Dermatology Flashcards
What is toxic epidermal necrolysis and Stevens-Johnson syndrome?
Blistering damage that occurs secondary to inflammation of the epidermis
Epidermal layer dies if severe, sheds, leaving exposed oozing dermis
What is the difference between toxic epidermal necrolysis and Stevens-Johnson syndrome?
Area of epidermal loss
TEN - >30%
SJS <10%
What are the features of Stevens Johnson syndrome?
Abrupt onset rash
Starting on trunk, extending rapidly
Mucocutaneous necrosis with at least 2 sites involved
Prodromal illness, flu like symptoms
What is erythema multiforme?
Target lesions
Initially seen on back of hands/feet before spreading to torso
Often of unknown cause Acute self-limiting Associated with HSV Infections or drugs Mucosal involvement absent or limited to one
What is the management of TEN/SJS and EM?
Early recognition, call for help Early referral, ITU or burns unit Supportive measures, maintain haemodynamics Fluid replacement, pain relief Stop drugs IV immunoglobulins, ciclosporins
What are some of the complications of TEN/SJS?
Sepsis
Electrolyte imbalance
Multi-system organ failure
What is erythroderma?
‘red skin’
Clinical state of inflammation of all the skin,
not a pathological diagnosis
What are the clinical features of erythroderma?
Skin is red, hot and scaly
May have generalised lymphadenopathy
Loss of control of temp
Bouts of shivering
Hypothermia from heat loss
High-output cardiac failure
Hypoalbuminaemia
Fluid loss
Capillary leak syndrome - cytokines released during inflammation cause vascular leakage - can lead to acute respiratory distress
What are the causes of erythroderma?
Dermatitis (eczema) including contact-allergic
Lymphoma
Drugs - sulphonamides, gold, sulphonylureas, penicillin, allopurinol
Psoriasis
Idiopathic
What is the management of erythroderma?
Treat underlying cause where known, stop drugs Methotrexate for psoriasis Keep patient warm Swab skin for infection Monitor vitals and serum albumin
Use emollients and wet wraps to maintain moisture
Mild topical steroids
What is the presentation of acute meningococcaemia?
Features of meningitis - headache, fever, neck stiffness
Septicaemia - hypotension, fever, neck stiffness
Non-blanching purpuric rash on trunk and extremities, may be preceded by blanching maculopapular rash
Can rapidly progress to ecchymoses, haemorrhagic bullae, tissue necrosis
What is the cause of acute meningococcaemia?
Gram negative diplococcus Neisseria meningitides
What is the sepsis 6?
Administer high flow oxygen Take blood cultures Give broad spec antibiotix e.g. benzylpenicillin Give IV fluid challaneges Measure serum Hb and lactate Measure accurate hourly urine output
What other management in meningococcaemia in important?
Prophylactic antibiotics e.g. rifampicin for close contacts, ideally within 14 days of exposure
What are the complications of acute meningococcaemia?
Septicaemic shock
Disseminated intravascular coagulation
Multi-organ failure
Death
What is necrotising fasciitis?
Rapidly spreading infection of the deep fascia secondary to tissue necrosis
Type 1 - aerobic and anaerobic bacteria seen post op (often in diabetes)
Type 2 - Group A streptococcus and can arise spontaneously in healthy individuals
What are risk factors for necrotising fasciitis?
Abdominal surgery, medical co-morbidities e.g. diabetes, malignancy
What is the presentation of necrotising fasciitis?
Often presents as rapidly worsening cellulitis with pain out of keeping with clinical features
Erythematous, blistering, necrotic skin
Systemically unwell, fever, tachycardia
Presence of crepitus - subcutaneous emphysema
X-Ray showing visible gas indicating gas-forming organism in soft tissue (absence does not exclude diagnosis)
What is the management of nec fasc?
Urgent referral, surgical debridement
IV antibiotics
Why are IV antibiotics alone ineffective in nec fasc?
The blood supply is compromised and vessels cannot deliver antibiotics to the necrotic tissues in sufficient concentration
What is eczema herpeticum?
Widespread eruption - monomorphic punched out erosions usually 1-3mm diameter
Serious complication of atopic eczema or other skin conditions e.g. pemphigus foliaceus
What is the presentation of eczema herpeticum?
Widespread eruption
Punched out erosions
History of preceding malaise and fever in patient known to have atopic dermatitis
Systemically unwell
What is the management of eczema herpeticum?
General supportive measures
IV antiviral therapy e.g. aciclovir
Antibiotics for bacterial secondary infection
Stop any non-essential therapies inc topical steroids
Ophthalmological review if any ocular involvement
What is angioedema?
Type 1 hypersensitivity reaction
Swelling of the dermis, subcut tissues and mucosae
Triggers can be allergic or non-allergic, but both cause release of inflammatory mediators
What can be causes of allergic reactions?
idiopathic Food - nuts, seeds, shellfish Drugs - penicillin, contrast media, NSAIDs, morphine Insect bites Contact e.g. latex Viral/parasitic infections Autoimmune Hereditary
What is the pathophysiology of urticaria?
Due to local increase in permeability of capillaries and small venules
Large number of inflammatory mediators
Leads to swelling involving the superficial dermis raising the epidermis
Leads to itchy wheals
What are the features of angioedema?
Deeper swelling involving dermis and subcut tissues
Swelling of tongue and lips
What are the features of anaphylaxis?
Bronchospasm
Facial and laryngeal oedema
Hypotensions
Can initially present with urticaria and angioedema
What is the management of urticaria?
Antihistamines e.g. chloramphenamine
What is the management of angioedema?
Corticosteroids
What is the management of anaphylaxis?
Oxygen
0.5 mg IM 1:1000 adrenaline
IV antihistamines, corticosteroids and IV infusion
What is erythema nodosum?
Hypersensitivity reaction to a variety of stimuli
What are the causes of erythema nodosum?
Group A beta haemolytic streptococcus Primary TB Pregnancy Malignancy Sarcoidosis Inflammatory bowel disease Chlamydia Leprosy
What is the presentation of erythema nodosum?
Nodular, discrete tender nodules, may become confluent
Lesions continue to appear for 1-2 weeks
Leave bruise like discolouration as they resolve, within 6 weeks usually
Lesions do not ulcerate, resolve without atrophy or scarring
Shins most common site
What is a comedone?
A plug in a sebaceous follicle containing altered sebum, bacteria, and cellular debris.
Can present as open (blackheads) or closed (whiteheads)
What are common pressure areas for distribution (pattern of spread of lesions)?
Sacrum, buttocks, ankles, heels
What is Koebner phenomenon?
A linear eruption arising at a site of trauma e.g. in psoriasis
What is a discrete lesion?
Individual lesions separated from each other
What are confluent lesions?
Lesions merging together
What is the appearance of target lesions?
Concentric rings, like a dartboard
e.g. seen in erythema multiforme
What is an annular lesion?
Like a circle or ring
Seen in e.g. tinea corporis - ringworm
What is a discoid lesion?
