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
What is the pathophysiology of psoriasis?
Hyperproliferation of keratinocytes in response to cytokines released by inflammatory cells produce characteristic changes in the epidermis and dermis, including:
- Reduced epidermal cell transit time (from 30 days to 2-3 days) causing epidermal thickening (acanthosis), elongated epidermal rete ridges (arrowheads), thickening of the cornified layer (hyperkeratosis), nuclei retained in stratum corneum (parakeratosis)
- Increased expression of intercellular adhesion molecule 1 (ICAM-1) in epidermis
- Thinned or absent granular layer
- Infiltration of neutrophils and activated lymphocytes
- Munro’s microabscesses – small aggregates of neutrophils transmigrate through the epidermis and forms microabscess
- Dilated, tortuous capillaries within outer dermal – papillary dermic layer
What are the risk factors for psoriasis?
Family history – having one parent increases risk, both increases it even more
Viral and bacterial infections
Stress – impacts immune system so increases risk
Obesity – excess weight increases the risk of psoriasis; lesions (plaques) associated with all types of psoriasis often develop in skin creases and folds
Smoking – increases risk of psoriasis but also may increase severity of disease
What are the potential differential diagnoses for psoriasis?
Systemic lupus erythematous - sub acute SLE may have clinical features of psoriasis but plaques less scaly and not lamellar. Skin biopsy including direct and indirect immunofluorescent tests will confirm SLE.
Pityriasis rosea - lesions may show features of guttate psoriasis but are in characteristic Christmas tree-shaped distribution. Usually subsides in 8 weeks.
What are the investigations for psoriasis?
Medical history
Examining scalp, skin and nails
Skin biopsy only if diagnosis is in doubt (doesn’t always show classical features)
- Intra epidermal spongiform pustules and Munro neutrophilic microabscess within stratum corneum
- Focal parakeratosis
- Epidermal acanthosis with dilated capillaries within dermal papillae
How to manage psoriasis?
MILD
- Topical corticosteroids
- Topical vit D analogues
MODERATE TO SEVERE
- Phototherapy
- Methotrexate - folic acid antagonist and works as antiproliferative and anti-inflam agent
- Oral retinoids - e.g. acitretin
- Ciclosporin - suppresses T cells and pro-inflam CKs (e.g. IL-2)
- Apremilast
- Biologics: Eternacept, Infliximab, Adalimumab, Certolizumab (all inhibiting TNF-a), Ustekinumab (inhibiting IL12 and 23), Secukinumab, Ixekinumab, Brodalumab (inhibiting IL 17A), Buselkumab, Guselkumab, Tildrakizumab (inhibiting IL 23).
What is Guttate psoriasis and how is it treated?
A type of psoriasis that shows up on your skin as red, scaly, small, teardrop-shaped spots.
1st line treatment phototherapy
2nd & 3rd line treatment oral systemic therapies
What is Erythrodermic or pustular psoriasis?
An uncommon, aggressive, inflammatory form of psoriasis. Symptoms include a peeling rash across the entire surface of the body. It can also occur at the onset of an episode of plaque psoriasis or alongside another rare type of psoriasis called von Zumbusch pustular psoriasis.
How would you treat Erythrodermic psoriasis?
Rapid and aggressive control essential
Initial treatment - ciclosporin around 3 wks to manage flare
Pts more stable can start with biological agent
Electrolyte monitoring and supportive care to all pts with erythrodermic psoriasis
How would you treat pustular psoriasis?
Pustular treated with oral retinoid acitretin or combination of acitretin and phototherapy (re-PUVA)
1st line treatment acitretin monotherapy
Re-PUVA - acitretin given night before enhancing efficacy of treatment
SE - inconvenient scheduling (2-3x per week), phototoxicity, burning
Provide electrolyte and supportive care to pts with extensive pustular psoriasis
What are the potential complications of psoriasis?
Carciovascular complications Psoriatic arthritis Depression Lymphoma Secondary infection
What is acne?
A skin disease affecting the pilosebaceous units characterised by comedones, papules, pustules, nodules, cysts and/or scarring primarily on face and trunk.
What are the causes of acne?
Excess sebum production and sebaceous gland hyperplasia
Abnormal follicular differentiation
Colonisation of follicles by Cutibacterium (Propionibacterium) acnes
Inflammation and immune response
External factors e.g. mechanical trauma, cosmetics, topical corticosteroids and oral meds (corticosteroids, lithium, iodine)
Endocrine disorders => hyperandrogenism
Genetics
What is the pathophysiology of acne?
Formation of microcomedo: follicular keratinocytes that exhibit increased cohesiveness do not shed normally leading to retention and accumulation. Androgens stimulate enlargement of sebaceous glands and increased sebum production and abnormal keratinaceous material and sebum collect in microcomedo, whorled lamellar concretions develop.
