Dermatology Flashcards
What is acanthosis nigricans?
Causes of acanthosis nigricans
Symmetrical, brown, velvety plaques on the neck, axilla and groin
Seen in: GI cancer, DM, obesity, PCOS, Cushings disease, acromegaly, hypothyroidism, familial, prader willi
Drugs: OCP, nicotinic acid
Features of acne rosacea
nose, cheeks and forehead Flushing Telangiectasia Later develops into persistent erythema with papules and pustules Rhinophyma Blepharitis Sunlight may exacerbate symptoms
Management of acne rosacea
Topical metronidazole for mild symptoms
Abx (oxytetracycline) for more severe disease
Laser therapy for telangiectasia
High factor sunscreen
Concealer
Pathophysiology of acne vulgaris
Follicular epidermal hyperproliferation -> keratin plug formation -> obstruction of pilosebaceous follicles -> colonisation by anaerobic bacteria (Proprionibacterium acnes) -> inflammation
Activity of sebaceous glands are controlled by androgen
Features of acne vulgaris
Comedones due to dilated sebaceous follicle (closed = whitehead, open = blackhead)
Papules and pustules (follicle bursts -> releases irritants -> inflammation)
Excessive inflammation -> nodules and cysts
Eventually leads to scarring -> ice-pick scars and hypertrophic scars
Classification of acne vulgaris
Mild - open and closed comedones +/- sparse inflammatory lesions
Moderate - widespread non-inflammatory lesions and numerous papules and pustules
Severe - extensive inflammatory lesions, nodules, pitting, scarring
Management of acne vulgaris
- Single topical therapy (topical retinoids, benzoyl peroxide)
- Topical combination therapy (topical abx, benzoyl peroxide, topical retinoid)
- Oral abx: tetracyclines (limecycline, doxycycline, oxytetracycline), erythromycin
Oral abx should be coprescribed with a topical retinoid or benzoyl peroxide.
COCP is an alternative in women - Oral isotretinoin under specialist supervision (C/I in pregnancy)
Features of actinic keratosis
Premalignant skin lesion as a result of chronic skin exposure
Small, crusty, scaly lesions
Pink/red/brown or same colour as skin
Typically on sun-exposed areas
Multiple lesions may be present
Management of actinic keratosis
Prevention of further risk: sun avoidance, sun cream
Fluorouracil cream Topical diclofenac Topical imiquimod Cryotherapy Curettage and cautery
Features and treatment of alopecia areata
Features - autoimmune condition, localised well de-marcated patches of hair loss with small broken exclamation mark hairs at the edge of the hair loss
Management - explanation is often sufficient as majority will regrow, other treatment includes topical/intralesional corticosteroids, topical minoxidil, phototherapy, dithranol, contact immunotherapy, wigs
Basal cell carcinoma features
Sun-exposed sites
Pearly, flesh-coloured papule with telangiectasia
May later ulcerate leaving a central crater
Slow growing and local invasion
Metastasis is rare
Management for basal cell carcinoma
Surgical removal Curettage Cryotherapy Topical cream: imiquimod, fluorouracil Radiotherapy
Bowen’s disease features and management
Squamous cell carcinoma in situ
More common in elderly females
Red, scaly patches
Often occurs on sun-exposed areas (eg. lower limb)
Management - topical 5-fluorouracil or imiquimod, cryotherapy, excision
Features of bullous pemphigoid
Autoimmune condition causing sub-epidermal blistering of the skin, secondary to antibodies against hemidesmosomal proteins
More common in elderly patients
Itchy, tense blisters typically around flexures
Blisters usually heal without scarring
Mouth is usually spared
Management of bullous pemphigoid
Referral to dermatologist for biopsy and confirmation of diagnosis
Oral corticosteroids are mainstay of treatment
Topical corticosteroids, immunosuppressants and abx are also used
Investigations for bullous pemphigoid
Skin biopsy -> immunofluorescence shows IgG and C3 at the dermoepidermal junction
Immediate management of burns (inc. heat burns, electrical burns and chemical burns)
A-E, analgesia
Heat burns: remove person from source, irrigate the burn with cool water for 10-30min, cover burn with clingfilm