Coin shaped/round lesion
Seen in for example - discoid eczema
What is purpura?
What is it due to?
Red or purple colour
Due to bleeding into the skin or mucous membranes
Does not blanch on pressure
There are petechiae - small pinpoint macules and ecchymoses - larger bruise like patches
What is a macule?
Flat area of altered colour e.g. freckles
What is a patch?
Larger flat area of altered colour or texture
for example, vascular formation - port wine stain
What is a papule?
Solid raised lesion <0.5cm in diameter
e.g. xanthomata - deposition of yellowish cholesterol rich material
What is a nodule?
Solid raised lesion >0.5cm in diameter, with a deeper component
What is a plaque?
Palpable scaling raised lesion >0.5cm in diameter
For example, psoriasis
What is a vesicle?
Small blister
Raised clear fluid filled lesion
<0.5cm in diameter
What is a bulla?
Large blister
Raised clear fluid filled lesion
>0.5cm in diameter
for example seen in a reaction to insect bites
What is a pustule?
Pus containing lesion
<0.5cm in diameter
For example in acne
What is an abscess?
Localised accumulation of pus in the dermis or subcutaneous tissue
What is a wheal?
Transient raised lesion due to dermal oedema
For example, urticaria
What is a carbuncle?
Staphylococcal infection of adjacent hair follicles
What is excoriation?
Loss of epidermis following trauma
What is lichenification?
Well defined roughening of the skin with accentuation of skin markings
For example seen in chronic rubbing in eczema
What are scales?
Flakes of stratum corneum
Seen in psoriasis - silvery scales
What is crust?
Rough surface consisting of dried serum, blood, bacteria and cellular debris
Exuded through an eroded epidermis e.g. burst blister
For example seen in impetigo
What is a scar?
New fibrous tissue
Occurs post wound healing
May be atrophic (thinning), hypertrophic (hyperproliferation within wound boundary)
or keloid scar - hyperproliferation beyond wound boundary
What is a fissure?
Epidermal crack often due to excess dryness
What are striae?
Linear areas which progress from purple to pink to white
Histopathological appearance of a scar
Associated with excessive steroid use and glucocorticoid production, growth spurts, pregnancy
What is hypertrichosis?
Non-androgen dependent pattern of excessive hair growth e.g. pigmented naevi
For example seen in hypertrichosis
When is koilonychia seen?
Spoon shaped depression of the nail plate
Iron deficiency anaemia, congenital, idiopathic
When is onycholysis seen?
Separation of the distal end of the nail plate from nail bed
Trauma, psoriasis, fungal nail infection, hyperthyroidism
When is nail pitting seen?
Punctate depressions of the nail plate
Psoriasis, eczema, alopecia areata
What are the major cell types in the epidermis?
Keratinocytes - produce keratin as a protective barrier
Langherhans - present antigens, activate T lymphocytes for immune protection
Melanocytes - produce melanin, gives pigment to skin and protects cell nuclei from UV damage
Merkel cells - contain specialised nerve endings for sensation
What are the layers of the epidermis?
Deepest - stratum basale
Stratum spinosum
Stratum granulosum - cells lose their nuclei and contains granules of keratohyaline
Stratum corneum - layer of keratin, most superficial layer
What are the components of the dermis?
Collagen, elastin, glycosaminoglycans
Synthesised by fibroblasts
Immune cells, nerves, skin appendages, lymphatic and blood vessels.
What are the main types of hair?
Lanugo - fine long hair in fetus
Vellus hair - fine short hair on all body surfaces
Terminal hair - coarse long hair on scalp, eyebrows, eyelashes, pubic areas
What stimulates sebaceous glands?
The conversion of androgens to dihydrotestosterone
Become active at puberty
What are the stages of wound healing?
Haemostasis - vasoconstriction, platelet aggregation, clot formation
Inflammation - vasodilation, migration of neutrophils and macrophages, phagocytosis
Proliferation - granulation tissue formation, angiogenesis, re-epithelialisation
Remodelling - collagen fibre re-organisation, scar maturation
What is the difference between cellulitis and erysipelas?
Cellulitis - deep subcutaneous tissue, spreading bacterial infection
Erysipelas - acute superficial form of cellulitis, involves the dermis and upper subcutaneous tissue
What are the causes of cellulitis?
Strep pyogenes and Staph aureus
What are risk factors for cellulitis/erysipelas?
Immunosuppression Wounds Leg ulcers Toeweb intertrigo Minor skin injury
What is the presentation of cellulitis?
Most common in the lower limbs
Local signs of inflammation - swelling, erythema, warmth, pain
May be associated with lymphangitis
Systemically unwell; fever, malaise, rigors; particularly with erysipelas
How can erysipelas be distinguished from cellulitis in clinical presentation?
Well defined red raised border
What is the management of cellulitis?
Antibiotics e.g. flucloxacillin, co-amoxiclav in severe cellulitis
Supportive care - rest, leg elevation, sterile dressings, analgesia
What are the complications of cellulitis?
Local necrosis
Abscess
Septicaemia
What is staphylococcal scalded skin syndrome?
Commonly seen in infancy and early childhood
Production of circulating epidermolytic toxins from phage group II, benzylpenicillin resistant staph
What is the presentation of scalded skin syndrome?
Develops within few hours to few days May be worse over the face, neck, axillae, groins Scald like skin appearance followed by large flaccid bulla Perioral crusting is typical Intraepidermal blistering Painful lesions Eruption can be more localised Recovery within 5-7 days
What is the management of scalded skin syndrome?
Antibiotics - systemic penicillinase resistant penicillin, fusidic acid, erythromycin or appropriate cephalosporin.
Analgesia
What is a superficial fungal infection?
Common and mild infection
Superficial layers of the skin, nails and hair
Can be severe in immunocompromised individuals
What is the cause of superficial fungal infections?
Dermatophytes - tinea/ringworm
yeasts e.g. candidas, malassezia
Moulds e.g. aspergillus
What is the presentation of the different types of ringworm?
Usually unilateral and itchy
Tinea corporis - trunk and limbs, itchy, circular or annular, clearly defined, raised edge
Tinea cruris - groin and natal cleft, very itchy, same presentation of lesions
Tinea pedis - athlete’s foot, moist scaling and fissuring in toewebs, spreading to sole
Tinea manuum - infection of hand, scaling and dryness in palmar creases
Tinea capitis - scalp, patches of broken hair, scaling and inflammation
If untreated, raised pustular spongy mass known as kerion can form.
Tinea unguuim - infection of nail, yellow discolouration, thickened, crumbly nails
Tinea incognito - inappropriate treatment of tinea infection with topical or systemic steroids, leads to ill-defined and less scaly lesions
What is the appearance of candidiasis?
Candidal skin infection
White plaques on mucosal areas
Erythema with satellite lesions in flexures
What is the presentation of tinea versicolour/pityriasis?
Infection with Malassezia furfur
Scaly pale brown patches in upper trunk that fail to tan on sun exposure, usually asymptomatic
What is the management of superficial fungal infections?
