Dermatology Flashcards
List the layers of the epidermis and describe them
- Stratum corneum
Made up of flattened, dead cells which have lost their nuclei and are filled with bundled keratin and lipids - Stratum lucidum
Only in thick skin e.g. palms of hands and soles of feet - Stratum granulosum
Cells containing keratohyalin granules - Stratum spinosum
> Several layers of keratinocytes held together by desmosomes - Stratum basale
> Mitotically active and contains stem cells responsible for repopulating all layers of the epidermis
> Cells are attached to basement membrane by hemidesmosomes
Describe the structure of the skin
Epidermis
> Made up of keratinocyters
> Stratified squamous keratinised epithelium
Dermis
> Consists, of fibroblasts, type I collagen, elastin
> Has immune cells, blood vessels and nerves
Subcutis / hypodermis
> Consists of loose connective tissue and adipose tissue
> Contains blood & lymphatic vessels, cutaneous nerves and sweat glands
Describe the embryological origin of the skin
Epidermis is derived from ectoderm
5th week – skin of embryo is covered by simple cuboidal epithelium
7th week – single squamous layer (periderm) & basal layer
4th month – intermediate layer, containing several cell layers is interposed between basal cells & periderm
Early foetal period – epidermis is invaded by melanoblasts (cells of neural crest origin)
Hair – 3rd month as an epidermal proliferation into dermis
Cells of the epithelial root sheath proliferate to form a sebaceous gland bud
Sweat glands develop as downgrowths of epithelial cords into dermis
Describe the skin immune system
Langerhans cells are members of the dendritic cell family
> Reside in basal layers
Specialise in antigen presentation
> Acquire antigens in peripheral tissues, transport them to regional lymph nodes
> Present them to naive T cells and initiate adaptive immune response
Activated T cells initiate cytokine release cascade
Involved in antimicrobial immunity, skin immunosurveillance, induction hypersensitivity and pathogenesis of chronic inflammatory diseases of the skin
Describe the cells involved in the different types of skin sensation
Cutaneous receptors can be
Encapsulated nerve endings
> Meissner corpuscle
> > Situated immediately below epidermis
Well-represented on palmar surfaces of the fingers and lips
Sensitive to light touch
> Pacinian corpuscle
> Mechanoreceptors present in the deep dermis
> Sensitive to deep touch, rapid deformation of skin surface and around joints for position/proprioception
> Ruffini’s corpuscle
> Located in the dermis and are sensitive to deep pressure and stretching
Free nerve endings
> Merkel cells
> Located at the base of the epidermis
> Respond to sustained gentle and localised pressure
> Assess shape/edge
> Other free nerve endings – pain, temperature
Describe the adnexal structures found in the skin
Hair
> Originate from invaginations of epidermis which form follicles that contain mitotically active cells or matrix cells, as well as melanocytes that give hair its colour
> Follicles found in reticular layer of dermis
Nails
> Located on distal phalanx of each finger and toe
> Composed of plates of heavily compacted, highly keratinised epithelial cells that form the nail plate, which lies on the nail bed & occupies the space of the stratum corneum.
Describe the effects of UV light on the skin, and how the skin protects itself from this
Damaging effects of ultraviolet light on skin – direct cellular damage and alterations in immunological function
> Photoaging
> DNA damage
> P53 TSG mutated by DNA damage
> Implicated in development of melanoma and non-melanoma skin cancers
> Carcinogenesis
Keratinocytes and melanocytes work together to protect cells from UV DNA damage
> Melanin is a pigment produced by melanocytes in organelles called melanosomes, which are then transferred to neighbouring keratinocytes
> The melanosomes within the keratinocyte then form a cap over the nucleus, protecting DNA from UV damage
Chronic UV exposure leads to
> Loss of skin elasticity/fragility
> Abnormal pigmentation
> Haemorrhage of blood vessels
> Wrinkles & premature ageing
Describe how vitamin D is synthesised in the skin and the associations of vitamin D deficiency
During exposure to sunlight, solar UVB photons (290-315 nm) are absorbed by 7-dehydrocholesterol in the skin and converted to previtamin D3
Previtamin D3 undergoes transformation within the plasma membrane to active vitamin D3
Associations vitamin D deficiency
> Increased risk of common cancers
> Autoimmune diseases
> Infectious diseases
> Cardiovascular disease
Which classification is used to determine skin colour?
