Dermatology Flashcards
Eczema
morphological descriptor for maculopapular erythematous rash ± scale/eroison/blistering, it is used in isolation usually to describe atopic eczema
Atopic dermatitis / atopic eczema
chronic relapsing inflammatory skin condition characterised by an itchy red rash that favours the skin creases e.g. fold of the elbow or behind knee
Epidemiology of atopic dermatitis / eczema
typically manifests in childhood (often improves in adolescence)
associated with other atopic disease e.g. asthma, allergic rhinitis, food allergies
affects ~10-30% of all children & up to 10% of all adults
Triggers for atopic dermatitis / eczema
irritants (e.g. soaps/detergents) heat very dry or very humid climate emotional stress dust mites pollen infections dietary factors (in ~50% of children) genetics
Associated conditions with atopic dermatitis / eczema
asthma
allergic rhinitis
food allergies
NB ~70% of cases have family history of atopic disease
Presentation of atopic dermatitis / eczema
intense pruritus & dry skin, redness ,swelling
distribution tends to vary with age
Infancy: face/scalp/extensor surfaces of limbs (nappy area generally spared)
Childhood: flexural creases, skin folds, extensor surfaces
adults/adolescents: flexural creases, lichenfied lesions & pruritus
Pompholyx eczema presentation
tiny vesicles on the palms and soles
intense pruritus ± burning sensation
once blisters burst skin may become dry and crack
Diagnostic criteria for eczema
Must have itchy skin condition + ≥3 of the following:
- hx of flexural itchiness
- hx of asthma / eczema
- dry skin for past year
- visible flexural eczema
- onset before 2 y/o
Investigations of atopic dermatitis / eczema
generally clinical diagnosis
consider allergy testing IgE level (↑) Radioallergosorbent test (RASTs)
Management of atopic dermatitis / eczema
Generally:
emollients & moisturisers (apply liberally & frequently, best on moist skin e.g. after shower, use 3-4/day)
soap substitutes
1st line: Topical steroids
2nd line: Topical tacrolimus / pimecrolimus
3rd line: systemic steroids
Finger tip unit
1 finger tip unit is ~0.5g
sufficient to treat area 2x size of flat adult hand
Mild topical steroids
e.g. hydrocortisone 0.5-2.5%
use in mild eczema and eczema on face
moderate strength topical steroids
e.g Eumovate, Modrasone
used in moderate eczema
potent topical steroids
e.g. Betnovate, Synalar, clobetasol
in severe eczema
NB super potent steroids include Dermovate
Eczema herpeticum
severe skin infection caused by herpes simplex virus (HSV) in a pt suffering from eczema
usually seen in children
Eczema herpeticum presentation
extensive disseminated & painful eruptions on head / upper body, erythematous skin with multiple round vesicles which may progress to pushed out lesions
the rash is painful & rapidly progressing
fever, malaise, lymphadenopathy
Eczema herpeticum investigations
may be a clincial diagnosis in those with know eczema & an acute eruption of a painful monomorphic clustered vesicle + fever & malaise
viral swabs /scrapings (for PCR of antibody fluorescence)
Eczema herpeticum management
Dermatological emergency
antiviral therapy e.g. aciclovir (PO/IV)
consider Abx for secondary bacterial infection
Discoid / Nummular eczema
chronic inflammatory skin condition charactersied by scattered well defined coin shaped & coin sized plaques of eczema
relatively common form of eczema, more frequently seen in men around the ages 50-65
Presentation of Discoid / Nummular eczema
2-5cm coin shaped / oval well demarcated erythematous plaques, pruritus, scale
primarily affects the extremities especially the legs
Investigations for Discoid / Nummular eczema
skin scrapping to exclude tinea (dermatophytosis)
Management of Discoid / Nummular eczema
rehydrate skin (shower/bathe in cool water)
emollients/moisturisers
soap substitutes
topical steroids (usually mild steroids sufficient e.g. hydrocortisone cream)
Urticaria (hives)
itchy, red, blotchy rash resulting from swelling of the superficial payer of the skin (dermis) due to mast cell degranulation & histamine release
NB angio-oedema occurs if the deeper tissues such as the lower dermis or subcutaneous tissue are involved & become swollen
Types of urticaria
Acute:
usually self limiting, causes include allergies, viral infections, skin contact with chemicals/nettles/latex, physical stimuli e.g. firm rubbing
Chronic:
maybe spontaneous, autoimmune or induced (e.g. by exercise, sun exposure etc)
Dermatographism
writing on skin with urticaria
i.e. urticaria develops when scratching the skin
Investigations for urticaria
clinical diagnosis
if chronic/recurring consider investigating (FBC, ESR/CRP, physical challenge testing, IgE tests, patch testing)
Management of urticaria
minimise non specific aggravating factors e.g. stress, alcohol
topical anti-pruritic agents e.g. calamine lotion, topical method
non sedating antihistamines e.g. cetirizine, loratadine
Psoriasis
chronic inflammatory skin condition characterised by erythematous, circumscribed scaly papules & plaques
affects ~2% of population, majority of cases present before age 35
Subtypes of psoriasis
plaque psoriasis:
90% of cases, usually well demarcated red scaly plaques on extensor surfaces/sacrum/scalp
flexural psoriasis:
skin is smooth, mainly affecting flexural surfaces & skin folds
guttate psoriasis:
widespread tear drop shaped psoriatic lesions triggered by streptococcal throat infection
pustular psoriasis:
commonly on palms & soles, associated with HLA-B27, confluent, white pustules
Guttate psoriasis
transient psoriatic rash usually triggered by streptococcal infection, presents as multiple widespread tear drop shaped lesions
more commonly seen in children
responds well to light therapy
Most common type of psoriasis
plaque psoriasis = ~90% of all cases
Risk factors for psoriasis
Family history (~30% of pts) infection (e.g. streptococcal) stress drugs (lithium, ACE-Is, beta-blockers, penicillins) smoking alcohol
Presentation of psoriasis
well demarcated erythematous plaques/papules with silvery-white scale (usually on scalp, extensor surfaces, back)
mild pruritus
pin point bleeding if scales scrapped of (Auspitz sign)
Nail involvement (~50% of pts) nail pitting, small round depression of nails, onycholysis, brittle nails, discolouration of nail bed
NB ↑ severity with alcohol consumption, ↓ severity with sunlight
conditions associated with psoriasis
psoriatic arthritis
IBD
metabolic syndrome
Investigations for psoriasis