Establish correct diagnosis with skin scrapings, hair or nail clippings, skin swabs if yeast
General measures - treat precipitating factors e.g. underlying immunosuppression, moist
Topical antifungals e.g. terbinafine
Oral antifungals e.g. itraconazole for severe widespread infections
Avoid use of topical steroids as can lead to tinea incognito
What is folliculitis?
Infection of the superficial part of a hair follicle with Staph aureus produces small pustule on erythematous base
What are common warts?
Raised cauliflower like lesions
Occur most frequently on hands, scattered or grouped
Cryotherapy to treat
Mainly due to HPV 2
What is molluscum contagiosum?
Due to poxvirus
Pearly pink papules
Central umbilication with keratin plug
Resolve spontaneously
What can cause a wart?
Infection - direct/indirect contact
Damaged epithelial barrier
What are the clinical findings of plantar warts?
Beneath pressure points
Either sharply defined rounded lesions or mosaic
Warts do not maintain skin markings
Can have rough keratotic surface
What is the appearance of anogenital warts?
Usually multiple
May have discomfort, bleed
Smooth, verrucous, lobules
Skin coloured or erythematous or hyperpigmented
Not all are sexually transmitted
However in children - possibility of sexual abuse
What is the management of warts?
Feet, hands, trunk - salicylic acid, cryosurgery
What lesions are seen in herpes simplex?
Type 1 HSV cold sore
Type 2 HSV genital herpes
Following primary infection, settles in sensory ganglia and then produces recurrent lesions by different stimuli
What are risk factors for candida infection?
Topical and systemic steroid therapy
Immunosuppression of any aetiology e.g. lymphoma, AIDS
Broad spectrum antibiotics
Diabetes mellitus
What is angular chellitis?
Inflammation at corners of mouth
Due to infection with candida or staph and prominent creases of the mouth
Saliva drawn into corners
Ill-fitting dentures
Modification of dentures may help
Treatment with imidazole/hydrocortisone
What is pityriasis versicolor?
Yeasts - malassezia
Normal skin commensals present in pilosebaceous follicles
On fair skin - pink/light brown macules
Pigmented skin - patchy hypopigmentation
What is the diagnosis and treatment of pityriasis versicolor?
Microscopic examination
Spores and hyphae
Selenium sulphide - shampoo on skin just before bathing
Topical imidazole antifungal creams
What is the aetiology of scabies?
Sarcoptes scabiei
From prolonged contact
Female scabies mite burrows in epidermis, lays eggs in the burrow
Itching begins 4-6 weeks after
What are the clinical features of scabies?
Itching, worse at night
Burrows - hands and feet, sides of fingers and toes
Often mild erythema around
Rash - inflammatory papules, occur mainly around axillae and umbilicus, and thighs
How can scabies be diagnosed?
Microscopy - mites, eggs etc
Skin scrapings
What is the treatment of scabies?
Topical agents from neck to toe
Malathion 0.5%, permethrin
Wash off after 8-12 hours
Topical antipruritic e.g. crotamiton 10% with hydrocortisone
What is crusted norwegian scabies?
Uncommon, lots of mites present in crusted lesions on the skin
What are the clinical findings of syphilis?
Primary stage:
Mainly glans penis, vulva or cervix
Solitary small firm red painless papule, becomes an indurated ulcer
Heals after 4-8 weeks with or without treatment
Secondary
Untreated infection manifests on skin and mucous membranes
Rash - not itchy, lesions distributed symmetrically, coppery red
Rounded oval macules
Systemic upset
Latent
No clinical signs of active infection
Tertiary
Affects approx 25% of untreated patients, slowly progressive
Solitary granulomatous plaque or nodule
CNS involvement
What can the herpes simplex virus cause?
Herpetic gingivostomatitis - HSV1 infection, 5-7 days and fully resolves within 2 weeks
Herpes labialis - cold sore
triggers e.g. UV, trauma, stress
Grouped vesicles on lips and perioral skin, crusts over
Herpes genitals
HSV-1 or 2
External genitalia, dysuria
Treat with prophylactic aciclovir
What causes chickenpox?
Varicella zoster
Highly contagious
Spread through contact with lesions or infected droplets - cough/sneeze
Become symptomatic 10 days - 3 weeks afterwards
No longer contagious when all lesions crusted over
What is the presentation of chickenpox?
Widespread erythematous
Raised, vesicular
Blistering lesions
Usually starts on trunk or face, spreads outwards
Affects whole body after 2-5 days
Lesions scab over
Fever first symptom
Itch
General fatigue and malaise
What are the complications of chickenpox?
Bacterial superinfection Dehydration Conjunctival lesions Pneumonia Encephalitis - ataxia
Can then lie dormant in dorsal root ganglion, reactivate later in life as shingles or ramsay hunt
What is the management?
Pregnant women not immune need varicella zoster immunoglobulins following exposure
Aciclovir for immunocompromised
Calamine lotion and chlorphenamine for itching
What is the morphology of herpes zoster virus?
Shingles rash
Closely grouped red papules
Become vesicular, then pustular, continuous band
Along dermatome
Lymph nodes draining the affected area are enlarged and tender
New vesicles continue to appear for several days
What is Ramsay Hunt syndrome?
Peripheral facial nerve palsy
Accompanied by an erythematous vesicular rash on the ear - HZ oticus or mouth
Infection involving the facial nerve, sensory nerve zoster causes pain and vesicles in affected distribution
Nerve palsy due to pressure on facial nerve motor fibres
What is herpes zoster ophthalmicus?
Hutchinson’s sign - tip of the nose, skin at inner corner of the eye, root and side of the nose
Without antiviral treatment can develop eye disorders, e.g. conjunctivitis, keratitis, uveitis, optic neuritis
What is the management of herpes zoster?
Oral antiviral therapy e.g. aciclovir, 800mg 5x a day for seven days
For postherpetic neuralgia - TCAs e.g. amitriptyline
What can be triggers of atopic eczema?
Soap and detergents
Overheating, rough clothes
Stress
Skin infection
Animal dander, house mites
Food
Aeroallergens - pollens
What differentials would you consider for itchy eruptions?
Eczema Scabies Urticaria Lichen Planus Tinea - pedis, capitis, corporis Candida Chicken pox
How would an eczematous lesion appear?
Dry, erythematous patches
Acute is erythematous, vesicular and exudative
Ill defined erythema
Dry skin, fine scale
Excoriations
Lichenification
How would you investigate eczema?
Patch testing
Serum IgE
Skin swab
What are the steps to management of atopic eczema?
Flare up - moderate to potent topical steroid e.g. Betnovate or Elocon
Sedating antihistamine e.g. chlorpheniramine if sleep disturbance
Long term management -
Emollient therapy; creams and gels moisturisers, soap substitutes e.g. Dermol
Topical steroids
Use lowest potency, moisturisers dry for 20 mins first e.g. hydrocortisone, Betnovate, Dermovate (strong)
Bandages, Clinifast, wet wraps
Consider topical calcineurin inhibitors e.g. tacrolimus
Can use light therapy or oral corticosteroids
Manage secondary infections with appropriate antibiotics
What is the step wise progression of topical corticosteroids for eczema?
