week 7-skin Flashcards
what is acne? treated
Very common
• Characterised by blackheads and whiteheads and pustules
• Mostly affects face, the upper part of the chest, and the back
where most sebaceous follicles
• Severe acne is inflammatory, but acne can also manifest in
non-inflammatory forms
• Lesions are caused by excess oil and dead skin cells clogging
up follicles – Propionibacterium acnae grow, triggering
inflammation and pus
• In adolescence, acne is usually caused by an increase in
testosterone, which accrues during puberty
• Acne scars are the result of inflammation within the dermis
brought on by acne (1 in 5 sufferers have scarring)
• Benzoyl peroxide, antiseptics, antibiotics, hormonal
treatments, retinoids
what are 3 main skin cancers?
Basal cell carcinoma
• Squamous cell carcinoma
• Malignant melanoma
what is basal cell cacinoma?
Slow-growing and locally invasive tumours
• 4 times more common than other skin cancers
• Caused by UV exposure and proliferation of basal
keratinocytes
• Commonly on head and neck
• Morbidity related to local tissue invasion and
destructions
• Imiquimod cream treatment
what is squamous cell carnioma?
• Malignant invasive proliferation of epidermal
keratinocytes
• Second most common skin cancer
• More common in men and the elderly
• Caused by UV exposure
• Common in white skin that burns easily
• Also caused by topical carcinogens – arsenic, or
chronic immunosuppression
• With treatment overall remission rate is 90%
what is maligant melanoma?
Malignant proliferation of melanocytes
• Incidence and mortality are increasing
• Highest incidence in Australia and New Zealand
• Caused by UV exposure
• Mortality rate of 25%
• ‘Limited’ treatment options
- recent high-profile successes of immune system
modulation
what ares some risk factors for melanoma?
UV exposure Intense short exposure in childhood Fair skin Red and blonde hair Blue eyes Difficulty to tan Freckles Benign naevi/dysplastic naevi
what are some signs of melanoma?
A Asymmetry B Border is irregular C Colour variegation D Diameter (>6 mm) E Evolving – any change size, shape, colour elevation bleeding, itching crusting
what actually happens causing melanoma?
- in the epidermis you have melanocytes in the basal layer
- when we get proliferation of them they can turninto beign moles
- but soemtiemes they grow our of controland you get dysplastic nevus
- overtime youll get radio growth phase they grow in epidermal layer
- they they exoand into dermal layer then evenually become metastatic melanoma and reach bood vessles and can move to otther to form metatsisis
what can affect the survival of the melanaoma?
the thickness more than 4mm 5years survival is 37-50%
less than 1mm 5 year survial is 95-100%
what is treatment for melanoma?
• Surgery – Simple or wide – Sentinel node biopsy • Chemotherapy – Dacarbazine iv infusion or Temozolomide oral – Taxanes (docetaxel, paclitaxel) and platinum agents – Targeted therapy • Interferon alpha 2b • IL2 • Ipilimumab (anti-CTLA4) • Anti-BRAF • Anti-PD1
what is warts and verrucas?
• Caused by human papillomavirus – causes excess keratin
production on epidermis
• Virus can spread through close skin to skin contact,
contaminated objects eg towels, shoes, communal
changing areas, more likely to spread if skin wet, soft and in
contact with rough surface
• Clear up after about 2 years
• Salicylic acid containing creams , gels and paints
• Cryosurgery
Genital warts - very common, sexually transmitted
• Months or even years to develop after HPV infection
• Liquids and creams, eg Imiquimod, a topical cream that
stimulates the immune system to fight papillomavirus by
encouraging interferon production
• Keratolysis and cryosurgery
what is impetigo?
• Common highly contagious skin infection causing sores
and blisters – often Streptoccocus/Staphylococcus
infections
• 2 types –
– Non-bullous – most common - nose and mouth, sores
quickly burst – leave yellow-brown crust
– Bullous – trunk, fluid-filled blisters that burst after few
days – leave yellow crust
• Very common in young -1/35 children in UK aged 0-4
• Topical antibiotics, stay away from other people.
• Severe cases – systemic antibiotics (eg. Flucloxacillin).
what are fungal infections?