Electrical burns: switch off power supply, remove person from source
Chemical burns: brush any powder off then irrigate with water
Assessing the extent of burns
Wallace’s rule of nines: Head+neck 9%, each arm 9%, each anterior leg 9%, each posterior leg 9%, anterior chest 9%, posterior chest 9%, anterior abdomen 9%, posterior abdomen 9%
The palmar surface is roughly equivalent to 1% of total body surface area
Different depths of burns and their features
Superficial epidermal = red and painful
Partial thickness (superficial dermal) = pale pink, painful, blistered
Partial thickness (deep dermal) = typically white, may have patches of non-blanching erythema, reduced sensation
Full thickness = white/brown/black in colour, no blisters, no pain
Burns referral to secondary care
- Deep dermal and full thickness burns
- Superficial dermal burns of more than 3% total body surface area (adults) or 2% (children)
- Superficial dermal burns involving face, hands, feet, perineum, genitalia, or any flexure, circumferential burns of the limbs, torso or neck
- Any inhalation injury
- Any electrical or chemical burn injury
- Suspicion of NAI
Calculating amount of fluids required following burns
Parkland formula:
Vol of fluid = total body surface area of the burn (%) x weight (kg) x 4
Half of the fluid should be administered in the first 8 hours
Urinary catheter inserted
What is an escharotomy and what are the indications
careful division of the encasing band of burn tissue to potentially improve ventilation, or relieve compartment syndrome and oedema
Indications: circumferential full thickness burns to the torso or limbs
Contact dermatitis two different types
Irritant contact dermatitis: common, non-allergic due to weak acids/alkalis, often on hands. Erythema is typical, crusting and vesicles are rare
Allergic contact dermatitis: type IV hypersensitivity. Uncommon, seen on the head following hair dye. Topical treatment with potent steroid is indicated
Features of dermatitis herpetiformis
Autoimmune blistering skin disorder, associated with coeliac disease
Caused by deposition of IgA in the dermis
Itchy, vesicular skin lesions of the extensor surfaces
Diagnosis and management of dermatitis herpetiformis
Diagnosis: skin biopsy -> direct immunofluorescence shows deposition of IgA in a granular pattern in the upper dermis
Management: gluten-free diet, dapsone
Eczema herpeticum
- Cause
- Risk factor
- Presentation
- Examination finding
- Management
Severe primary infection of the skin caused by herpes simplex virus 1 or 2
Commonly seen in children with atopic eczema
Often presents as a rapidly progressing painful rash
O/E: monomorphic punched out erosions (circular, depressed, ulcerated lesions), usually 1-3mm in diameter
Potentially life-threatening, so children should be admitted for IV aciclovir
Management of eczema
Emollients and soap substitutes
Topical steroids
UV radiation
Immunosuppressants (ciclosporin, antihistamines, azathioprines)
Topical steroids ranked by potency
Mild: hydrocortisone
Moderate: betnovate RD, eumovate
Potent: betnovate, cutivate
Very potent: dermovate
1 finger tip (0.5g) should treat a skin area about twice that of the flat of an adult hand
Features of erythema multiforme
Hypersensitivity reaction commonly triggered by infections
Divided into minor and major forms
Target lesions
Initially seen on the back of hands/feet before spreading to torso
Upper limbs more commonly affected than lower limbs
Pruritus occasionally seen and usually mild
Causes of erythema multiforme
Viruses (herpes simplex virus) Idiopathic Bacteria (mycoplasma, streptococcus) Drugs (penicillin, sulphonamides, carbamazepine, allopurinol, NSAIDs, OCP) Connective tissue disease (SLE) Sarcoidosis Malignancy
Causes of erythema nodosum
Infection (streptococci, TB), systemic disease (sarcoidosis, IBD, Behcets), malignancy/lymphoma, drugs (penicillins, sulphonamides, COCP), pregnancy
Erythema nodosum features
inflammation of subcut fat Typically causes tender, erythematous, nodular lesions Usually occurs over shins Usually resolves within 6 weeks Lesions heal without scarring
What is erythroderma?
