FBC and auto-Abs
U&E, BP, urine dip
Cutaneous Vasculitis - Triggers
- Infection – Meningococcus, strep, URTI, hep C
- Autoimmune – RA, Lupus, IBD
- Medications – ABX, NSAIDs, diuretics
- Haematological disorders/malignancies
Pre-tibial Myxoedema
= accumulation of excess glycosaminoglycans in the dermis and subcutis of the skin.
Most commonly seen on the shins (pretibial areas)
Characterised by swelling and waxy/ lumpiness of the lower legs.
Associations = Grave’s disease
What skin changes can occur in SLE?
Acute = malar (butterfly) rash Subacute = discrete ring lesions => red & scaly Chronic = discrete discoid lesions => thick & scarring
+/- photosensitivity, arthritis, Raynaud’s, renal disease
Diagnostic criteria for SLE
Malar skin rash
Antiphospholipid / ANA / Anti-DNA antibodies
Persistent thromocytopaenia
Persistent proteinuria
What skin changes can occur in diabetes?
Granuloma Annulare:
=> Small papules in annular configuration
Necrobiosis Lipodica:
=> Symmetrical plaques with telangiectasia +/- ulceration
Diabetic ulcer / gangrene / candidiasis
Acanthosis nigricans
Rubeosis & vitiligo
Benign pigmented lesions
- Freckles
- Congenital Melanocytic Naevi (Moles)
- Acquired Melanocytic Naevi (Moles)
- Atypical Melanocytic Naevi (Moles)
What is a mole?
A proliferation of melanocytes
Can be congenital or acquired (UV exposure, hormones, age)
Atypical Melanocytic Naevi - features and risk factors
Mole, which looks similar to melanoma
RFs – FHx, UV exposure, <30 years.
Features: • 5+ mm • Irregular border • Variable pigmentation • Asymmetrical • Flat or raised
Atypical Melanocytic Naevi - management
- Monitor for changes
- Sun protection advice
- Excision if suspicious
Features of malignant melanoma
- Asymmetrical
- Border = IRREGULAR
- Colour/pigmentation = VARIED
- Diameter >6 mm
- Evolution (ABCDE changes or bleeding/itching)
Risk factors for Melanoma
GENETIC PHx or FHx melanoma Pale skin / red hair Many/large atypical naevi Increasing age
ENVIRONMENTAL Sun/UV exposure Phototherapy Tanning beds Immunosuppression
Differentials of melanoma
Pigmented BCC
Seborrheic Keratosis
Atypical Mole
Melanoma - Ix
2WW referral to dermatology!!
- History & Examination
- Excision for biopsy – if suspected melanoma
- Histopathology – Breslow Thickness = best prognostic factor.
Breslow Thickness
= the thickness of the tumour, measured from the granular layer of epidermis to the deepest point of invasion.
Melanoma - Mx
Breslow Thickness <1mm = WIDE LOCAL EXCISION (1cm margins)
Breslow Thickeness 1-4 mm = WIDE LOCAL EXCISION (1-3cm margins) + SENTIAL LN BIOPSY
=> +ve biopsy = total LN dissection + chemo/radiotherapy
=> -ve biopsy = monitor
Breslow Thickness >4mm = WIDE LOCAL EXCISION (3cm margins)
+/- LN Biopsy
What are signs of poor prognosis for melanoma?
Breslow Thickness (most important prognostic factor) Ulceration
Sun protection advice
Sunscreen – at least SPF 30 (UVB protection) and high star rating (UVA protection), applied as per manufacturers advice.
Wear protective clothing in sunny weather
Direct sunlight:
=> Spend time in the shade between 11am and 3pm when it is sunny
=> Keep babies and young children out of direct sunlight
Avoid sunbeds
What risk factors are there for both BCC and SCC?
UV Exposure
Fair skin
Immunosuppression
Sites of inflammation/infection/wounds
What risk factors are there for SCC only (i.e. not necessarily BCC)?
