Wk10 - Dermatology Flashcards
3 main functions of the skin
Three main functions: Protection, Regulation and Sensation
Primary function as a barrier (physical and immunological)
- mechanical impacts
- protects and detects pressure
- detects variations in temperature,
- barrier to micro-organisms
- barrier to radiation / chemicals
Physiological regulation - body temperature via sweat, hair and changes in peripheral circulation - fluid balance via sweat and insensible loss - synthesis of Vitamin D
Network of nerve cells that detect and relay changes in the environment (heat, cold, touch, and pain)
Layers of epidermis
Stratum corneum Stratum lucidum Stratum granulosum Stratu spinosum Stratum basale
Embryology of the skin
Epidermis is derived from the ectoderm
5th week, the skin of the embryo is covered by simple cuboidal epithelium
7th week single squamous layer (periderm), and a basal layer
4th month, an intermediate layer, containing several cell layers, is interposed between the basal cells and the periderm
Early fetal period the epidermis invaded by melanoblasts, cells of the neural crest origin
Hair- 3rd month as an epidermal proliferation into dermis.
Cells of the epithelial root sheath proliferate to form a sebaceous gland bud. Sweat glands develop as downgrowths of epithelial cords into dermis.
Recognise interactions between immune system and skin and how this can manifest as skin disease
Langerhans cells are members of the dendritic family, residing in basal layers.
They specialise in antigen presentation:
- Acquire antigens in peripheral tissue and transports to lymph nodes
- Presents them to naive T cells which initiate cytokine cascade
- This initiates an adaptive immune response
Langerhans cells are also involved in microbial immunity, induction of hypersensitivites and pathogenesis of chronic inflammatory diseases of the skin
Skin allergy
- Skin irritation by nonallergenic and allergenic compounds induces - Langerhans cell migration and maturation
Langerhans cells migrate from epidermis to draining lymph nodes - Initial sensitization takes 10-14 days from initial exposure to allergen (nickel, dye, rubber etc)
- Once an individual is sensitized to a chemical, allergic contact dermatitis can then develop within hours of repeat exposure exposure
Ultraviolet effects on skin
Damaging effects of ultraviolet on skin - direct cellular damage and alterations in immunologic function. Direct effects include photoaging, DNA damage and carcinogenesis
- P53 tumour suppressor genes are mutated by DNA damage, developing melanoma and non melanoma skin cancers (UV light switches off p53)
Keratinocytes and melanocytes work together to protect cells from UV DNA damage - keratinocytes flood between cells to provide protective cover
Chronic UV exposure in humans leads eventually to loss of skin elasticity, fragility, abnormal pigmentation and hemorrhage of blood vessels. Wrinkles and premature ageing
Vitamin D and the skin
During exposure to sunlight, solar UVB photons
(290-315 nm) are absorbed by 7-dehydrocholesterol in the skin and converted to previtamin D(3)
Pre-vitamin D(3) undergoes transformation within the plasma membrane to active vitamin D(3)
During our winter there is minimal pre-vitamin D(3) production in the skin. Few foods naturally contain Vit D
Associations of vitamin D deficiency - increased risk of common cancers, autoimmune diseases, infectious diseases, and cardiovascular disease
Skin sensation - Merkel cells
Merkel cells at the base of the epidermis, respond to sustained gentle and localised pressure, assess shape /edge
Skin sensations - Meissner corpuscels
Meissner corpuscles situated immediately below epidermis and are particularly well represented on the palmar surfaces of the fingers and lips They are especially sensitive to light touch
e.g. cotton wools
Skin sensation - Ruffinis corpuscles
Ruffini’s corpuscles , situated in the dermis are receptors sensitive to deep pressure and stretching
Skin sensation - Pacinian corpuscles
Pacinian corpuscles are mechanoreceptors present in the deep dermis, sensitive to deep touch, rapid deformation of skin surface and around joints for position/proprioception
Other free nerve endings – Pain, temperature
Dermatology descriptions: Macule Papule Pustule Plaque Vesicle Bulla Ulceration
