Common skin disorders

What is dry skin

• lack of water in stratum corneum

• epidermis lose flexibility → roughness, fissures and inflammation

• scaling and flakiness of skin

Why is brittle stratum corneum at risk in dry skin?

• risk of stress fractures → further impairs barrier function of skin

Causes of dry skin

• Humidity

• soaps and deterdegents

• UV radiation

• Natural moisturising factor

How does humidity cause dry skin

• balance between desquamation and production of new keratinocytes disturbed by humidity (reduced in cold weather)

• reduce the water content of skin to less than 10% and

• decreases the activity of the protease enzymes so corneodesmosomes are not degraded efficiently

• accumulation of corneocytes on skin surface (causes flakiness)

How do soaps and detergents cause dry skin

• reduce activity of protease enzymes

• disrupt structure of intercellular lipids → affects barrier function of stratum corneum so decrease level of hydration

How does UV radiation cause dry skin

• irradiation impairs stratum corneum barrier

• increased water loss bc interfere w/ structure of intercellular lipid matrix

How does ageing cause dry skin

• stratum corneum becomes thinner

• reduction in natural moisturising factor (NMP)

What is difference and similarity between eczema and dermatitis

• endogenous cause - eczema

• external cause - dermatitis

• both = inflammatory response of skin

How does do both eczema and dermatitis present on the skin

• dry cracked inflamed skin

• often in elbow/knee creases

• in adults: thickened plaques may affect hands and face

What unique symptoms may appear in people w/ darker skin tones

• dark circles under eyes

• papular eczema (small bumps on torso, arms, or legs),

• bumps around hair follicles

What does atopy mean in relation to eczema and what is the atopic march

• genetic predisposition to develop allergic symptoms that affect skin gut sinuses and airways

• atopic march → progression of allergic symptoms, starting with skin symptoms, followed by food allergies, allergic rhinitis, and then asthma.

What are the diagnostic criteria for atopic eczema

• itchy skin condition within the past 12 months and three or more of the following:

  • Onset before age 2

  • History of flexural involvement

  • History of generally dry skin

  • Personal or family history of atopic disease

• if skin not itchy then unlikely to be eczema

Primary suspected cause of AE (atopic eczema)

• combination of altered skin barrier function and immune dysregulation

What is the outside in theory of AE

• genetic susceptibility leads to defective skin barrier

• allowing allergens/irritants to provoke inflammatory response

• mutations in filaggrin gene (FLG) causes ichthyosis and predispose individuals to AE

What is filaggrin and its role in skin health

• protein needed for intact skin barrier

• contributes to NMF → help to maintain skin hydration

What is the inside-out theory for AE

• immune dysfunction lead to local inflammation so defective skin barrier

• theory proposed bc not everyone w/ FLG mutations developed AE

How does scratching affect AE

• damages the skin

• releases inflammatory cytokines that intensify scratch itch cycle

• increase skin permeability

What are emollients and how do they work

• e.g. ointments/creams

• form protective barrier over skin

  • prevents water loss

  • protect against allergens and irritants

What is an alpha-hydroxyacid?

• e.g. lactic acid

• described as keratolytic BUT do not dissolve keratin

• enhance desquamation

What is the recommended treatment for AE and how to use it

• emollients

• used frequently after washing or bathing

• applied to whole skin not just affected areas

• continue to use in absence of symptoms

How should emollients and topical steroids be used together in treating skin conditions

• used together

• but do not apply at same time → wait 30 mins after applying emollient before applying steroid

General advice to patients on use of emollients

• use emollients to wash and bath - avoid soaps and detergents

• frequent use even when skin appears normal

• after showering/bathing pat the skin dry and immediately apply emollient

• dot emollient onto skin and spread in downward direction

• pump dispensers are best bc give specific amount of emollient, if using tubs then DO NOT use hands - risk of contamination

What are some examples of mild potency steroid and when to use

• hydrocortisone acetate at a concentration of 0.5, 0.1, 1 and 2.5%

• mild eczema

• for facial genital or axilla eczema

What are some examples of moderate potency steroid and when to use

• Clobetasone 0.05%

• Betamethasone valerate 0.025%

• moderate eczema

What are some examples of potent steroid

• Beclomethasone dipropionate 0.025%

• Hydrocortisone butyrate 0.1%

• severe eczema

What are some examples of very potent steriod

• Clobetasol 0.05%

• Diflucortolone valerate 0.3%

What does potency depend on

• steroid molecule itself

• its physiochemical properties (e.g., solubility, lipophilicity)