Hydrocortisone
Eumovate - Clobetsone Butyrate 0.05%
Betnovate - Betamethasone Valerate 0.1%
Dermovate - Clobetasol Propionate 0.05%
What features may be associated with scabies?
Secondary eczema
Impetigo
What is lichen planus?
Fairly common non infectious rash in adults
Lichen - small bumps on the skin, planus - flat
As flat topped papules
What are the clinical findings in lichen planus?
Most common on flexural aspects of wrists, ankles, lumbar region
Shiny flat topped papules
White lines - Whickham’s striae transverse skin
Linear grouped lesions in scratch marks - Koebner’s
Papules flatten over few months, replaced by hyperpigmentation
Where can lichen planus be found?
Wrists, ankles, back
Mucosal lesions - mouth and vulva
White lacework pattern
Can arise due to contact allergic dermatitis to mercury in fillings
How would you investigate lichen planus?
Skin biopsy
How would you manage lichen planus?
Corticosteroids - topical, oral if extensive
Antihistamines
Benzydamine mouth wash if oral
Which drugs can cause lichenoid eruptions?
Thiazides
Gold
Quinine
What are the timescales for SSSS?
Develop within few hours to few days
Recover within 5-7 days
What nail changes can be seen in eczema?
Nail pitting and ridging
How is mild eczema treated?
Reduce exposure to the trigger
Regular use of emollients - generous use!
Intermittent corticosteroids - 1% hydrocortisone
How long should 1% hydrocortisone be used for in mild eczema?
48 hours after the flare up has calmed down
How is moderate eczema treated?
as above
Moderately potent topical steroid - 0.025% betamethasone
Non-sedating anti-histamine to help with itch
Topical calcineurin inhibitors for prevention- tacrolimus
How is severe eczema treated?
Potent corticosteroid - 0.1% betamethasone or 0.05% clobetasone
Flexural areas and face - 0.025% betamethasone
Antihistamine
How are infected wounds in eczema treated?
Swab all infected area
Empirical Antibiotics - flucloxacillin or clarithromycin if pen allergic
Pick antibiotic based on sensitivity from swab
What is herpetic whitlow?
Painful blisters on fingers or thumb
What is psoriasis?
A chronic inflammatory skin disease due to hyperproliferation (abnormal T cell proliferation) of keratinocytes and inflammatory cell infiltration
What are common triggers in psoriasis?
Stress Alcohol - heaving drinking Smoking - palmoplantar pustulosis and chronic plaque Trauma Strep infections Drugs - lithium, certain anti-malarials e.g. hydroxychloroquine Pregnancy Sunlight
Severe psoriasis identified as HIV indicator condition
What are some of the types of psoriasis?
Chronic plaque - most common Seborrheic - naso-labial and retro-auricular Flexural (body folds) Pustular Erythrodermic
What is the morphology of psoriasis?
Large plaque or small plaque psoriasis
Ruby red
Well defined
With silvery surface scale
Lesions can sometimes be itchy, burning or painful
50% have associated nail changes e.g. pitting, onchyolysis
What is Auspitz sign?
When adherent psoriatic scales are scraped or picked off - causes bleeding
What is the management of psoriasis?
General measures - avoid triggers
Emollients to reduce scale
Topical therapies, spray foam version Enstilar - Vitamin D and corticosteroid (betamethasone)
Continue Vit D analogues, coal tar, retinoids, keratolytics
Phototherapy for extensive disease
Oral therapies if severe - methotrexate, ciclosporins
CVD and arthritis risk
What complications are associated with psoriasis?
Erythroderma
Psychological/social changes
What are the four major features of acne vulgaris?
Androgen induced seborrhoea, excess grease
Comedone formation - due to abnormal proliferation, controlled by androgens
Colonisation of pilosebaceous duct with cutibacterium acnes
Production of inflammation
Androgens lead to seborrhoea and comedone formation, leads to changes in ductal micro environment results in P acnes colonisation and inflammation
What factors can modify acne?
Hormonal factors e.g. PCOS, endocrine disorders UV light can benefit Stress Diet Cosmetics
Topical and oral corticosteroids Anabolic steroids Lithium Ciclosporin Iodides taken orally
What are the clinical findings of acne vulgaris?
Greasy skin - seborrhoea Non inflamed lesions e.g. comedones Inflamed lesions Scarring - loss of tissue, increased fibrous tissue Pigmentation
How is acne managed?
General measures
Topical therapies for mild acne
Oral therapies for moderate to severe acne
Oral retinoids
What general measures are suggested for acne?
Don’t over clean
Choose make up cleaners appropriately
Avoid squeezing spots - scar
Maintain healthy diet
What treatment is recommended dependent on the severity of acne?
Mainly comedonal - a topical retinoid e.g. adapelene, with benzoyl peroxide or isotretinoin
Mild to moderate papular/pustular - fixed combination treatment, ideally containing. benzoyl peroxide
adapalene + BPO, clindamycin, tretinoin
If not responding to treatment or more widely distributed - antibiotic e.g. lymecycline or doxycycline
Ideally 3 months treatment, patients need to remain on topical treatment
Initially single topical therapy then combo
Must prescribe with oral antibiotics, and COCP
What topical therapies can be given for acne?
Benzoyl peroxide
Topical clindamycin (antibiotic based on guideline)
Topical retinoids
What oral therapies can be given for acne?
Oral abx - doxycycline
Anti-androgen - female
What do you have to be aware of with prescribing oral retinoids?
Oral retinoids such as Isotretinoid are teratogenic - girls must be on contraception and have regular LFT and lipid checks
What complications are associated with acne vulgaris?
Post inflammatory hyperpigmentation
Scarring
Deformity
Psychological and social effects
What is a pilar cyst?
Common benign cyst
Usually found on the scalp
Contains keratin and its breakdown products
Is lined by walls resembling the external root sheath of hair
What are the clinical findings of a pilar cyst?
Most arise on the scalp
Smooth mobile firm round nodule
No punctum - unlike an epidermoid cyst
What is the management of a pilar cyst?
Be aware of possibility of dermoid cyst - can present from birth to early childhood
Surgical treatment if problematic, complete excision
What is an epidermoid cyst?
Very common cyst, contains keratin and its breakdown products, surrounded by an epidermoid wall
What is the cause of epidermoid cyst?
Inflammation around a pilosebaceous follicle
Can therefore follow on from more severe lesions of acne vulgaris
Can result from deep implantation of the epidermis by a blunt penetrating injury
What are the clinical findings of an epidermoid cyst?
Common on the face, neck, shoulders and chest
In dermis, raises epidermis to create firm elastic dome shaped protuberance
Mobile over deeper structures
Cysts found near skin are yellow-white
Lesions enlarge slowly
Infected cysts enlarge, become red and tender and discharge pus
What is the management of epidermal cysts?
