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