Dermatology - Inflammatory skin conditions Flashcards
What is eczema?
Eczema (or dermatitis) is an inflammatory skin condition characterised by papules and vesicles on an erythematous base.
Atopic eczema is the most common type - usually develops by early childhood and resolves during teenage years (but may recur).
Approximately 20% prevalence in <12 year olds in the UK.
What causes eczema?
The aetiology of eczema is not fully understood, but a positive family history of atopy (e.g. eczema, asthma, allergic rhinitis) is often present.
A primary genetic defect in skin barrier function (i.e. loss of function variants of the protein filaggrin) appears to underlie atopic eczema.
Exacerbating factors such as infections, allergens (e.g. chemicals, food, dust, pet fur), sweating, heat and severe stress may play a role.
How does eczema present?
Commonly presents as itchy, erythematous dry scaly patches. These are more common on the face and extensor aspects of limbs in infants, and flexor aspects in children and adults. Acute lesions are erythematous, vesicular and weepy (exudative).
Chronic scratching/ rubbing can lead to excoriations and lichenification.
Patients may show nail pitting and ridging of the nails.
What criteria are required to diagnose eczema?
An itchy skin condition in the last 12 months, plus three or more of:
- onset below the age of 2 years
- history of flexural involvement *
- history of generally dry skin
- personal history of other atopic disease
- visible flexural dermatitis*
- or extensor aspects in infants under 18 months
How should eczema be treated?
- General measures - avoid known exacerbating agents, frequent emollients +/- bandages and bath oil/soap substitute
- Topical therapies – topical steroids for flare-ups; topical
immunomodulators (e.g. tacrolimus, pimecrolimus) can be
used as steroid-sparing agents - Oral therapies - antihistamines for symptomatic relief, antibiotics
(e.g. flucloxacillin) for secondary bacterial infections, and
antivirals (e.g. aciclovir) for secondary herpes infection - Phototherapy and immunosuppressants (e.g. oral prednisolone, azathioprine, ciclosporin) for severe non- responsive cases
How should steroids be used to treat eczema?
Topical steroids should be used for flare ups. The weakest steroid cream should be used to control the patients symtoms:
- Mild = hydrocortisone
- Moderate = betamethasone or clobetasone butyrate
- Potent = fluticasone propionate or betamethasone valerate
- Very potent = clobetasol proprionate
The finger tip rule:
- 1 finger tip unit (FTU) = 0.5g, should be sufficient to treat a skin area about twice that of the flat of an adult hand (e.g. hand and fingers is 1 FTU, whereas an entire leg and foot is 8 FTU)
What are the complications of eczema?
Secondary bacterial infection (crusted weepy lesions)
Secondary viral infection - molluscum contagiosum (pearly papules with central umbilication), viral warts and eczema herpeticum.
What is acne vulgaris?
Acne vulgaris is a common skin disorder which usually occurs in adolescence. It typically affects the face, neck and upper trunk and is characterised by the obstruction of the pilosebaceous follicle with keratin plugs which results in comedones, inflammation and pustules.
What are the key epidemiological features of acne?
Affects around 80-90% of teenagers, 60% of whom seek medical advice.
Acne may also persist beyond adolescence, with 10-15% of females and 5% of males over 25 years old being affected.
What is the pathophysiology of acne?
Pathophysiology is multifactorial:
- follicular epidermal hyperproliferation resulting in the formation of a keratin plug. This in turn causes obstruction of the pilosebaceous follicle. Activity of sebaceous glands may be controlled by androgen, although levels are often normal in patients with acne
- colonisation by the anaerobic bacterium Propionibacterium acnes
- inflammation
What are the features of acne?
Acne is a disease of the pilosebaceous unit. Several different types of acne lesions are usually seen in each patient.
Comedones are due to a dilated sebaceous follicle
- if the top is closed a whitehead is seen
- if the top opens a blackhead forms
Inflammatory lesions form when the follicle bursts releasing irritants
- papules
- pustules
An excessive inflammatory response may result in:
- nodules
- cysts
This sequence of events can ultimately cause scarring
- ice-pick scars
- hypertrophic scars
In contrast, drug-induced acne is often monomorphic (e.g. pustules are characteristically seen in steroid use).
Acne fulminans is very severe acne associated with systemic upset (e.g. fever). Hospital admission is often required and the condition usually responds to oral steroids.
How is acne vulgaris managed?
Acne may be classified into mild, moderate or severe:
i) mild: open and closed comedones with or without sparse inflammatory lesions
ii) moderate acne: widespread non-inflammatory lesions and numerous papules and pustules
iii) severe acne: extensive inflammatory lesions, which may include nodules, pitting, and scarring
A simple step-up management scheme often used in the treatment of acne is as follows:
- single topical therapy (topical retinoids, benzyl peroxide)
- topical combination therapy (topical antibiotic, benzoyl peroxide, topical retinoid)
- oral antibiotics: e.g. Oxytetracycline, doxycycline. Improvement may not be seen for 3-4 months. Minocycline is now considered less appropriate due to the possibility of irreversible pigmentation. Gram negative folliculitis may occur as a complication of long-term antibiotic use - high-dose oral trimethoprim is effective if this occurs
- oral isotretinoin: only under specialist supervision
There is no role for dietary modification in patients with acne.
What is isotretinoin?
Isotretinoin is an oral retinoid used in the treatment of severe acne. Two-thirds of patients have a long term remission or cure following a course of oral isotretinoin
Adverse effects:
- teratogenicity: females should ideally be using two forms of contraception (e.g. Combined oral contraceptive pill and condoms)
- dry skin, eyes and lips: the most common side-effect of isotretinoin
- low mood*
- raised triglycerides
- hair thinning
- nose bleeds (caused by dryness of the nasal mucosa)
- benign intracranial hypertension: isotretinoin treatment should not be combined with tetracyclines for this reason
- photosensitivity
What is psoriasis?
A chronic inflammatory skin condition due to hyperproliferation of keratinocytes and inflammatory cell infiltration. Psoriasis is a common (prevalence around 2%) and chronic skin disorder. It generally presents with red, scaly patches on the skin although it is now recognised that patients with psoriasis are at increased risk of arthritis and cardiovascular disease.
What is the pathophysiology of psoriasis?
Multifactorial and not yet fully understood
1) genetic: associated HLA-B13, -B17, and -Cw6. Strong concordance (70%) in identical twins
2) immunological: abnormal T cell activity stimulates keratinocyte proliferation. There is increasing evidence this may be mediated by a novel group of T helper cells producing IL-17, designated Th17. These cells seem to be a third T-effector cell subset in addition to Th1 and Th2
3) environmental: it is recognised that psoriasis may be worsened (e.g. Skin trauma (Koebner phenomenon), stress), triggered (e.g. Streptococcal infection) or improved (e.g. Sunlight) by environmental factors