Smoking
Actinic keratosis / Bowen’s disease
What is the most common skin cancer?
Basal Cell Carcinoma
Where does BCC originate?
From basal cells of epidermis.
BCC - features
- Slow Growth (months/years)
- Locally invasive but decreased mets
- Generally asymptomatic
- Shiny or pearly nodule with a smooth surface (may have central depression or ulceration)
- Blood vessels cross the surface
BCC - Management
If elderly, may not treat.
- Simple Surgical Excision – margins 4mm
- Moh’s Micrographic Excision
- Curettage & Cautery – scrape & cauterise to stop bleed
- Cryotherapy – only if low-risk tumour
- Photodynamic Therapy (PDT) – only superficial BCC
What is Moh’s Micrographic excision
Remove a layer of the lesion at a time & re-examine
Photodynamic therapy for skin lesions
photosensitiser + UV => phototoxic reaction destroys lesion
Where does SCC originate?
From keratinocytes.
SCC - features
- Rapid Growth (weeks/months)
- Highly metastatic
- Present as enlarging scaly or crusted lumps
- May ulcerate
- Often tender/painful
- Present on sun-exposed areas
Risk factors for metastasis of SCC
- > 2cm or deep
- Poorly differentiated
- Lip/ear lesions
- Previous Tx failure
- Immunocompromised
SCC - management options
- Simple surgical excision – margins 5mm
- Moh’s Micrographic Excision
- Radiotherapy – if extensive surgery not an option
SCC - 5-year survival
Non-metastatic – 75-90%
Metastatic – 25%
Malignant non-pigmented skin lesions
BCC
SCC
What is Bowen’s Disease?
SCC in situ = epidermal dysplasia (considered SCC if penetrate basement membrane)
Bowen’s Disease - features
Erythematous, scaly plaque/patch
Bowen’s Disease - differentials
- Psoriasis
- Eczema
- Actinic Keratosis
- Superficial BCC
Bowen’s Disease - Mx
- 5-flurouracil cream
- Cryotherapy
- Curette & cautery
- Photodynamic Therapy
Actinic Keratosis - features
Also “solar keratosis”
=> Results from long-term exposure to UV radiation
- Often appear as small dry, scaly or crusty patches of skin
- May be red, light or dark tan, white, pink, flesh-toned or a combination of colours and are sometimes raised
- Often easier to feel than see
- Common on sites often exposed to the sun
What are the risks/complications of actinic keratosis?
Can develop into SCC (~10% of AK)
Actinic Keratosis - Mx
excision / curettage / cryotherapy
When and where does Seborrhoeic Keratosis occur?
A common sign of skin aging (~90% of adults aged >60 years)
Can arise on any area of skin, with the exception of palms and soles and mucous membranes
Why is the name of seborrhoeic keratosis misleading?
not limited to a seborrhoeic distribution;
not produced by sebaceous glands;
not associated with sebum.
Seborrhoeic Keratosis - features
- Flat or raised papule or plaque
- 1 mm to several cm in diameter
- Skin coloured/ yellow/ grey/ light brown/ dark brown/ black or mixed colours
- Smooth, waxy or warty surface
- Solitary or grouped in certain areas, such as within the scalp, under the breasts, over the spine or in the groin
Is seborrhoeic keratosis malignant?
Not malignant or pre-malignant, but are sometimes hard to tell apart from malignant tumours.
(Very rarely, eruptive seborrhoeic keratoses may denote an underlying internal malignancy, most often gastric adenocarcinoma)
Seborrhoeic Keratosis - Mx
Can be left alone or removed – reasons for removal may be that it is unsightly, itchy, or catches on clothing.
- Cryotherapy for thinner lesions (repeated if necessary)
- Curettage and/or electrocautery
- Ablative laser surgery
- Shave biopsy
- Focal chemical peel with trichloracetic acid
What are the normal bacterial skin commensals?