generally clinical diagnosis
ESR/CRP (↑ if arthropathy)
consider skin biopsy if diagnosis in doubt
Management of psoriasis
1st line: OD potent topical steroid + OD topical Vit D analogue e.g. calcipotriol
2nd line: Vit D analogue BD
3rd line: potent corticosteroid BD / coal tar preparation
Secondary care:
narrow band UV B light theory
Systemic therapy:
methotrexate = 1st line
Exacerbating & relieving factors for psoriasis
↑ severity with alcohol consumption
↓ severity with sunlight
Erythema nodosum
common cuteness hypersensitivity reaction leading to inflammation of the subcutaneous fat
most commonly affects women in early adulthood
Aetiology of erythema nodosum
NB most common cause = underlying streptococcal infection
Causes include: sarcoidosis* IBD Behcet syndrome COCP pregnancy TB infection (e.g. streptococcal)
Presentation of erythema nodosum
painful subcutaneous nodules, firm, erythematous, fluctuant & blueish in colour usually on bilateral shins
self resolves in ~6 weeks
fever, arthralgia, aches
Investigations for erythema nodosum
to exclude serious underlying cause
anti-streptococcal (ASO) titre FBC ESR (↑↑) CXR (for TB/Sarcoidosis) Ca2+ / ACE (↑ in sarcoidosis) intradermal skin test (for TB)
Management of erythema nodosum
generally self limiting condition so only symptomatic relief i.e. hot/cold compresses, NSAIDs, potassium iodide
treat underlying disease
Erythema multiforme
rare acute hypersensitivity reaction leading to mucocutaneous inflammation which is usually self limiting but often relapsing
most pts are <40y/o
Aetiology of erythema multiforme
NB most common cause is Herpes simplex virus (HSV) infection
Infections:
HSV
mycoplasma pneumoniae
Medications:
phenytoin, beta-lactam Abe e.g. penicillin, NSAIDs, allopurinol, carbamazepine
Others:
sarcoidosis, SLE
Presentation of erythema multiforme
generally acute onset of rash characterised by target / iris lesions
3 zones, inner (dark red/brown), middle (pale) outer (erythematous ring)
starts on back of hands / feet then spreads to torso
may have mucous involvement e.g. mouth lesions
NB rash may be preceded by 3-14 by infection e.g. cold sores
management of erythema multiforme
treat underlying cause e.g. infection or stop offending drug
consider antiretrovirals if recurrent disease due to HSV
Characteristic lesion of erythema multiform
Target lesions
Pruritus
an unpleasant itching sensation leading to intense scratching, may be localised or general
NB localised usually dermatological cause, generalised pursuits usually systemic/psychogenic cause
Management of pruritus
moisturisers
calamine lotion
topical steroids/calcineurin inhibitors e.g. tacrolimus
antihistmamines
Erythoderma
term used to describe when >95% if the skin is involved in a rash of any kind
Causes of erythroderma
eczema
psoriasis
drugs
lymphomas/leukaemia
Eryhtrodermic psoriasis
most common cause of erythroderma in adults, either due to progressively worsening plaque psoriasis or unstable psoriasis triggered by infection/drugs
NB dermatological emergency
Eryhtrodermic psoriasis presentation
whole skin is erythematous & hot
dermatological features of psoriasis are often lost, scale is usually finer & flakier
usually painful & pruritic
pt systemically unwell
Management of Eryhtrodermic psoriasis
emergency admission to hospital
emollients & cool wet dressing
methotrexate or cyclosporin & infliximab
Steven-Johnson syndrome (SJS) & Toxic epidermal necrolysis (TEN)
spectrum of rare immune mediated skin reactions resulting in blistering of the skin & epidermal detachment
SJS & TEN are the same entity but depend on the extend of skin involved
<10% = SJS
10-30% = overlap between SJS & TEN
>30% = TEN
Aetiology of Steven-Johnson syndrome (SJS) & Toxic epidermal necrolysis (TEN)
drug induced (75%) allopurinol, phenytoin, sulfalazine, pencillin, carbamazepine, other anticonvulsants
infections / other causes (25%)
viral (HSV, EBV), bacterial (group A haemolytic strep), Hep B vaccination
Presentation of Steven-Johnson syndrome (SJS) & Toxic epidermal necrolysis (TEN)
ill defined red burning / painful macular/papular rash develops that forms into bull which then coalesce
mucous membrane involvement (90% of pts)
Nikolsky sign +ve
NB mucous membrane involvement differentiates this from SSSS
Management of Steven-Johnson syndrome (SJS) & Toxic epidermal necrolysis (TEN)
stop offending drug
supportive therapy:
IV fluids, Abx if septic, electrolyte replacement
ITU/burns unit admission
Necrotising fasciitis
life-threatening sub-cutaneous soft tissue infection that may extend to the deep fascia, usually progresses rapidly
NB Fournier gangrene is necrotising fasciitis of the external genitalia / perineum
Types of necrotising fasciitis
Type I (most common) polymicrobial, usually in pts with chronic disease e.g. diabetes
Type II:
caused by strep pyogenes
Risk factors for necrotising fasciitis
skin injury e.g. insect bites/trauma/surgical wounds
diabetes*
IVDU
immunocompromise
Presentation of necrotising fasciitis
pt systemically ill with disproportionately severe pain & only minor skin changes in early phase
pain swelling & erythema of affected site (often presents as rapidly worsening cellulitis)
later skin necrosis, gas gangrene
Management of necrotising fasciitis
Surgery (should no be delayed if necrotising fasciitis is suspected)
urgent surgical debridement, repeated daily until infection controlled
high dose broad spectrum Abx
Bullous pemphigoid vs Pemphigus vulgaris
Pemphigus = S for superficial blisters, usually younger people, +ve Nikolsky sign
Pemphigoid = D for deep blisters, usually old people, -ve Nikolsky sign
Bullous pemphigoid
chronic acquired autoimmune blistering disease (subepidermal) characterised by autoantibodies against hemidesmosomal antigens (BP180 & BP230)
most common type of blistering dermatosis
usually seen in pt aged >80 yrs (i.e. a disease of the elderly)
Presentation of Bullous pemphigoid
initially pruritus (weeks-months before blisters)
large tense sub epidermal (deep) blisters on normal/erythematous skin, usually on flexor surfaces of arms/legs, axillae, groin, abdomen
heal without scars
NB mucous involvement is rare
Investigations for Bullous pemphigoid
skin biopsy + direct immunofluorescence (sub epidermal blisters, dermal inflammatory cell infiltrates rich in eosinophils, IgG & C3 deposition)
antibody tests (BP180 & BP230)
Management of Bullous pemphigoid
1st line: potent topical steroids e.g. clobetasol (if localised disease) otherwise systemic steroids + osteoporosis cover
