Dermatology

Question 1

What are the stages of wound healing

Answer 1

Haemostasis: vasoconstriction and platelet aggregation, clot formation
Inflammation: vasodilation, migration of neutrophils + macrophages, phagocytosis of debris and bacteria
Proliferation: granulation tissue formation (fibroblasts) and angiogenesis, re-epithelialisation (epidermal cell proliferation + migration)
Remodelling: collagen fibre reorganisation, scar maturation

Question 2

Urticaria patho, Px, Mx

Answer 2

Local increase in permeability of capillaries + small venules, histamine and inflammatory mediators, induced by immunological or non mechanisms

Px: itchy wheals (superficial swelling, epidermis raised), angioedema (swelling of tongue + lips)

Mx: antihistamines;+ corticosteroids

Question 3

Anaphylaxis patho, Px, Mx

Answer 3

Anaphylaxis: primarily IgE mediated hypersensitivity, sensitisation during initial exposure to allergen (antigen presenting cells, T cells, T helper 2 (cytokines), IgE antibodies, mast + basophils), effector phase (mast + basophils)

Anaphylaxis: bronchospasm, facial + laryngeal oedema, hypotension. Swelling of throat / tongue - hoarse + stridor, wheeze, dyspnoea, hypotension, tachycardia. Generalised pruritus, widespread rash

anaphylaxis: IM adrenaline (adults 500 micrograms / 0.5ml 1 in 1000) every 5 minutes; more than 2: IV fluids, senior help +/- IV
Following anaphylaxis: chlorphenamine, serum tryptase can be used to determine, new diagnoses to specialist allergy clinic. Can discharge after 2h if good response, 6h-12 depending

Question 4

Erythema nodosum patho, Px

Answer 4

IV hypersensitivity response to: Group A beta-haemolytic strep, primary TB, pregnancy, malignancy, sarcoidosis, IBD, chlamydia, leprosy
Px: discrete tender nodules (may become confluent), appear for 1-2w and leave bruise like discolouration when resolve, shin most common site

Question 5

Erythema mulitforme / SJS / toxic epidermal necrolysis description, Px, Mx, causes

Answer 5

Erythema multiforme: often unknown cause, acute self limiting inflammatory condition, herpes simplex virus main precipitating factor (other infections, drugs), mucosal involvement maximum one surface
Target lesions (central necrosis surrounded by erythema), hands / feet / torso. Major = mucosal involvement, and systemic sx

SJS: mucocutaneous necrosis with at least 2 mucosal sites, skin involvement ranges, drugs or infections + drugs. Extensive necrosis (seen on histopathology with few immune cells)
Px: painful burning eruption, loss of epidermis, prodromal illness (URTI), nikolsky sign positive - soft rubbing of skin results in removal

Hospital admission, supportive care with fluids

TEN: extensive skin and mucosal necrosis accompanied by systemic toxicity, usually drug induced. Histopathology has full thickness with subepithelial detachment
Nikolsky sign positive, fever + tachycardia, leads to sepsis and hypovolaemic shock
IV abx and IV IG

Common drugs: antibiotics (sulfonamides, penicillins, cephalosporins), antiepileptics (phenytoin, carbamazepine, lamotrigine), allopurinol, nevirapine (antiviral), piroxicam (NSAID)

Question 6

Erythroderma description, Px, Mx

Answer 6

Exfoliative dermatitis involving at least 90% skin surface; previous skin disease, lymphoma, drugs, idiopathic
Px: inflamed, oedematous, scaly, systemically unwell (lymphadenopathy, malaise
Mx: treat cause, emollients, wet wraps, topical steroids

Question 7

Eczema herpeticum Px, Mx, complications

Answer 7

Px: rapidly worsening painful eczema, vesicular (blistering) rash, punched-out uniform erosions 1-3mm, starts in affected areas then spreads to normal skin 1-2w, systemically unwell (fever, malaise)

Mx: aciclovir 5* 10-14d, antibiotics for secondary infection if required. Referral to dermatologist, same day ophthalmologist if eye involvement