Fitzpatrick Skin Colour Types
1 - very fair
2 - fair
3 - medium
4 - olive
5 - brown
6 - black
Describe the pathophysiology of acne
Keratin and thick sebum block sebaceous gland
Androgenic increase during puberty leads to increased sebum production and viscosity
Proprionibacterium acnes inflammation
List the clinical features of acne, including signs and symptoms and distribution
Signs and symptoms
> Papules
Pustules
Comedones
Erythema
Nodules
Cysts
Scarring
Hyperpigmentation in darker skin types
Distribution
> Face
> Chest
> Back / shoulders
> Legs, scalp
List the subtypes of acne
> Papulopustular
Nodulocystic
Comedonal
Steroid-induced
Acne fulminans
Acne rosacea
Hidradenitis ( acne inversus)
Which system is used to grade the severity of acne?
Leeds Acne Grading System
> Grade 1-12
Describe the treatment of acne
Reduce plugging
> Topical retinoid
> Topical benzoyl peroxide
Reduce bacteria
> Topical antibiotics – erythromycin, clindamycin
> Oral antibiotics – tetracyclines, erythromycin
> Benzoyl peroxide reduces bacterial resistance
Reduce sebum production
> Hormones – anti-androgen i.e. Dianette / OCP
Side-effects
> Topical agents – irritant, burning, peeling, bleaching
> Oral antibiotics – gastro upset
> OCP – DVT risk
Dietary modification (controversial)
> Reduced dietary glycaemic load e.g. chocolate, milk
Describe the treatment of acne with oral isotretinoin, including standard course and side-effects
Oral retinoid licensed for severe acne vulgaris
> Isotretinoin is a concentrated form of vitamin A
> Reduces sebum, plugging and bacteria
Standard course
> 16 weeks - 1m/kg
> Remission in 80%
Side-effects
- Mild
> Dry lips, dry skin, nosebleeds
> Myalgia - Severe
> Deranged liver function
> Raised lipids
> Mood disturbance
> Teratogenicity
» Pregnancy prevention program
Expensive and consumes a lot of clinical time
Define eczema and its subtypes and pathophysiology
Inflammation in eczema is primarily due to inherited abnormalities in the skin - barrier defect
> Leads to increased permeability and reduces its antimicrobial function
- Atopic eczema
- Contact dermatitis
- Seborrhoeic dermatitis
- Varicose eczema
Describe atopic eczema including symptoms and complications
> Itchy inflammatory skin condition
> Associated with asthma, allergic rhinitis, conjunctivitis, hayfever (atopy)
> High IgE immunoglobulin antibody levels
> Genetic and immune aetiology
> Infant atopic eczema
> Itchy, occasionally vesicular – small blisters
> Secondary infections common
> 10-15% of infants affected
> Remission occurs in majority by 15 years
> Disproportionately affects face (perioral sparing)
> Occasionally aggravated by food i.e. milk
> Flexural folds often affected
> Diffuse margins
> Exaggerated skin markings (thickened)
> Superficial ulceration
> Relatively symmetrical
> Presentation on darker skin types
> More scaling and surface dryness
> More white-appearing scales
Describe the complications of atopic eczema
> Bacterial infections: staph aureus
> Viral infections
> > Molluscum – umbilicated papules
> Viral warts
> Eczema herpeticum (HSV virus in pre-existing eczema)
> Hospital admission + IV acyclovir
> Tiredness
> Growth reduction
> Psychological impact
Describe the management of atopic eczema
> Emollients
> Topical steroids
> Bandages
> Antihistamines
> Antibiotics / antivirals
> Education for parents / child
> Avoidance of exacerbating factors
> Rarely dietary avoidance/house dust mite
> Very severe systemic eczema
> Systemic drugs e.g. ciclosporin, methotrexate
> Newest biologic agent IL4/13 blocker - dupilumab
Describe seborrhoeic dermatitis
Chronic, scaly inflammatory condition
Often thought to be dandruff
Face, scalp and eyebrows, occasionally upper chest
Overgrowth of Pityrosporum ovale yeast
Can be worse in teenagers
Occasionally confused with facial psoriasis
Can be severe in HIV
Describe the management of seborrhoeic dermatitis
Scalp – medicated anti yeast shampoo i.e. antifungal ketoconazole: Nizoral, Selsun