Can be dissected
Any recent infection must settle for at least 6 weeks
What is seborrheic keratosis?
Benign overgrowth of epidermal keratinocytes
What are the clinical findings of seborrheic keratosis?
Frequently asymptomatic, occasionally itch
Part/all of lesion can come away with minimal trauma
Trunk and face commonly affected
Lesions vary from brown to black, traumatised lesions are inflammed
Thickened acanthotic lesion - irregular verrucous surface, greasy appearance, stuck on lesion, 1-3cm in diameter
Leser-Trelat sign - abrupt appearance of multiple seborrhoeic keratoses that rapidly increase in their size and number
What dermoscopic features are seen in seborrheic keratosis?
Acanthotic SK - thickened epidermis, scattered milia like cysts
Multiple fissures and ridges and cerbiform pattern
Grouped skin coloured globules with a central blood vessel
What is the management of SK?
Do not usually need treatment, or can be treated by. liquid nitrogen
What is a dermatofibroma?
Benign skin lesion
Believed to represent a traumatic reaction e.g. to an insect bite
What are the clinical findings of dermatofibromas?
Commonly on limbs
Multiple lesions common
Most approx 5mm in size and slightly elevated
Tends to be red-brown
Pinching results in central dimpling
Central scar like white area
Very fine brown rounded peripheral pigment network
What is a lipoma?
Common benign tumour of adipose tissue
Usually found in the subcutaneous tissue, and less commonly in internal organs
Usually solitary lesions or multiple, usually of no significance
What are the clinical findings of a lipoma?
Subcutaneous nodule
Often lobulated
Soft doughy consistency
Overlying skin surface normal
Freely mobile over the lipoma
What are the differentials for a lipoma?
Angiolipomas - lots of capillary proliferation
Lipomatosis - diffuse infiltration of structures with non-encapsulated adipose tissue
Dercum’s disease - deposits of tender adipose, ecchymoses and obesity
Cutaneous sarcomas
What is the management of lipomas?
Most do not require treatment
Surgical excision can be for symptomatic lesions
What are angiomas?
Cherry angioma or Campbell de Morgan spots - small numerous lesions
Soft red/purple nodules/papules
What are infantile haemangiomas?
inc strawberry naevi
Rapidly growing, benign proliferations of endothelial cells
Tumours can be localised, segmental, superficial or deep
Usually most lesions do not need treatment
Urgent referral if likely to grow into important structure, interfere with feeding, on scalp leading to intracranial complications
What is a pyogenic granuloma?
Common benign and rapidly growing vascular lesion, possibly resulting from trauma
What are the clinical findings of a pyogenic granuloma?
Can arise on any part of the body, most common sites
Lesion is sudden in onset, grows rapidly and bleeds after minimal trauma
Starts as small red spot, quickly enlarges into a nodule
What is the management of pyogenic granuloma?
Apply vaseline to surrounding skin to prevent irritation, keep dry
Main differential is hypomelanotic melanoma - so may need excision if suspicious
What is impetigo?
Superficial bacterial skin infection
Usually caused by staph aureus, or less commonly streptococcus pyogenes
Can be bullous or non bullous
Passed on from an infected individual, or arise with no clear source of infection, enters skin at site of minor skin injury or secondarily to another skin condition e.g. chickenpox
What are the clinical findings in non bullous impetigo?
Multiple lesions arise
Most commonly on exposed sites such as the face
Particularly around nose and mouth, limbs, in flexures
Initial lesion - thin walled vesicle, ruptures easily
Exudate dries, forms golden yellow or yellow-brown crusts; thicker if strep infection
Lesions extend gradually without healing, resolves without scarring in 2-3 wks
Lesions can become more widespread if underlying skin condition
What is the presentation of bullous impetigo?
Small or large bullae arise over short period of time
Usually spread locally on face, trunk, buttocks, extremities
Bullae rupture less easily than non-bullous form
Initially contain clear fluid, then become cloudy
Buccal mucous membrane can be informed
What are the investigations for impetigo?
Swabs of the vesicles can confirm diagnosis, bacteria and antibiotic sensitivities
What is the management of impetigo?
Cover affected areas, wash hands regularly
Avoid school until lesions are healed and crusted over, or 48 hrs after abx started
Consider hydrogen peroxide 1% cream for people with localised non-bullous and not systemically unwell
OR topical fusidic acid for 7-10 days, or mupirocin if resistant
For more widespread infection - use systemic antibiotic for 7 days either flucloxacillin or erythromycin/clarithromycin
What are some examples of paraneoplastic conditions?
Paraneoplastic dermatoses - group of skin conditions that have strong associations with internal malignancies
Malignant acanthosis nigricans - adenocarcinoma of stomach, GI tract, lung
Acanthosis palmaris/tripe palms
Paraneoplastic pemphigus
Carcinoid syndrome
What is paraneoplastic pemphigus?
Rare group of immunobullous conditions affecting skin or mucous membranes
Painful blisters, denuded areas of the mouth, lips, oesophagus, skin
What are the clinical features of paraneoplastic pemphigus?
Associated malignancy
Painful oral erosions
Generalised cutaneous eruption
Oral erosions severe, crusting on lips
Respiratory and GI tract complications
What are the investigations for paraneoplastic pemphigus?
Skin antibodies
Skin biopsy - intact blister excised, peri-lesional skin for direct immunofluorescence
Histology - acantholytic cells, blisters, dead keratinocytes
DIF - IgG antibodies
What is the management of paraneoplastic pemphigus?
Supportive
Identify and treat underlying malignancy
What is bullous pemphigoid?
Blistering skin disorder
Autoantibodies against antigens between epidermis and dermis, causes sub-epidermal split in the skin
What is the presentation of bullous pemphigoid?
Tense fluid filled blisters
On an erythematous base
Lesions often itchy
May be preceded by non specific itchy rash
Usually affects trunk and limbs, mucosal involvement less common
What is the management of bullous pemphigoid?
General measures. - wound dressings where required, monitor for signs of infection
Topical therapies for localised disease - topical steroids
Oral therapies for widespread disease - oral steroids, oral tetracyclines, nicotinamide, immunosuppressive agents
What is pemphigus vulgaris?
Blistering skin disorder
Usually affects the middle aged
Autoantibodies against antigens within the epidermis causing an intra-epidermal split in the skin
What is the presentation of pemphigus vulgaris?
General measures, wound dressings, monitor for signs of infection
Good oral care if oral mucosa is involved
Oral therapies, high dose oral steroids, immunosuppressive agents e.g. methotrexate, azathioprine, cyclophosphamide
What is generalised pustular psoriasis?
Rare
Presents with flares of widespread sterile pustules on a background of red and tender skin
What are possible triggers for flares of pustular psoriasis?
Sudden withdrawal of injected or oral corticosteroids
Drugs e.g. lithium, aspirin, indomethacin, iodide and some beta blockers
Infection
Pregnancy
What is the presentation of pustular psoriasis?