- Staph. epidermidis
- Corynebacteria
- Micrococci
- Propriobacteria
What bacteria tend to cause skin infections?
Staphylococci
(Staph. Aureus = ALWAYS pathogenic)
Streptococci
(Strep. pyogenes (group A strep) = ALWAYS pathogenic.)
What skin infections do staphylococci cause?
Primary Infections:
- Folliculitis
- Cellulitis
- Impetigo
Secondary Infections:
- Cellulitis
- Wound/ulcer/eczema infection
Infections due to bacterial toxins:
- Bullous impetigo
- Staphylococcal Scalded Skin Syndrome
- Toxic Shock Syndrome
What skin infections do streptococci cause?
Primary Infections:
- Erysipelas
- Necrotising Fasciitis
- Impetigo
Secondary Infections:
- Cellulitis
- Wound/ulcer/eczema infections:
Infections due to bacterial toxins:
- Scarlet Fever
Hypersensitivity Reactions (group A strep):
- Erythema Nodosum
- Vasculitis
Impetigo - cause and features
Stalphyococci/streptococci
Primary infection, affects young children
=> Golden crust +/- oozing blisters
CONTAGIOUS
Impetigo - Mx
- Soak crust with soap and water
- Topical antiseptic / ABX
- Systemic ABX if widespread
CONTAGIOUS – no school for 48 hours after starting oral ABX or until wounds are crusted (topical ABX)
Bullous Impetigo - features
Toxin reaction – specifically from Staph. aureus
2-3cm blisters (bullae)
Usually in areas with skin folds
Bullous Impetigo - Mx
Oral flucloxacillin
Bullous Impetigo - Complications
Can develop into a more severe and generalized form called staphylococcal scalded skin syndrome (SSSS)
RFs – Newborns/children (<5), immunocompromise, kidney failure
Folliculitis - features
Primary infection
Erythematous pustules around hair follicles
Folliculitis - Mx:
Screen and treat nasal carriage (mupirocin cream)
Topical or systemic ABX
Staphylococcal Scalded Skin Syndrome
Toxin reaction
Presentation:
- Erythema & sheets of peeling skin
- Malaise and fever
Why is Staphylococcal Scalded Skin Syndrome mostly seen in neonates and children <5 ?
Protective antibodies against staphylococcal exotoxins are usually acquired during childhood which makes SSSS much less common in older children and adults
Staphylococcal Scalded Skin Syndrome - Mx
ADMIT (emergency)
Supportive management (fluids & analgesia)
IV flucloxacillin/erythromycin
Toxic Shock Syndrome - features and associations
Toxin reaction
Presentation:
- Septic shock
- Days 1-3: widespread macular erythema
- Days 10-21 – desquamation, mucosal oedema & ulceration
Associations:
- Tampon use
- GI tract infection
Toxic Shock Syndrome - management
Supportive (fluids & analgesia)
IV flucloxacillin/erythromycin
What ABX are typically used for staphylococcal skin infections?
Topical ABX – fusidic acid, mupirocin
Oral ABX – flucloxacillin, clindamycin
What ABX are typically used for streptococcal skin infections?
Topical ABX – clindamycin
Oral ABX – penicillin V (Phenoxymethylpenicillin)
Erysipelas - features
Primary infection
= a specific form of cellulitis caused by strep
Affects the upper layers of the skin
Presentation:
- Unilateral “beefy” red plaque
- PAINFUL
Erysipelas - Mx
Oral ABX – Penicillin V
Necrotising Fasciitis - cause
group A strep
+/- S. aureus
+/- others
Necrotising Fasciitis - presentation
Rapidly spreading erythema & necrosis
Systemic sepsis – high fever, intense pain, vomiting
Necrotising Fasciitis - Mx
Surgical debridement IV ABX (vancomycin +/- gentamicin)
What is Cellulitis?
