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
Types of psoriasis and basic pathology
- Chronic plaque psoriasis = most common.
- Guttate psoriasis = raindrop lesions, can affected anywhere on body, post-strep infection.
- Seborrheic
- Flexural = psoriasis at folds of skin.
- Pustular = at palms and soles of foot, Rx with retinoid.
- Erythrodermic = total body redness, rare but can be life threatening.
- Nail psoriasis seen with psoriatic arthritis.
Pathophysiology behind psoriasis
Autoimmune condition with T cell infiltration stimulating keratinocyte proliferation. Unregulated keratinocyte turnover leads to plaque formation, parakeratosis (retain nuclei), poor adhesion and increased keratin.
Triggers/ precipitants to psoriasis
Trauma e.g. burns, surgery, piercings. Infection Stress Alcohol Drugs e.g. lithium, chloroquine. Guttate psoriasis = streptococcal infection associated esp RTI.
Someone gets a new piercing 👩🎤 and now they have psoriasis
Koebner phenomenon.
Presentation of psoriasis
Clearly delineated/well circumscribed.
Erythematous, silvery scaly plaques
Itchy, burning or painful
Symmetrical distribution
Common on extensor surfaces of the body and scalp
- Scratch off plaque causes pinpoint capillary bleeding = Auspitz sign
- Halo around the plaque due to vasoconstriction = Woronoff’s ring
- Nail changes (pitting, onycholysis)
- S+S of associated disease e.g arthritis, IBD
How can you assess the impact of a skin condition on the patient?
Dermatology Life Quality Index - self- administered questionnaire.
‘Difficult to treat’ sites with chronic plaque psoriasis
Face, flexures, genitalia, scalp, palms and soles.
Psoriasis in these areas has a high-impact on patient.
Care when prescribing topical Rx.
May be v difficult to treat.
Management of chronic plaque psoriasis
Clinical ∆. Advise on use of emollients, smoking cessation, weight loss.
- topical corticosteroid, vitamin D analogue e.g. Calcitriol, coal tar preparations.
- phototherapy.
- methotrexate, oral retinoids, biologics.
Inflammation on cheeks, nose shin, eyes and forehead of a fair-skinned 35 year old European female…?
Acne rosacea.
High density of Demodex mites could be contributing factor.
S+S = facial flushing, persistent erythema, telangiectasia, papules, pustules, ocular rosacea eye symptoms.
Rx = topical metronidazole if mild, oral tetracycline if more severe.
Ocular problems with rosacea
Blepharitis
Conjunctivitis
Inflammation of Meibomian gland.
Keratitis
Triggers for rosacea
Alcohol Caffeine Spicy foods Drugs e.g. CCB Topical corticosteroids Heat and sunlight Emotional stress.
Impetigo
Superficial infection of skin. Highly contagious.
- Non-bullous or Bullous (fluid filled lesions).
- Common organism is Staph aureus.
- Golden/brown crusted lesion, dry and fall off leaving erythema which fades with time.
- Urgent assessment if infant with bullous impetigo.
- Good hygiene to prevent spread.
- PHE recommends that children and adults stay away from school, childcare facilities or work until lesions crusted over and dried / 48hrs after starting Abx.
- Topical fusidic acid or oral flucloxacillin.
Blistering skin disorder in an elderly patient, on trunk and limbs
Bullous pemphigoid.
- Chronic, autoimmune acquired disease.
- Autoantibodies against antigen between epidermis and dermis causing sub-epidermal splitting in skin.
- Itchy prodrome and then formation of tense, sub-epidermal bull. Usually symmetrical. Common on trunk, flexure aspects of legs.
- Rx with topical corticosteroids e.g. hydrocortisone
Blistering skin disorder of middle-aged patient, on mucosal areas
Pemphigus vulgaris.
- Autoantibodies against antigens within epidermis.
- Intra-epidermal splitting of skin.
- Flaccid, easily to rupture bullae form. Can develop erosions and crusts.
- PAINFUL.
- Affects mucosal areas before skin involvement.
- Rx with high-dose oral steroids or immunosuppressants e.g. methotrexate.
What is the most common Candida species
Candida albicans
Common areas for Candisiasis
At skin folds = intertrigo Oral mucosa = oral candidiasis Genital = Balanitis / Vulvovaginal candidiasis Nappy rash At nail fold At nail plate.
Presentation fo Candial skin infection and management
Sore and itch in affected area
Thin walled pustules with red base
Whitey curd like substance over affected area
Rx = topical anti-fungal e.g. imidazole, ketoconazole, terbinafine, clotrimazole
Kid with fever, malaise and now itchy red rash…?
Chickenpox!
- Small erythematous macules which progress to papules and pustules over 12hrs.
