Dermatology Flashcards
What is the origin of basal cell carcinomas.
Do they metastasise?
Epidermal keratinocytes. Rarely metastasises but most common malignant skin tumour. Locally invasion.
RFx and causes of BCC
UV exposure in sunlight. Frequent sun burning and type 1 skin (easy burn, rarely tans) Immunosuppression Ionizing radiation Genetic predisposition
Presentation of a basal cell carcinomas
Most seen on head or neck.
Ulcer like papule with a raised, rolled edge and central depression.
Prominent fine blood vessels around the lesion (telangiectasis)
Pearly or waxy nodules on the skin.
Different types including cystic, morphoeic, superficial, nodular.
Ix and Mx for basal cell carcinoma
Ix = biopsy for histopathology.
Rx = routine referral time, unless significant impact will arise from delay.
1. Surgical excision
2. Mohs micrographic surgery for higher risk lesions to ensure microscopically free of tumour.
3. Radiotherapy is not appropriate for surgery, other options include curettage and cautery, cryotherapy.
Origin of squamous cell carcinoma
Tumour of epidermal keratinocytes or appendages.
Has potential to metastasise.
RFx for SCC
UV exposure
Pre-malignant skin conditions such as actinic keratosis
Immunosuppression
Genetic predisposition
Presentation of a squamous cell carcinomas
Nodular, keratinising/crusted/scaly lesions.
Can ulcerate.
Ill-defined border
Fleshy-coloured
Ix and Mx for squamous cell carcinoma
Ix = biopsy, consider CT for lymphadenopathy and metastasis.
Mx = 2 week wait.
1. Surgical excision
2. Mohs micrographic surgery if large and ill-defined.
3. Radiotherapy for very big, non-resectable.
Different stages of SCC
Actinic keratosis (more pinky coloured and small) Bowmen's disease = SCC in situ, confined to outer layer of skin. More red that AK and sometimes larger. Invasive SCC = in deeper layers of skin. Metastatic SCC.
3 variants of a squamous cell carcinoma
- Keratoacanthoma = rapidly growing, dome-shaped nodule with keratin filled centre.
- Verrous carcinoma = fumigating, verrucous nodules, local invasion, less metastasis.
- Marjolin ulcer = aggressive, metastatic, ulcerating SCC from burn/scar/ulcer/chronic wound
What pre-malignant disease can increase risk of squamous cell carcinoma. Describe it 🔬
- Actinic keratosis.
- Skin-coloured, ill-defined scaly macules or plaques at sun-exposed areas.
- Dermascopy as clinical diagnosis, can send for biopsy if ?cancer.
- Rx = cryosurgery with liquid nitrogen.
Origin of malignant melanoma
Invasive, malignant tumour of epidermal melanocytes. Potential to metastasise.
RFx for malignant melanoma
UV exposure/sunlight
Type 1 skin
Atypical or multiple moles
FHx and genetic predisposition.
Presentation of a malignant melanoma
Asymmetrical shape Irregular Border Colour irregularity Diameter >6mm Evolution of lesion - change in size or shape. Symptoms such as bleeding, itchy, oozing
Signs of metastasise such as weight loss, headache, cough, night sweats.
Location of malignant melanomas
Legs in females
Trunk in males.
When to refer a ?malignant melanoma for 2 week wait
Dermascopy suggests MM. Weighted 7 point checklist has score >3. 2 points for: - change in size - irregular shape - irregular colour. 1 point for: - diameter >6mm - inflammation - oozing - change in sensation.
Ix for malignant melanoma
- Biospy. Assess invasion thickness with Breslow’s thickness or Clark’s level.
- Staging using AJCC staging system.
- Consider investigating for metastasis e.g. lymph node biopsy, CXR, head CT.
Management of a malignant melanoma
Stages 0-II = local excision, topical Imiquimod.
Stages III = lymph node removal + chemo or immunotherapy.