= infection of the deeper layers of skin and the underlying tissue
Erisypelas vs Cellulitis
Erysipelas affects the upper layers of skin and is specifically caused by streptococci
Cellulitis is an infection of the deeper layers of skin and the underlying tissue and can be strep or staph infection
Cellulitis - presentation
Gross oedema, erythema, heat
PLUS pain
Cellulitis - Mx
Elevate affected limb
UNCOMPLICATED cellulitis (no signs of systemic illness or extensive infection) => oral ABX, analgesia, fluids
COMPLICATED cellulitis (severe / systemic upset / limb threatened) => admission, fluids, IV penicillin-based ABX
Scarlet Fever - cause and features
Toxin-mediated, follows strep throat infection.
Presentation:
- Widespread pink/read papules
- Preceding sore throat, fever, lymphadenopathy
- Strawberry tongue
When can a child with scarlet fever go back to school?
Can go back to school 24 hours after starting ABX
Scarlet fever - Mx
Oral penicillin
How do viral warts spread?
Via direct contact or indirect contact (e.g. swimming)
Management options for viral warts
- Topical Paints – salicylic acid + lactic acid
=> 5 mins soak in warm water, apply Tx, nail file away dead skin - Cryotherapy – painful & may cause blisters
- Curettage & cautery – need local anaesthetic
- Formalin soaks / podophyllin – for RESISTANT warts
Types of viral wart
Common Warts (HPV 2):
- Elevated papules
- Dorsum of hands
- Common in children
Plane Warts (HPV 3):
- Flat-topped
- Face and back of hands
Plantar Warts (HPV 1, 2, 4, 57):
- May be uncomfortable to put pressure on
- Tend to be quite Tx resistant
Anogenital Warts (HPV 6 & 11):
- RF for cervical neoplasia in women
- Refer for STI screen
Chicken Pox - cause
= infection caused by varicella zoster virus
Usually an uncomplicated, self-limiting disease
=> More severe in adults
Chicken pox - presentation
Widespread rash
Itchy red papules progressing to vesicles on the stomach, back and face, and then spreading to other parts of the body.
Fever, headache, malaise
Chicken pox - complications
Pneumonia
Hepatitis
Encephalitis
Secondary bacterial infection of skin lesions caused by scratching
Chicken pox - Mx
Calamine lotion and oral antihistamines may relieve itching.
Only if immunocompromised – Oral/IV acyclovir
Shingles - cause
= herpes zoster
=> reactivation of dormant VZV (anyone who has had chickenpox may subsequently develop shingles)
Shingles - presentation
Dermatomal distribution of vesicles
DOES NOT CROSS MIDLINE
Preceding pain/tingling
Shingles - complications
Persisting pain, Scarring
Ramsay Hunt Syndrome
Ophthalmic Shingles
Deafness/dizziness
Encephalitis
Shingles - Mx
Oral acyclovir if:
- within 72 hours of onset
- mod/severe pain or mod/severe rash
- Immunocompromise
- Non-truncal involvement
Analgesia
If severely immunocompromised, consider admission.
What can HSV infection cause?
What is the presentation and management of these?
- Cold Sores (HSV 1):
- 30-50% recur
- Pain, tingling, vesicular eruption
- Mx = topical acyclovir - Genital Herpes (HSV 2):
- 95% recur
- Pain, tingling, dysuria
- Mx = oral acyclovir
Molluscum Contagiosum - cause and features
Caused by Molluscipox virus (MCV)
Presentation:
- Small, umbilicated papules (mainly trunk)
- Erythema, pus, crusting
Common in infants/children = contagious
Molluscum Contagiosum - Mx
Mx = self-limiting (if not, cryotherapy/topical podophyllin)
Hand, foot & mouth disease - cause and presentation
Caused by Coxsackie Virus
Presentation:
=> Erythematous vesicles on hands, soles of feet, mouth
Common in infants/young children
Hand, foot & mouth disease - Mx
self-limiting (5-7 days)
Pityriasis Rosea - cause
Unknown cause
?herpes virus
Pityriasis Rosea - presentation
Initially – herald patch (oval erythematous plaque + scaling)
5-15 days later – generalised, smaller, well-defined erythematous macules (CHRISTMAS TREE DISTRIBUTION)
Pityriasis Rosea - Mx
if symptomatic/itchy => topical steroids or UVB
What are dermatophytes?
fungi that require keratin for growth.