Macule - flat area of skin (different colour) Papule - raised from skin Pustule - raised and full of pus Plaque - raised, big Vesicle - small blister Bulla - large blister Erythematous - red Ulceration - epidermis has been removed, could be traumatic ulceration
Aetiology of acne
Acne is caused by:
- Keratin and thick sebum blockage of sebaceous gland
- Androgenic increased –> sebum production and viscosity
- Proprioni bacterium inflammation
- -> marked inflammation and scarring
Clinical features of acne
Papules Pustules Erythema Comedones (black heads - oxidised sebum; White heads - not oxidised (closed) Nodules Cysts Scarring
Distribution of acne vulgaris
Face
Chest
Back / Shoulders
Occassionally legs, scalp
Subtypes of acne & grading scale
Acne vulgaris:
Papulopustular (most common subtype), Nodulocystic, Comedonal
Steroid induced
Acne fulminans
Acne rosacea - mainly on face
Acne Inversus - mainly in armpits or groin (Hidradenitis suppuritiva)
Grading scale - Graded using Leeds acne grading system - Grades 1-12
Treatment options for acne
Reduce plugging through a topical retinoid or topical benzoyl peroxide
Reduce bacteria Topical antibiotics (erythromycin, clindamycin) or oral antbiotics (tetracyclines, erythromycin) - Benzoyl peroxide reduced bacterial resistance
Reduce sebum production using hormones – anti androgen ie Dianette / OCP (Change viscoity and quantity of oil produced)
Side effects
Topical agents – irritant, burning, peeling, bleaching
Oral antibiotics – gastro upset
OCP- possible DVT risk
Oral Isotretinoin is an oral retinoid for severe acne.
Dietary modification controversial
Reduced dietary/ glycaemic load eg milk, choc
Oral isotretinoin for Tx of acne
Is the only oral retinoid licensed for severe acne vulgaris
Concentrated form of vitamin A
Reduces sebum, plugging and bacteria
Remission of acne in around 80% teenagers
Standard course for 16 weeks 1mg/kg
Multiple side effects – most are trivial - Dry lips, nose bleeds, dry skin, myalgia
Serious side effects - Deranged liver function, raised lipids,
mood disturbance , teratogenicity
Pregnancy Prevention Program - Women have to be contraceptive
Pregnancy test done every 4 weeks
Expensive , consumes lots of clinical time
Eczema - Definitions & aetiology
Terms eczema and dermatitis interchangeable
Dermatitis - inflammation of the skin
Aetiology - combination of genetic, immune and reactivity to a variety of stimuli
Inflammation in eczema primarily due to inherited abnormalities in skin so called “barrier defect”.
Leads to increased permeability and reduces its antimicrobial function
An inherited abnormality in filaggrin expression considered a primary cause of disordered barrier function. Filaggrins are proteins which bind to keratin fibres in the epidermal cells (form the barrier defect).
The gene for filaggrin is on Chromosome 1 (if have genetic defect - more likely to get eczema)
Name the subtypes of eczema
Endogeneous - Atopic, Seborrhoeic, Discoid, Varicose (Venous), Pompholyx
Exogeneous - contact (allergy, irritant), Photoreaction (allergic, drug)
Atopic eczema
Itchy inflammatory skin condition
Associated with asthma, allergic rhinitis, conjunctivitis, hayfever (atopy)
High Ig-E immunoglobulin antibody levels
Genetic and immune aetiology
10-15% of infants affected
Remission occurs in 75% by 15 years
2/3 have a family history of atopy
Infant atopic eczema
Itchy Occasionally vesicular (small blisters) Often facial component Secondary infection < 50% still have eczema by 18 months occasionally aggravated by food (ie milk)
Complications of atpic eczema
Break in barrier defect - risk of infection
Bacterial infection - Staph. aureus
Viral infection - Molluscum - Viral warts - Eczema herpeticum
Tiredness
Growth reduction
Psychological impact
Management of atopic eczema
Emollients
Topical steroids (to reduce the inflammation)
Bandages (to prevent them from scratching)
Antihistamines (to try suppress itch response)
Antibiotics / anti-virals
Education for parents /child National Eczema Society
Avoidance of exacerbating factors
rarely dietary avoidance / house dust mite etc
Systemic drugs eg ciclosporin (immunosuppressive),methotrexate
Newest biologic agent IL4/13 blocker Dupilumab
Contact dermatitis
Precipitated by an exogenous agent