- Occur in crops on scalp, face, trunk and proximal limbs.
- Intense itch
- Crust over within 5 days and fall off within 2 weeks.
When is chickenpox infectious
From 1-2 days BEFORE rash appears and until the vesicles are dry and crusted over.
Where does the virus in chickenpox go?
Sensory nerve root ganglia. Can reactive to cause Shingles years later.
Management of chickenpox
Adequate fluid intake Smooth cotton fabric clothes Cut nails to prevent scratching damage. Consider paracetamol Calamine lotion to relieve itch - 7 days of acyclovir may be needed.
Difference between erysipelas, cellulitis and necrotising fasciitis.
Erysipelas =
- Infection of dermis and upper subcutaneous tissue.
- More superficial.
- Involve lymphs.
- Sharply demarcated.
Cellulitis =
- Deep subcutaneous tissue infection.
- Rapidly spreading infection with indistinct margins.
Necrotising fasciitis =
- Deep dermis, adipose tissue and subcutaneous fascia.
- V V V quick spreading, necrosis, bullae, high mortality.
Common causes of skin and soft tissue infections
Group A, beta-haemolytic strep - S.pyogenes
Also S.aureus
Hot tub, nail parlours and spas = Pseudomonas aeruginosa.
RFx for soft tissue and skin infections
Lymphoedema and leg oedema Diabetes mellitus Increasing age Obesity Malignancy Venous insufficiency
Presentation of cellulitis and Erysipelas
Common in lower limbs.
Acute onset
Swelling, erythema, warmth, pain.
Fever, malaise, rigors
Erysipelas = more well-defined borders to affected area, more lymph involvement.
Classification for cellulitis
Eron classification
Ix and Mx for cellulitis
Ix = swab of area for mc+s, FBC, ESR, CRP, USS for ?abscess, blood cultures. Mx = Abx (flucloxacillin for staph, BenPen for Strep) and supportive care.
Necrotising fasciitis
S+S = Severe pain, blistering, necrotic skin, systemically VVVV unwell (fever, TC), surgical emphysema.
Surgical debridement and ABx (tazosin)
Causes of onycholysis
Psoriasis
fungal nail infection
Hyperthyroidism
Functions of the skin
Protective barrier against environmental insult.
Thermoregulation.
Neurological = sensation of pain, touch, vibration, heat.
Vitamine D synthesis.
Immunosurveillance
Cosmetic/asthetic.
Cell for sensation in skin
Merkel cell in epidermis
Stages of wound healing at the skin
- Haemostasis - vasoconstriction, platelet aggregation and clot formation.
- Inflammation - more immune cell migration and phagocytosis of debris.
- Proliferation - granulation tissue formation, angiogenesis and re-epithelialisation.
- Remodelling - collagen re-organisation and scar maturation.
What you can tell a patient when they ask how much emollient is enough emollient
Finger-tip unit.
Squeeze of cream onto tip of index finger = enough to cover area for one hand.
Name some topical steroids in ascending order of potency
Hydrocortisone
Eumovate
Betnovate
Dermovate
Side effects of topical steroids
Skin atrophy
Telangectasia
Brusing
Worsening of condition
Baby has red blistering skin lesions, fever and irritable ….?
Staphylococcal scalded skin syndrome
- caused by release of epidermolytic toxin A and B from phage group II, benzylpenicillin resistant Staphylococci e.g. S.aureus.
- S+S = red cloistering skin (scald appearance) which goes on to form flaccid bullae, pain, fever, irritable baby. Nikolsky sign +ve.
- Ix = clinical ∆ but can take swabs for mc+s.
- Recovery within a week.
- Rx = good hydration, fusidic acid, flucloxacillin.
Nikolsky sin
Positive when gentle stroking of the skin causes upper epidermis to slip.
+ve in:
Steven-Johnson syndrome and Toxic epidermal necrolysis.
Staph scalded skin syndrome
Pemphigus vulgaris (but not bullous pemphigoid)
What causes verruca
HPV - can mimic SCC.
Linear burrows in between fingers …?
Scabies.
Ix = microscopic visualtions of mites or their eggs on skin scrapings.
TREAT THE WHOLE FAMILY AND WASH EVERYTHING
Rx = Topical permethrin + antihistamine.
- Urticaria
- Angioedema
- Rx for anaphylaxis
- Increased permeability of capillaries
- Deeper dermis and subcutaneous tissue swelling.
- A-E resus. IM Adrenaline 1:1000, IV Chlorphenamine, IV Hydrocortisone.
What is erythema nodosum
Inflammation of subcutaneous fat causes erythematous lumps on shins.
Seen in IBD, Sarcoidosis, group A beta-haemolytic strep throat infections, primary TB, COCP.