Cause tinea / ringworm (most common fungal infections).
Wood’s UV lamp
= a light that uses long wave ultraviolet light
When an area of scalp that is infected with tinea is viewed under a Wood’s light, the fungus may glow.
What are the genera of fungi in the dermatophyte group?
Microsporum,
Trichophyton,
Epidermophyton
Dermatophyte infection - Ix
Skin scrapings, Hair pluckings, Nail clippings => microscopy & culture
Or view under wood’s lamp
Dermatophyte infection - Tx
Topical Anti-fungals for LOCALISED INFECTION
=> Miconazole, ketonazole, terbinafine, nystatin
Systemic anti-fungals for WIDESPREAD INFECTION or HAIR/SCALP/NAILS or IMMUNOCOMPROMISED
=> Terbinafine, itraconazole, griseofulvin (for <12 years)
Candida
A yeast that causes the fungal infection thrush (can affect genitalia, periungual, oral).
Candidiasis - features
Erythema extending from body folds (unclear border)
Small satellite lesions +/- pustules at edges of eruption.
Candidiasis - risk factors
Extremes of age
Immunocompromise
Candidiasis - Mx
- Topical Azoles – clotrimazole
- Systemic Azoles – fluconazole
- Nystatin / amphotericin B
What are the fungal skin commensals?
Malassezia (formerly known as Pityrosporum)
What infections can be caused by Malassezia/Pityrosporum?
- Pityriasis Versicolor
2. Seborrhoeic Dermatitis
Pityriasis Versicolor - features and treatment
Features:
- Finely scaled, yellow/brown macules on trunk
- Hypo/hyperpigmented
Treatment:
- Topical antifungal – miconazole
- Selenium sulphide shampoo
- Systemic itraconazole if immunocompromised.
Seborrhoeic Dermatitis - features and Tx
Affects scalp, eyebrows, paranasal/periorbital areas.
Features:
- Yellow/white flaking
- +/- erythematous, itchy, GREASY/WET-looking skin
- +/- patchy hair loss.
Treatment:
- Topical azoles
- Low potency steroids (rapid, short-term Tx)
Tinea Corporis
Affects body
Erythematous ANNULAR SCALY PLAQUE
Central clearing
Very itchy
Tinea Cruris
Affect genitals
Well-demarcated, erythematous plaque
Very itchy
Tinea Manum
Affects hands
Scaling that spreads proximally
Asymmetrical involvement
Tinea Unguium (onchomycosis)
Very common => often with atheletes foot
Hyperkeratosis of nail
White discolouration
Loss of nail plate and lifting from bed (oncholysis)
Athlete’s foot
= Tinea Pedis
White maceration between toes
RFs – communal floors, occlusive shoes, wet feet.
Moccasin foot
= severe form of Tinea Pedis / Athlete’s foot
Erythema, scaling, pustules, widespread
Tinea Capitis
Affects scalp
More common in afro-Caribbean’s & children
Patchy hair loss
Scales, erythema, pustules
Kerion
= complication of tinea capitis
Boggy, painful swelling (honey-coloured)
+ alopecia/lymphadenopathy
(Occurs due to epidermal invasion & inflammatory response)
Skin infestations
= parasites living on the host’s skin
Scabies
Head lice
Scabies - cause and features
Caused by the sarcoptes scabies mite.