Irritant - direct noxious effect on skin barrier
Contact dermitis - common allergensAllergic - Type IV hypersensitivity reaction
Contact dermatitis - common allergens
Nickel - Jewellery, zips, scissors, coins
Chromate - Cement, tanned leather
Cobalt - Pigment /dyes
Colophony - Glue, adhesive tape, plasters
Fragrance- Cosmetics, creams, soaps
Features of Seborrhoeic dermatitis
Chronic, scaly inflammatory condition
Often thought to be “dandruff”
Face, scalp, and eyebrows, occ upper chest
Reaction due to overgrowth of Pityrosporum Ovale yeast
Can be worse in teenagers
Occasionally confused with facial psoriasis
Can be severe in HIV - should do HIV test
Management of Seborrhoeic Dermatitis
Scalp - medicated anti yeast shampoo
(ie Antifungal ketoconazole -Nizoral, Selsun)
Face - anti-microbial, mild steroid
(ie Daktacort cream)
Simple moisturiser
Rarely systemic antifungals
Often improves with UV / sunlight
(can give medical sunbed treatment)
Features of Venous Dermatitis
Underlying venous disease
Affects lower legs
Incompetence of deep perforating veins
Increased hydrostatic pressure
More severe - Deposits iron and haemosiderin - brown appearance
Management of venous dermatitis
Emollients
Mild / moderate topical steroid
Compression bandaging / stockings
Consider early venous surgical intervention
Definition of Psoriasis
Definition -
a chronic relapsing and remitting scaling skin disease which may appear at any age and affect any part of the skin
Prevalence 1.5 - 3%
Age onset often two peaks age 20-30y or 50-60y
What causes psoriasis?
Caused by T-cell mediated autoimmune disease- Abnormal infiltration of T Cells causes release of inflammatory cytokines (interferon, interleukins and TNF)
which cause increased keratinocyte proliferation.
Environmental and genetic factors (PSORS1 on chromosome 6)
Genes associated with psoriasis
PSORS genes (e.g. PSORS1, Chromosome 6) and HLA-Cw0602 associated in certain subtypes
Types of psoriasis
Plaque Guttate Pustular Erythrodermic Flexural / Inverse Palmar/plantar pustulosis
Psoriasis at sites of trauma / scars – Koebner phenomenon
(not Auspitz) - this has came up in exam previously
Nail findings with psoriasis
Oncholysis (painless separation of the nail from the nail bed)
Nail pitting
3 features seen with psoraisis
Salmon-pink colour
Well de-markated
Scaling on top
Relationship between psoriasis and arthritis
Up to 20% of patients with psoriasis develop psoriatic arthritis
Treatments for psoriasis
In order of increasing effectiveness (and toxicity)
Topical creams and ointments (moisturises will reduce dryness and flakiness; steroids will reduce inflammation and redness; Vit D analogues and topical retinoid treatment will slow keratinocyte proliferation)
Phototherapy light treatment (this reduces T cell proliferation, encourages Vit D production (reducing skin turnover); UV-B light most commonly used
UV-A with psoralen photosensitiser) - risks include burning and inc. risk of cancer)
Oral retinoids such as Acitretin (slows down turnover of keratinocytes)
Immunosuppressant - Methotrexate or Ciclosporin (often targets TNF)
Biologic therapies Adalumimab or Infliximab (anti TNF) Ustekinumab (anti IL12/23)
Secukinumab
Brodilumab
Fumaric acid esters
Most drugs have potent side effects i.e. liver dysfunction, hypertension, risk of infection - so need to be tailored to patient
Are screened for TB
UV Phototherapy is different to Photodynamic therapy PDT used in skin cancer
At least 2 dinstinct pathways interact or converge to cause skin cancer
- Direct action of UV on target cells (keratinocytes) for neoplastic transformation via DNA damage (This can cause immune suppression –> leads directly to skin cancer; Can also cause p53 mutation –> cancer)
- Effects of UV on the host’s immune system
(UV causes trans-UCA transformation into cis-UCA –> causes immunosuppression
What are the 3 main skin cancer types?
Basal cell carcinoma
Squamous cell carcinoma
Malignant melanoma
Features of Basal-cell carcinoma
The most common type of skin cancer
The process of creating new skin cells is controlled by a basal cell’s DNA.
A mutation in the DNA causes a basal cell to multiply rapidly and continue growing when it would normally die. Eventually the accumulating abnormal cells may form a tumour.