2nd line: immunotherapy e.g. azathioprine
NB topical steroids usually better tolerated by the pt than systemic steroids
Pemphigus vulgaris
autoimmune blistering condition that involved the epidermal surfaces of skin / mucosa or both, associated with antibodies to demoglein 3 (DSG3) an epithelial cell adhesion molecule
rare conditions, usually seen in those aged 30-70
Presentation of pemphigus vulgaris
spontaneous onset painful, flaccid intraepidermal (superficial) blisters that easily rupture, so erode & crust over
blisters usually first present on oral mucosa
pruritus usually absent Nikolsky sign (spread of blisters/loss of top layer of skin from moderate lateral pressure on healthy skin
NB often blisters pop before pt presents so generally presents as eroded skin
Nikolsky sign
occurrence of blisters or loss of top layer of skin when slight lateral pressure is applied to healthy skin(by rubbing)
Investigations of pemphigus vulgaris
skin biopsy with direct immunofluorescence (DIF):
intraepidermal vesicles, acantholysis, IgG deposition in intracellular spaces of epidermis, IgG in reticular pattern around epidermal cells
antibody tests (DSG3)
Management of pemphigus vulgaris
topical steroids e.g. beclometasone if mild/oral disease
1st line:systemic steroids
2nd line: electrophoresis
Dermatitis herpetiformis
autoimmune blistering skin disease associated with coeliacs disease & may be considered the cutaneous manifestation of coeliacs, due to IgA deposition in dermis
very rare, usually seen in younger people (age 20-40)
Presentation of dermatitis herpetiformis
tense grouped sub epidermal vesicles / papule and/or bullae with herpetiform appearance
lesions grow in centrifugal pattern with vesicles predominating the peripheries
intense pruritus
NO mucosal involvement
Investigations for dermatitis herpetiformis
skin biopsy & DIF (sub epidermal vesicles, deposition of granular IgA)
coeliac disease screen (anti-TTG / anti-endomysial antibodies)
Management of dermatitis herpetiformis
gluten free diet
Dapsone
topical steroids for pruritus
Cellulitis
acute spreading infection of the skin with visually distinct borders that principally involves the dermis & subcutaneous tissue
Erysipelas
a distinct form of superficial cellulitis with notable lymphatic involvement
Causative organism of cellulitis
strep pyogenes
staph aureus
Risk factors for cellulitis
insect bites elderly alcohol misuse IVDU obesity/overweight pregnancy diabetes immunocompromised
Presentation of cellulitis
erythema, oedema, warmth, tenderness over affected area
usually affects lower limbs (usually unilateral)
Rash = poorly defined with induction (NB erysipelas is well demarcated raised lesions)
lymphadenopathy, fever, chills, nausea, headache etc
criteria guiding cellulitis treatment
ERON criteria
Management of cellulitis
analgesia (paracetamol, ibuprofen)
Abx:
1st line: flucloxacillin (erythromycin/clarithromycin if penicillin allergy)
2nd line (if severe): co-amoxiclav, ceftriaxone
Impetigo
a superficial predominately paediatric skin infection caused by staph aureus, either as a primary infection or secondary to other skin conditions e.g. eczema
Causative organism of impetigo
Staph aureus (80%) strep pyogenes
Presentation of non-bullous impetigo
70% of cases
papules which turn into small vesicles with surrounding erythema, ooze secretions that dry to from honey-coloured crusts
often seen around mouth & nose or on limbs
rapidly spreads
local lympahdenopathy
Presentation of bullous impetigo
30% of cases
vesicles that grow in large flaccid bullae that tend to be thin roofed & spontaneously rupture
no regional lymphadenopathy
more likely to have systemic upset & pain than non bullous impetigo
Investigations for impetigo
generally clinical diagnosis
consider swab for culture especially if MRSA is suspected
Management of impetigo
Localised non bullous impetigo:
hydrogen peroxide 1 % cream or topical Abx (e.g. fusidic acid)
extensive disease:
oral Abx e.g. flucloxacillin (erythromycin if penicillin allergy)
School exclusion:
until all lesion are dry/scabbed over or after 48h of Abx
School exclusion for impetigo
stay off school/work until all lesion are dry/scabbed over or after 48h of Abx
Dermatophyte infection / tinea
fungal infections of the skin/hair/nails caused by dermatophytes - a group of fungi that invade & grow in dead keratinocytes
tend to grow outward on skin producing a ring like pattern hence the name ring worm, often itchy & erythematous
Tinea pedis (athletes foot)
most common tinea infection
particularly in between webs of toes where skin may be marcated & erythematous
itchy, peeling skin between toes
common in adolescence
Tinea corporis (ringworm)
dermatophyte infection anywhere on body excluding feet/scalp/nails/groin
well defined annular erythematous lesions with pustules & papules
lesions have annular scaly plaques with raised edges
Tinea capitis
dermatophyte infection of the head & scalp mainly seen in children
round pruritic scalp plaques with broke hair shafts or alopecia in affected area
cause of scarring alopecia
post auricular lymphadenopathy
NB if untreated a kerion may form = deep, boggy plaque with pustule formation
Tinea unugvium (onychomycosis)
fungal nail infection usually affecting toe nails
discoloured white/grey/yellow nails, very brittle nails
separation of nail from nailed common
nail dystrophy & thickening
Tinea cruris (jock itch)
Ringworm affecting genital area
Risk factors for tinea infection
diabetes immunocompromise exposure to infected individuals/animals public bathing/swimming pools chronic steroid use
Investigations for Tinea
KOH (potassium hrydoxide) microscopy:
hyphae (branching red-shaped filament sou infirm with with septa) + spores
UV light (Wood's light) specifically for tinea = blue-green fluorescence of causative microsporum species
Management of Tinea
1st line: Topical antifungals e.g. fluconazole / terbinafine / itraconazole
2nd line: systemic antifungals (as above) used for tinea Capitis & extensive disease
NB for tinea capitis use oral griseofulvin or terbinafine + Topical ketoconazole shampoo
Tinea vesicolor / Pityriasis vesicolor
common superficial fungal infection of the stratum corneal (outer layer of epidermis) commonly caused by malassezia furfural or other malassezia species
usually seen in teenagers & young adults usually in hot & humid climates
Risk factors for Tinea vesicolor / Pityriasis vesicolor