Face – Anti-microbial, mild steroid i.e. hydrocortisone: Daktacort
Simple moisture
Systemic antifungals (rarely - itraconazole)
Often improves with UV/sunlight
Describe varicose or venous dermatitis
Underlying venous disease
Affects lower legs
Incompetence of deep perforating veins
Increased hydrostatic pressure
More hyperpigmentation in darker skin types
Describe the management of varicose or venous dermatitis
Emollients
Mild / moderate topical steroid
Compression bandaging / stockings
Consider early venous surgical intervention
Describe contact dermatitis including common allergens causing it
> Precipitated by exogenous agent
> Irritant – direct noxious effect on skin barrier
> Allergic – type IV hypersensitivity reaction (delayed T cell mediated)
> Common allergens
> Nickel – jewellery, zips, scissors, coins
> Chromate – cement, tanned leather
> Cobalt – pigment / dyes
> Colophony – glue, adhesive tape, plasters
> Fragrance – cosmetics, creams, soaps
Name a mild steroid and a very potent steroid
Very potent - dermovate aka clobetasol propionate 0.05%
Mild - hydrocortisone 1%
Describe psoriasis and its pathogenesis
> Chronic relapsing and remitting scaling skin disease
> May appear at any age and affect any part of the skin
> Prevalence 1.5-3%, age onset often 2 peaks 20-30y or 50-60y
> Cause
> > T cell mediated autoimmune disease
> > Abnormal infiltration of T cells
> Release of inflammatory cytokines including interferon, interleukins & TNF
> Increased keratinocyte proliferation
> > Environmental and genetic factors
>PSORS genes e.g. PSORS1, chromosome 6 and HLA – Cw0602 associated in certain subtypes
> Linked to
> Psoriatic arthritis
> Metabolic syndrome
> Liver disease / alcohol misuse
> Depression
List the different types of psoriasis
- Plaque
- Guttate (teardrop/raindrop)
- Pustular
- Erythrodermic (more inflammatory)
- Flexural / inverse
- Palmar / plantar pustulosis
- Psoriasis at sites of trauma/scars: Koebner phenomenon
> Not Auspitz: pinpoint bleeding after scratching psoriasis scale
Describe the features of psoriasis
Well-defined
Hyperkeratosis
>If significant, plaque appears white
Characteristic sites: nape of neck, back, extensor surfaces of elbows/knees
Symmetrical distribution
Nails: pitting
Describe the management of psoriasis
> Depends on severity, patient wishes, presence of arthropathy
> Scoring systems –
> DLQI (Disease Life Quality Index) - impact on patients
> PASI – psoriasis area severity index; clinician index
> PEST – psoriasis epidemiology scoring tool; marker of psoriatic arthritis
> 20% of patients with psoriasis develop arthritis
Treatments for psoriasis
> In order of increasing effectiveness (and toxicity)
> Topical creams and ointments
> Moisturisers – help reduce dryness, flaking
> Steroids – reduce autoimmune response, redness, itching, inflammation
> Salicylic acid – dissolve thick dead skin
> Slow down keratinocyte proliferation
> Vitamin D analogues
> Coal tar
> Dithranol
> Phototherapy light treatment
> Uses UV-B commonly – non-specific immunosuppressant therapy
» UV-A with psoralen photosensitiser
> Encourages vitamin D and reduces skin turnover
> Risks: short-term - burning; longer term - cancer
> Systemic drugs/immunosuppressants
> Immunosuppressants: methotrexate, ciclosporin
> Acitretin (oral retinoid / vitamin A)
> Dimethyl fumarate
> Apremilast: anti-phosphodiesterase inhibitor
> Biologic therapies
> Adalimumab – anti-TNF
> Ustekinumab – anti-IL12/23
List benign skin lesions
> Moles
> Fibroepithelial polyps aka skin tags
> Seborrheic warts / keratosis
> Elderly patients
> Raised, rough lesions
> Found in back commonly
> Well-defined
> Cauliflower like appearance
> Viral warts (verrucae)
> Vascular spots
Describe the pathogenesis of skin cancer
At least 2 distinct pathways interact or converge to cause skin cancer
Direct action of UV on target cells (keratinocytes) for neoplastic transformation via DNA damage