Causes of erythroderma
A term used when more than 95% of the skin is involved in a rash of any kind
Eczema, psoriasis, drugs (gold), lymphomas, leukaemias, idiopathic
Causes and risk factors of fungal nail (onychomycosis)
Causes: dermatophytes (Trichophyton), yeasts (candida), non-dermatophyte moulds
Risk factors: DM, increasing age
Features of onychomycosis (fungal nail)
Unsightly nails
Thickened, rough, opaque nails
Investigations of fungal nail (onychomycosis)
Nail clippings
Scrapings of the affected nail
Management of fungal nail (onychomycosis)
No treatment required if asymptomatic
Dermatophyte infection: oral terbinafine first line, oral itraconazole second line. 6wks-3m for fingernails, 3-6m for toenails
Candida infection: topical antifungal (amorolfine) for mild disease, oral itraconazole for 12 weeks for more severe infection
Guttate psoriasis features
2-4 weeks after streptococal infection
Tear drop papules on trink and limbs
Management of guttate psoriasis
Most cases resolve spontaneously in 2-3 months Regular emollients Potent topical corticosteroid Topical vitamin D analogue UVB phototherapy
Hereditary haemorrhagic telangiectasia
- inheritance pattern
- diagnostic criteria
Autosomal dominant
If the patient has 2 then they are said to have a possible diagnosis of HHT, if they have 3+ then they are said to have definite diagnosis of HHT
- Spontaneous recurrent epistaxis
- Telangiectases at the lips/oral cavity/fingers/nose
- Visceral lesions (eg. GI telangiectasia, pulmonary arteriovenous malformations, hepatic AVM, cerebral AVM, spinal AVM)
- Family history (first degree relative with HHT)
What is herpes zoster?
Features and cause
Management of herpes zoster
Shingles.
Acute, unilateral, painful blistering rash caused by reactivation of varicella zoster virus
Management: oral aciclovir
Shingles vaccine
- who is it offered to?
- what type of vaccine is it?
- vaccine contraindication
Offered to all patients aged 70-79 yrs
Live-attenuated and given subcutaneously
C/I in immunosuppression as it is live-attenuated
Causes of hirsutism
Cushing’s syndrome, congenital adrenal hyperplasia, androgen therapy, obesity (insulin resistance), adrenal tumour, androgen secreting ovarian tumour, drugs (phenytoin, corticosteroids)
Management of hirsutism
Weight loss if overweight
Waxing/bleaching
COCP
Management of hyperhidrosis
Topical aluminium chloride is first line (S/E = skin irritation)
Iontophoresis
Botulinum toxin (for axillary symptoms)
Surgery
Causes and spread of impetigo
Superficial bacterial skin infection - Staphylococcus aureus or Streptococcus pyogenes
It can be a primary infection or a complication of an existing skin condition (eg. eczema, scabies, insect bite)
Common in children, particularly during warm weather
Spread by direct contact with discharges from the scabs
Features of impetigo
Golden crusted skin lesions typically found around the mouth
Very contagious
Management of impetigo
Limited, localised disease:
- Topical fusidic acid is first line
- Topical mupirocin if MRSA
Extensive disease:
-Oral flucloxacillin first line
Oral erythromycin is pen-allergic
Children should be excluded from school until the lesions are crusted and healed, or 48hrs after starting abx
Adverse effects of isotretinoin
Teratogenicity (use two forms of contraception)
Dry skin, eyes, lips/mouth (most common side effect)
Low mood
Raised triglycerides
Hair thinning
Nose bleeds
Photosensitivity
Intracranial hypertension (avoid prescribing with tetracyclines)
Features and management of a keratocanthoma
Looks like a volcano/crate
Initially a smooth dome-shaped papule
Rapidly grows to become a crater centrally-filled with keratin
Spontaneous regression within 3 months usually, however should be excised urgently as it is clinically difficult to exclude form a SCC
What is the Koebner phenomenon? What conditions is it seen in?