warm & humid climates excessive sweating (hyperhidrosis) occlusive clothing malnutrition immunosuppression
Presentation of Tinea vesicolor / Pityriasis vesicolor
usually affects trunk/chest
round well demarcated macule that reveal fine subtle scale with gentle scrapping
patches of altered pigmentation (hypo or hyper pigmented)
NB lesions do not tan so are often more apparent after sunbathing e.g. on holiday
Management of Tinea vesicolor / Pityriasis vesicolor
1st line: ketoconazole shampoo
2nd line: other topical anitfungals e.g. clotrimazole or miconazole used as shampoos / creams
3rd line: oral itraconazole (if resistant to topical treatment)
NB hypo/hyper pigmented patches may take several months to disappear after treatment
Acne rosacea / Rosacea
chronic inflammatory skin condition with unclear aetiology characterised by recurrent episodes of facial flushing with persistent erythema, telangiectasia, papules & pustules
Epidemiology of Rosacea
primary seen in white population
more common in women
triggers associated with ↑ body temp
Triggers for rosacea
alcohol consumption hot weather consuming spicy food stress nicotine caffeine sun exposure steroids
Presentation of rosacea
often long history of intermittent flushing
persistent erythema on face with telangiectasia, usually on forehead, nose & cheeks ± papules / pustules
Rhinophyma: enlarged bulbous nose usually seen in men
NB if any comedones present = not rosacea
Rhinophyma
associated with acne rosacea
enlarged bulbous nose (looks like brain) almost exclusively seen in men
Management of acne rosacea
avoidance of triggers
daily application of high factor sunscreen
Mild to moderate:
1st line: topical metronidazole
2nd line: azelic acid gel
moderate to severe: oral Oxytetracycline (Abx)
Symptomatic:
laser therapy for telangiectasia
surgery for rhinophyma
Acne vulgaris
common skin condition that affects the pilosebaceous unit, will affect most individuals at some point in their lives
related to ↑ sebum production in response to ↑ androgen levels during puberty
more common in boys especially in teenagers years
Presentation of acne vulgaris
usually in areas with sebaceous glands (face, shoulders, upper chest, back)
non inflammatory comedonal acne: closed comedones (white heads) open comedones (black heads)
inflammatory lesions when follicles burst = erythema, papules, pustules, pain
ultimately scars develop ( ice pick or hypertrophic scars)
Nodulocystic acne
affects chest/face/back
usually seen in males
characterised by multiple inflamed & uniflammed nodules with scarring
topical treatment is usually not effective
Drug induced acne
usually monomorphic e.g. pustules characteristically seen in steroid use
Management of acne vulgaris
Topical preparations: e.g. topical retinoids, benozylperoxide, topical Abx
1st line: single therapy
2nd line: combination therapy
Systemic treatment:
Abx e.g. tetracyclines. oxytetracycline, doxycycline + topical agent e.g. topical retinoids, benozylperoxide
give single Abx for max 3 months
COCP in women
Specialist therapy:
isoretinoin (teratogenic so females but be on effective contraception & have negative pregnancy test)
Specific treatment for acne vulgaris in women
COCP
Pityriasis rosea
acute self limiting inflammatory condition usually affecting young adults (10-35yrs), more commonly women
Presentation of pityriasis rosea
prodrome of fever, mailasie, joint pain
herald patch:
2-5 cm diameter oval/round patch with central salmon coloured area, fine white scale on outside
secondary rash appears after herald patch, erythematous, oval scaly patches appear along Langers lines (Christmas tree / fir tree)
Management of pityriasis roscea
self limiting
disappears in 6-12 weeks
Seborrhoeic dermatitis / eczema
chronic inflammatory skin condition that affects areas with high sebaceous activity e.g. scalp / face / chest
peaks in infancy & puberty
Presentation of Seborrhoeic dermatitis
infants:
affects scalp (cradle cap), nappy area, face, limb flexures
erythematous plaques with patchy coarse yellow scale & greasy yellow crusts
adults:
erythematous greasy areas with fine scaling often on nasolabial folds, bridge of nose, behind ear
dandruff on scalp
may develop blepharitis or otitis externa
Management of Seborrhoeic dermatitis
infants:
baby shampoo & baby oil
if severe mild topical steroids e.g. hydrocortisone
adults:
scalp = 1st line: zinc pyrithione shampoo
2nd line: ketoconazole shampoo
face/body = topical antifungals e.g. ketoconazole & topical steroids
Seborrhoeic keratosis
common benign skin tumour mostly found on torso, due to being growth of immature keratinocytes usually seen in older people (90% of >60y/o have at least 1)
Seborrhoeic keratosis presentation
multiple darkly pigmented papules/plaques, have a stuck on appearance, greasy, wav like, sharply demarcated soft
may have keratitis plugs on surface
most commonly seen on trunk & face
Management of Seborrhoeic keratosis
reassurance usually no treatment required
may consider dermoscopsy & biopsy to rule out cancer
may remove for cosmetic purposes
Pyogenic granuloma
common benign vascular lesion of the skin & mucosa which are characterised by rapid growth & tendency to bleed easily
unknown aetiology
more common in women
presentation of pyogenic granuloma
most commonly found on head/neck, upper trunk & hands
solitary red/purple/yellow papule or nodules arising from normal skin, usually soft & round, very friable (bleeds easily), has polypoid appearance i.e. develops stalk
usually erupts & growth over a few weeks
NB very common in pregnancy (may be seen on oral mucosa)
Investigations for pyogenic granuloma
biopsy ( for histological confirmation)
dermoscopy
Management of pyogenic granuloma
pregnancy related lesions generally self resolve post partum
removal of lesions e.g. cryotherapy, curettage, excision
Dermatofibroma
fibroblast proliferation resulting in a small fibrous, benign growth, more frequent in women
presents as single nodule that develops on an extremity, freely moving, firm to hard nodule with smooth skin surface
clinical diagnosis (pinch test)
managed with reassurance or removal for cosmetic reasons
Solar lentigo (liver spots)
flat brown macules/patches found on back of hands or cheeks that are induced by sun exposure (UV light) usually seen in older fair skinned people
no treatment necesary
Moles / Nevi / melanocytes naevi
a benign collection of pigment producing cells (melanocytes) in there epidermis/dermis or both