PTCH gene mutation may predispose to tumour development
Clinical presentation:
80 percent of basal-cell cancers are found on the head and neck / UV exposed sites
Rarely metastasis or kills
Basal cell carcinoma subtypes
1) Nodular - Circular, nodule (i.e. >0.5cm raisde lesion), shiny (‘pearly’), broken blood vessels (Telangiectasia), central ulceration often
2) Superficial - No raised nodule Roled margin Broken blood vessels No ulceration Presence of sun-damaged skin --> freckles, redness etc.
3) Pigmented - slightly raised edge, tend to be in darker skin, pigmented sections
4) Morphoeic/sclerotic - more invasive, harder to diagnose, harder for patient to pick up, the biopsy needs to be bigger as often infiltrates beneath skin –> makes it difficult to excise
Treatment of basal cell carcinoma
Gold standard – Surgical excision 3-4mm margin
Curettage and cautery
Cryotherapy - liquid nitrogen
Photodynamic therapy (painful, long and needs repeating)
Topical imiquimod / 5-fluorouracil cream (SBCC responds better, causes an immune response)
Mohs micrographic surgery (time consuming and expensive)
Features of squamous cell carcinoma
May occur in normal skin or in skin that has been injured (burns) or chronically inflamed
Originates from keratinocytes
2nd commonest skin cancer
Pre malignant variants - actinic keratoses, Bowens disease
Most SCC occur on skin that is regularly exposed to sunlight or other ultraviolet radiation
Risk of metastasis from a high risk SCC from
10 to 30% (high risk sites- ears, lips)
Treatment of squamous cell carcinoma
Gold standard – Surgical excision 4-5mm margin
Curettage and cautery
Pre-malignant /squamous cell in-situ (faint, scaley patch)
Topical imiquimod / 5-fluorouracil cream
Cryotherapy (operator dependent - usually only used on small lesion)
Photodynamic therapy (LED lamp and photosensitiser - takes about 3 hours)
Sun protection
Features of melanoma
Malignant tumour of melanocytes
Most common in skin as where most of the melanocytes are (but can be bowel/ eye)
Rarest type of skin cancer
Accounts for 75% of deaths from skin cancer
Often affects young, fit people
Pathophysiology:
- Cause through DNA damage - mainly UV, rarely genetic element
- Radial growth phase, then vertical growth (want to catch at radial phase)
- Depth of presentation determines prognosis
- Spread via lymphatics
- Premalignant form
Risk factors for developing melanoma
Genetic markers (e.g. CDKN24 mutations) Family history of dysplastic nevi or melanoma Ultraviolet irradiation Sunburns during childhood Congenital nevi Number of atypical nevi (>5) High socioeconimc status - travel to warm countries Skin type I, II Immunosuppression
What system is used to determine survival rates for malignant melanoma
Breslow Depth (mm) - according to thickness of the cancer (most are less than 1mm - 97% clearance; 71% for >4mm) Clark - tells where the skin lesion is
Melanoma subtypes
Superficial spreading malignant melanoma (common) Nodular melanoma Acral melanoma (hands and feet) Subungual melanoma (under a nail) Amelanotic melanoma (dont have any pigment - can be confused with BCC) Lentigo maligna (pre-malignant) Lentigo maligna melanoma Melanoma in-situ
Melanoma Treatment
- Surgical excision (Breslow < 1mm) – 1cm margin
(Breslow > 1mm) – 2cm margin - Immunotherapy ipilimumab
- Immune check point / MEK inhibitors
- Biologic antibodies eg BRAF genetic defects (debrafanib) - BRAF inhibitor
- Imaging /scanning CT / MRI / PET
- Long term follow up up to 5 years
- Assessment for Lymph node / organ spread
- Genetic testing in families, multiple primary melanomas
Cutaneous tumour syndromes
These often present with skin tumours:
Gorlin’s syndrome
(multiple BCCs, jaw cysts, risk of breast ca)
Brook Spiegler syndrome
(multiple BCCs, trichoepitheliomas)
Gardner Syndrome – soft tissue tumours, polyps, bowel ca
Cowden’s Syndrome – multiple hamartomas, thyroid, breast ca
Changes in the skin can be a marker of…
Know the conditions associated with psoriasis
Marker of: Endocrine disease Internal malignancy Nutritional deficiency Systemic infection Systemic inflammatory disease
Psoriatic arthritis - up to 20% will develop this
Metabolic syndrome
Liver disease/Alcohol Misuse
Depression - psychological factor of appearance
Hutcheson’s sign –> ?