• Several types of infections eg dermatophytes and yeasts,
result in inflammation
• Fungi invade and grow in dead keratin
• Dermatophytes
– Athletes foot –
• Ringworm growing between toes
• Itchy flaky red skin
• Contaminated floors
– Nail infections – usually toenails – start from edge to base
– Ringworm – body, scalp, groin
• Small areas treated with topical application of imidazoles
(2%)
• Severe cases with systemic antifungal agents (griseofulvin, itraconazole)
• Immunocompromised patients (Candida and Aspergillus).
what is vitiligo?
Also called leucoderma
• Loss of skin colour in patches – discoloured
areas usually get bigger with time
• Affects any part of the body, hair and inside
the mouth but more often around eyes,
nostrils, mouth, navel, knees and elbows
• Melanocytes die or stop functioning leading
to loss of melanin
• Affects people of all races and all skin types
• 95% develop it before age 40
• Not contagious or life threatening and not
linked to cancer
• No cure
• 3 Types
– Focal, Segmental, Generalised
• Aetiology
– Autoimmune component
– 30% of patients have a family history
– 15-24% have autoimmune disease
– Immune system attacking its own melanocytes
– Triggers – stress, skin damage, hormonal changes, chemical
exposure (phenol) , liver/renal disease
• Pathogenesis
– Autoimmune component
– Body makes autoantibodies to tyrosine hydroxylase in nonsegmental vitiligo
– Increase in ROS production also in mitochondria of affected cells
what is Psoriasis?
Chronic autoimmune, inflammatory skin disease with periods of remission and relapse • Affects 2-3% UK population • Equally in men and women, any age • Peaks in late teens-early 30s and 50-60 • Normal skin cells produced faster than they are shed resulting in itchy, skin lesions/plaques – pink/red with white scales, variety of shapes and sizes – can split – painful • Can develop psoriatic arthritis
whats plaque psoriasis?
Most common
• Alone or in combination with other type(s)
• Red, itchy, sore plaques with white or silvery
scales – well demarcated
• Occurs anywhere on body – usually different
type if on palms or soles or where skin
touches skin
what is the aetiology of psorosis?
• Genetic predisposition
– Complex inheritance but 1/4 children of affected
parent
– Several susceptibility loci
• Keratinocytes normally take 3-4 weeks from
basal layer to shedding – 3-4 days in psoriasis
• Inflammatory cells increased in all layers
• Trigger often outside event – eg throat infection
(streptococcal) , stress or injury to skin, virus (HIV
or HPV) or withdrawal of corticosteroids
what is the treatment for psorosis?
• Unique to each individual
• Topical treatments
– Moisturisers and emollients
– Vitamin D derivatives (calcipotriol, tacalcitol, calcitriol)
– Topical steroids (eumovate, betnovate, dermovate),
– Dovobet (betamethasone and Vit D derivative)
– Coal Tar preps – scalp
– Dithranol – for well-defined plaques not on sensitive
areas
– Calcineurin inhibitors
• Phototherapy
• Systemic treatments
– Immunosuppressants – methotrexate and ciclosporin
– Vitamin A derivative (Acitretin)
– Apremilast – inhibits phosphodiesterase 4
– Dimethyl fumarate – activates Nrf2
– Anti-TNF (infliximab, adalimumab, etanercept, certolizumab)
– Anti-IL23 (ustekinumab (anti-Il12/Il23), guselkumab, rizankizumab, tildrakizumab)
– Anti-IL17/IL17A (secukinumab, brodalumab, ixekizumab)
what is psoriatic arthritis? and treatment
• Inflammatory joint disease affecting both joints (eg knees, hands and feet) and tendons (eg heel and lower back) • Relapsing and remitting • Generally occurs after skin lesions • Not linked to severity of psoriasis • Joints become tender, swollen and stiff – worse in morning and ease with exercise • Inflammation of tendons without joints • Often associated with nail psoriasis Treatment of psoriatic arthritis • Painkillers • NSAIDs – ibuprofen, diclofenac, COX-2 inhibitors • Corticosteroids • DMARDS – leflunomide • Biologicals – Anti-TNF – adalimumab, etanercept, certolizumab – Apremilast – anti-PDE4 – Tofacitinib – JAK inhibitor
what is the aetiology for atopic eczema?
Genetic predisposition – atopic families
• Defects in the skin barrier – repair and maintain
• Lack of anti-microbial peptides
• Defect in the filaggrin gene - important for maintaining
the skin barrier – in most eczema patients
• Abnormalities in the normal inflammatory and allergy
responses
• Barrier defects makes the skin in affected patients
much more susceptible to infection and to irritation
and allows allergy-inducing substances to enter the
skin, causing itch and inflammation