Causes the proliferation of C acnes, which metabolises triglycerides and releases free FAs. This activates complement which produces pro-inflammatory mediators including neutrophil chemo-attractants.
Depending on the specific inflammatory cells present, suppurative pustules or inflamed papules, nodules or cysts may develop. Scarring may result.
What are the risk factors for acne?
Age – most common in teens 12-14 years
Medications – exacerbated by some meds e.g. androgens, corticosteroids (topical, oral or injected), antiepileptic meds, isoniazid, lithium, and adrenocorticotropic hormone
Family history – genetics
Greasy skin/increased sebum production
What are the potential differential diagnoses for acne?
Acne keloidalis nuchae – most likely in black people; lesions localised to posterior neck; begin as papules and pustules and may progress to confluent keloids
Acneiform eruptions – abrupt onset of lesions within days of exposure, widespread involvement, atypical locations, atypical age, improvement with cessation of meds or exposure
What are the clinical features of acne?
Usually begins as a puberty commences but the clinical course is highly variable.
Non-inflammatory acne manifests as whiteheads and blackheads.
Inflammatory lesions begin as microcomedones but may develop into papules, pustules, nodules or cysts.
May affect only the face but the chest, back and upper arms are often involved.
Post-inflammatory hyperpigmentation and/or atrophic scars may be present.
What are the investigations for acne?
Usually clinical features are enough
Hormonal evaluation is rarely required – free testosterone is the most sensitive test to establish the presence of hyperandrogenism
Bacterial culture is rarely required – ordered only when standard treatments are not efficacious and there is clinical suspicion of gram –ve folliculitis
How would you manage acne?
Mild acne (no inflammation): topical retinoid or salicylic acid Mild acne (with inflammation): topical retinoid + topical antibiotic with additional topical benzoyl peroxide or topical azelaic acid if needed Moderate acne (no inflammation): topical retinoid Moderate acne (with inflammation): topical retinoid + oral antibiotic with additional topical benzoyl peroxide or topical azelaic acid if needed Severe or resistant acne: oral retinoid with additional oral corticosteroid if needed
What is the treated for hormone-related acne?
Oral hormonal therapy If inflammatory: Adjunct – topical retinoid + oral antibiotic Adjunct – topical benzoyl peroxide Adjunct – topical azelaic acid
What are the complications of acne?
Scarring
Dyspigmentation
Why are doctors difficult patients?
Drs don’t like being on the “wrong” side of the dr-patient divide
Many ignore or downplay health problems
Help is often sought late
Notion that illness is a patient’s prerogative and falling prey to it is an admission of weakness
What is the legal stance of self-prescribing?
In UK it is legal for Drs to self prescribe or provide prescriptions for people they know.
GMC states to avoid providing medical care to yourself or anyone with whom you have a close personal relationship
What are the dangers of self-prescribing and prescribing for others?
Risk of misdiagnosis Lacks rigour of independent assessment May involve drugs of addiction Accompanied by failure to keep adequate notes Subversion of patient-dr relationship Pressure from certain people/situations
When is prescribing for others appropriate?
No other person with legal right to prescribe is available to assess and prescribe without delay which would put your or your patient’s life or health at risk or cause unacceptable pain or distress
Treatment is immediately necessary to
- Save a life
- Avoid serious deterioration in health
- Alleviate otherwise uncontrollable pain or distress
How to assess a skin lesion for malignant melanoma?
A – asymmetry B – border C – colour D- diameter E – elevations or enlargement Other symptoms – bleeding, itching and crusting
What are the types of malignant melanoma?
Superficial spreading Nodular Lentigo maligna Acral letiginous Amelanotic
When would you refer for malignant melanoma?
Urgent referral if patient presents with suspicious pigmented skin lesion that has weighted 7 point checklist score of 3 or more or dermoscopy suggest malignant melanoma or if suggests nodular melanoma
What are the types of non-malignant melanoma?
Basal cell carcinoma – caused by overexposure to UV light
Common on face and other exposed skin surfaces
Small round area of skin thickening, like red scaly patch with no itching, pain or changes in skin colour.
Squamous cell carcinoma
Appear as scaly or crusty raised area of skin with red, inflamed base
Often ulcerated keratanised
Can be sore or tender and may bleed
How to treat non-malignant melanoma?
Consider urgently referring if patient has skin lesion raising suspicion of BCC with worrying size or site or SCC.
Treatment: Excision of tumour, can include cryotherapy and radiotherapy.
How will occupational health help with employees with skin conditions?
Encouraging employees and colleagues to seek advice from their GP if it’s noted they have a skin condition.
Reduce tissue damage which can become a problem in healthcare environment as it leads to broken skin and increased risk of infection.
Encourage use of moisturisers
Using specialist creams and hand washes