Does the pigmentation spill over from nail to finger?
to do with malignant melanoma
Thyroid causes of skin changes
Dry skin (hypothyroidism) Thyroid dermopthy (peritibial myxoedema) - (Grave’s disease) Thyroid acropachy (e.g. clubbing) (Grave’s disease)
Skin conditions associated with diabetes mellitus
Necrobiosis lipoidica Diabetic dermopathy Scleredema (not scleroderma) Leg ulcers Granuloma annulare
Features of necrobiosis lipoidica
Waxy shiny appearance
Usually yellow discolouration
Often Shins
Occassionally ulcerates and scars
Features of sclerederm
Unusual texture to the skin (woody) - harder to squeeze the skin
Thicker skin
Inflammation and reddness
Features of granuloma annulare
Infiltration into the skin –> circular patches
Backs of hands and dorsum of foot is common site
Can get as precursor to diabetes
One patch = probably not associated with diabetes
Skin changes associated with steroids
Cushings / steroid excess:
Acne, Striae, Erythema, Gynaecomastia
Addisons /steroid insufficiency:
Hyperpigmentation, Acanthosis nigracans
Skin changes assoicated with excess sex hormones
Excess Testosterone: Acne, Hirsutism (e.g. in Polycystic Ovarian Syndrome Testicular tumours Testosterone drug therapy)
Excess Progesterone:
Acne, Dermatitis
(e.g. in Congenital adrenal hyperplasia
Contraceptive treatment)
What internal malignancies can cause skin changes>
Necrolytic migratory erythema
Erythema gyratum repens
Acanthosis nigricans
Erythema annulare
Sweet’s Syndrome
Sister Mary Joseph Nodule
Features of necrolytic migratory erythema
Necrolytic migratory erythema (glucagonoma syndrome)
Rare disease
Erythematous, scaly plaques on acral, intertriginous, and periorificial areas
Association with an islet cell tumour of the pancreas
Other signs hyperglycemia, diarrhoea, weight loss, glossitis
Treatment is removal of the tumour
Features of erthema gyratum repens
Rare
Very distinctive skin disease
Reddened concentric bands whorled woodgrain pattern
Severe pruritus and peripheral eosinophilia
Strong association with lung cancer
Association with breast, cervical, GI cancers less strong
Treatment of the underlying malignancy treats skin disease
Features of acanthosis nigricans
Smooth, velvet-like, hyperkeratotic plaques in intertriginous areas (e.g., groin, axillae, neck)
Three types of acanthosis nigricans have been recognized
Type I associated with malignancy
adenocarcinoma, especially of the gastrointestinal tract (60% gastric). Sudden onset and more extensive
Type II familial type, autosomal dominant Very rare, appears at birth, no malignancy Type III associated with obesity and insulin resistance. Most common type
DEficient in what nutrients can cause skin changes
Vitamin B
B6 pyridoxine Dermatitis
B12 cobalamin Angular chelitis
B3 niacin Pellagra
Zinc - Acrodermatitis Enteropathica:
Inherited or acquired condition
Pustules, bullae, scaling (acral and perioral distribution)
Inherited- mutation in SLC39A, which encodes an intestinal zinc transporter
In infants, deficiency can follow breast-feeding, when breast milk contains
low levels of zinc
In adults, disease can occur after total parenteral nutrition without zinc supplementation;
alcoholism, malabsorption states, inflammatory bowel disease, bowel surgery
Differential diagnosis- nutritional deficiencies, necrolytic migratory erythema
Treatment is zinc supplementation
Vitamin C - Scurvy Punctate purpura / bruising “Corkscrew” spiral curly hairs Patchy hyperpimentation Dry skin Dry hair Non healing wounds Inflamed gums
Causes of erythema nodosum
(Severe pain
Piniculitis - inflammation of subcutaneous fat causing red bumps and patchesf)
Shins are common place
Streptococcal infection Pregnancy / Oral contraceptive Sarcoidosis Drug induced Bacterial / Viral infection Others
Causes/triggers of pyoderma gangrenosum (
Often on shin
Purple raised overhanging edge with central ulceration)
Inflammatory Bowel Disease Crohn’s disease , Ulcerative colitis Rheumatoid arthritis Myeloma Others
Types of skin drug reactions
Maculopapular Urticaria Morbilliform Papulosquamous Photo-toxic
Less common: Pustular Lichenoid Fixed drug rash Bullous Itch (no rash)