Pathology of Steven-Johnson Syndrome and Toxic Epidermal necrolysis.
Causes.
Type 4, T cell mediated hypersensitivity reaction. T cell attack on epithelial cells causing cell death, inflammation and detachment from basement membrane.
Causes: mostly drugs. Beta-lactams e.g. penicillin Sulfonamides Allopurinol Anti-convulsants e.g. carbamazepine, phenytoin NSAIDs PCM
S+S of Steven-Johnson Syndrome
Prodromal period of fever, sore throat, conjunctivitis, general malaise, runny nose.
Tender red skin rash starting on trunk and extending rapidly. VERY PAINFUL.
- Skin lesion = macular, diffuse erythema, flaccid bullae.
- +ve Nikolsky’s sign.
- At least 2 mucosal involvement areas e.g. eyes, mouth, pharynx, genitalia.
Toxic epidermal necrolysis
- Severe manifestation of SJS with greater than 30% of body surface area involved.
- Extensive skin and mucosal necrosis and detachment.
- Systemic toxicity
Lichen planus
Chronic inflammatory condition.
More common in females.
Attack on keratinocytes.
- Intense itch
- Eruption of shiny flat topped papules and plaques.
- Plaques have network of crosses = Wickham’s striae
- Mostly on extremities, can be oral, vulval, penile, scalp, nail or on other mucosa.
- Rx with topical steroids, calcineurin inhibitors, topical retinoids.
Name 3 different types of leg ulcers.
- what predisposing conditions do they have?
- where do they commonly occur?
- Venous ulcer = Hx of DVT or varicose veins. Malleolar region.
- Arterial ulcer = Hx of PAD and atherosclerotic disease. At a trauma or pressure site or distal areas e.g. toes.
- Neuropathic ulcer = Hx of diabetes. At a pressure site e.g. heel, toe.
Venous ulcers
- Large, shallow ulcer with irregular border.
- Exudate, warmth, oedema.
- Poor pedal pulses.
- Signs of venous eczema.
- Pain relieved on elevation
- Rx with compression bandaging.
Arterial ulcers
- Small, sharply defined ulcer.
- Nocturnal pain, relieved by hanging leg out of bed.
- Deep.
- Necrotic base.
- Cold skin, shiny/pale appearance, atrophy of hair.
- Rx with vascular reconstruction.
Neuropathic ulcers
- Punched-out appearance.
- Peripheral neurological deficit e.g. poor sensation.
- Pedal pulses present unless co-morbid ischaemia.
Differentials for purpura
- Meningococcal septicaemia
- DIC
- Vasculitis e.g. Henoch-Schonlien purpura
- Senile in elderly.
Ix and Mx for SJS/TEN
- Ix = elevated serum granulysin, skin biopsy to exclude scalded skin. Signs of dehydration in U+E.
- Mx = SCORTEN assessment for prognosis. Stop causative drug, analgesia, haemodynamic support. Can give antihistamines and steroids to decrease immune response.
Complications of SJS and TEN
Infection from broken skin barrier = sepsis.
Dehydration from fluid loss.
Lots of red, well defined bordered lesions on back of hands…
- Erythema multiforma from HSV.
- Hundreds of lesions erupt within 24hrs. Start on hand and spread to limbs and trunk.
- Start as macules then develop to papules and plaques with central darkness.
- TARGET LESION = 3 coloured plaque seen in EM.
- Can occur at trauma sites = Kobner phenomenon.
- Major and minor forms.
- Can give steroids and emollients.
Rash seen in Lyme disease
Erythema migrans.
Small papule at site of a tick bite delves into a large erythematous ring with central fading.
Rash seen in rheumatic fever
Erythema marginatum.
Pink coalescent rings
Pyoderma gangrenosum
Nodulo-pustular ulcers on leg, abdo and face.
Large, tender, necrotic edge, purulent discharge.
Associated with IBD, granulomatosis with polyangiitis.
White patches and hyper pigmented borders ∆
Vitiligo
On sunlight = itch.
Associated with premature ovarian failure and autoimmune diseases.
Skin manifestation of IBD
Erythema nodosum
Pyoderma gangrenosum
Skin manifestation of dermatomyositis
Gottron’s papules on knuckles and extensor surfaces.
Helitrope on eyelid.
Associated malignancy.
Skin manifestation of DM
Acanthosis nigricans
Neuropathic ulcers
Recurrent candidiasis
Skin manifestation in coeliac disease
Dermatitis herpetiformis
Itchy blisters in knees, elbow and scalp
∆∆ for eczema.
Rx with gluten free diet, Dapsone
Skin manifestation of hyperthyroidism
Pretibial myxoedema (Grave's) Sweating, facial flushing. Thinned hair Pruritis Thyroid acropachy causing onycholysis
