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