Complications: herpes hepatitis, encephalitis, DIC, recurrent herpes

Question 8

Necrotising fasciitis description, Px, Ix, Mx

Answer 8

Severe and rapidly progressive soft tissue infection causing necrosis of subcutaneous tissues and fascia (sometimes muscle). Most commonly in diabetes, following trauma / surgery. Can affect limbs, perineum, genitals (Fournier’s gangrene) or abdominal wall

Px: swelling, severe pain, erythema / blistering / necrotic, induration. Rapid progression, blistering and bullae, failure to response to abx, grey skin, skin crepitus. Systemic: diarrhoea + vomiting, tachycardia, fever, hypotension, tachypnoea, sepsis

Ix: NF score bloods (Hb, WCC, Na, creatinine, glucose, CRP); Xray may show subcutaneous gas, CT / MRI, incisional biopsy

Mx: urgent surgical debridement - fasciotomy, IV abx depending on organism (flucloxacillin, benzylpenicillin)

Question 9

Eysipelas vs cellulitis, Px, Ix, Mx

Answer 9

Erysipelas is acute superficial form of cellulitis involving dermis and upper subcutaneous tissue. Cellulitis is infection of deep subcutaneous. Usually strep pyogenes or staph aureus

Px: usually unilateral and leg, swelling, erythema, warmth pain. Systemically fever, malaise, rigours. Erysipelas has well defined raised red border
Bilateral or slowly progressive less likely, rapidly progressive blistering consider necrotising fasciitis

Ix: bloods (FBC, U+Es, CRP / ESR), wound swab, blood cultures in IC or atypical

Mx: analgesia, oral flucloxacillin (clarithromycin); severe: co-amoxiclav / clindamycin / cefuroxime. Elevate area, sterile dressings, mark areas to check progression

Referral: Eron class III or IV: significant systemic upset, unstable comorbidities, is immunocompromised, significant lymphoedema, facial / periorbital cellulitis

Question 10

Staph scladed skin syndrome Px, Mx

Answer 10

Px: develops quickly, face / neck / axillae / groin, scalded appearance followed by large flaccid bulla, perioral crusting, painful lesions

Mx: flucloxacillin, erythromycin, analgesia

Question 11

What are the 3 main groups of fungal infections, Ix, Mx

Answer 11

3 main groups: dermatophytes (tinea / ringworm), yeasts (candidiasis, malassezia), moulds (aspergillus)

Ix: clinical, skin scrapings / nail or hair clippings, skin swabs (yeast)

Mx: topical terbinafine, oral itraconazole (fluconazole) in systemic or nail, correct predisposing factors

Question 12

Px of tinea corporis / pedis / manuum / capitis / unguium / incognito / vesicolour, candidiasis

Answer 12

Tinea corporis: trunk + libs, itchy, circular / annular lesions, clearly defined, scaly edge
Tinea pedis (athlete’s foot): moist scaling + fissuring in toewebs, spreads to sole + dorsum
Tinea manuum: hands, scaling + dryness, palmar creases
Tinea capitis (scalp ringworm): patches of broken hair, scaling and inflammation
Tinea unguium: nail, yellow discolouration, thickened and crumbly nail
Tinea incognito: inappropriate treatment with steroid, ill defined and less scaly
Pityriasis / tinea vesicolour (malassezia furfur): scaly brown patches on upper trunk, fail to tan in sun, asymptomatic
Candidiasis: white plaques on mucosal surface, erythema with satellite lesions in flexures

Question 13

Scabies patho, Px, Mx

Answer 13

Mite sarcoptes scabiei colonises skin and lays eggs in epidermis, T4 hypersensitivity to eggs (up to a month after exposure - skin to skin), inflammatory cytokine release

Px: pruritus, worse at night, linear burrows (thread like grey lines with small vesicle and black dot at end), erythematous papules on side of fingers / web spaces / under nails

Mx: whole household, whole body permethrin (8-12h) or malathion (24h); severe: topical insecticide and oral ivermectin

Question 14

Squamous cell carcinoma Patho, RF, Px, Mx

Answer 14

Locally invasive malignant tumour of epidermal keratinocytes or appendages, potential to metastasise

RF: UV exposure, premalignant conditions (actinic keratoses), chronic inflammation, IC

