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
