Dermatology Flashcards
Functions of skin?
Barrier to infection, thermoregulation, protection against trauma, protection against UV, vitamin D synthesis, regulate H20 loss
Normal proliferation occurs in what layer? To balance new cells in the basal layer of the epidermis, what are shed from the surface of the stratum corneum? Process called what? This involves what? Normal pH of the skin?
Just in the basal layer
Mature corneocytes
Degradation of the extracellular corneo-desmosomes under the action of protease enzymes= desquamation
5.5(allows proteases to remain on the skin)
3 layers of skin?
1) Epidermis
2) Dermis
3) SC tissue
Layers of the epidermis?
Stratum corneum(keratin layer,) lucidum, granulosum, spinous, basale(dividing cells)
What’s in the dermis? SC layer?
Meissner’s corpuscle- light touch, Pacinian corpuscle- coarse touch/ vibration
Fat
What is the stratum corneum made up of in the epidermis? What do the corneo-desmosomes keep together? Increased/ decreased numbers in what conditions?
Corneo-desmosomes + desmosomes
Corneocytes
Psoriasis/ atopic eczema
Cell types of the epidermis?
Keratinocytes- produce keratin
Langerhans cells- present antigens + activate T cells
Melanocytes= produce melanin
Merkel cells- specialised nerve endings for sensation
Common causes of itch with a rash? Without a rash?
Urticaria, atopic eczema, psoriasis, scabies
Renal failure, jaundice, iron deficiency, lymphoma, polycythaemia, pregnancy, drugs, diabetes, cholestasis, skin ageing
What does acne affect? Epidemiology?
Expansion + blockage of the hair follicle
Usually starts in adolescence, often resolves in mid-20s, prevalence= 70-87% in teenagers, affects face, back and chest, usually seen in 13-20 y/o
Pathophysiology of acne?
Narrowing of hair follicle–> hypercornification blocking entrance–> increased sebum production, some becomes trapped, stagnates–> propionibacterium acnes multiply, breaks down triglycerides in sebum–> fatty acids–> neutrophils attraction–> pus + inflammation
Sx of acne?
Whiteheads= closed comedones
Blackheads= open comedones
Skin-coloured papules
Inflammatory lesions= the closed wall of comedones ruptures
Papules
Pustules- white/ yellow spots
Nodules- large red bumps
(Commonly face, chest and upper back)
Ix for acne? Tx for mild and severe acne?
Usually clinical Ix, skin swabs for microscopy + culture. females= hormonal tests
Mild: benzyl peroxide gel/ cream(increases skin turnover, clears pores + reduces bacterial count, causes dryness due to keratolytic effect)
Topical ABx= clindamycin/ erythromycin gel
Topical retinoids= tazarotene gel(inhibit formation + reduce number of microcomedones)- S/E= burning, stinging, dryness + scaling
Severe: oral doxycycline–> oral minocycline- 4 months, CI in pregnancy + children
Hormonal: failed/ menstruation control required, anti-androgen= suppresses sebum production e.g. oral Co-cyprindiol(acetate + ethinylestradiol,) oral retinoids e.g. isoretinoin= last-line, highly teratogenic, S/E= dry skin + lips, photosensitivity to sunlight, suicidal ideation, rarely= SJS and toxic epidermal necrolysis
What is mild acne classed as? Moderate acne?
<20 comedones, <15 inflammatory lesions, /total lesion count<30
20-100 comedones, 15-50 inflammatory lesions/ total lesion count 30-125
> 5 pseudocysts, total comedo count>100 count, total inflammatory count>50, total lesions count>125
What should people with acne be advised of?
To avoid over-cleaning the skin, use a non-alkaline synthetic detergent cleansing product x2 daily on acne-prone skin, avoid oil-based comedogenic skin care products, make-up + sunscreens, picking/ scratching can increase scarring risk, tx takes time to work
Urgent referral for who with acne? Referral to consultant dermatologist for who?
Those with acne fulminans on the same day to the on-call hospital derm team to be assessed within 24 hours
Mild-moderate not responded to 2 completed courses, moderate-severe not responded to previous tx includes oral ABx, acne with scarring/ persistent pigmentary changes, psychological distress/ mental health disorder
Epidemiology of eczema/ dermatitis? Aetiology? RFs?
Genetically complex, familial with strong maternal influence, up to 40% in their lifetime
Endogenous(atopic)- due to hypersensitivity
Exogenous(contact dermatitis from chemicals, sweat and abrasives)
PP not full understood- damaged filaggrin–> exogenous allergens can invade more easily
Family hx, initial TH2 lymphocyte activation–> inflammation
Sx of eczema? Ix?