Effects of UV on the host’s immune system – immune suppressant (indirect effect)
Describe the characteristics of basal cell carcinoma
Most common type of skin cancer
Process of creating new skin cells is controlled by a basal cell’s DNA
PTCH gene mutation may predispose (rare)
Commonly found on head and neck / UV exposed sites
Rarely metastasises or kills – unless neglected/untreated
Appearance
> Pearly rolled margin with a shoulder
> Dipped centre which may ulcerate
> Telangiectasia – lightning bolt blood vessels
Describe the different subtypes of basal cell carcinoma
Nodular
> Most common
> Raised lesion - shiny “pearly”
> Telangiectasia
> Often ulcerated centrally
Superficial
> Tiny thread like rolled shoulder
> Lightning bolt blood vessels
> Crusting - suggests ulceration
> Flatter
> Often on neglected areas i.e. back
Pigmented
> May be confused with melanoma or seborrhoeic warts
> Same features just pigmented - more melanin deposited in basal cell
Morphoeic / sclerotic
> Barely visible, usually extends further below surface
Describe the treatment of basal cell carcinoma
> Gold standard – surgical excision 3-4mm margin
> Curettage and cautery
> Circular scalpel used to scrape away damaged tissue
> Usually used in diagnostics
> Cryotherapy
> If surgery not suitable
> High recurrence rate
> Photodynamic therapy
> Immune based treatment
> Apply a photosensitiser which provokes an immune reaction when you shine LED light on it
> Preferentially taken up by tumour cells – high recurrence rate – painful (burns skin)
> Topical imiquimod / 5-fluorouracil cream
> Immune triggers to provoke immune system to kill cancer cells
> Inflammatory burn reaction in area applied to
> Mohs micrographic surgery
> Pathology technician ensures all tumour is removed (histological checking)
> Saucer-like sections taken around tumour
> Time-consuming, only used when tissue sparing would be useful e.g. morphoeic tumour where margin is unclear
Describe the characteristics of squamous cell carcinoma and its pre-malignant variants
May occur in normal skin or skin that has been injured (burns) or chronically inflamed – damaged skin (UV or other)
Originates from keratinocytes
Pre-malignant variants
> Actinic keratoses
» Patches of skin damage
> Bowen’s disease
» SCC in situ
Most SCC occur on skin that is regularly exposed to sunlight or other ultraviolet radiation
Risk of metastasis from a high-risk SCC is 10-30%
High risk sites
> Ears, lips
Appearance
> Slight central dip
> Centre heavily keratinised – crust
> Tumour lumps
> On very damaged skin i.e. skin damage
Describe the treatment of squamous cell carcinoma
Gold standard – surgical excision 4mm margin
Curettage and cautery (frail & elderly)
Pre-malignant: squamous cell carcinoma in situ
> Topical imiquimod / 5-fluorouracil cream
> Cryotherapy
> Photodynamic therapy – also used in Bowen’s disease
Describe the characteristics of malignant melanoma
Malignant tumour of melanocytes
Higher risk of metastasis and recurrence
Most common in skin but can be found in bowel or eye
DNA damage – mainly UV, rarely genetic
Radial growth phase then vertical growth downwards (more aggressive)
Depth of presentation determines prognosis
Spread via lymphatics (also via blood vessels)
Goes into subcutaneous fat, spreads to distant sites i.e. lungs and liver via lymph nodes
Describe the subtypes of melanoma
- Superficial spreading melanoma
- Nodular melanoma
- Acral melanoma
> Poorer prognosis
> Found late, quite hidden
> Very dark, satellite drifting
> More common in darker skin types - Subungal melanoma
- Amelanotic melanoma
> Red nodule (very rare) - does not look like melanoma
Describe the premalignant precursors to melanoma
- Lentigo maligna
> Premalignant precursor
> Usually unique to very sun damaged head and neck skin (usually elderly) - Lentigo maligna melanoma
- Melanoma in situ
Why are Breslow thickness and Clark level used in the diagnosis of melanoma?
