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Acne vulgaris
Papule
https://t.me/med1917
Common inflammatory skin disorder commonly affecting ages 14–19y
Pathophysiology
• Abnormal keratinisation of follicle = pore blockage
• Sebum production = due to androgens at puberty
• Overgrowth of Cutibacterium acnes = Gram +ve commensal
▶ releases pro-inflammatory mediators
▶ follicles rupture & contents leak into surrounding dermis
Lesions of acne
1. Non-inflammatory
• Closed comedones (whiteheads) – small papules that may burst
• Open comedones (blackheads) – flat or raised with impacted keratin
2. Inflammatory
• Papules – burst comedones cause inflammation
• Pustules – papules containing pus
• Nodules – painful swellings lasting weeks–months
Chapter 7: Dermatology 227
Risk factors for acne
• Male
• Cosmetic/hair products
• Excess washing
• OCP/steroids
• Endocrine disorders – PCOS
Sequelae of acne
1. Non-scarring
• Hyper-/hypopigmentation
• Erythematous macules
2. Scarring
• ‘ICE-PICK’ scars (atrophic) – collagen loss
• ‘KELOID’ scars (hypertrophic) – collagen formed
Management
→ depends on severity, psychological impact, response to previous Tx
1. TOPICAL TX = 1st-line for mild/moderate acne
• Retinoids = affect keratin production
• Antibacterials e.g. benzyl peroxide
• Antibiotics e.g. erythromycin/clindamycin
2. SYSTEMIC ABX = 2nd-line OR 1st-line for severe acne
• Lymecycline/doxycycline (teratogenic / yellow teeth in kids)
3. ORAL ISOTRETINOIN (ROACCUTANE) = retinoid (s sebum made)
Indicated in:
• Nodulocystic acne
• Tx-resistant subtypes
• Visible scarring or risk of bad scarring
• Significant psychological distress
4. HORMONAL TX = Tx-resistant females / cyclical flares / hirsutism
• Combined oral contraceptive pill
5. SCAR TREATMENT
• Microdermabrasion (removes dead skin) – superficial scars
• Laser resurfacing – atrophic scars
• Punch biopsy/excision – ice-pick scars
• Intralesional steroids – keloid scars
2
NICE (2021) Acne vulgaris [NG198]
2
CIs:
pregnancy/lactation, PHx or FHx VTE
Pustule
Nodule
Fig. 7.2
All Tx may cause irritation/erythema &
photosensitivity
Side-effects of Roaccutane (key parameters
to monitor in parentheses)
• Teratogenic – 2× contraception + monthly
pregnancy test
• Hepatitis – avoid alcohol (LFTs)
• Photosensitivity & dry skin – protection
• Muscle aches
• Mood changes
• Anaemia & thrombocytopenia (FBC)
• Triglycerides & cholesterol (fasting lipids)
important monitoring requirements
Contraindications to Roaccutane
• Pregnancy
• Severe liver/renal disease
• Severe depression
• Peanut allergy
228 Chapter 7: Dermatology
https://t.me/med1917
Eczema
Causes/risk factors:
• Genetics
▶ mutated filaggrin gene
▶ PHx/FHx atopies
• Environmental
▶ irritants (chemicals, soap, nylon)
▶ allergens (pets, dust, food)
▶ illness/infection/stress
▶ cold weather
Lotion → cream → gel → ointment
(become more oily from left to right = better
moisture trapping BUT greasier)
Itchy skin condition characterised by erythema, dry skin, scaling
± vesicles & blisters (acute)
↳
± fissures & lichenification (chronic)
Atopic eczema
Prevalence: 20–30% schoolkids & 5–10% adults
Onset: usually <2y
Features: red, dry, scaly skin → affects flexures
Complications: susceptible to infection
S. aureus / Strep:
• Weeping pustules / crusting
• Fever/malaise
↳
HSV (eczema herpeticum)
• Pain, fever, lethargy
• Clustered blisters & punched-out erosions
*EASI/DLQI scores: assess severity & impact
Management of eczema3
→ assess impact on life / psychological impact*
MILD ATOPIC ECZEMA
1. Emollients (e.g. Cetraben cream) – for dry skin: liberally as often as needed
2. Mild potency topical steroids – for active areas: ‘finger-tip’ portion 1/2 × daily
MODERATE ATOPIC ECZEMA
1. Emollients
2. Moderate potency topical steroids – for active areas
3. Topical calcineurin inhibitors e.g. tacrolimus, pimecrolimus (warn about
stinging/burning sensation in first 2w of use)
MODERATE ATOPIC ECZEMA
1. Emollients
2. Potent topical steroids – for active areas
3. Topical calcineurin inhibitors
4. Phototherapy + emollients & topical steroids
5. Immunosuppressants: ciclosporin,
methotrexate, azathioprine
GENERAL: avoid irritants/allergens/triggers
ADDITIONAL TREATMENTS
• Systemic ABX – if infection (flucloxacillin/
erythromycin or aciclovir)
• Antihistamines
• Dupilumab (monoclonal antibody)
Fig. 7.3 Atopic eczema.