Acute drug rashes - common drugs
Antibiotics ie penicillins (generalised redness, swollen and puffy), trimethoprim NSAIDs Chemotherapeutic agents Psychotropic chlorpromazine Anti-epileptic lamitrigine, carbamaz Cardiac
Features of vasculitis
Triggers -
Infection
Drugs
Connective tissue disease ie RA
Check for systemic vasculitis ie renal BP / Urinalysis
Often localised and not rapidly progessive
Less unwell than in meningococcal rash
Drug induced psoriasiform rash
Psoriasis–like
Well demarcated pink erythema with scale
Sudden onset, no FHx
Lithium, Beta blockers
Blistering disorders
Drug induced:
Steven Johnson Syndrome
Toxic epidermal necrolysis
Immunobullous diseases:
Bullous pemphigoid
Bullous pemphigus
Toxic epidermal necrolysis (TEN)
Dermatological emergency Majority drug induced ? Disease spectrum SJS TEN If < 10% skin involvement -SJS Most severe mucous membrane involvement Stop suspect drug
Analgesia Fluid balance SCORTEN severity scale (works out mortality likelihood) Special mattress, sheets Infection control / prophylaxis Non adherent dressings Urology, Gynae, Ophthalmology input Some reports > 50% mortality rate
Features of erythema multiforme
Self–limiting allergic reaction HSV, EBV, occassionally drug No or mild prodrome Target lesions Never TEN
Types of immunobulloues disorders
Bullous pemphigoid (more common)
Mucous membrane pemphigoid
Paraneoplastic pemphigoid
Pemphigus (more common)
Autoantibodies to various skin component
ie basement membrane proteins in BP
Dermatitis herpetiformis (coeliac disease)
Treatment for immunobullous disorders
Reduce autoimmune reaction – oral steroids
Steroid sparing agents ie azathioprine
Burst any blisters
Dressings and infection control
Check for oral / mucosal involvement
Consider screen for underlying malignancy
Dermatitis herpetiformis (coeliac disease)
Topical steroids
Gluten free diet
Oral dapsone
FEatures of urticaria
Itchy, wheals (hives) Lesions last < 24 hours Non-scarring Commonest skin disorder to present A&E Acute < 6 weeks Chronic > 6weeks
Immune-mediated
type 1 allergic IgE response
Non-immune-mediated
direct mast cell degranulation
eg opiates, antibiotics, contrast media, NSAIDs
Treatment of urticaria
antihistamines, steroids, immunosuppression, omiluzimab
Causes of acute urticaria
Unknown Viral infections Medication NSAIDS, Aspirin, ACE Foods & food additives Parasitic infections Physical stimulants – cold, pressure, solar, cholinergic, aquagenic
Features of erythroderm
- Causes
- Treatment
Descriptive term
>80-90% involvement, erythema
Causes – Psoriasis
Eczema
Drug reaction
Cutaneous lymphoma
others
Treat underlying skin disorder, supportive
Fluid / temperature balanceDifferential diagnosis of chronic, red scaly skin?
Eczema (dermatitis)
Psoriasis
Seborrhoeic dermatitis
What factors might influence a patients risk of developing plaque psoriasis
Multigenetic factors (PSORS gene, e.g. PSORS1 on chromosome 6), family history, occasionally infection (e.g. streptococcal throat infection provoking guttate psoriasis). Rarely triggered by drugs e.g. Lithium and BetaBlockers, paradoxical reaction to biologic agents e.g. adalimumab
How might psoriasis impact on a patients lifestyle?
Limits leisure activities e.g. gym, swimming, holidays
Difficulty travelling (tubs of creams, bedding etc.)
Flaky skin/dandruff may limit clothing types e.g. can’t wear dark tops
May be hesitant with relationships and sexual activity
Can lead to low mood, alcohol misuse, reduced exercise and thus weight gain
What tests can be done to help confirm the diagnosis of psoriatic arthritis
Xray
Exclusion of other inflammatory arthropathies e.g. Rheumatoid (blood RF), Autoantibodies e.g. ANA, US joints, MRI joints
What Tx for plaque psorasis and psoriatic arthritis
Combined Chronic Plaque Psoarises and Inflammatory Psoiatic Arthropathy, should have Disease Modifying Therapy such as EMthotrexate, Apremilast, Biologic agents e.g. Adalimumab
A 21 yo F beauty therapist with known atopy presents with her skin on her hands and face. This tends to be itchy and often improves when she is on holidays.