Breslow thickness - how deeply tumour cells have invaded
Measured from most superficial aspect of granular cell layer (or from base of ulcer) to deepest point of invasion
Important for prognosis
> Also mitotic rate, ulceration & extent of metastatic disease
> Lymphatic or vascular invasion, perineural infiltration
> Family history
> Sun exposure, tanning beds
> Molecular mutational gene expression (immunogenetics)
Clark level - staging system that describes the depth of melanoma as it grows in the skin
Describe the treatment of melanoma
Surgical excision
> Breslow < 1mm : 1cm margin
> Breslow > 1 mm : 2 cm margin
Immunotherapy – ipilimumab, nivolumab
Immune checkpoint / MEK inhibitors – trametinib
Biologic antibodies – BRAF genetic defects (debrafanib) involved in predisposition to melanoma
> Can reduce risk of recurrence
Imaging / scanning CT / MRI / PET
> Staging from head to pelvis, brain scan
Long-term follow up up to 5 years – to look for metastatic spread
Assessment for lymph node or organ spread
> Clinically, US or CT
Genetic testing in families, multiple primary melanomas
> Multiple melanomas at a young age
> CKDN2 genetics
Describe cutaneous tumour syndromes
Gorlin’s syndrome
> Multiple BCCs, jaw cysts, risk of breast cancer
Brook Spiegler syndrome
> Multiple BCCs, trichoepitheliomas
Gardner syndrome
> Soft tissue tumours, polyps, bowel cancer
Cowden’s syndrome
> Multiple hamartomas (benign or malignant), thyroid, breast cancer
List drugs which cause acne
- Corticosteroids
- Lithium
- Vitamin B12
- Thyroid hormones
- Iodine-containing drugs
- Antibiotics e.g. tetracyclines, streptomycin
Describe skin changes associated with thyroid disease
Dry skin – hypothyroidism
Thyroid dermopathy – pretibial myxoedema
> Grave’s disease
> Velvety texture, exaggerated skin markings
Thyroid acropachy – Grave’s disease
> Soft tissue swelling of distal digits and around nail resulting in bowing or “clubbing”
Describe skin changes associated with diabetes
Necrobiosis lipoidica
> Waxy yellow appearance surrounded by erythema
> Bilateral appearance on shins
> Occasionally ulcerates and scars
Diabetic dermopathy
> Inflammatory papules and patches
> Mild itch healing with hyperpigmentation
> Affects lower legs
Scleredema
> Woody inflammatory infiltrate in skin
> Warm to touch – cannot squeeze skin due to lack of elasticity
> Often affects upper back
Leg ulcers
> Pressure calluses
> Venous ulcers
Granuloma annulare
> Round plaques
> Granulomatous histological appearance
> Appear on dorsum of hands & feet usually
Describe skin changes associated with steroid excess
- Acne
- Striae
- Erythema
- Gynaecomastia
Describe skin changes associated with steroid insufficiency
Hyperpigmentation - Addison’s disease
> Mucosal surfaces
> Bronzing of skin
> Acanthosis nigricans
Describe skin changes associated with excess sex hormones and causes of this
Testosterone
> Symptoms
> Acne
> Hirsutism
> Causes
> Polycystic ovarian syndrome
> Testicular tumours
> Testosterone drug therapy
Progesterone
> Symptoms
> Acne
> Dermatitis
> Causes
> Congenital adrenal hyperplasia
> Contraceptive treatment
Describe the presentation of Cushing’s disease
Excessive production of cortisol in the body leads to
> Increased central adiposity
Moon faces and buffalo hump
Global skin atrophy, epidermal and dermal components
Striae on abdominal flanks, arms, thighs
Purpura with minor trauma – reduced connective tissue
Describe the skin syndrome associated with islet cell tumours of the pancreas
Necrolytic migratory erythema
Aka glucagonoma syndrome
Very rare
Erythematous, scaly plaques on acral, intertriginous and periorificial areas
Association with islet cell tumour of the pancreas
Other signs
> Hyperglycaemia
> Diarrhoea
> Weight loss
> Glossitis
Describe the characteristics of erythema gyratum repens
Rare
Very distinctive skin disease
Reddened concentric bands whorled woodgrain pattern