may be present at birth or shortly thereafter or acquired throughout childhood
most important differential is melanoma
Common acquired melanocytes naevi
Types:
- Junctional melanocytes naevi (circular macules, flat, darkly pigmented)
- Compound naevi (domed pigmented nodules, usually smooth + uniform colour)
- Intradermal naevi (raised mole with same pigmented as surrounding skin)
all associated with fair skin
all have potential for malignant transformation
Congenital melanocytes naevi
mongolian spot
congenital, usually >1cm diameter, blue-grey hyper pigmented
disappear in childhood
Spitz naevus
develops over few months in children
pink/red, may grow rapidly
usually excised
dysplastic/atypical naevi
ugly duckling sing (naves not in keeping with other moles on same pt)
treated with excision
Strawberry naevus / infantile haemangioma
benign vascular skin tumour that usually develops rapidly in first months of life, usually occur on head/neck
often solitary erythematous, raised, painless multilobulated tumours
usually self resolve but if symptomatic e.g. periorbital causing visual problems or in oral cavity = propanolol
Cherry haemangioma / Campbell de Morgan spots
usually seen in middle aged adults, usually found on trunk
presents as bright red cherry red dome shaped papules/macules, often multiple lesions, non blanching
no treatment required
Keloid scars
skin lesion caused by high fibroblast proliferation & collagen production as excessive tissue response to minor injury, more common in dark skinned individuals
presents as brownish-red scar tissue of varying consistency with claw like appearance growing beyond boundaries of original lesion, most common on sternum
may require excision or intralesional steroids
Lipoma
common benign tumour of subcutaneous soft tissue
presents as slow growing, round, rubbery non tender nodule
no management needed unless painful / cosmetic removal wanted
Sebaceous gland hyperplasia
enlarged sebaceous glands surrounded by yellowish lobules
no treatment required
sebaceous adenoma
benign overgrow of sebaceous gland presenting as yellowish papule
Epidermoid cyst
cells lining cyst come from epidermal cells that line top of the hair follicle, seen on face/neck/upper back
presents as slow growing firm, mobile, painless mass
no treatment if asymptomatic
Pilar cyst
derived from cells at bottom of hair follicle, often seen in middle aged women on scalp
presents as slow growing firm, mobile, painless mass
Common location of keloid scars
Sternum > shoulder > neck > face > extensor surfaces of limb > trunk
Lichen planus
chronic pruritic inflammatory skin condition of unknown origin commonly seen in middle age
associated with Hep C*, Hep B, primary biliary cirrhosis
Presentation of lichen planus
usually cute onset on flexor surfaces of arms, palms, soles, genitalia, scalp
pruritic, planar, purple well demarcated papuples/plaques, polygonal shape with white line pattern on surface (wickham’s striae usually on oral mucosa)
Koebeners phenomenon = new lesions at site of trauma
NB if on scalp may cause scarring alopecia (lichen planapilaris)
7 Ps of Lichen planus
Planus = pruritic, polygonal, planar purple papules & plaque
Investigations for lichen planus
usually clinical diagnosis
skin biopsy (saw tooth pattern of epidermal hyperplasia, hyperkeratosis, hypergranulosis)
Management of lichen planus
1st line: potent topical steroids e.g. betnovate/dermovate
2nd line: systemic steroids
NB benzydamine mouthwash for oral lichen planus
drug induced lichen planus
may be caused by quinine, thiazides, ACE-Is
stop offending drugs
only distinguished histological
Lichen sclerosus
chronic inflammatory dermatosis primarily affecting the anogenital region in women & the glans penis / foreskin in men
more common in post menopausal women
Presentation of lichen sclerosus
white thickened patches (porcelain white papules & plaques), may progress to crinkled white patches
women may present with vaginal discharge
active lesions may have areas of ecchymosis, hyperkeratosis, bullae
pruritus is severe especially in women (may disrupt sleep)
Investigations for lichen sclerosus
usually clinical diagnosis
biopsy if uncertain/no response to treatment/suspected SCC
Management of lichen sclerosus
topical steroids & emollients e.g. clobetasol
NB need to follow up as ↑ risk of vulval cancer
Scabies
parasitic skin manifestation caused by the sarcoptes scabiei mite, spreads by prolonged skin-to-skin contact
highly contagious
Risk factors of scabies
overcrowding poverty poor nutritional status poor hygiene institutions e.g. care homes, prisons
Presentation of scabies
symptoms develop 3-4 weeks post infection
wide spread pruritus, worse at night (if multiple household members affected = indicative)
linear burrows (thread like whitish-grey lines on skin) on side of fingers, interdigital webs, flexor aspects of wrists
excortications, papules, vesicles
Investigations for scabies
largely clinical diagnosis
ectoparasitic presentation (from skin biopsy) = presence of mites/eggs/faecal material
Management of scabies
1st line: premetherin 5%
2nd line: malathion 0.5%
happy head to toe & repeat after 7 days
treat all household members & close contacts
tumble dry/wash/launder all clothing & bedding on day 1 of treatment
NB: symptoms develop 3-4 weeks post infection (contacts may be asymptomatic during this period so empirical treatment is vital)
crusted (norwegian) scabies
seen in immunosuppressed pts e.g. HIV, infection with thousands of mites
hyperkeratotic crusted lesions on hands/feet/nails/scalp/ears
treatment = ivermectin
Candidiasis
candida spp is a species of yeast like fungi, usually part of normal body flora but may become an invasive pathogen
candida albicans = most common species
severe disease is associated with immunosuppression
Oral candidiasis
oral thrush (curd like white patches in mouth) may be followed by marked erythema & soreness, especially on tongue
usually treated with topical/oral miconazole
candidial skin infections
soreness & itching, red moist skin area with ragged peeling edge ± pustules / papules at margin, yellow-white curd like scale
treated with topical imidazole cream e.g. miconazole / ketoconazole
Viral warts
hyperkeratosis & hyperplasia of epidermis usually caused by human papillomavirus (types 1,2,3,4,10,27,57)
very common, up to 30% of children & young adults affected, peak in teenage years
Presentation of viral warts
common wart (verruca vulgaris): papules/nodules with keratotic papillomatous surface, skin coloured/whitish, rough, usually on hands/fingers/knees/elbows