Px: keratotic, scaly, crusty, ill defined nodule which may ulcerate

Mx: surgical excision (or Mohs micrographic), radiotherapy for non resectable

Question 15

Malignant melanoma patho, Px, Ix, prognosis indicator, Mx

Answer 15

Invasive malignant tumour of epidermal melanocytes. Radial growth along epidermis + superficial dermis, vertical growth into deep dermis

Px: starts as unusual freckle / mole, becomes abnormal (ABCDE): asymmetry, borders irregular, colour not uniform, diameter >6mm, evolution of lesion. Bleeding, itching
(Superficial spreading (70%): limbs and torso of young people. Nodular: most aggressive, bleeds. Lentigo maligna: slowly progressive in situ. Acral lentiginous: rare form with pigmentation under nails / palms / soles of black and asian people)

IX: biopsy and sentinel lymph node mapping

Prognosis - depth of tumour (Breslow thickness) most important factor: <1mm 95% 5y survival, >4mm 50%

Mx: surgical removal (second wide local excision often needed) +/- sentinel lymph node biopsy, chemo / radio / targeted therapy

Question 16

Atopic eczema patho, Px, Mx

Answer 16

Primary genetic defect in skin barrier function (filaggrin protein), mediated by increased Th2 cells, promoted pathogen specific IgE (TI hypersensitivity) - eosinophils and mast cells. Irritants enter easier and cause inflammatory response
Exacerbating factors: infections, allergens (chemicals, food, dust, pet fur), sweating, heat, occupation, stress

Px: acute: erythematous fissuring, itchy papules + vesicles, weepy; chronic: dry, clay patches; distribution: babies - face and torso, older - flexor surfaces + face creases (sweat concentration)
Chronic scratching leads to lichenification, hypopigmentation, nail pitting / ridging

Mx: avoid exacerbating agents, frequent emollients (hydromol, diprobase) +/- bandages. Topical steroids for active areas (10:1 with emollient, 1 fingertip for double area of hand); hydrocortisone (weakest), eumovate, betnovate (potent), fucidin H (hydrocortisone + fusidic acid for infections)

Tacrolimus (calcineurin inhibitor), for maintenance in severe, phototherapy and immunosuppression (azathioprine) in severe non responsive

Question 17

Px of eczema secondary infections, discoid, sebhorrhoeic, contact, dyshidrotic

Answer 17

Secondary infections: bacterial (crusted, weepy) - flucloxacillin, eczema herpeticum (extensive crusted papules, blisters, swollen lymph glands + fever, untreated can lead to eyes / brain / lung) - aciclovir. Molluscum - pearly papules with central umbilication

Discoid eczema: round erythematous patches, arms and legs, starts as red spots that merge together. Mild steroids

Seborrheic: chronic in sebum rich areas (scalp and face), abnormal response to malassezia furfur leading to inflammation. Yellow scale on scalp (cradle cap), regular shampoo, ketoconazole in severe. Adults will be pink thin scaly plaques in folds, mild steroids in flare, ketoconazole

Contact: redness, dryness, swelling, fissuring, only areas exposed (usually hands). Avoid contact, less soap, better gloves, emollients, steroids

Dyshidrotic: blisters on fingers / palms / soles, unknown cause but related to seasonal allergies. Intense itching, burning, large painful blisters which flake off, lasts up to 3w. Emollients + steroids

Question 18

Psoriasis patho and types

Answer 18

Chronic inflammatory condition due to hyperproliferation of keratinocytes and T cell activity. Genetic predisposition and environmental triggers (stress, trauma, infection, medications)

Plaque: most common (90%), well defined, red, scaly patches, extensor surfaces + head
Flexural (inverse): smooth, well defined plaques, folds + genitals
Guttate: self resolving teardrop lesions, following strep infection
Generalised pustular: flares of pustules superimposed of red painful skin

Question 19

Psoriasis Px, Ix, Mx

Answer 19

Px: red salmon rash, plaque formation, nail changes (pitting, onycholysis), auspitz sign (removal of scales leads to pinpoint bleeding), Koebner phenomenon (new plaques at sites of skin injury), psoriatic arthritis in roughly 30%

Ix: mostly clinical, skin biopsy, bloods, rheumatology screening. Psoriasis area severity index (PASI) - extent of surfaces, intensity of redness, thickness and scaling

