Beauty is skin deep Flashcards
What are the psychosocial impacts of having a skin condition?
Poor quality of life Stigmatism Decreased sense of body image Lower self-esteem Avoid exposing skin Anxiety Withdraw from social interactions Sexual and relationship issues Shame and disgust about appearance Depression OCD – scratching, compulsive hand washing, hair pulling, skin picking Stress itch cycle
What are common triggers for skin conditions?
Environmental factors or allergens Cold and dry weather Dampness House dust mites Pet fur Pollen Moulds Cows’ milk Eggs Peanuts Soya or wheat Wool and synthetic fabrics
What is eczema?
A common, itchy skin disease characterised by erythema and vesicle formation, which may lead to weeping and crusting. It is endogenous (outside agents do not play a primary role).
Usually develops in early childhood. Occurs in atopic individuals i.e. those who have capacity to hyper-react to common environmental factors.
Associated with asthma and hay fever.
What is the atopic march?
The natural history or typical progression of allergic diseases that often begin early in life. These include atopic dermatitis (eczema), food allergy, allergic rhinitis (hay fever) and asthma.
What are the causes of eczema?
Alterations in their skin barriers, and overly reactive inflammatory and allergic responses.
Environment factors include contact with soaps, detergents, and any other chemicals applied to skin, exposure to allergens, and infection with certain bacteria and viruses.
Genetics - gene that makes skin barrier more susceptible to infection and allows irritating substances/particles to enter the skin, causing inflammation and itching.
What is the pathophysiology of eczema?
Genetic alterations such as null mutations in the fillagrin gene. Fillagrin plays a crucial role in skin barrier integrity: it cross-links keratin filaments into tight bundles and moisturises the stratum corneum through natural moisturising factors.
Disturbed epidermal barrier, caused by mutations in fillagrin, leads to dry skin as a consequence of a high transepidermal water loss on the one hand and to enhance penetration of irritative substances and allergens into the skin on the other side.
Other genetic alterations include:
- Homerin involved in epidermal differentiation complex
- Mutations in IgE receptor, leading to Th2 prevalence and Th2 cells induce the production of IgE antibodies by plasma cells.
How do acute and chronic stages of atopic eczema differ?
Th2 skewed immune response is predominant in the acute phase, but switched to a more Th-1 like profile in chronic profile. Both acute and chronic phases of AE contain significant amount of Th-2 creatine kinase compared with normal skin.
What are the risk factors for eczema?
Genetic
Diet – e.g. milk and eggs
Environmental factors associated with development and urbanisation
Exacerbating factors – e.g. heat, humidity, drying out of skin, contact with wool
Association between AE and various congenital conditions
What are the potential differential diagnoses for eczema?
Seborrheic dermatitis - characteristic greasy scale not pruritic; affects cheeks on face, scalp, extremities, trunk. Clinical examination allows differentiation
Irritant contact dermatitis - common in nappy area, face and extensor surfaces in children resulting from exposure to irritating substance. Less pruritic than eczema. Elimination of irritant = clinical improvement
Patch testing = +ve for relevant irritant
What are the clinical features of eczema?
Chronic, relapsing course Pruritis Redness Swelling – papules or oedema Blisters Lichenification (from continued scratching) Dry skin Abnormal sweating Prominent skin creases Fissures or splits – especially on palms or soles Flexural pattern – in latter stages
What are the investigations for eczema?
Serum IgE levels - elevated
Skin prick tests - positive to common allergens
Radioallergosorbent testing (RAST)
Skin biopsy – chronic inflammation involving lymphocytes, mast cells, histiocytes, eosinophil degranulation
White dermographism – rubbing skin elicits a simple white linear streak along the site
How to educate a patient with eczema about their condition?
Fully inform the patient and child about disease course and effects of treatment.
No therapy can completely prevent relapse.
Avoidance of triggers - wearing cotton underclothes instead of wool, the avoidance of heat, reducing exposure to house mites, and lightly bandaging limbs at night.
A milk free diet is advised by some but care must be taken to ensure malnutrition doesn’t occur.
May use an egg-free diet in infants with suspected egg allergy who have positive specific IgE to eggs.
What is first-line treatment for eczema?
- Emollients – combats dry skin (soaps, bath, shower, topical)
- Topical corticosteroids – used to suppress inflammatory response. Common to use a potent steroid and then reduce. Alongside emollients. Usually once daily.
- Antibiotics: control of staphylococcal overgrowth e.g. a seven day course of flucloxacillin or erythromycin if signs of moderate to severe infection
- Antihistamines: to combat itching
- Pimecrolimus, topical cream
- Topical tacrolimus: moderate to severe AE that is not controlled by topical corticosteroids
- Cotton bandages and dressings: wet wrapping with emollient and sometimes topical steroid at night-time
- Coal tar and ichthammol: Most suitable for chronic lichenified eczema. May be applied as crude coal tar, tar-containing creams or in combination with zinc paste either as a cream or a bandage.
- Salicylic acid – may be used in combination preparations.
What is second-line treatment for eczema?
- Phototherapy – UV or PUVA (psoralen and UVA): Psoralens work by photosensitising skin. Can cause burning or increased risk of skin cancer.
- Immunosuppressants
Oral corticosteroids, e.g. prednisolone 30mg daily for 1 week. Immunosuppressive drugs e.g. azathioprine, ciclosporin used only in secondary care setting - Alitretinoin: for adults with severe chronic hand eczema that has not responded to potent topical corticosteroids. Closely monitored.
What are the complications of eczema?
Psychological stress Systemic SE of topical corticosteroids Malignancy related to use of topical calcineurin inhibitors Systemic SE of ciclosporin Bacterial cutaneous infection and colonisation Systemic SE of methotrexate Systemic SE of azathioprine Eczema herpeticum
What is Psoriasis?
A common chronic skin disease characterised by cutaneous inflammation and epidermal hyperproliferation – lesions appear on any part of the skin, particularly the scalp, lumbosacral area, and over the extensor aspect of the knees and elbows.
How does Psoriasis present?
Well defined, raised, erythematous and scaly lesions which are “salmon pink” or “full rich red” in colour; surface silvery scale which may be easily removed often leading to pin-point capillary bleeding; they may or may not itch but usually not a prominent feature.
How does acute and chronic psoriasis differ>
Acute disease may manifest as inflammation and erythema while chronic lesions present as typical plaques. In most of the patients, psoriasis presents in a chronic course with periods of remission.
What are the causes of psoriasis?
Genetic
Infection – streptococcal pharyngitis, AIDS/HIV, Reiter’s syndrome
Stress
Trauma
Drugs
Treatment methods of psoriasis e.g. anthralin and phototherapy
Smoking and alcohol