Severe pruritus and peripheral eosinophilia
Strong association with lung cancer
Also breast, cervical, GI cancers
Treatment of underlying malignancy treats skin disease
Describe the characteristics and types of acanthosis nigricans
Smooth, velvet-like hyperkeratotic plaques in intertriginous areas (groin, axillae, neck)
3 types
> Type I
> Associated with malignancy
> Adenocarcinoma, especially gastric
> Sudden onset and more extensive
> Type II
> Familial type – AD
> Very rare
> Appears at birth – no malignancy
> Type III
> Associated with obesity and insulin resistance
> Most common type
Describe Sweet’s syndrome
Affects head and neck
Juicy, infiltrated, red, inflammatory (sometimes ulcerated) plaques and nodules
Associated with haematological malignancy
Name the skin lesion associated with an umbilical tumour
Sister Mary Joseph Nodule
Describe the conditions arising from different types of vitamin B deficiency
B6 – pyridoxine
>Dermatitis
B12 – cobalamin
>Angular cheilitis
B3 – niacin
>Pellagra – dementia, dermatitis, diarrhoea, death
Describe the skin condition associated with zinc deficiency
Acrodermatitis enteropathica
> Inherited or acquired
> Results in pustules, bullae, scaling (acral and perioral distribution)
> Inherited – mutation in SLC39A – encodes an intestinal zinc transporter
> In infants – deficiency can follow breastfeeding when breastmilk contains low levels of zinc
> In adults, disease can occur after total parenteral nutrition without zinc supplementation
> > Alcoholism
Malabsorption states
Inflammatory bowel disease
Bowel surgery
Describe the condition caused by vitamin C deficiency
Scurvy
> Punctate purpura / bruising
> Corkscrew spiral curly hairs
> Patchy hyperpigmentation
> Dry skin
> Dry hair
> Non-healing wounds
> Inflamed gums
Describe the causes, characteristics and distribution of erythema nodosum
Causes
> Streptococcal infection
Pregnancy / oral contraceptive
Sarcoidosis
Drug-induced
Bacterial / viral infection
Others
Distribution – lower legs
Deep red/purple bruise-like discolouration
Patient will be extremely uncomfortable and cannot tolerate touch
Describe the causes, characteristics and distribution of pyoderma gangrenosum
Deep ulcer with purple overhanging edge
Treating underlying disorder leads to improvement
50% idiopathic
Autoimmune – responds to immunosuppression
Linked to
> Inflammatory Bowel disease
> Crohn’s disease
> Ulcerative colitis
> Rheumatoid arthritis
> Myeloma
Name the condition which causes autoimmune patchy hair loss
Alopecia areata
List conditions that cause hair thinning
B12 deficiency
Iron deficiency
Lupus
Hypothyroidism
Which conditions cause nail fold telangiectasia?
Scleroderma and dermatomyositis
List types of skin drug reactions
Maculopapular
> Areas of flat colour change with small papules
Urticaria
> Nettle like rash
Morbilliform
> Measle like rash
Papulosquamous
> Raised areas with dry flakiness
Phototoxic
> Exposed skin in response to UV light
> Areas covered from sun spared – T shirt distribution
> Can be caused by bendroflumethiazide or quinine
> Chronic phototoxic rash
Pustular
Lichenoid (like lichen planus)
Fixed drug rash
Bullous
Itch – no rash
List common drugs that can cause a rash
Antibiotics e.g. penicillins, trimethoprim
NSAIDs: urticaria, angioedema
Chemotherapeutic agents
Pyschotropic – chlorpromazine, alanzapine, risperidone
Anti-epileptic – lamotrigine, carbamazepine
Cardiac drugs – BB, ACE, anticoagulant
Describe vasculitis, including triggers and complications
Inflammation of blood vessels
Triggers
> Infection
> Drugs
> Connective tissue disease e.g. RA, SLE
Investigations – systemic vasculitis
> Renal BP
> Urinalysis
Localised, not rapidly progressive
Less unwell than in meningococcal rash
Describe a drug-induced psoriasiform rash
Psorasis-like
Well demarcated pink erythema with scale
Sudden onset, no family history
Lithium, beta blockers
Which clues point towards a fixed drug reaction?