What is the most likely diagnosis?
Atopic eczema (dermatitis) (or Allergic Contact dermatitis)
What investigations may you wish to request in a patient with suspected atopic dermatitis or contact dermatitis
Consider bacterial skin swb is skin is broken
Fungal mycology skin scrape to exclude skin fungal infection
Latex IgE RAST blod test if glove aggravation
Consider allergic contact dermatitis patch testing with extras inc acrylics
Occasionally further blood IgE RAST tests, skin prick tests, Eosinophil count
If standard emolients etc. aren’t working for dermatitis, what other Tx options might hospital dermatology be able to offer her?
Oral corticosteroids for quick relief (e.g. 7 days prednisolone PO)
Systmeic immunisuppressives e.g. azathioprine, ciclosporin, methotrexate
Oral retinoids e.g. alitretinoin
Ultraviolet phototherapy e.g. UVB or P-UVA
Name some types of skin allergy testing and discuss the place for each
RAST tests - not very sensitive, useful single agents e.g. one foot type, exepnsive
Contact patch testing - chemical contact allergy e.g. nickel, rubber, fragrance
Skin prick testing - used more in children e.g. food allergy milk, eggs, peanut
What are the implications of using oral isotretinoin in a teenage girl?
Known significant teratogen, birth defects. Pregnancy Prevention Program 4 weekly drug dispensing (hospital only). Female consetn form to sign, regular pregnancy testing for prescriptions, two forms of contraception e.g. OCP and condoms.
Discuss need for pregnancy prevention program with topical retinoid use
What is the significance of irregular menstruation and excess hari associated with acne vulgaris? What tests may you consider?
Acne can be associated with PCOS (insulin resistance, overweight, hirsitusim, irregular periods, difficultly conceiving)
Blood profile, LH/FSH, progesterone, testosterone, free androgen index, sex hormone binding globulin, prolactin
Gyna transvaginal US
A 78 year old female presents with purple brown discoloration of both lower legs and around the ankles, there is some dryness on the surface of the skin and a deep 3cm break in the skin over in the inner aspect of the ankle
What diagnosis might be relevant?
Venous dermatitis with venous ulcer
Features of venous ulcer
Tends to be less painful than arterial, usual more superficial and fdiffuse with mroe surrounding skin cahnges (arterial punched out and deep). Peripheral circulation likely intact.
Most seen in ‘gaitor’ area
What are the social/lifestyle factors involved in development of venous ulcer
Multiple pregnancies put pressure and stress on venous system
Varicose veins
Obesity and standing in a shop at work puts pressure on venous valves
History of DVT- likely damage to veins and valves
What medication can provoke peripheral oedema (thus venous dermatitis, vneous ulcer)
Ca+ antagnoists such as amlodipine
Most important initial investigation for venous ulcer
Ankle Brachial Pressure Index ABPI (blood pressure comparison between upper and lower limbs) should be roughly equal 0.8 ratio might suggest occlusion and need vascular arterial assessment >1.1 ration might suggest calcification
Bacterial skin swab only if deteriorating, spreading cellulitis or smelling
Vascular Surgery Assessment - arterial circulation eg MRI angiography
Skin biopsy incase inflammatory skin disease ie pyoderma gangrenosum or to exclude skin tumour
Bacterial swabs for unusual bacteria ie MRSA (wouldn’t routinely swab)
Exclude drug induced ulceration ie Nicorandil
Patch testing to bandages, dressings and steroids
(if well defined dermatitis to bandage distribution site)
Name some other causes for leg ulceration (other than venous dermatitis)
Arterial disease Connective Tissue Disease ie Lupus
Diabetic Pressure sores Skin cancer – eg basal cell ca
Neuropathic Infection, deep fungal
Trauma Sickle Cell Disease Necrobiosis lipoidica
Drug induced ie Nicorandil, hydroxycarbamide Pyoderma gangrenosum
68y F is anxious about a mark on her leg. She is concerned that it has seemed to inc in size over the last year.
Give some suggestions of lesions in this age group that could be found on a leg
Moles/melanocytic naevi
Seborrhoeic keratosrs/warts
Dermatofibroma/histiocytoma
Actinic keratoses, Bowen’s syndrome (squamous cell carcinoma - in situ)
Skin cancer e.g. melanoma, basal cell carcinoma, squamous cell carcinoma
Irregular pigmented lesion on sun exposed UV damaged skin most likely to be…
malignant melanoma
How would you confirm the diagnosis of suspiscion of malignant melanoma
Ideally a full excision o fthe whole lesion for diagnosti cbiopsy and histology.