Face + flexure surfaces of limbs, itchy, erythematous, scaly patches on elbows, knees, ankles, wrists and around the neck. increased dryness. infants= often cheeks–> the body, acute may weep/ exude, recurrent s.aureus may be common
Atopic= clinical, 80%= high serum IgE, must have itchy condition in past 6 months + 3/ more of: hx of involvement of skin creases, personal hx of asthma/ hayfever/ family hx, hx dry skin, onset in first 2y of life
Tx of eczema?
Avoid irritants/ allergens, keep nails short, complete emollient therapy e.g. E45 cream
Occlusive emollients= trap moisture in the skin)eczema= loss of NMF + abnormal lipid bilayer)–> increasing hydration, artificial permeability barrier above stratum corneum preventing water loss between corneocytes
Apply every 4 hours/ 3-4 times per day- x2 at least
250-500g child, 500-750g for adult
Topical therapies for eczema?
Topical corticosteroids= 1st line
Topical calcineurin inhibitors= 2nd line
Moderate- severe/ non-responsive= oral immune-modulators, oral steroids, ABx, phototherapy with UV A, antihistamines
E.g. corticosteroids for eczema?
Very potent(only on thick skin)= DERMOVATE (CLOBETASOL PROPIONATE 0.05%,)
Potent= BETNOVATE,
Moderate= EUMOVATE (CLOBETASONE BUTYRATE,)
Mild= HYDROCORTISONE 0.5%, 1% and 2.5%
(HEBDO- oral)
Directly + indirectly inhibit pro-inflammatory cytokines e.g. IL-1, IL-2, -6, TNF- alpha
S/E= skin atrophy, suppression skin barrier homeostasis, telangiectasia, skin thinning, acne, striae
ONLY INFLAMED SKIN
E.g. topical calcineurin inhibitors for eczema?
Pimecrolimus(mild,) tacrolimus(moderate) ointment
Inhibits calcineurin which induces transcription factors for many interleukins which activate Th cells and induces production of other cytokines- reduce inflammation
(Less effective, less SEs, more useful for sensitive areas, don’t cause skin atrophy- face + eyelid option)
S/E= burning/ stinging following application
Oral immune-modulators for eczema? Oral steroids? ABx? Antihistamines?
Ciclosporin(calcineurin inhibitor,) azathioprine
Oral prednisolone
Flucloxacillin
Chlorphenamine(sedates the patient so they can sleep)
Thin emollient creams for eczema? Thick emollient creams?
E45, diprobase cream, oilatum cream, Aveeno, cetraben, epaderm
50:50 ointment, hydromol/ diprobase/ cetraben/ epaderm ointments
Most common bacterial infection in eczema? Other viral infection? Tx for bacterial? Sx of eczema herpeticum? Tx?
S.aureus–> weeping, crusting, pustules w/ fever or malaise
HSV-1 (eczema herpeticum)
Oral ABx, flucloxacillin, more severe= admission + IV ABx
Widespread, painful, vesicular rash with systemic symptoms e.g. fever, lethargy, irritability + reduced oral intake, lymphadenopathy
Viral swabs–> aciclovir, oral–> IV for mild–> severe
Immediate hospital admission for eczema? Consider referral when? Referral to immunologist, paediatrician/ dermatologist when?
Suspected eczema herpeticum
Diagnosis uncertain, not controlled with current treatment, recurrent secondary infection, high risk of comps, tx advice needed
Food allergy trigger suspected, can’t manage in primary care
Epidemiology of psoriasis? Aetiology/ RFs?
Affects 2% of the UK population, peak prevalence in early adulthood, second peak= 50-60 y/o, equally in men and women
Is polygenic- infection with group A strep, drugs e.g. lithium, UV light, high alcohol use, stress, family hx
PP of psoriasis?
T-cell activation–> upregulation of Th1 types cell cytokines e.g. interferon gamma, interleukins, growth factors and adhesion molecules–> increased uncontrolled hyperproliferation of the keratinocytes in the epidermis with increase in epidermal cell turnover rate
Sx of psoriasis?
Pitting + onycholysis, chronic plaque psoriasis= most common–> well-demarcated disc-shaped salmon-pink silvery plaques on exterior surface of limbs(elbows + knees,) scalp common, thickened epidermis, new plaques at sites of skin trauma
Tx for psoriasis?
Emollients e.g. E45
Topical vitamin D analogues- stimulate keratinocyte differentiation e.g. calcipotriol cream
Topical corticosteroids e.g. hydrocortisone
Topical retinoids e.g. tazarotene gel
UVB
Coal tar
Anti-mitotic e.g. dithranol cream(large plaques)
Extensive plaques= phototherapy with UVA, DMARDs(inhibits folic acid production + DNA replication, GIVE FOLIC ACID SUPPLEMENTS 48 HOURS AFTER TX e.g. oral methotrexate, immunosuppressants e.g. ciclosporin
Occurrence of flexural psoriasis? Sx? 1st + 2nd line tx?