3
NICE (2007, updated 2021) Atopic eczema in under 12s [CG57]
Skin infestations
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Scabies
→ Sarcoptes scabies mite
FEATURES
• ITCHY papules (worse at night)
• Burrows / small tracts
• Usually symmetrical
Common sites:
• Finger webs
• Breasts
• Ankles
• Axillae
• Scalp
• Feet
Chapter 7: Dermatology 229
Public health must be informed if it occurs
in an institution such as a nursing home
Risk factors for scabies
1. Close contact – dorms, wards, care homes
2. Elderly, young, immunocompromised
→
‘crusted scabies’
elderly/immunocompromised
= severe form in
Fig. 7.4
Confirm Dx with microscopy
MANAGEMENT
1. Permethrin/malathion creams
• Apply to whole body for 8–24h
• Repeat in 1w
• TREAT ALL CLOSE CONTACTS AT SAME TIME
→ For crusted scabies: ivermectin 200mcg/kg single dose
2. Wash all bedding/clothing
Head lice
→ live on hair, feed on blood, spread via close contact
FEATURES
• Persistent itching of scalp
• Redness & excoriated papules
MANAGEMENT
1. Fine comb wet hair & conditioner REGULARLY = most important
2. Physical insecticide gels/sprays/lotions OR chemical insecticide (e.g. malathion
0.5% aqueous liquid) – apply from roots to tips of hair, leave on for 12h and
then wash out using shampoo
4
4
NICE (2016) Scenario: Head lice management
230 Chapter 7: Dermatology
https://t.me/med1917
Bacterial skin infections
Classification of skin infection
Normal skin commensals
• Staph. epidermidis
• Corynebacteria
Key to colours used in table
Primary infections
Secondary infections
Infections due to bacterial toxins
Hypersensitivity reactions (Group A Strep)
• Micrococci
• Propionibacteria
Staphylococcus Streptococcus
Folliculitis Erysipelas
Cellulitis Necrotising fasciitis
Bullous impetigo Scarlet fever
Staphylococcal scalded skin syndrome Erythema nodosum
Toxic shock syndrome Vasculitis
Impetigo, erysipelas
Wound/ulcer/eczema infection
Both
Cellulitis
Staphylococcal infections can be 1° or 2° via toxins
Mx of Staph infections: take swab
→ Topical ABX: fusidic acid, mupirocin
→ Oral ABX: flucloxacillin, clindamycin
Impetigo = contagious – no school for 48h
after starting ABX or until wounds crusted
Staphylococcal infections
→ Over 10 types of commensal staph on skin
→ Staph. aureus = PATHOGENIC when associated with disease flares
IMPETIGO
Sx: golden crust ± oozing blisters (affects young children)
Mx:
• Soak crust with soap + water
• Topical antiseptic/ABX
• Systemic ABX if widespread
BULLOUS IMPETIGO (specific strain of Staph. aureus)
Sx: 2–3cm blisters
Mx: oral flucloxacillin
FOLLICULITIS
Sx: erythematous pustules around hair follicles
Mx:
• Screen & treat nasal carriage (mupirocin cream)
• Topical or systemic ABX
Fig. 7.5
Fig. 7.6
STAPHYLOCOCCAL SCALDED SKIN SYNDROME
Sx: erythema & sheets of peeling skin, malaise & fever
(affects children <5y, especially neonates)
Mx: ADMIT (emergency)
• Supportive (fluids & analgesia)
• IV flucloxacillin/erythromycin
TOXIC SHOCK SYNDROME
Sx: septic shock
Days 1–3: widespread macular erythema
Days 10–21: desquamation, mucosal oedema & ulceration
Mx:
• Supportive (fluids & analgesia)
• IV flucloxacillin/erythromycin
Associations:
• Tampons
• GIT infection
Fig. 7.7
Fig. 7.8
Streptococcal infections
https://t.me/med1917
→ Usually more acute onset & more severe than staph infections
→ Strep. pyogenes (group A strep) = always PATHOGENIC
Chapter 7: Dermatology 231
Streptococcal infections can be 1° or 2° via
toxins or hypersensitivity
ERYSIPELAS
(Infection involving the dermis only – not
extending to the subcutaneous tissue)
• unilateral ‘beefy’ red plaque = painful
Mx: penicillin V
NECROTISING FASCIITIS 1° or 2° infection
Sx:
• Rapidly spreading erythema & necrosis
• Systemic sepsis: high fever, intense pain, vomiting
Cause: group A strep ± S. aureus ± others
Mx:
1. Surgical debridement
2. IV ABX (vancomycin ± gentamycin)
CELLULITIS
Sx: gross oedema, erythema, heat PLUS pain
Mx:
• Elevate
• IV flucloxacillin
• Bloods if systemically unwell
SCARLET FEVER: toxin-mediated following
STREP THROAT
Sx:
• Widespread pink/red papules
• Preceding sore throat, fever,
lymphadenopathy
• Strawberry tongue
Mx: systemic penicillin
ERYTHEMA NODOSUM
= panniculitis
Sx: red, tender nodules
+ fever, malaise, arthralgia
Mx of Strep infections: take swab
→ Topical ABX: clindamycin
→ Oral ABX: penicillin V
Fig. 7.9
Fig. 7.10
Fig. 7.11
Fig. 7.12
VASCULITIS
Sx:
• Widespread purpura
• Arthralgia, arthritis, haematuria
• ± other organs
Fig. 7.13
Fig. 7.14
232 Chapter 7: Dermatology
https://t.me/med1917
Viral skin infections
Viral warts (HPV)
Consider testing for HIV if widespread
facial or perianal warts
→ 5min soak in warm water, apply Tx, nail file
→ VERY COMMON (spread via direct or indirect contact e.g. changing room floor)
MANAGEMENT: most warts disappear without treatment
1. Topical paints – salicylic acid + lactic acid
2. Cryotherapy – painful & may cause blisters
3. Curettage & cautery – need local anaesthetic
4. Formalin soaks / podophyllin – for resistant warts
FILIFORM WARTS
→ common on eyelids, face, neck, body folds
Recommended Tx:
• Most disappear without treatment
• Keratolytic agents containing 10–26%
salicylic acid
• Curettage
↳ (warn patient about recurrence due to
latent virus in the skin)
Fig. 7.15 Filiform warts.