flat warts (verruca plana): slightly elevated flat topped warts often on face/back of hands/legs
plantar warts (verruca plana): on soles of feet, firm, flat flesh colours hyperkeratotic lesions
Management of viral warts
may resolve spontaneously without therapy
1st line: topical salicylic acid (treat daily for ≥12 weeks)
2nd line: cryotherapy
herpes simplex virus (HSV) infection
infection with the major strains of HSV (type 1 or type 2), which manifests as oral/genital/occular ulcers
very common, worldwide seroprevalence ~90%
Labial/oral herpes (cold sores)
cold sores - recurring erythematous vesicles that progress to painful ulceration
usually found on oral mucosa & lip border
may be preceded by burning/tingling/pain
Genital herpes
redness, swelling, tingling, pain pruritus
painful lymphadenopathy
single/disseminated painful red bumps / white vesicles that later ulcerate
Investigations for herpes
often clinical diagnosis (especially cold sores)
nucleic acid amplification tests (NAAT) = test of choice for genital herpes
consider serology if recurrent genital ulcers
Management of herpes
cold sores:
usually self limiting
symptomatic management with choline salicylate gel
genital ulcers:
GUM clinic referral, oral aciclovir (within 5 days of onset)
if recurrent (>6 attacks/year) = oral aciclovir as long term suppressive therapy
Herpes Zoster infection
shingles (herpes zoster) is a dermatomal rash with painful blistering caused by reactivation of varicella zoster virus (VZV)
NB initial VZV infection usually in childhood as chickenpox after which the virus remains in the dorsal root ganglia
Risk factors for herpes zoster
↑ age immunocompromise HIV malnutrition chronic corticosteroid use malignancy
Presentation of herpes zoster (shingles)
dermatomal distribution usually affecting 1-3 dermatomes unilaterally, i.e. does not cross midline
most commonly T1-L2
prodrome of burning, itching, paraesthesia in one dermatome lasting 2-3 days
rash = erythematous macular rash over affected dermatome that quickly becomes vesicular
NB any rash crossing midline = not shingles
Management of herpes zoster (shingles)
avoidance of immunosuppressed & pregnant people (infections until all lesions crusted over)
analgesia (paracetamol / ibuprofen)
oral antivirals e.g. aciclovir (within 72h of onset)
Complications of herpes zoster (shingles)
Zoster opticus
post hepatic neuralgia (usually resolved in 6 months, chronic neuropathic pain treated with amitriptyline or pregabalin/gabapentin
Ramsay-Hunt syndrome (Zoster oticus)
VZv reactivation in geniculate ganglion CN VII
presents with facial paralysis, loss of taste, pain, vestibulocochlear dysfunction (vertigo/tinnitus), rash, auricular pain, facial nerve palsy
treated with oral corticosteroids & aciclovir
Alopecia
hair loss form any hair bearing area but most often of the scalp
Types of alopeica
Scarring alopecia:
also know a cicatricial alopecia
hair loss accompanies by scarring & irreversible destruction of hair follicles
i.e. irreversible hair loss
Non-scarring alopecia:
also known as noncicatricial alopecia
loss of hair without the presence of scarring & the preservation of hair follicles
i.e. potential for hair regrowth
Androgenic alopecia
progressive non scarring alopecia affecting area of scalp with most androgen sensitive hair follicles resulting in characteristic pattern of balding, most common type of alopecia
↑ incidence with age
age of onset may be as early as puberty in males, and usually postmenopausal in women
↑ androgen insensitivity of hair follicles is genetically predisposed to
Male pattern baldness
bitemporal M pattern of hairless (receding hair line) & loss of crown hair
affectes 1/2 men >50y/o
negative hair pull test (i.e. not pulling out multiple hairs)
treatment = mostly nothing, minoxidil, finasteride or hair transplant
Female pattern baldness
more diffuse hairloss particularly at top of scalp (vertex), more diffuse shining of hair on entire scalp
usually in post menopausal women
treatment = reassurance, minoxidil, spironolacton or finasteride
Telogen effluvium
when physiological/hormonal stress triggers many hairs to move into telogen phase (sheding), as new hairs appear in anagen phase the telogen hairs are pushed out ~4-12 weeks post insult
may be caused by physiological stress, childbirth, crash dieting, anorexia, chronic illness etc
presents as ↓ hair density >50%, does not progress to baldness
hair pull test = >50% of the hairs in telogen phase
managed by reassurance & treating underlying condition
Anagen effluvium
hair production arrested in anagen phase e.g. secondary to chemo therapy, immunotherapy or radiotherapy casing rapid hair loss
hair grows back within months of stopping offending treatment
Alopecia areata
autoimmune disease that’s causes inflammation of hair follicles leading to non-scarring alopecia of scalp & body hair, usually seen ages 15-29
presents as well defined patches of non scarring alopecia, with small, broken, ‘exclamation mark”’ hairs around outside
usually abrupt onset with circular patterns of hair loss
NB may have nail involvement e.g. pitting/onycholysis)
management is generally reassurance (~90% of pts eventually have regrowth)
may consider topical corticosteroids if severe
Trichotillomania
hair pulling disorder, usually a behavioural disorder linked to OCD, often starting in adolescence
presents as asymmetrical hair loss with unusual shape, broke hairs across bald patch & minimal inflammation
psychotherapy & CBT = management
Scarring alopecia
discoid lupus erythematous:
itch, scale & hair loss, usually in women aged 30-50
lichen planopilaris (lichen planus affecting scalp): perifollicular redness & minimal scale, pruritus + hair loss often seen in postmenopausal women
acquired scarring alopecia:
e.g. from burns, chemical burns or viral disease
folliculitis decalvans:
inflammation of hair follicle characterised by redness, swelling & pustules around hair follicles, triggered by staph aureus
tinea capitis:
often seen in children, round pruritic scaly plaques with broken hair shaft & alopecia
Hirsutism
androgen dependant hair growth in women, i.e. excessive growth of thick hair to an androgen dependant pattern in women where hair growth is normally minimal
Causes of hirsutism
PCOS (most common) idiopathic (often familial) Cushings congenital adrenal hyperplasia androgen therapy obesity adrenal tumour drugs e.g. phenytoin, corticosteroids, danazol, valproate