Mx: avoid triggers, emollients; FL: topical steroids + calcitriol (Vit D) for 4w; add phototherapy; methotrexate, etanercept, apremilast for refractory disease

Question 20

Acne vulgaris Px, Mx, referral

Answer 20

Px: early: open (blackheads) and closed (whiteheads) comedones; inflammatory: papules, pustules; severe: nodules, cysts. Face / chest / back as highest concentration of sebaceous glands
Leads to ice-pick and hypertrophic scars
Drug induced: monomorphic - steroids cause pustules

Mx (12w): mild: adapalene / tretinoin (retinoid) + benzoyl peroxide; inflammatory: add topical clindamycin or azelaic acid; moderate: tretinoin / adapalene and oral lymecycline or doxycycline; severe: oral isotretinoin +/- oral / injection steroids
Hormonal in women: COCP, spironolactone

Referral: any not responded to 2 courses, not responded to oral abx, scarring / persistent pigmentary changes, persistent psychological distress. Only dermatologists can prescribe oral retinoids

Question 21

Roascea Px, Ix, Mx

Answer 21

Px: nose / cheeks / forehead, flushing, telangiectasia, erythema with papules + pustules, rhinophyma (large, red, bumpy), sunlight exacerbates

Ix: clinical diagnosis, exclusion of acne / seborrhoeic dermatitis / lupus

Mx: high factor suncream; erythema / flushing - brimonidine (alpha agonist); papules / pustules: ivermectin, severe ivermectin + oral doxycycline
Referral for persistent or rhinophyma

Question 22

Bullous pemphigoid Px, Mx

Answer 22

Autoantibodies against antigens between epidermis and dermis causing subepidermal split in skin, typically elderly

Px: tense, fluid filled blisters, erythematous base, itchy, trunk and limbs (sometimes mucosa)

Mx: wound dressings, monitor infection, topical steroids; systemic: oral steroids, tetracycline + nicotinamide

Question 23

Pemphigus vulgaris Px, Mx

Answer 23

Autoantibodies against antigens within epidermis - intraepidermal split in skin, typically middle aged

Px: flaccid, easily ruptured blisters forming erosions and crusts, painful, mucosal most common

Mx: wound dressing, monitor infection, high dose oral steroids, methotrexate / azathioprine

Question 24

Vitiligo Px, Mx

Answer 24

AI condition resulting in loss of melanocytes. Unknown cause, associated with: T1DM, addison’s, AI thyroid, pernicious anaemia, alopecia

Px: any age, well demarcated patches of depigmented skin (often symmetrical), face / hands / feet / body folds / genitalia, Koebner phenomenon

Mx: minimise injury, suncream +/- makeup for affected areas, potent topical steroids (mometasone) can reverse if applied early enough, tacrolimus and phototherapy also used. Severe: methotrexate, oral dexamethasone, surgery

Question 25

Melasma Px, Mx

Answer 25

Acquired increased skin pigmentation by melanocytes, triggers: sun exposure, hormonal changes

Px: brown macules or larger patches with irregular border, symmetrical distribution, usually face

Mx: lifelong suncream, discontinuation of hormonal treatments, cosmetic. Topical hydroquinone can depigment skin

Question 26

Neurofibromatosis T1 / 2, tuberous sclerosis Px

Answer 26

Px: >5 cafe au lait marks (uniformly pigmented brown macules) >1.5cm, freckles in axilla + groin, peripheral neurofibromas
Other organs: scoliosis, lisch nodules in eye, pheochromocytoma
Associations: learning difficulties, hypertension (renal artery stenosis, phaeochromocytoma), neurofibromas + optic nerve gliomas

Bilateral acoustic neuromas (sensorineural hearing loss, tinnitus, vertigo) - benign but can cause raised ICP; schwannomas + meningiomas

Px: hypopigmented ‘ash-leaf spots’ (fluoresce under UV), angiofibroma in butterfly pattern around nose (adenoma sebaceum), connective tissue naevus (Shagreen patch, elevated skin on back), subungual fibromata (under nails)
Other organs: rhabdomyomas (benign muscle) of heart, PCKD + benign kidney tumours, haematomas in eye, hematoma in CNS