Same area, same drug, e.g. paracetamol
Describe Steven Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN)
Steven Johnson Syndrome (SJS)
> Can be drug induced or viral (HSV)
Causes blistering and ulceration around mouth and mucosal surfaces
Up to 30% skin involvement
Toxic epidermal necrolysis (TEN)
> Dermatological emergency
> Majority drug-induced
Disease spectrum from SJS to TEN
> Most severe mucous membrane involvement
> Stop suspect drug
> Top of the full thickness of the epidermis sloughs off
In-patient management
> Derm
> ITU
> Burns
> Analgesia
> Fluid balance
SCORTEN severity scale
> Special mattress, sheets
Infection control, prophylaxis
Non-adherent dressings
Urology, gynae, ophthalmology inputs
> 50% mortality rate
Describe bullous pemphigoid and pemphigus vulgaris
Bullous pemphigoid
> Rare autoimmune skin condition that affects mainly older people
> Starts with an itchy raised rash
> As it develops large tense fluid-filled blisters can form
> Tend to be stable as lesions are subepidermal and unlikely to erode
> Lesions most commonly on flexures
Pemphigus vulgaris
> Mucosal erosions are an early sign often preceding the cutaneous
> Cutaneous lesions typically affect chest, back and scalp
> Erythematous macules appear first later evolving into flaccid blisters
> Blisters are intraepidermal so are weak and rupture easily resulting in painful erosions
Describe staphylococcal scalded skin syndrome
Flexural folds first
Younger patients
Toxin from Staph aureus infection causes rash
Treatment is antibiotics for underlying infection
Describe erythema multiforme
> Self-limiting allergic reaction
HSV, EBV, occasionally drug
No or mild prodrome
Target lesions
Never to TEN
List the different types of immunobullous disorders
- Bullous pemphigoid
- ## Pemphigus vulgaris
Describe dermatitis herpetiformis
Skin rash associated with coeliac disease
Tiny vesicle blisters in very distinctive sites
Treatment
> Topical steroids
> Gluten free diet
> Oral dapsone
Describe the treatments for immunobullous disorders
Reduce autoimmune reaction – topical / oral corticosteroids
Steroid sparing agents e.g. azathioprine, anti-inflammatories, tetracyclines
Burst any blisters
Dressing and infection control
Check for oral / mucosal involvement
Consider screen for underlying malignancy
Describe the clinical features of urticaria
Itchy, wheals (hives)
Lesions last <24 h
Non-scarring, common skin disorder to present to A&E
Acute < 6 weeks, chronic > 6 weeks
Can have angioedema but no anaphylaxis
Describe the pathophysiology of urticaria and its treatments
Immune-mediated
> Type 1 IgE response
Non-immune mediated
> Direct mast cell degranulation e.g. opiates, antibiotics, contrast media, NSAIDs
Investigations
> Often none
> Not normally allergy driven
> Don’t do allergy testing, no patch testing
Treatment
> Antihistamines
> Steroids
> Phototherapy
> Immunosuppression
> Omalizumab
Causes
> Unknown
> Viral infections
> Medication – NSAIDs, aspirin, ACE
> Foods & food additives
> Parasitic infections
> Physical stimulants – colds, pressure, solar, cholinergic, aquagenic
Describe erythroderma, including clinical features, causes and management
> 80-90% involvement, erythema
- Associated with exfoliation – skin peeling off in scales or layers
- Intense itch
- Temperature dysregulation
- Fluid loss
- Oedema
Causes
> Psoriasis
> Eczema
> Drug reaction
> Cutaneous lymphoma
> Others
Treatment
> Treat underlying skin disorder
> Supportive
> Fluid / temperature balance important
Describe dermatomyositis
Rare disease that causes muscle weakness and skin rash
Symptoms
> Red or purple rash on sun exposed skin and eyelids
> Calcium deposits under the skin
> Muscle weakness
> Trouble talking or swallowing
Describe acute generalised exanthematous pustulosis (AGEP)
Acute febrile pustular eruption on erythematous background
> 90% drug induced (other causes – HS to mercury, enteroviral infection)
Short time between drug and eruption <2- 4/7
Clinical features
- High fever, usually onset same day as rash
- Numerous small, non-follicular, sterile pustules arising within large areas of oedematous erythema +/- burning, pruritus
- Lesions start face and arimpits & groins then disseminate over a few hours
Drugs causing AGEP: “BAD FACE”-mostly penicillins and macrolides
- Bactrim
- Antibiotics and antifungals(Vanc/Penicillins/Cephalosporins/Macrolides/terbinafine/itraconazole)
- Diltiazem
- Frusemide
- Allopurinol/antimalarials
- Cimetidine
- Epileptics
Treatment
> Stop offending drug
> Supportive – rest, bland emollients, topical steroids
List the different types of inflammatory skin rashes
Psoriaform e.g. psoriasis
> Histology
» Hyperkeratosis: thickened keratin layer
» Parakeratosis: nuclei within keratin layer
» Acanthosis: thickened epidermis
Spongiotic e.g. eczema
> Space between epidermal keratinocytes due to increase in fluid between cells
> Scattering of eosinophils in dermis
Lichenoid e.g. Lichen planus, lupus
Vesiculobullous e.g. pemphigus
Granulomatous e.g. Tuberculosis, sarcoidosis
Vasculopathic e.g. Leukocytoclastic vasculitis
Drug rashes