• formulation of vehicle

• interact to influence potentcy

How do topical steroids work

• binding with a steroid receptor on the cellular surface

• so modulates transcription of genes responsible for inflammation and other proteins that have vasodilatory effects

What effects do topical corticosteroids have

• anti-inflammatory

• immunosuppressive

• anti-proliferative

• vasoconstrictor

How are topical steroids anti-inflammatory

• bind to glucocorticoid receptor

• suppression of pro-inflammatory agents like prostaglandins and leukotrienes via arachidonic acid pathway

• decrease pop of polymorphonuclear leucocytes and monocytes at site of inflammation

How are topical steroids immunosuppressive

• reduce number of Langerhans cells present and APC function

How are topical steroids vasconstrictors

• may occur through blockage of vasodilators like histamine and bradykinins

How are topical steroids anti-proliferative

• reduction in mitosis in epidermis

• so reduction in basal cell layer thickness

• keratinocyte proliferation and growth factors are reduced

• dermis = atrophy due to inhibition of fibroblast proliferation and reduced synthesis of collagen and glycosaminoglycans

• overall effect is reduction in volume of dermis which is hallmark of topical steroid induced skin atrophy

Symptoms of infected AE

• Red, “angry”, weepy with yellow-coloured crusts

• Pustules and papules

• Fever, malaise

• Skin that is itchy, hot and sore

What is is the treatment option for infected Ae

• oral antibiotics

• flucloxacillin

• restricted use = 2 weeks

What are the 2 currently available Calcineurin Inhibitors (CI)

• Tacrolimus (Protopic®)

• Pimecrolimus (Elidel®)

MoA for CI

• macrolactams w/ immunosuppressive effects

• CI bind to intracellular immunophilins

• complex binds to calcineurin → preventing T cell activation and release of inflammatory cytokines (IL-2, IL-3, IL-4, IL-12, TNF-α, and IFN-γ) and mediators from mast cells

Who and what are the CI licensed for

• Protopic® 0.03% (maintenance therapy to prevent flares) and Elidel® cream from age 2

• Protopic® 0.1% from age 16

When should CI be used in eczema treatment

• second line for moderate to severe

• 1st line being topical steroids

Who can prescribe CI

• dermatologists or GP w/ special dermatology experience

What is wet wrap therapy

• use of emollient under wrapping gives lasting emollient effect

• used in primary and secondary care

What are some oral therapies for eczema and when can they be used

• Ciclosporin

• Azathioprine

• Oral corticosteroids

• Mycophenolic mofetil

• Methotrexate

• short term in primary care for severe flares

What benefits does phototherapy have for patients with AE

• immunosuppressive effects, by altering cytokine production

• causing apoptosis of infiltrating T-cells

• inhibiting antigen-presenting function of Langerhans cells

• induces epidermal hyperplasia → limits eczematous reactions and entry of allergens and prevents skin colonisation

What are the different types of phototherapy and how is it used

• narrow-band UVB

• broad-band UVB

• administered 3-5 times a week for up to 3 months

• can be used in conjunction w/ topical therapies and 2nd line if pt not respond to topical treatment

Describe biologic agents

• management of psoriasis

• Dupilumab licensed for use of moderate to severe AE

What is irritant contact dermatitis (derm)

• chemical or physical agents damage skin quicker than it can repair itself

• chemicals like solvents/detergent/polishes

• can occur in young children who dribble and nappy rash

• hands = most commonly affected area

Symptoms of irritant contact derm

• presents at site of contact w/ irritant

• well-demarcated (organised - kind of) inflamed area of skin

• may look blistered or scaled and very pruritic (itchy)

Management of irritant contact derm

• removal of irritant

• can take up to 12 weeks for symptoms to resolve

• liberal use of emollients and topical steroid use to control symptoms which do not resolve with use of emollients

What is allergic contact dermatitis

• specific allergen contact w/ skin

• delayed reaction sometimes 48-72 hrs after

• allergens e.g. nickel → watch, jewellery etc

• condition may present at other sites like eyelids, genitals bc of transmission from fingers

Symptoms of allergic contact dermatitis

• pruritic papules and vesicles on an erythematous base

• The site of inflammation = clue to the potential allergen

Management of allergic contact derm

• emollients and topical steroids

• if cant find allergen then refer to secondary care for patch testing