Stage IV = surgical excision of systemic melanoma metastasis, immunotherapy e.g. Ipilimumab.
How to determine reoccurrence of a malignant melanom
Use Breslow thickness score. If >1.5mm = high risk.
Classification of skin types
Fitzpatrick skin type. Type 1 = increased risk of cancer.
Common places for a malignant melanoma to metastasise to
Lung
Liver
Brain
Name some benign tumours of the skin
Seborrhoeic keratosis
- on torso. Most people over the age of 50 get them.
- well circumscribed, plaques which appear ‘stuck-on’.
- painless. No Rx needed.
Name 3 inflammatory skin conditions
Acne
Psoriasis
Eczema
Types of eczema and basic pathology
Atopic - common, early childhood.
Seborrheic dermatitis - overgrowth of yeast.
Venous eczema - poor venous return.
Discoid eczema
Allergic contact dermatitis - type 4 hypersensitivity reaction to previously sensitised allergen.
Irritant contact dermatitis - non-immunological inflammatory reaction, no previous exposure needed.
RFx for atopic eczema
Genetic predisposition + environmental triggers.
- mutation in filaggrin gene.
- other atopic diseases such as hayfever, asthma, nasal polyps, food allergies.
Complications of eczema
Infection e.g S.aureus
Sleep disturbance
Depression and psych problems.
Triggers for an eczema exacerbation
Food Dust Pet fur Chemical contact Heat Severe stress
Presentation of eczema
Acute = Itchy, erythematous, scaly, vesicles. May weep.
Chronic = lichenified skin from repeated scrathcing.
Xerosis
Infants = cheeks, forehead, scalp and extensors of limbs.
Children + adults = wrist, ankle, popliteal fossa and flexures of limbs.
Name for dry skin
Xerosis
Mx for eczema
Clinical ∆.
Mild = emollients + mild potency topical corticosteroid Mod = emollients + mod potency topical corticosteroid + topical calcineurin inhibitor Severe = emollients + potent topical corticosteroid + topical calcineurin inhibitor + phototherapy |+ oral corticosteroid.
- Bandages and dressing where appropriate.
- Emollients e.g. E45, Oilatum, Eucerin Intensive.
- Corticosteroid of varying potency e.g. Hydrocortisone.
- Calcineurin inhibitor e.g. Tacrolimus
- Consider ABx if ?infection e.g. flucloxacillin.
Pathophysiology of acne vulgaris
Inflammation of pilosebaceous unit.
What makes up the pilosebaceous unit
Hair follicle
Hair shaft
Sebaceous gland
Difference between black heads and white heads
Open comedone = blackhead
Closed comedone = white head.
Both are non-inflammatory lesions.
Bacteria which can cause acne
Propionibacterium acnes.
Pathology and RFx for acne vulgaris
Sebacesous gland hyperplasia + abnormal follicular differentiation + P.acnes colonisation + inflammation and immune response.
RFx = Genetic predisposition Proliferation of P.acnes Puberty and hormones Endocrine disorder such as PCOS, Cushing's
Presentation of acne vulgaris
Non-inflammatory = comedones
Inflammatory lesions = papules, pustules, cysts, nodules.
Face, chest and back.
Management of acne vulgaris
Clinical ∆.
Advise = avoid over-cleansing skin, avoid picking spots, health diet, use products close to skin’s pH (4.7 - 5.75), smoking cessation.
Rx =
- Topical retinoid
- Topical retinoid + topical antibiotic
- Oral retinoid by dermatology e.g Isotretinoin
Consider use of COCP in females.
Name a topical retinoid and when can’t you use it
Isotretinoin, Adapalene.
CI in pregnancy and breastfeeding.
Name a topical antibiotic and how to prescribe it.
Clindamycin 1% + benzoyl peroxidase to prevent resistance.
Azelaic acid 20%
Fusidic acid
Name a calcineurin inhibitor
Tacrolimus