consider PO valaciclovir as it has better
bioavailability than PO aciclovir
COMMON WARTS (HPV 2)
→ elevated papules
→ dorsum of hands
→ common in children
PLANE WARTS (HPV 3)
→ flat-topped
→ face & back of hands
VZV infections
CHICKENPOX → 10–14d
Sx:
• Widespread rash
• Vesicles & crusted papules
• Fever, headache, malaise
Mx5:
Children: symptomatic treatment
with paracetamol, calamine lotion and
chlorphenamine if ≥1y
Adults: consider PO aciclovir in
immunocompromised adult or adolescent
if presenting within 24h of rash
(800mg 5 times a day × 7d)
PLANTAR WARTS (HPV 1, 2, 4, 57)
→ may be uncomfortable to put pressure on
→ tend to be quite Tx-resistant
ANOGENITAL WARTS (HPV 6 & 11)
→ risk factor for cervical neoplasia in women
→ refer patient for STI screen
Fig. 7.16
Complications of shingles
• Persisting pain
• Ramsay Hunt
• Eye disease
• Deaf/dizzy
• Encephalitis
SHINGLES → reactivated HSV in
neural tissue
Sx:
• Dermatomal distribution of vesicles
• Preceding pain/tingling
Mx with 7d PO aciclovir if:
• >72h pain/tingling
• Involves the eyes/perineum
• Immunocompromised
• Moderate/severe pain or rash
5
NICE (2018) Scenario: Chickenpox management
6
NICE (2021) Scenario: Shingles management
6
Fig. 7.17
HSV infections
https://t.me/med1917
HERPES SIMPLEX VIRUS (HSV)
• Cold sores (HSV 1) 30–50% recur
▶ Sx: pain, tingling, vesicular eruption
▶ Mx: topical aciclovir/valaciclovir
• Genital herpes (HSV 2) 95% recur
▶ Sx: pain, tingling, burning on urinating
▶ Mx: oral aciclovir/valaciclovir
Other infections
MOLLUSCUM CONTAGIOSUM –
Molluscipoxvirus (MCV)
Sx:
• Small, umbilicated papules (mainly trunk)
• Erythema, pus, crusting
→ common in infants/children & is contagious
Mx: self-limiting
(if not use cryotherapy or topical 1% hydrogen
peroxide or 5% potassium hydroxide solution)
Chapter 7: Dermatology 233
Fig. 7.18
Fig. 7.19
COXSACKIE VIRUS – hand, foot & mouth
disease
Sx: erythematous vesicles on hands, soles of
feet, mouth
→
common in infants / young children
Mx: self-limiting (5–7d)
PITYRIASIS ROSEA (thought to be caused
by HHV6/7 virus)
Sx initially:
Herald patch (oval erythematous plaque +
scaling)
Sx 5–15d later:
Generalised, smaller, well-defined
erythematous macules
→ ‘Christmas tree’ distribution
Mx: the rash usually clears in 8w
→ if symptomatic/itchy, topical steroid can be
used
Fig. 7.20
Fig. 7.21
234 Chapter 7: Dermatology
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Fungal skin infections
Candidiasis
Levels of infection
Superficial: stratum corneum, hair, nails
Deep: subcutaneous tissue, dermis
Systemic: blood-borne
Risk factors for candida
→ Young/old
→ Immunocompromised e.g. steroids, ABX, DM
→ causes THRUSH (genitalia, periungual, oral)
Features:
• Erythema extending from body folds
→ unclear border
• Small satellite lesions ± pustules at
edges of eruption
Treatment
1. Topical azoles – clotrimazole
2. Systemic azoles – fluconazole
3. Nystatin / amphotericin B
Malassezia/pityrosporum
→ skin commensals
Fig. 7.22 Genital candida.
PITYRIASIS VERSICOLOR
Features: on trunk
→ finely scaled, yellow/brown macules
→ hypo-/hyperpigmented
→ asymptomatic or slightly itchy
Treatment
1. Topical treatment
→ Ketoconazole shampoo – lather on affected areas for 10min before washing
off – daily × 5d
2. Systemic treatment: widespread/resistant cases
→ Oral itraconazole – 200mg daily × 7d
Warn patients that it will take several months for skin colour to return to its original state
• Scaly in active phase
• Macular post-inflammatory
hypopigmentation may persist for months,
until melanocytes are stimulated by sun
exposure
Fig. 7.23 Pityriasis versicolor.