Features:
- Itchy papules (worse at night)
- Burrows/small tracts
- Usually symmetrical
Common sites – Finger webs, Axillae, Breasts, Scalp, Ankles, Feet
Scabies - RFs
- Close contact – dorms, wards, care homes
- Extremes of age or immunocompromise
=> risk of “crusted scabies” = severe form
Scabies - management
- Permethrin / Malathion creams (insecticides)
- Apply to whole body for 12 hours
- Repeat in 1 week
- TREAT ALL CLOSE CONTACTS AT SAME TIME - Wash all bedding/clothing.
Head lice - features
Live on hair, feed on blood, spread via close contact.
Features:
- Persistent itching of scalp
- Redness & excoriated papules
Head lice - Mx
- Fine comb & conditioner REGULARLY = most important
2. (Malathion/ Permethrin) = not very effective
What is important to remember in a dermatology history?
Identify site, onset, character, exacerbating/relieving factors, associated Sx, time course.
Any treatments tried already?
Any previous episodes similar to this?
Contact Hx with infectious diseases (e.g. chickenpox)
PMHx (especially skin cancer)
DHx, Allergies
FHx of skin conditions or cancers
Travel Hx
Sun exposure (including sunbed use)
Occupation
Recent changes (in diet, washing powder, etc.)
Inspection of an eruption
=> DCM
D – Distribution
• Where is it?
• E.g. flexures/extensors, sun exposed/covered
C – Configuration
• Shape or outline of rash
• Symmetrical/asymmetrical
• Any articular patter? e.g. diffuse, linear, grouped or scattered
M – Morphology • The form and structure of the rash • E.g. papules, plaques, etc. • Weeping, crusting, bleeding, excoriations • Odour
Inspection of a pigmented lesion
=> ABCDE
A – Asymmetry B – Border C – Colour D – Diameter E – Elevation / evolution
Inspection of a non-pigmented lesion
Site and Side Shape (macule, papule, plaque, nodule, cyst, etc.) Size Symmetry Surface Surrounding Skin Colour
What is important to palpate for in examination of a skin eruption/lesion?
Tenderness
Surface texture
Scaling
Elevation
Skin thickness
=> Any atrophy (tissue loss)?
=> Wrinkling or dimpling (loss of fat)?
Firmness
=> Solid or fluctuant?
Tethering
Blanching (if necessary)
Temperature
How can you differentiate between erythema and purpura?
Erythema - blanches with light pressure
Purpura - non-blanching
Flat vs palpable purpura
Flat purpura suggests leakage without inflammation
Palpable purpura suggests associated inflammation (likely to be caused by a small-vessel cutaneous vasculitis)
Why is it important to compare temperature of skin abnormality to normal skin?
Inflamed skin is hot
Poorly perfused skin is cold
Where are flexures?
Inside of elbows
Front of neck
Back of knees
Under buttocks
How would you counsel a patient about emollients?
Moisturiser - creates a barrier on the skin to prevent water loss
Apply liberally to the skin, following direction of hair growth
Use MINIMUM twice a day - no limit to how much you can use them
Use even when you have no flare-ups
Re-apply after bathing/showering
Most contain paraffin which is EXTREMELY FLAMMABLE => avoid contact with open flames/cigarettes
Important things to remember about use of ointments as a topical formulation
Best option for dry skin
BUT - more greasy and less cosmetically acceptable for the patient
How much topical steroid should be applied?
Finger-tip units are a useful way to explain to a patient how much topical steroid should be applied.
How would you counsel a patient for applying topical steroid?
Used more sparingly (not liberally like the emollient).
Try to leave 30-60 minutes between applying any emollients and the steroid
Side effects are usually with prolonged/ regular/ inappropriate use and are rare with topical use.
=> skin thinning
=> with potent/very potent steroids, sometimes adrenal suppression and Cushing’s
How long are topical steroids used for?