Skin is dry, fiery red, tender
Within hours, 2-3mm pustules
Pustules then coalesce
Systemic symptoms, fever, chills, headache, rapid pulse rate, loss of appetite and nausea
What is the management of generalised pustular psoriasis?
Hospitalisation usually required, prevent further fluid loss, stabilise temp
Antibiotics Aciretin Systemic corticosteroids Ciclosporin Methotrexate
What is vitiligo?
Acquired depigmenting disorder, complete loss of pigment cells/melanocytes
Thought to be autoimmune
Can present at any age
What is the presentation of vitiligo?
Single or multiple patches of depigmentation, often symmetrical
Common sites are exposed areas e.g. face, hands, feet, body folds, genitalia
Favours sites of injury - Koebner phenomenon
What is the management of vitiligo?
Minimise skin injury as cut, graze, sunburn etc can trigger new patch
Topical treatments e.g. topical steroids and calcineurin inhibitors e.g. tacrolimus and pimecrolimus
Phototherapy - UVB
Oral immunosuppressants e.g. methotrexate, ciclosporin, mycophenolate mofetil
What is melasma?
Acquired chronic skin disorder, increased pigmentation in the skin
What is the cause of melasma?
Thought to be due to genetic predisposition
Triggered by factors such as sun exposure, hormonal changes e.g. pregnancy and contraceptive pills
Pigmentation is caused by overproduction of melanin by melanocytes
What is the presentation of melasma?
Brown macules - freckle like spots, or larger patches with an irregular border
Symmetrical distribution
Common sites - forehead, cutaneous upper lips and cheeks
What is the management of melasma?
Lifelong sun protection Discontinue hormonal contraceptive pills Cosmetic camoflauge Topical treatments - inhibit formation of new melanin, e.g. hydroquinone, azelaic acid, kojic acid, Vit C Laser treatments with caution
What is alopecia areata?
Chronic inflammatory disease affects hair follicle
Causes patchy non-scarring hair loss on the scalp
What is the presentation of alopecia areata?
Most probably an autoimmune disorder
Characteristic initial lesion - circumscribed totally bald smooth patch, normal skin
Short broken hairs, exclamation mark hairs - seen around the margins
Initial patch may regrow, or further patches appear, can go on to lose all hair
Nail pitting
What is the treatment of alopecia areata?
Patient more likely to have full regrowth, but most likely have more than one episode
Topical steroids e.g. dermovate, evidence limited
Intralesional steroids for patchy hair loss e.g. triamcinolone
Contact immunotherapy
Wigs, integrated hair systems, hats, false eyelashes
What are the types of lupus?
Discoid lupus erythematous
Subacute cutaneous lupus erythematous
Systemic lupus erythematous
What is the aetiology of lupus?
Autoimmune of unknown cause
Some cases can be drug-induced
Frequently provoked by UV exposure, tends to be more severe in smokers
What are the features of SLE?
Common cutaneous features - Photosensitivity Butterfly rash Raynaud's phenomenon Urticaria Mouth ulceration Non-scarring alopecia Chillblain lupus
Non erosive arthritis Episcleritis Renal involvement Cardiac - HTN, pericarditis Pulmonary e.g. pleurisy NS - migraine, epilepsy
What are the investigations for lupus?
Autoantibodies ANA
Anaemia, leucopenia, thrombocytopenia
RF, ESR, (normal CRP)
Lupus anticoagulant
What is the management of lupus?
SLE - systemic steroids, antimalarials in photosensitivity, immunosuppressive drugs
DLE and SCLE - first line potent topical steroid e.g. betnovate or dermovate
Hydrochloroquine, chloroquine
What are some examples of vasculitis?
Small vessel - Henoch Schonlein purpura, septic, urticarial
Larger vessel - Polyarteritis nodosa, Wegeners (granulomatosis with polyangiitis) Churg-Strauss (allergic granulomatous angiitis) Giant cell arteritis
What are the causes of vasculitis?
Idiopathic infection - viral Hep B and C, bacterial - strep infections Medications - penicillins, quinolones, NSAIDs, thiazides, anticonvulsants Connective tissue disorders Abnormal proteins Inflammatory bowel disease Haematological, malignancy Physical factors - exercise
What are the cutaneous clinical features of vasculitis?
Capillaritis - red brown discolouration of skin
Palpable purpura
Ulceration and necrosis
Nodules - subcutaneous, tender, discoloured, ulcerated
Livedo reticularis - livedoid discolouration of the skin in a reticular pattern
Urticaria
Subungal haemorrhages
What is seen in the history of a venous ulcer?
Often painful
Worse on standing
History of venous disease e.g. varicose veins, DVT
What is seen in the history of an arterial ulcer?
Painful, especially at night
Worse when legs elevated
History of atherosclerosis
What is seen in the history of a neuropathic ulcer?
Often painless
Abnormal sensation
History of diabetes or neurological disease
What are common sites for venous ulcers?
Malleolar areas, more common over medial than lateral malleolus
What are common sites for arterial ulcers?
Pressure and trauma sites e.g. pretibial, supramalleolar, distal points e.g. toes
What are common sites for neuropathic ulcers?
Pressure sites
Soles, heels, toes, metatarsal heads
What are the clinical features in arterial ulcers?
Small, sharply defined deep ulcer, necrotic base
Cold skin
Weak or absent peripheral pulses
Shiny pale skin
Loss of hair
What are the clinical features of venous ulcers?
Large, shallow irregular ulcer
Exudative and granulating base
Warm skin
Normal peripheral pulses
Leg oedema, haemosiderin, melanin deposition
Lipodermatosclerosis
Atrophie blanche - white scarring with dilated capillaries
What are the clinical features of a neuropathic ulcer?
Variable in size and depth
Granulating base
May be surrounded by or underneath hyperkeratotic lesion e.g. callus
Warm skin
Normal peripheral pulses - unless a neuroischaemic ulcer
Peripheral neuropathy
What are some investigations for the different types of ulcers?
Venous - normal ankle brachial pressure index of 0.8-1
In arterial ulcers - ABPI <0.8 suggesting arterial insufficiency - Doppler studies and angiography
Neuropathic ulcers - ABPI <0.8 - neuroischaemic
X-Ray excludes osteomyelitis
What is the management of venous ulcers?
Compression bandaging after excluding arterial insufficiency
What is the management of arterial ulcers?
Vascular reconstruction
Compression bandaging
What is the management of neuropathic ulcers?
Wound debridement
Regular repositioning, appropriate footwear, good nutrition
What are some differentials for an itchy eruption?
Eczema
Scabies
Urticaria
Lichen planus
What are some differentials for a changing pigmented lesion?
Melanocytic naevi - develop during infancy, asymptomatic
Seborrhoeic wart
Malignant melanoma - features of ABCDE, >6mm
Treatment based on breslow thickness
What are the differentials for a purpuric eruption?
Meningococcal septicaemia
Disseminated intravascular coagulation
Vasculitis
Actinic purpura - arises in elderly population with sun damaged skin, on extensor surfaces
What are the differentials for a red swollen leg?