Skin lesions which appear at the site of injury
Seen in: psoriasis, vitiligo, warts, lichen planus, lichen sclerosus, molluscum contagiosum
Leukoplakia
- features
- diagnosis
- management
Premalignant condition, presents as white, hard spots on mucous membranes in the mouth
Common in smokers
Diagnosis of exclusion, rule out candidiasis and lichen planus
Biopsies often performed to exclude SCC
Regular follow up to exclude malignant transformation into SCC
Lichen planus features
Itchy, papular rash most common on palms, soles, genitalia and flexor surfaces of arms
Rash is polygonal in shape, with a ‘white-lines’ pattern on the surface (Wickham’s striae)
Koebner phenomenon (new lesions at the site of trauma)
Oral involvement (white lace pattern on buccal mucosa)
Thinning of nail plate, longitiduinal ridging
Management of lichen planus
Topical steroids
Benzydamine mouthwash/spray for oral lichen planus
Oral steroids/ immunosuppression for extensive lichen planus
Lichen sclerosus features
Inflammatory condition usually affecting the vagina
More common in elderly females
Leads to atrophy of the epidermis with white plaques forming
Very itchy
Lichen sclerosus diagnosis and management
Diagnosis is usually clinical, but biopsy may be done it atypical features are present
Management - topical steroids and emollients
Follow up due to increased risk of vulval cancer
Features, diagnosis and management of lipoma
Smooth, mobile, painless lump
Generally found in the subcutaneous tissues
Clinical diagnosis
Mx: observation. Remove if diagnosis uncertain or if compressing surrounding structures
4 main types of malignant melanoma (frequency, typically affected body part, appearance)
Superficial spreading: Commonest. Affects arms, legs, back and chest in young people. Growing moles with change in size/ shape/ colour/ discharge
Nodular: second commonest. Sun-exposed skin in middle-aged people. Red or black lump which bleeds/ oozes
Lentigo maligna: less common. Chronically sun-exposed skin in older people. Growing mole with change in size/shape/ colour/ discharge
Acral lentiginous: rare. Nails, palms, or soles in african-americans or asians. Subungal pigmentation (Hutchinsons sign) or on palms/ feet
Margins of excision
Breslow thickness 0-1mm thick = 1cm margin 1-2mm thick = 1-2 cm 2-4mm thick = 2-3 cm >4 = 3 cm
Management of malignant melanoma
Suspicious lesion -> excision biopsy (remove lesion completely with a 2mm margin)
Once diagnosis is confirmed, Breslow thickness should be assessed to determine whether further re-excision of margins is required
Malignant melanoma risk factors
Increased UV exposure, sunburn, fair complexion, lots of moles, positive family history, previous melanoma, elderly
Signs of malignant melanoma
ABCDEF Asymmetry Border irregularity or blurring Colour variation Diameter >6mm Evolution of mole Funny looking mole
Prognosis of malignant melanoma
Depends on Breslow thickness <1mm = 95-100% 5-yr survival 1-2mm = 80-96% 2.1-4mm = 60-75% >4 mm = 50%
Cause of molluscum contagiosum
Skin infection caused by molluscum contagiosum virus
Transmission occurs directly by close personal contact, or indirectly via contaminated surfaces
Majority of cases occur in children (esp children with atopic eczema), often 1-4 yrs
May occur around the genitals in adults as a result of sexual contact
Features of molluscum contagiosum
Characteristic pink/pearly white papules with a central umbilication which are up to 5mm in diameter
Lesions appear in clusters anywhere on the body, with sparing of the palm and sole
Management of molluscum contagiosum
No treatment usually, as it is self limiting
Spontaneous resolution within 18 months
Contagious so avoid sharing towels/clothing/baths
Encourage not to scratch lesion
If lesions are troublesome then use cryotherapy or squeeze the lesion following a bath
No need to exclude form school/swimming
Prescribe an emollient and a mild topical corticosteroid if itchy
Prescribe a topical abx (fusidic acid) if skin looks infected
Causes of nail pitting
Psoriasis
Alopecia areata
Causes of leuconychia
Hypoalbuminaemia
Fungal disease
Lymphoma
Features of pellagra
Causes of pellagra
Dermatitis, diarrhoea, dementia (3 Ds)
Also depression, and death if not treated
Caused by nicotinic acid deficiency, may occur as a consequence of isoniazid therapy. More common in alcoholics
Cause of pemphigus vulgaris
Autoimmune disease caused by antibodies ageinst desmoglein 3
More common in Ashkenazi jewish population
Features of pemphigus vulgaris
Mucosal ulceration, oral involvement
Skin blistering - flaccid, easily ruptured vesicles and bullae
Lesions are painful but not itchy
Diagnosis and management of pemphigus vulgaris
Acantholysis on biopsy
Management - steroids first line, immunosuppressants
What is pityriasis rosea? Who does it tend to affect? What causes it?