Once or Twice daily for maximum 14 days
5 days on the face
Maintenance topical steroids
Initiated by specialist
use of topical steroids twice weekly as a preventative measure for patients who suffer frequently from flare ups
Methotrexate - important drug interactions
Trimethoprim / co-trimoxazole - FATAL IMMUNIOSUPPRESSION
NSAIDs - increases risk of toxicity
Penicillins / ABX - increased risk of toxicity
Can increase the risk of nephrotoxicity if given alongside nephrotoxic drugs
Nikolsky’s sign
Positive when slight rubbing / mild lateral pressure of the skin results in separation of the epidermis
almost always present in SJS/ TEN and SSSS
How would you differentiate Spider naevi from telangiectasia?
When pressure is applied to blanch the area, spider naevi refill from the centre and telangiectasia refills from the edges.
Erythema Nodosum - Mx
Treat underlying cause
Analgesia and follow-up
Usually resolves within 6 weeks and lesions heal without scarring
How long do children with Molluscum contagiosum need to stay off school for?
Not required to stay off school
Contagious but the chances of passing it on during normal school activities are low.
Advice should be given to limit spread amongst family members e.g. no sharing towels.
What can trigger/exacerbate rosacea?
Sunlight,
Pregnancy,
Certain drugs and food
Koebner phenomenon
= the appearance of new skin lesions of a pre-existing dermatosis on areas of cutaneous injury in otherwise healthy skin.
Hutchinson’s Sign
a rash on the tip, side, or root of the nose in a patient with shingles
Representing the dermatome of the nasociliary nerve
=> prognostic factor for subsequent eye inflammation and permanent corneal denervation.
Guttate psoriasis
= a form of acute psoriasis described as a shower of small, pink-red, scaly ‘raindrops’ that has fallen over the body.
Typically develops 1–2 weeks after a streptococcal URTI, and some viral URTIs
Lichen Planus - presentation
planus = Ps
=> purple, pruritic, papular, polygonal rash on flexor surfaces.
Oral involvement common
Cutaneous manifestations of SLE
Photosensitive ‘butterfly’ rash
Discoid lupus (coin-shaped lesions)
Alopecia
Livedo reticularis (net-like rash)
What is Vitiligo?
Autoimmune condition which results in the loss of melanocytes and consequent depigmentation of the skin
Features:
- well-demarcated patches of depigmented skin
- peripheries tend to be most affected
- trauma may precipitate new lesions (Koebner phenomenon)
Types of BCC
- Nodular BCC
- Superficial BCC – shallow plaques, pink to almost skin coloured, that slowly expand over many years.
- Sclerosing BCC – can look like a small white scar on the skin (can expand to a very large size before it is clinically obvious as a skin cancer)
- Pigmented BCC – occurs in darker skinned individuals.
Skin Type I
Pale white skin, blue/green eyes, blond/red hair
Always burns, does not tan
Skin Type II
Fair skin, blue eyes
Burns easily, tans poorly
Skin Type III
Darker white skin
Tans after initial burn
Skin Type IV
Light brown skin
Burns minimally, tans easily
Skin Type V
Brown skin
Rarely burns, tans darkly easily
Skin Type VI
Dark brown or black skin
Never burns, always tans darkly
Alopecia Atreata
Presumed to be an autoimmune condition
Features:
- Localised, well demarcated patches of hair loss.
- At the edge of the hair loss, there may be small, broken ‘exclamation mark’ hairs
Hair will regrow in 50% of patients by 1 year, and in 80-90% eventually.
Pompholyx eczema
Characterised as an itchy vesicular rash over the palms and soles of feet and is associated with sweating.
Heat often exacerbates the rash.
Dermatofibroma
A solitary firm papule/nodule that dimples when pinched.
Tend to occur following injury
Lichen Planus - Mx
POTENT topical steroids are the mainstay of treatment
Benzydamine mouthwash or spray is recommended for oral lichen planus
Extensive lichen planus may require oral steroids or immunosuppression