Later in life, well-demarcated red, glazed non-scaly plaques, scaling= ABSENT, confined to flexures, mistaken for candida intertrigo
1st line= topical mild-moderate corticosteroids e.g. hydrocortisone/ clobetasol butyrate(short course prevent atrophy)
2nd line= topical vit D analogue e.g. calcipotriol cream
Who gets guttate psoriasis? Sx? Tx?
Children + young adults
Trunk, upper arms and legs- small circular/ oval plaques over trunk 2 weeks after strep sore throat
Topical mild-moderate corticosteroids e.g. hydrocortisone/ clobetasol butyrate, UVB, coal tar
What is palmoplantar psoriasis? Tx?
Thickening of palms and soles
Emollients, keratolytic agents e.g. salicylic acid, potent topical corticosteroids e.g. flucinonide, phototherapy with UVA, oral retinoid e.g. oral acitretin= anti-proliferative, alongside phototherapy, S/E= dry lips, eyes and mucosa, hyperlipidaemia, disturbed liver functions, TERATOGENIC
IF SYSTEMIC THERAPY FAILED= anti-TNF biologics e.g. IV infliximab, IV etanercept/ IV adalimumab
Types of psoriasis is an emergency?
Pustular- pustules form under areas of erythematous skin(not infectious)
Erythrodermic= extensive red inflamed areas covering most of the surface of the skin- comes away in large patches–> raw + exposed
Specific signs of psoriasis?
Auspitz sign- small points of bleeding when plaques are scraped off
Koebner phenomenon= psoriatic lesions affected by trauma
Residual pigmentation after lesions resolve
What is a venous ulcer defined as?
Loss of skin below the knee on the leg/ foot that takes more than 2 weeks to heal from sustained HTN in the superficial veins
Epidemiology and aetiology of venous ulcers?
Most in developed world, common in later, most on lower leg in triangle above the ankles
Incompetent valves in deep/ perforating veins, previous DVT, atherosclerosis, vasculitis
Varicose veins/ DVT
PP of venous ulcers? Sx?
Increased pressure–> extravasation of fibrinogen through capillary walls–> perivascular fibrin deposition–> poor oxygenation of surrounding skin
Sloping + gradual edges, ulcer= large, superficial, irregular and exudative, oedema of lower leg, venous eczema, brown pigment from haemosiderin, less painful than arterial- relieved by elevation
Ix of venous ulcers? Tx?
ABPI= normal, Doppler USS exclude arterial disease
High compression 4 layered bandage, leg elevation, ABx for infection, analgesia- ibuprofen/ morphine, support stockings for life
Epidem and RFs for arterial ulcers? Sx?
Claudication, HTN, angina/ smoking, arterial disease, hypercholesterolaemia, diabetes
Punched out, painful ulcers higher up leg/ on feet, intense pain worse on elevation + at night, leg= cold, pale, shiny skin, loss of hair, absent peripheral pulses, arterial bruits, NO OEDEMA
Ix and tx for arterial ulcers?
Doppler USS, ABPI= arterial insufficiency
Keep clean + covered, analgesia, vascular reconstruction, never use compression bandaging
Score used for estimating a patient’s risk of developing a pressure ulcer?
Waterlow Score
Sx of neuropathic ulcers? Tx?
Often painless, over pressure areas of the feet, common in diabetes + neurological disease, leprosy= common cause in developing countries, variable size, may be surrounded by callus, warm skin + normal pulses
Keep ulcer clean, remove pressure/ trauma from area, correctly fitting shoes + specialist podiatrist for diabetes
Most common cutaneous vasculitis? Usually appears where? Causes? Sx? Tx?
Leucocytoclastic vasculitis/ angiitis
On lower legs as symmetrical palpable purpura
Idiopathic, drugs, infection, inflammatory/ malignant disease
Haemorrhagic papules, pustules, nodules, plaques, DON’T BLANCH with glass slide pressure, pyrexia + arthralgia
Analgesia, support stockings, dapsone(antibiotic)// prednisolone
Things to ask in a skin cancer hx?
Sunlight/ sun exposure, occupation, foreign travel, radiation exposure, burn easily/ sun protection, smoking, family hx- benign/ malignant, genetic, PMH- immunosuppression?, previous skin cancer, moles, growing, bleeding, itching
Examination for a skin lesion/ ulcer?