Acute, self-limiting rash
Tends to affect young adults
Thought to be due to Herpes hominis virus 7 (HHV 7)
Features of pityriasis rosea
Majority of patients have no prodrome, but some patients give a history of a recent viral infection
Pruritus
Herald patch usually on trunk
Herald patch is followed by erythematous, oval, scaly patches
Oval patches follow a characteristic distribution with the longitudinal diameters of the oval patches running parallel to the line of Langer (fir-tree appearance)
Management of pityriasis rosea
Self-limiting, usually disappears after 6-12 weeks so no treatment needed
Pityriasis versicolor
- what is it
- cause
- predisposing factors
Superficial cutaneous fungal infection caused by Malassezia furfur
Predisposing factors: occurs in healthy individuals, immunosuppression, malnutrition, Cushing’s
Pityriasis versicolor features
Most commonly on the trunk Hypopigmented, pink or brown patches May be more noticeable following a suntan Scale is common Mild pruritus
Management of pityriasis versicolor
Topical antifungal (ketoconazole shampoo)
If failure to respond, consider alternative diagnoses (send scrapings) + oral itraconazole
Causes of pruritus
Liver disease Iron deficiency anaemia Polycythaemia Chronic kidney disease Lymphoma
Other causes: Hyper/hypothyroidism DM Pregnancy Urticaria Skin disorders: eczema, scabies, psoriasis, pityriasis rosea
Subtypes of psoriasis
Plaque psoriasis: most common. typical well demarcated red scaly patches on the extensor surfaces
Flexural psoriasis: smooth skin
Guttate psoriasis: transient psoriatic rash triggered by Strep infection. Red teardrop lesions
Pustular psoriasis: usually on palms and soles
Features and complications of psoriasis
Raised red plaques with silver scaling, typically on extensor surfaces
Nail signs: pitting, onycholysis
Arthritis
Complications: Psoriatic arthropathy Metabolic syndrome Cardiovascular disease VTE Psychological distress
Exacerbating factors of psoriasis
Trauma
Alcohol
Drugs (beta blockers, lithium, antimalarials, NSAIDs, ACEI, infliximab)
Withdrawal of systemic steroids
Streptococcal infection may trigger guttate psoriasis
Management of psoriasis
Regular emollients to reduce scale loss and pruritus
First line: potent topical corticosteroid and topical vit D analogue OD for up to 4 weeks as initial treatment
Second line: if no improvement after 8 weeks then offer vit D analogue BD
Third line: if no improvement after 8 weeks then offer either: potent topical corticosteroid BD for up to 4 weeks, or a coal tar preparation OD/BD
Short acting dithranol may be used
Secondary care:
- Phototherapy
- Systemic therapy (oral methotrexate first line)
Advice for using topical corticosteroids in psoriasis
Aim for a 4 week break between courses of topical corticosteroids
Use potent topical corticosteroids for no longer than 8wks at a time
Vitamin D analogues
- examples
- MoA
- Side effects
Examples: calcipotriol, calcitriol, etc
MoA: reduce cell division and differentiation. they tend to reduce the scales and plaque thickness but not the erythema
SE: uncommon. Avoid in pregnancy
Unlike corticosteorids they may be used long term
Unlike coal tar prep and dithranol they do not smell or stain
Systemic therapy used in secondary care for the management of psoriasis
Methotrexate - first line
Ciclosporin
Systemic retinoids
Biological agents: infliximab, etanercept
Phototherapy for psoriasis
- type of phototherapy
- how often
- side effects
Narrow band UV B light is now the treatment of choice
Can be given 3 times a week
Adverse effects include skin ageing and squamous cell carcinoma
Childhood causes of purpura
Meningococcal septicaemia Acute lymphoblastic leukaemia Congenital bleeding disorders Immune thrombocytopenic purpura Henoch-Schönlein purpura NAI
Adulthood causes of purpura
Immune thrombocytopenic purpura
Bone marrow failure
Senile purpura
Drugs (quinine, antiepileptics, antithrombotics)
Nutritional deficiency (vit B12, C, folate)
Pyoderma gangrenosum features
Typically on lower limbs
Initially small red papules
Later deep, red, necrotic ulcers with a violaceous border
May be accompanied with systemic symptoms (fever, myalgia)