Cellulitis - painful spreading rash, systemically unwell, do skin swabs, antibiotics
Venous thrombosis - pain, swelling, redness, risk factor, usually systemically well, do D dimer and doppler USS, give anticoagulants
Chronic venous insufficiency - heaviness or aching of leg, worse on standing, relieved by walking, discoloured oedematous leg, haemosiderin deposition, doppler USS, leg elevation, compression stockings, sclerotherapy
What are local side effects from topical corticosteroids?
Skin atrophy Telangiectasia Striae May mask, cause or exacerbate skin infections Acne, allergic contact dermatitis
What are some systemic side effects from oral corticosteroids?
Cushing's syndrome Immunosuppression Hypertension Diabetes Osteoporosis Cataracts Steroid induced psychosis
What are some of the side effects of oral aciclovir?
GI upset, raised liver enzymes
Reversible neurological reactions
Haematological disorders
What are the side effects of oral antihistamines?
Sedation
Anticholinergic effects - dry mouth, blurred vision, urinary retention, constipation
What are some of the systemic side effects of topical/oral antibiotics?
Local skin irritation, allergy
GI upset, rashes, anaphylaxis, vaginal candidiasis, antibiotic associated infections e.g. C diff
What are the side effects of oral retinoids?
Mucocutaneous reactions e.g. dry skin, dry lips, dry eyes, disordered liver function, hypercholesterolaemia, hypertriglyceridaemia, myalgia, arthralgia, depression
Teratogenicity - effective contraception one month before, during and one month after isotretinoin
Two years after Acitretin
What are the local and systemic side effects of biological therapies?
Local - redness, swelling, bruising at site of injection
Allergic reactions, antibody formation, flu-like symptoms, infections, hepatitis, demyelinating disease, heart failure, blood problems, rare reports of cancers
What adverse effects are associated with methotrexate?
Mucositis Myelosuppression Pneumonitis Pulmonary fibrosis Liver fibrosis
What are the rules surrounding methotrexate use and pregnancy?
Women - avoid pregnancy for at least 6 months after treatment stopped
Men - use effective contraception for at least 6 months after treatment stop
How should methotrexate be prescribed?
Weekly
Folic acid 5mg once weekly co-prescribed - more than 24hrs after methotrexate dose
Methotrexate Mondays Folate Fridays
How should patients on methotrexate be monitored?
FBC
U&E
LFT
Before treatment
Weekly until stabilised
Every 2-3 months thereafter
What interactions with methotrexate should you be aware of?
Avoid trimethoprim/co-trimoxazole - increase risk of marrow aplasia
High dose aspirin increase risk of methotrexate toxicity secondary to reduced excretion
Should a patient have a methotrexate toxicity, how should it be managed?
Folinic acid
What is pityriasis rosea?
Generalised self limiting rash
May be caused by human herpes virus, but unsure
What is the presentation of pityriasis rosea?
Characteristic herald patch - more than 2cm in diameter
Occurs on torso
Widespread faint red or pink, slightly scaly oval shaped lesions rash
Christmas tree arrangement along lines of the ribs
Generalised itch
Low grade pyrexia
Headache
Lethargy
What is the management of pityriasis rosea?
Rash resolves without treatment in 3 months
Can leave discolouration of skin
Emollients, topical steroids, sedating antihistamines at night to help with sleep - chlorphenamine
What occurs in head lice?
What is the management?
Due to close contact
Itchy scalp
Detection combing
Dimeticone 4%
What are the characteristics of basal cell carcinoma?
Slow-growing, locally invasive, malignant epidermal basal layer skin tumour
What are the risk factors for BCC?
Exposure to UV light is main aetiological factor
Fitzpatrick skin types I & II: light skin, tans poorly
Male Mutations in PTCH, p53, ras Albinism Gorlin's syndrome Xeroderma pigmentosum Increasing age Previous skin cancers Immunosuppression e.g. AIDs, transplantation Carcinogens - ionising radiation, arsenic, hydrocarbons
What is Gorlin-Goltz syndrome?
Nevoid basal cell carcinoma syndrome
Rare autosomal dominant condition, mutation of PTCH1 gene
Early onset BCCS Broad nasal root Palmar and plantar pits Bifid ribs Hypertelorism - wide spaced eyes Calcification of faux cerebri
What are the clinical features of a typical nodular BCC?
TURP
Presence of irregular pink/skin coloured lesion
Commonly on face/neck
Telangiectasia
Ulceration
Rolled edges
Pearly edge
What are the clinical sub-types of BCC?
Nodular
Superficial
Morphoeic
Pigmented
Basosquamous
What are the features of nodular BCC?
Most cases of BCC
Occur mostly on head
Flesh/red coloured
Well defined borders
Overlying telangiectasias
Rodent ulcer - central ulceration
What are the features of superficial BCC?
Erythematous plaque
Mostly on trunk/limbs
Slow-growing
May be dry/crusted
May have bluish tinge
Numerous of these may indicate arsenic exposure
What are the features of morphoeic infiltrative BCC?
Scar-like lesion or indentation
Commonly occur on upper trunk or face
Whitish, compact
Poorly defined plaque/scar
Deeply invasive
What are the features of pigmented BCC?
Difficult to distinguish from melanoma
Pigmentation due to melanin production, why it is hard
Often excised with 2mm margin as a result
What are the features of basosquamous BCC?
Rare but agressive
Increased risk of recurrence and metastasis
Differentiation towards SCC
Has macro and histopathological features of both
What surgical management is available for BCC?
Excision - wide local or Moh’s micrographic surgery for high risk lesions
Destructive - curettage, cautery, cryotherapy, carbon dioxide laser (these don’t provide histological sample, so low risk lesions only)
What non-surgical management is available for BCC?
Radiotherapy -
Adjuvant
Prevent recurrence e.g. incompletely excised margins
Recurrent BCC
High risk BCCs; and surgery not appropriate
NB risk of radiation induced BCC in those with Gorlin’s
Topical immunotherapy e.g. Imiquimod
PDT
What are the features of a high risk BCC lesion?
Size > 2cm
Site - around eyes, lips, ears
Poorly defined margins
Histological sub-type - morpoeic, infiltrative, micro nodular, basosquamous
Histological features - perineural, perivascular inv
Previous tx failure
Immunosuppression
What are the surgical excision margins for BCC?
Lesions should be excised down to subcutaneous fat to ensure entirety of skin; epidermis and dermis is included in sample
Low risk lesions - (small <2cm, well defined) margin of 4-5mm = 95% clearance
High-risk lesions - (large >2cm poorly defined) 5mm provides 83% clearance
Recurrent lesions - referral to Skin MDT, re-excision of scar 5-10mm margins or Moh’s surgery and radiotherapy
What is Moh’s surgery?
Surgical removal of tissue
Free margin removed can be less
Mapping piece of tissue, freezing and cutting, staining
Interpretation of slides, determines if any more needs to be removed
Possible reconstruction of surgical defect
What is the system used to describe a skin lesion?