SEBORRHOEIC DERMATITIS
Features: scalp, eyebrows, paranasal/periorbital
→ yellow/white flaking
→ ± erythematous, itchy, greasy skin
→ ± patchy hair loss
Treatment
→ Ketoconazole 2% shampoo – use 2–4 times a week then once every 2w as
maintenance therapy
→ Low potency steroids e.g. Daktarin for a week
→ If more extensive and recalcitrant disease, use systemic itraconazole – 200mg
OD × 7d
Consider HIV in patients with more severe symptoms
Dermatophytes
https://t.me/med1917
→ cause TINEA/RINGWORM (most common fungal infections)
Causes: Microsporum, Trichophyton, Epidermophyton
Investigations: skin scrapings, hair pluckings, nail clippings → microscopy &
culture or under Wood’s UV light
Treatment:
Examples Indications
Topical antifungals Miconazole, ketoconazole,
terbinafine, nystatin
Systemic antifungals Terbinafine, itraconazole,
griseofulvin for those aged <12y
TYPES OF DERMATOPHYTE INFECTION
TINEA CORPORIS = BODY
• Erythematous annular scaly plaque
• Central clearing
• Very itchy
Localised infection
Widespread or hair/scalp/nails or
immunocompromised
Chapter 7: Dermatology 235
TINEA CRURIS = GENITALS
• Well-demarcated, erythematous
plaque
• Very itchy
TINEA UNGUIUM (ONYCHOMYCOSIS)
= NAILS
• Very common → often with athlete’s
foot
Hyperkeratosis:
• White discolouration
• Loss of nail plate & lifting from bed
(onycholysis)
TINEA CAPITIS = HEAD/SCALP
• Patchy hair loss
• Scales, erythema, pustules
More common in Afro-Caribbeans &
children
Fig. 7.24 Tinea corporis.
TINEA MANUUM = HAND
• Scaling that spreads proximally
• Asymmetrical involvement
TINEA PEDIS = FEET
Athlete’s foot: white maceration between toes
RFs: common floors, occlusive shoes, wet feet
Moccasin foot: more severe form
(erythema, scaling, pustules, widespread)
KERION = complication of tinea capitis
Boggy, painful swelling (honey-coloured)
+ alopecia/lymphadenopathy
(due to epidermal invasion & inflammatory response)
236 Chapter 7: Dermatology
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Melanocytic (pigmented) lesions
Benign lesions
1. FRECKLES – overproduction of melanin due to UV
exposure
2. CONGENITAL MELANOCYTIC NAEVI (MOLES) –
proliferations of melanocytes
Causes: genetics, UV exposure, hormones
( with age to peak at 30y)
3. ACQUIRED MELANOCYTIC NAEVI (MOLES) –
proliferations of melanocytes
4. ATYPICAL MELANOCYTIC NAEVI (MOLES)
Features: similar to melanoma
• ≥5mm
• Irregular border
• Variable pigmentation
• Asymmetrical
• Flat or raised
Management
1. Monitor for changes
2. Sun protection advice
3. Excision if suspicious
Risk factors: FHx, UV, <30y
Malignant lesions
Fig. 7.25 Atypical naevus.
Differentials of melanoma
• Pigmented BCC
• Seborrhoeic wart
• Atypical naevus
Stage of melanoma is determined by histopathologic
features such as Breslow thickness
POSITIVE SLNB
Discussion in SSMDT:
Total LN dissection + chemo-/radiotherapy
NEGATIVE SLNB
Discussion in SSMDT:
Monitoring as per SSMDT discussion
MELANOMA
FEATURES:
Asymmetrical
Border = IRREGULAR
Colour/pigmentation = VARIED
Diameter >6mm
Evolution (ABCD changes or
bleeding/itching)
INVESTIGATIONS: 2ww referral to dermatology
1. History & skin examination
2. Excision – if suspected melanoma (2mm margins)
3. Histopathology – Breslow thickness = depth of invasion → best prognostic
factor
MANAGEMENT
Breslow thickness <1mm
= WIDE LOCAL EXCISION (1cm margins)
Breslow thickness 1–4mm
= WIDE LOCAL EXCISION (1–3cm margins) ± SLNB
Breslow thickness >4mm
= WIDE LOCAL EXCISION (3cm margins) ± SLNB
Patients are usually followed up for 2–5y depending on the MDT
decision / Breslow thickness
7
: MDT (plastics, radiology, histopathology, oncology)
Risk factors
Genetic Environmental
• PHx or FHx melanoma
• Pale skin / red hair
• Many/large atypical naevi
• Increasing age
• Sun/UV exposure
• Phototherapy
• Tanning bed
• Immunosuppressed
Fig. 7.26 Malignant melanoma.
7
British Association of Dermatologists Guidelines (2010) Revised UK guidelines for the management
of cutaneous melanoma
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