Causes of pyoderma gangrenosum
Idiopathic (50%) IBC RA, SLE Myeloproliferative disorders Lymphoma, myeloid leukaemias Monoclonal gammopathy Primary biliary cirrhosis
Management of pyoderma gangrenosum
Oral steroids are first line
Ciclosporin and infliximab have a role in difficult cases
Features of pyogenic granuloma
Most common sites: head/neck, upper trunk and hands (oral mucosa is common in pregnancy)
Initially small red/brown spot
Rapidly progresses within days/weeks forming raised red/brown lesions which are often spherical in shape
Lesions may bleed profusely and ulcerate
Management of pyogenic granuloma
If pregnancy-related they often resolve spontaneously post-partum
Other lesions usually persist
Removal methods: curettage and cautery, cryotherapy, excision
Scabies pathophysiology
Caused by the Sarcoptes scabiei mite and is spread by prolonged skin contact
Scabies mite burrows into the skin, laying its eggs in the stratum corneum
Intense pruritus due to a delayed type 4 hypersensitivity reaction to the mites/eggs about 30 days after initial infection
Features of scabies
widespread pruritus
Linear burrows on the side of fingers, interdigital webs and flexor aspects of the wrist
Secondary features due to itching: excoriation, infection
Management of scabies
Permethrin 5% is first line
Malathion 0.5% second line
Pruritus persists for up to 4-6 weeks post eradication
Avoid close contact with others
All household and close contacts should be treated
Launder, iron and tumble dry clothing, bedding and towels on the first day of treatment
Seborrhoeic dermatitis in adults
- cause
- features
- associated conditions
- cause: chronic dermatitis thought to be caused by an inflammatory reaction related to proliferation of a normal skin inhabitant, Malassezia furfur
- features: eczematous lesions on sebum-rich areas (scalp-> dandruff, periorbital, auricular, nasolabial folds), otitis externa, blepharitis
0Associated with HIV and parkinsons disease
Management of adult seborrheic dermatitis
Scalp disease:
First line: OTC preparations containing zinc pyrithione (head and shoulders) and tar (neutrogena T gel)
Second line: ketoconazole shampoo
Selenium sulphide and topical corticosteroid may be useful
Face and body management:
Topical antifungals (ketoconazole)
Topical steroids
Difficult to treat, recurrence is common
Seborrhoeic keratoses
- what is it
- features
- management
benign epidermal skin lesions seen in older people
Features: stuck-on appearance, large variation in colour from flesh colour to light brown or black, keratotic plugs on the surface
Management: reassurance (benign), may remove (curettage, cryotherapy, shave biopsy)
Polymorphic eruption of pregnancy
- what is it
- features
- management
Pruritic condition associated with last trimester
lesions often first appear in abdominal striae
Management: emollients, mild potency topical steroids, and oral steroids depending on severity
Pemphigoid gestationis
- features
- when does it develop
- management
Pruritic blistering lesions, often develop in peri-umbilical region, later spreading to the trunk, back, buttocks and arms
Usually presents in 2nd or 3rd trimester and rarely seen in first pregnancy
Management: oral corticosteroids
5 types of basal cell carcinoma
Nodular BCC - commonest. Raised translucent papule, usually on face
Superficial BCC - superficial erythematous macule on the trunk, may show spontaneous regression
Morpheaform BCC - flat, slightly atrophic lesion or plaque without well-defined borders, high recurrence rate
Cystic BCC - clear or blue-grey appearance, may resemble nodular BCC
Basosquamous carcinoma - atypical, features resemble BCC and SCC, biologically more aggressive and more destructive, metastatic disease may occur
Skin types
Fitzpatrick classification
1 - never tans, always burns (red hair, freckles, blue eyes)
2 - burns easily, tans poorly
3 - may burn, tans poorly
4 - burns minimally, tans easily (olive)
5 - rarely burns, always tans (asian)
6 - never burns, tans darkly (black african)
Spider naevi
- what are they
- where are they found
- vs. telangiectasia
- associated conditions
Central red papule with surrounding capillaries which blanch upon pressure