Presentation of hirsutism
excessive terminal hair growth in masculine pattern i.e. moustache / beard /chest / areola / line alba / buttocks
signs if hyperandrogenism (acne, alopecia, truncal obesity, clitoromegaly, deepening of voice)
investigations for hirsutism
assessed using Ferriman-gallway scoring system (9 body areas assigned score of 0-4)
testosterone level* free androgen index FSH/LH 24h urine cortisol prolactin pregnancy test TFTs HbA1c lipid profile CT/MRI (if tumour suspected)
Actinic keratosis / solar keratosis
common premalignant skin lesion that develop as a consequence of chronic sun exposure and may develop into squamous cell carcinoma (SCC) of the skin
usually seen in fair skinned people, uncommon in <45y/o
Risk factors for solar / actinic keratosis
pale skin ↑ age male sex chronic sun exposure lifestyle / ↑ time spent outdoors being closer to equator
Presentation of solar / actinic keratosis
small papule/plaque with rough, sand paper like texture, which may grow & become erythematous & scaly
usually on sun exposed parts of body e.g. face, ears, scalp, forearms, back of hands
other features of solar damaged e.e.g telangiectasia, elastosis, pigmented lentigo
Investigations for solar / actinic keratosis
dermoscopy (strawberry pattern)
skin biopsy (if features with high risk of malignant change)
Management of solar / actinic keratosis
sun avoidance & use of sunscreen
fluorouracil cream (for single/small lesions)
topical diclofenac
cryotherapy, curettage & cautery
Squamous cell carcinoma (SCC) of the skin
cutaneous SCC is the proliferation of atypical, transformed keratinocytes in the skin with malignant behaviour
2nd most common skin cancer after BCC
Epidemiology of cutaneous SCC
2nd most common skin cancer after BCC
more common in caucasian
more common in men
↑ incidence with age
Risk factors for cutaneous SCC
chronic exposure to UV radiation fair skin blonde hair outdoor occupations use of tanning beds immunodeficiency actinic keratosis Bowen's disease (SCC in situ) HPV closeness to equator smoking (for SCC on lip)
Bowen’s disease
SCC in situ, usually seen as erythematous scaling plaques on sun exposed skin
pathological = full thickness atypic of dermal keratinocytes
Presentation of cutaneous SCC
presents as indurated nodular keratinise or crusted over tumour that eventually ulcerates
painless non healing ulcer, which may bleed
ulcer is indurated with hard raised edges
slow growth (but faster than BCC)
most common on face/neck/hands
Investigations for cutaneous SCC
skin biopsy (full thickness keratinocyte atypia) usually excisions skin biopsy done i.e. tumour removal
CT/MRI for metastasis (if advanced)
Mangement of cutaneous SCC
complete surgical excision + histopatholigcal examination e.g. via cryotherapy or surgical excision
radiotherapy if surgery not possible
Metastatic risk of cutaneous SCC
locally invasive cancer
generally low metastatic potential but ↑ risk if on earl/lip/scalp or if immunocompromised
Basal cell carcinoma (BCC)
slow growing, locally invasive malignant epidermal skin tumour, predominantly effects caucasians
most common type of skin cancer
Risk factors for Basal cell carcinoma (BCC)
↑ UV exposure ↑ age male sex fair skin previous BCC immunosuppression basal cell naevus albinism
Presentation of Basal cell carcinoma (BCC)
small very slow growing, painless non healing ulcer with central depression & rolled non tender borders (rodent ulcers), i.e. have central crater with pearly, rolled borders
usually in sun exposed areas e.g. head/neck (80% of cases)
Investigations for Basal cell carcinoma (BCC)
skin biopsy (palisading nuclei) CT/MRI (if metastases suspected)
Mangement of Basal cell carcinoma (BCC)
surgical excision with safety margin
cryotherapy, curretage
radiotherapy (if incomplete excision or large tumours)
Melanoma
highly malignant tumour arising from melanocytes, more common in females, with 1/3 pts having premalignant lesions e.g. atypical naevi
much less common than BCC & SCC
Risk factors for melanoma
Moles (strongest risk factor for cancer) UV exposure light skin immunosuppression genetics (BRAF gene or CDKN2A gene) Family history solar keratosis
Superficial spreading melanoma
most common type (70% of cases)
on arms/legs/chest/back
flat irregular tumour with variable pigmentation
nodular melanoma
2nd most common type of melanoma sun exposed areas in middle age reddish-brown/black, smooth nodule verrous surface / ulceration with bleeding most aggressive form of melanoma
lentigo maligna
melanoma in-situ
sun exposed area on older people
large & irregular shaped patch
irregular pigmentation
Acral lentiginous
rare
more common in dark skinned population
irregular shaped brown-black pigmentation + Hutchinson sign (subungal pigmentation)
may be below nail (subungal) which is more aggressive
Presentation of melanoma
generally a persistently pruritic bleeding skin lesion similar to a mole
exhibits ugly duckling sign (i.e. a mole that is no in keeping with the other moles the pt has)
change in size, colour, shape, irregular border, indistinct margins
subungal melanoma
tends to be more aggressive
usually hyperpigmentation below nail
may metastasis to lymph nodes, liver, lung, brain, bone
Investigations for melanoma
7 point checklist ABDCE assessment (asymmetry, border irregular, colour irregular diameter >7mm, evolving)
Assessment of pigmented skin lesions
7 point checklist (change in size, change in colour, change in shape, diameter >7mm, inflammation, oozing / bleeding, altered sensation)
ABDCE assessment (asymmetry, border irregular, colour irregular diameter >7mm, evolving)
7 point check list (Glasgow 7 point score) for melanoma
- Change in size
- change in colour
- change in shape
- diameter >7mm
- inflammation
- oozing / bleeding
- altered sensation
7 point check list (Glasgow 7 point score) for melanoma
- change in size
- change in colour
- change in shape
- diameter >7mm
- inflammation
- oozing / bleeding
- altered sensation
Investigations for melanoma
ABCDE assessment / Glasgow 7 point score
complete excisional skin biopsy (abnormal melanocytes proliferation)
staging (USS / CT)
Management of melanoma
excision with narrow margin followed by a wider margin local excision after Breslow index staging
lymph node resection
adjuvant radiotherapy
Breslow index
Breslow thickness: is the measurement of the depth of the melanoma from the surface of your skin down through to the deepest point of the tumour.