Question 27

Venous / arterial / neuropathic ulcers Px, Ix, Mx

Answer 27

Venous: pain worse on standing, venous history (varicose veins, DVT), malleolar area most common (medial>lateral), large / shallow / irregular, exudative + granulating base
Associated: warm skin, normal pulses, leg oedema
Normal ankle/brachial pressure index. Compression bandaging

Arterial: pain worse at night / legs elevated, history of arterial disease, pressure sites / distal points (toes), small / sharply defined / deep, necrotic base
Associated: cold skin, weak / absent pulses, shiny pale skin, loss of hair
ABPI <0.8, doppler studies + angiography. Vascular reconstruction, compression bandaging is contraindicated

Neuropathic: often painless, abnormal sensation, history of neuropathy (diabetes), pressure sites, variable size + depth, granulating base, may be surrounded by callus
Associated: warm skin, normal pulses, peripheral neuropathy
Normal ABPI unless neuroischaemic, X ray to exclude osteomyelitis. Wound debridement, regular repositioning, appropriate footwear

Question 28

Melanocytic naevi + seborrhoeic wart Px, Mx

Answer 28

Melanocytic naevi: asymptomatic, develop before adulthood, variable location. Only remove if symptomatic with excision

Seborrhoeic wart: multiple, asymptomatic, arise in later age, face and trunk. Warty / greasy papules or nodules, stuck on appearance with well defined edges. Only remove if symptomatic with crete and cautery / cryotherapy

Question 29

How to take a derm history

Answer 29

Pc: nature, site and duration
HPc: Initial appearance + evolution, aggravating + relieving, previous + current treatments, causes (contact, stress, illness, travel, sunburn / tanning beds)
PMHx: atopy, previous conditions, suspicious lesions
FHx
SHx: occupation (worse / better at work), impact on life
Meds

Question 30

Describe a derm exam

Answer 30

General observation, pigmentation / skin type, site + number of lesions = pattern
S(s)CAM(m): size (widest diameter) / shape, colour, associated secondary change, morphology / margin
If pigmented ABCDE: asymmetry, border is irregular, colours (2+), diameter >6mm, evolution
Surface, consistency, mobility, tenderness, temperature (especially important in dark skin)
Nails, scalp, hair, mucous membranes. General systems exam relevant to symptoms

Question 31

Lichen planus Px, Ix, Mx

Answer 31

Unknown aetiology, chronic inflammatory condition affecting skin, hair, nails, mucous membranes. Thought that response to viruses or drugs

Px: papular rash (often polygonal) with white lines (Wickham’s striae), itchy, palms / soles / genitalia / flexor surfaces of arms, Koebner phenomenon, thinning + ridging of nails. Oral in 50%

Ix: biopsy FL; direct immunofluorescence, bloods (FBC, LFTs, viral serology)

Mx: topical steroids, benzydamine mouthwash; extensive - oral steroids / immunosuppression

Question 32

Describe superficial, partial thickness and full thickness burns

Answer 32

First degree - superficial, epidermis + erythema only, should not slide over layers when rubbed
Red and painful, no blisters, CRT normal

Second degree - partial thickness, dermal layers; subdivided into superficial / mid / deep dermal), indicated by blistering
Superficial partial: red / pale pink with blistering, CRT slow
Deep partial: dry / blotchy / mottled, may be blisters, CRT does not blanch

Third degree - through dermis and deeper layers
White / brown / charred, no blisters, dry / leathery / waxy, painless, CRT does not blanch

Question 33

How are non complex and complex burns managed

Answer 33

Non complex burns can be managed in primary care: wound management, cold water, emollient, simple analgesia, good hydration, assess need for tetanus vaccine

Complex burns: all electrical + chemical, thermal affecting critical area (face, hands, feet, perineum, genitalia), more than 15% TBSA (10% in children)

Wallace rule of nines (estimating total body surface area of 2nd+3rd); 9% of body: full head and neck, entire arm, chest, abdomen, upper back, lower back; legs 18% each, genital area 1%
Calculated for fluid requirements

Fluid requirements (modified parkland formula): 4mls * weight kg * TBSA burn %, Hartmann’s, ½ fluid in first 8h, 2nd ½ over 16h
Burns lead to lots of skin oedema and hypovolaemic shock