Almost always found on upper part of body
Can be differentiated from telangiectasia by pressing on them and watching them fill - spider naevi fill from the centre, telangiectasia fill from the edge
Associations - liver disease, pregnancy, COCP
Squamous cell carcinoma risk factors
Excessive exposure to sunlight Actinic keratosis/ bowens disease Immunosuppression Smoking Long standing leg ulcers Genetic conditions
treatment of squamous cell carcinomas
Wide local excision for diagnostic biopsy, then repeat surgery to gain adequate margins
Surgical excision with 4mm margin if lesion <20mm in diameter, and 6mm margin if lesion >20mm diameter
Moh’s micrographic surgery used in high-risk patients and in cosmetically important sites
Poor prognostic factors of squamous cell carcinoma
Poorly differentiated
>20mm in diameter
>4mm deep
Immunosuppression
Invasive SCC features
Erythematous keratotic papule or nodule on a background of sun exposure
Ulceration may occur
Regional lymphadenopathy may be present
May metastasise
Tinea capitis
- features
- cause
- diagnosis
- management
Scalp ringworm (dermatophyte fungal infection) Scarring alopecia, mainly seen in children If untreated, a raised, pustular, spongy/boggy mass (kerion) may form
Most common cause: Trichophyton tonsurans)
Diagnosis: scalp scrapings
Management: oral antifungal (terbinafine), topical ketoconazole shampoo for the first two weeks to reduce transmission
Tinea corporis
- causes
- features
- management
Ringworm (dermatophyte fungal infection)
Causes: Trichophyton rubrum and Trichophyton verrucosum (contact with cattle)
Well-defined annular, erythematous lesions with pustules and papules
Management: oral fluconazole
Tinea pedis features
Athletes foot (dermatophyte fungal infection) Itchy, peeling skin between toes Common in adolescence
Toxic epidermal necrolysis (TEN)
- causes
- features
Potentially life-threatening skin disorder, commonly seen secondary to a drug reaction
Examples: phenytoin, sulphonamides, allopurinol, penicillins, carbamazepine, NSAIDs
Scalded appearance over an extensive area
Systemically unwell (pyrexia, tachycardia)
Positive Nikolsky sign (epidermis separates with mild lateral pressure)
Toxic epidermal necrolysis management
Stop precipitating factor
ITU supportive care
IV Ig first line
Other options: ciclosporin, cyclophosphamide, plasmapharesis
Venous ulceration
- features
- risk factors
- investigations
- management
features: medial malleolus, shallow ulcer with granulated base
risk factors: varicose veins, DVT, venous insufficiency, poor calf muscle function, AV fistulae, obesity, leg fracture, trauma over medial malleolus
Ix: Duplex USS, ABPI normal (0.9-1.2)
Mx: compression bandaging (four layers)
Oral pentoxifylline (peripheral vasodilator)
Features of vitiligo and associated conditions
Autoimmune
Well-demarcated patches of depigmented skin
Peripheries tend to be most affected
Trauma may precipitate new lesion (koebner phenomenon)
T1DM, Addisons, autoimmune thyroid disease, pernicious anaemia, alopecia areata
Management of vitiligo
Sunblock
Camouflage makeup
Topical corticosteroids may reverse changes if applied early
Topical tacrolimus and phototherapy may be helpful
Arterial ulceration
- features
- ix
- mx
Features: small deep lesions, well-defined borders, evidence of arterial insufficiency, found at distal sites
Ix: ABPI either reduced (<0.9) or raised (due to calcification, >1.2), duplex USS, CT angiography
Mx: lifestyle advise, statin, aspirin, optimise BP and DM, angioplasty or bypass grafting, amputation
Neuropathic ulceration
- features
- ix
- mx
Features: painless, over areas of abnormal pressure, often secondary to joint deformity in DM
Ix: blood glucose levels, ABPI normal, duplex USS, swab if ?Infection, X-ray if ?osteomyelitis, neuro foot exam
Mx: optimise DM control, improve diet, increase evercise, regular chiropody, abx for any infection, surgical debridement, amputation
What is Charcot’s foot?
Neuroarthropathy whereby a loss of joint sensation results in continual unnoticed trauma and deformity
Neuropathic ulcers can be seen alongside Charcot’s foot
Patients present with swelling, distortion, pain, and loss of function