A - asymmetry
B - border irregularity
C - colour (varies)
D - diameter (greater than 6mm)
E - evolving (change in shape, size or shade)
F - funny looking
Describe how BCC grow
Slow growing
Locally Invading
Very rarely metastasis
What cells do BCCs arise from?
Epidermal tumours arising from hair follicles
Describe the appearance of solar (actinic) keratoses:
On sun-exposed skin
Crumbly, yellow-white crusts
What is the risk associated with actinic keratoses?
Malignant change to squamous cell carcinoma may occur after several years
How should actinic keratoses be managed?
Cryotherapy or fluorouracil/imiquimod cream
Describe the appearance of Bowen’s disease:
Slow growing red/brown scaly plaque
How should Bowen’s disease be managed?
Cryo, topical fluorouracil, photodynamic therapy
Describe the appearance of keratoacanthoma:
Dome-shaped erythematous lesions that grow rapidly and often contain a central pit of keratin
name 3 genetic conditions associated with increased risk skin ca
- gorlins syndrome (PTCH1 gene mutation leading to increased risk nevoid BCC)
- xeroderma pigmentosa
- albinism
How should a suspected BCC be referred?
- routine referral if suspect BCC
- 2WW if concern that delay would have impact either bc or site or feature of the lesion
How should BCC be investigated?
- excision biopsy
- incision biopsy before non surgical treatment to confirm diagnosis
- examine for lymphadenopathy
- MRI or CT only when bony involvement suspected or tumour invaded major nerves, orbit or parotid gland
What is squamous cell carcinoma?
Malignant tumour
Keratinising cells of the basal layer of the epidermis
Locally invasive
Potential to metastasise
What are the risk factors for SCC?
UV light
Fair skin
Chemical carcinogens - arsenic, chromium, soot, tar and pitch oils
HPV
Ionising radiation exposure
Immunodeficiency
Chronic inflammation - near chronic ulcers, lupus vulgaris
Genetic conditions e.g. albinism, xeroderma pigmentosum
Pre-malignant conditions e.g. Bowen’s disease
What are the features of actinic keratosis?
Macule or patch
On areas that receive large amounts of sunlight: head and neck, dorsum of hands, forearms
Erythematous base
Overlying scale
Typically non tender
Where can invasive cutaneous SCC occur?
Arise from any cutaneous surface
Most frequently head and neck
Legs, hands, forearms, shoulder, back, chest, abdomen
What are the characteristics of a well differentiated invasive cSCC?
Papule, plaque or nodule
0.5-1.5cm or larger
Erythematous base
Rough scale, crusting
May have ulceration
Firm, indurated on palpation
How do invasive cutaneous cSCC lesions evolve?
Grows over period of months
Becomes increasingly tender
More likely to ulcer and bleed
May present as a non-healing wound, asymptomatic
What are the differential diagnoses for invasive cSCC?
Actinic keratosis
Superficial BCC
Warts
Pyogenic granuloma
What are the investigations for SCC?
Visual inspection and removal for histology where necessary
Excision biopsy - whole lesion excised
Incisional or punch biopsy if lesion in large, in cosmetically sensitive areas, close to vital structures
If advanced disease - imaging including CT scanning for bone or soft tissue spread, MRI scan
Clinically enlarged nodes should be examined histologically e.g. by fine needle aspiration
At which sites can squamous cell carcinoma of the skin develop from (predisposing sites)?
Actinic keratoses, lips of smokers, or in long standing ulcers (Marjolin’s)
What are the features of suspicious of melanoma?
ABCDE
Asymmetry Border - irregular Colour - alterations Diameter >6mm Evolving lesions
What are risk factors for melanoma?
Exposure to UV light
Severe sun burn
Immunosuppression
Skin types I and II
Family history
Genetic mutations
What biopsy is available for melanoma?
Excision biopsy of the suspicious lesions
Completely excised with a margin of 1-2mm of healthy surrounding skin
Includes portion of subcutaneous fat to ensure full-thickness of dermis sampled
Orientation important - longitudinal lesions preferred on the limbs
Incisional biopsy - punch or incision for small sample for large lesions or close to vital structures - eyes, ears, nose
What are the major subtypes of melanoma?
Superficial spreading - initial radial growth progresses to vertical growth
Nodular - transition quickly to vertical growth
Acral lentiginous - under nails, hands and feet, black line on nail = Hutchinson’s sign
Lentigo maligna - common in elderly, chronically sun-exposed sites
Desmoplastic - very rare, due to abnormal deposits of collagen
What are the features of histological analysis of melanoma?
Clark level:
I-V histological classification for depth of invasion
Breslow thickness (mm): Measured from stratum granulosum of epidermis or from bottom of ulceration to the point of maximum infiltration
Ulceration:
Absence of intact epithelium overlying the lesion
Correlates with poorer prognosis, suggestive of aggressive tumour phenotype
Mitotic index
Indicator of cell turnover
Important histological finding
Number of mitoses per mm2
What are the investigations for melanoma?
Careful skin and lymph node examination
FNA and cytology if suspicious lymph node
Total body CT or PET-CT for high-risk lesions - those with aggressive lesions, or presence of known lymph node spread
LDH (lactate dehydrogenase blood marker of cell turnover) for risk stratifying
What is the surgical management of melanoma?
Wide local excision for primary melanoma, removal of biopsy scar, margin depends on Breslow thickness
Senital lymph node biopsy under GA at same time as WLE - radio-labelled tracer and CT identifies hot spots, further shown in surgery with blue dye
Positive SLNB results in subsequent lymphadenectomy
Electro-chemotherapy
For locally advanced melanoma
Chemo agent given IV or injected into the tumour, then powerful pulses of electricity applied to the tumour
Increases permeability of tumour cell membranes so chemo agent can pass through
What is the medical management of melanoma?
Adjuvant therapy e.g. interferon alpha
Chemo, radio, immuno
Describe the clinical features of melanoma
- lesion changed in size
- irregularity of pigmentation (may need dermatoscope to appreciate)
- irregularity of outline
- size >6mm
- inflammation
- oozing or bleeding
- itch or altered sensation
- risk factors identified
- not all melanomas are pigmented but most are
what are the criteria for melanoma 2WW
- 2WW if 3 or more points from:
2 points: - change in size
- irregular shape
- irregular colour
1 point: - > 6mm
- inflammation
- oozing
- change in sensation
Describe the breslow scale
about depth of invasion at biopsy, strongly correlated with survival
- Tis= top layer of skin
- T1= 1mm thick or less
- T2= melanoma between 1 and 2mm thick
- T3= 2-4mm thick
Describe the Glasgow 7-point checklist for malignant melanoma and when you should refer:
Major (2pts): change in size, shape, colour
Minor (1pt): inflammation, sensory change, diameter >6mm, crusting/bleeding
Refer if 3+
Where do malignant melanomas metastasise?
Bone, brain, lung, liver
What are some poor prognostic indicators for malignant melanoma?
High Breslow thickness
Ulcerated
Node involvement
Location of head, neck, back of arms