prognostic & staging index for melanoma
Granuloma annulare
associated with diabetes & hyperlipidaemia
papular lesions that are often centrally depressed & slightly hyper pigmented, which may coalesce to forms rings / arcs
usually on back of hands/ankles/knees/elbows
no treatment needed
Acanthosis nigricans
associated with diabetes / insulin resistance, obesity, acromegaly, PCOS, GI cancers
symmetric hypertrophic papillomatous velvety hyper pigmented plaques
found on neck/axillae/groin
Necrobiosis lipoidica
inflammatory granulomatous skin conditions associated with diabetes & glucose tolerance problems
very painful, rapidly progressing red papules that progress to deep red necrotic ulcers
on extensor surfaces of lower limbs
Splinter haemorrhage
associated with endocarditis
red/brown linear haemorrhage lying parallel to long axis of nail
Janeway lesions
associated with infective endocarditis
small non tender erythematous macules on palms & soles
microabscess & haemorrhage caused by septic emboli
Osler nodes
associated with endocarditis
painful nodules on pads of fingers & toes
due to immune complex deposition
Spider naevi / spider angiomas
associated with liver disease, pregnancy, COCP
central red papules with surrounding capillaries (blanches on pressing, refill from centre) usually found on upper body
NB telangiectasia fill from edge after blanching
Xanthelasma
associated with hyperlipidaemia
typically bilateral yellow, flat plaques found around eyes & upper eyelids or on palmar surfaces of hands
Staphylococcal scalded skin syndrome (SSSS)
potentially serious acute skin condition caused by the exfoliative toxins of staph aureus, toxins are serine proteases that break down the epidermal cell adhesion molecule desmoglein 1
typically seen in neonates & children <5yrs
Presentation of staphylococcal scalded skin syndrome (SSSS)
usually preceded by mucocutaneous staphylococcal infection e.g. pharyngitis
starts as fever, mails, irritability, skin tenderness
then extremely tender, flaccid bullae (large superficial blisters) which easily rupture with red skin underneath that have scalded appearance
widespread sloughing of epidermal skin
Nikolsky sign positive (gentle shearing force on intact skin causes upper epidermis separate)
NB: no mucous involvement unlike in TEN / SJS
Management of staphylococcal scalded skin syndrome (SSSS)
Abx (flucloxacillin 1st line)
hospitalisation & isolation of pt
analgesia (paracetamol)
supportive care (fluids, electrolytes, nutrition)
physio (as flexors often affected which may restrict movement)
Palmoplantar pustulosis (PPP)
crops of sterile pustules on hands & feet associated with thickened scaly skin that easily develops cracks & fissures
managed with plenty of thick emollients, salicylic acid ointment & urea cream
Melasma
common acquired skin condition presentation as bilateral brownish facial pigmentation, more common in women
managed is year long sun protection
Hyperhydrosis
excessive sweat production, can be generalised or focal e.g. palms of hands / axillae / soles
may present as bilateral, symmetrical abnormal amounts of sweating, sweating while sleeping, lasting > 6months
management is topical aluminium chloride (1st line), botulinum toxin, surgery
Steroid induced skin atrophy
thinning of skin due to prolonged steroid exposure usually in its with psoriasis taking steroids for >1year
also presents as easy bruising, telangiectasia, purpurs & striae
treated by stopping steroids
Macule
flat, distinct, coloured area of skin <1cm in diameter
does no include changes in skin texture/thickness
cannot be felt when running finger over it
e.g. freckles, moles, malignant melanoma
Patch
a macule > 1cm in diameter i.e. flat, distinct, coloured area of skin >1cm in diameter, no change in skin texture / thickness
e.g. cafe au lait spots in neurofibromatosis
Papule
a solid raised lesion that has distinct borders, <1cm in diameter
may have a variety of shapes & profiles (domed, flat topped) & may be associated with secondary features such as scales and crusts
e.g. acne vulgaris
Nodule
a raised solid lesion >1cm in diameter
e.g. warts, sebaceous cysts, lipomas
Plaque
a solid, raised, flat topped lesion >1cm in diameter
e.g. psoriasis
Vesicle
raised lesion <1cm in diameter filled with clear fluid
e.g. chickenpox
Bullae
circumscribed fluid filled lesions >1cm in diameter
e.g. epidermolysis bullosa
Wheal
area of oedema of the upper epidermis
e.g. during allergic reaction
Pustule
cricumscribed elevated lesions that contain pus, most commonly infected e.g. in folliculitis but may also be sterile e.g. pustular psoriasis
e.g. acne vulgaris, pustular psoriasis
Burrows
linear lesions produced by infestation of skin & formation of tunnels
e.g. scabies, cutaneous larva migrant
Lichenification
thickening of epidermis seen with exaggerated skin lines usually due to chronic rubbing & itching
Excortications
traumatised / abraded skin caused by acute scratching / itching
Scars
permanent fibrous changes of skin following damage to the dermis
Purpura
blood that has leaked from dermal blood vessels so cannot be blanched by pressure
e.g. Henoch-Schonlein purpura, Meningococcal septicaemia
Petechiae
pin points sports of purport / vasculitis / thrombocytopenia / leukaemia
Pyoderma gangrenosum
typically on the lower limbs, initially small red papule, later deep, red, necrotic ulcers with a violaceous border
may be accompanied systemic symptoms e.g. fever
associated with IBD, SLE,
oral steroids as first-line treatment
Herpes zoster opthalmicus
reactivation of the varicella-zoster virus in the area supplied by the ophthalmic division of the trigeminal nerve (V1). It accounts for around 10% of case of shingles
Presents as vesicular rash around eye, may have Hutchinson’s sign (rash on tip/side of nose indicates nasociliary involvement) may involved eye
oral antiviral treatment for 7-10 days (ideally started within 72h of rash onset)
Vitiligo
autoimmune condition which results in the loss of melanocytes and consequent patchy depigmentation of the skin.
usually presents before age 30
Vitiligo associated disease
type 1 diabetes mellitus Addison's disease autoimmune thyroid disorders pernicious anaemia alopecia areata
Vitiligo presentation
well-demarcated patches of depigmented skin, more common on peripheries
usually no other symptoms i.e. no pain/pruritus
Koebener phenomenon (i.e. new lesions at site if injury)
Vitiligo management
sunblock for affected areas of skin
camouflage make-up
topical corticosteroids
topical tacrolimus and phototherapy,