If unable to easily removed the whole lesion could take a large diagnostic representative sample through the most irregular area
What risk factors may have predisposed Mrs Nicholson to developing malignant melanoma
Type 1 skin, natural sun exposure, history of sun bed use, previous drug induced immunocompression (allows more UV damage)
Discuss prognostic factors in melanoma
Clinical appearances -
Size of presenting lesion, depth of clinical pigmentation (Blue / grey colours)
Anatomical location (eg poor prognosis for late presentation acral melanoma eg sole foot)
Evidence of clinical ulceration
Evidence of resorption eg regression
Obvious local metastases / satellites (eg in transit)
Histological appearances -
Breslow thickness (physical depth measurement in mm) < 1mm good prognosis
Clark Level (actual anatomical level within skin) less commonly used now
Evidence of high mitotic rate - poorer prognosis
Involvement of lymphovascular tissues - poorer prognosis
Genetic BRAF mutation on skin tissue – may mean more susceptible to benefits of some new chemo agents
Controversial – Sentinel Lymph node assessment (carries no improved prognosis)
AJCC Staging system eg good prognosis thin melanoma - Stage 1A
Discuss some of the treatment options for emlanoma
Surgical excison with wide local excision
Surgical excision margin based on Breslow thickness 1cm margin Breslow <1mm
Lymph node dissection if LN involved
Chemotherapuetic agents eg BRAF inhibitors,
Immunotherapy eg nivolumab, ipilimumab
What is the main differential diagnosis in any hair loss, differentiate between scarring and non-scarring hair loss and those that are generalise or localised
Non-scarring - alopecia areata, telogen effluvium (hair cycle disorder)
Drug induced e.g. chemotherapy, androgenic alopecia, anorexia/vitamin deficiency, syphilis
Scarring hair loss - discoid cutaenous lupus, follicultis, fibrosing alopecia, lichen planua, fungal inefction
Localised - alopecia areata, fungal infection. Rest tend to be generalised
What aetiologists are involved in the developmentof alopecia areata
Immune phenomenon, against hair follicles and follicular melanocytes
What areas can be affected by alopecia areata
Scal hair, eyelashes, eyebrows, facial/beard hair, body hair, pubic hair
What are the different types/classifications of alopecia areata
Alopecia Totalis (whole scalp hair loss) Alopecia Universalis (whole body hair loss)
What intiial treatment option could you start with for alopecia areata.
Other known treatments.
Super potent topical corticosteroid e.g. clobetasol (liquid, foam, cream)
Others:
Intralesional corticosteroid injections/trimcinolone
High dose oral corticosteroids (in very rapid onset progressive AA)
Allergic contact immunotherapy - e.g. diphencyperone DCP Tx
New generation biologic agents e.g. Jak2 inhibitors
Possible use of Minoxidil
Discuss other causes of hair loss (other than AA)
Primary skin conditions eg psoriasis, eczema
Scarring skin diseases eg cutaneous discoid lupus, frontal fibrosing alopecia
Fungal infection/ringworm
Syphilis
Secondary medical causes hair loss -
Thyroid disease, systemic lupus, vitamin deficiencies eg iron, B12, zinc blood tests
Hormonal – androgen excess eg polycystic ovarian syndrome
Male pattern / Female pattern androgenic hair loss (most genetic)
Male- typical pattern crown balding and temporal recession
Female pattern- frontal and crown thinning
Minoxidl topical treatment
Hair cycle disorders eg after illness or pregnancy eg Telogen Effluvium
Hair cycle phases – anagen, telogen, catogen
Chemotherapy induced hair loss (arrests growing phase of hair)
Psychological/psychiatric – Trichotillomania (self induced hair pulling)
Consider any investigations in hair loss
Dermoscopy (exclamation hairs in alopecia areata)
Associated autoimmune bloods eg Thyroid, Glucose, B12
Fungal mycology Hair sample or skin if tinea capitis / ringworm , scaly, inflammatory
ANA / lupus (scarring alopecia discoid lupus, generalised hair loss SLE
Syphilis serology (multi patch moth eaten hair loss)
Diagnostic skin biopsy including hair follicles