Look, feel, move, regional lymphatic drainage, special tests
Look: single/ multiple, size, site, shape, margin, edge, floor, discharge, surrounding skin, whole limb(if limb,) consider dermatoscope
Feel: tenderness, temp, edge-induration, bleeding?
Move: tethering?
Regional lymphatic drainage: lesion in lower limb, trunk, upper limb, head + neck
Special tests: peripheral pulses, light touch and pressure sensation, bony involvement, relevant examinations if systemic features
Epidemiology and RFs for melanoma? 5 year survival rate?
Excessive sun exposure + sunburn in childhood, more affluent people, heavy alcohol drinking(alcohol carcinogenic to melanocytes,) red hair, high density freckles, skin type 1: tends to burn and not tan, atypical moles, multiple melanocytic naevi, sun sensitivity, immunosuppression, family hx, pale skin
90%
Sx of melanoma?
Men= back/ chest, women= lower legs, more in younger people
>95%= dark colour, black/ almost black
ABCDE: asymmetrical, border irregular, colour irregular, diameter>6mm, elevation/ evolution
Major features for a lesion scoring 2 points? Minor scoring 1? Lesions above/= to what are suspicious and need referring?
Change in size, shape, border/ colour
Largest diameter 7mm/ more, inflammation, oozing/ crusting of the lesion, change in sensation- itching
3, low suspicion= monitor over 8 weeks
Most common type of melanoma? Most aggressive?
1)Superficial spreading(SSMM)- trunk in males, legs in females
2) Nodular- most common= trunk, head and neck
3) Lentigo: common= face, more common in elderly
4) Acral: palms/ soles, most common in darker skin types, often presents late, worse prognosis
DDx for melanoma? Tx? Prognosis?
Benign pigmented naevus, seborrheic wart, pyogenic granuloma- small warty lesion bleeds easily, non-pigmented- minor trauma, benign lesion grows quickly
Tx? Prognosis of melanoma?
2WW
Surgical= curative in early cases, metastatic= remove lymph nodes, isolated limb perfusion, radiotherapy, immunotherapy and chemo
Distant= commonest to lung, liver, CNS
Diagnostic excision of the pigmented skin lesion with a 2mm peripheral margin
Wide local excision - margins dependent on staging
Thin lesions<1mm- Breslow= best, >60= <5y survival, female advantage, ulceration= late sign, poor= trunk vs limbs
What is dermoscopy useful for? 3-point checklist?
Distinguishing between benign and malignant pigmented lesions
Asymmetry of colour/ structure, atypical pigment network, blue-white structures
What are pre-malignant keratinocyte tumours which can turn into SCC? RFs for non-melanocytic skin cancer?
Actinic keratosis and Bowen’s disease
UV exposure, Fitzpatrick skin types I-II, increasing age, immune suppression, ionising radiation, chronic wounds, smoking, HPV, genetics
Sx of actinic keratosis? Tx?
Develops over years, sun exposed sites, no hx of rapid growth/ pain/ bleeding/ ulceration, base not raised
Field change= topical treatments(5- flurouracil, imiquimoid, diclofenac,) PDT
Discrete lesions= cryotherapy, C&C, topical treatments
Sx of Bowen’s disease(in situ SCC confined to the epidermis)? Tx?
Develops over years, sun exposed sites, no hx of rapid growth/ pain/ bleeding/ ulceration, base not raised
5- flurouracil, cryotherapy, C&C, PDT
What is a SCC? Sx?
Locally invasive malignant tumour of the squamal keratinocytes, more aggressive than BCC, higher met potential- part to lymph nodes
Sun-exposed sites in later-life, keratotic, ill-defined nodules may ulcerate, grow very rapidly, raised base, may be painful, ulcerates lesions on lower lip/ ear= often more aggressive
Tx of SCC? DDx for SCC?
Surgical excision with minimal margin of 5mm, radiotherapy if non-resectable
Keratocathoma- may shrink, tx surgically, solid core filled with keratin, arise from hair follicle skin cells
Most common malignant skin cancer? Sx?
BCC< metastatic + aggressive than SCC
Border= raised with pearly appearance, slowly enlarging shiny nodule on head and neck which bleeds following minor trauma, local destruction if not tx
BCC tx?
Surgical excision with wide borders + histology to ensure margins
Superficial= cryotherapy, photodynamic therapy, radiotherapy if can’t tolerate surgery
What is the thick skin found over the palms, soles of the feet and flexor surfaces of the fingers that is free from hair called? Hair follicles and sebaceous glands combine to form what? They release their glandular secretions via what mechanism into the hair follicle shaft? The hair follicle is associated with what?
Glabrous skin
Pilosebaceous unit
Holocrine mechanism
Arrector pili- contract to cause the follicle to stand upright
2 types of sweat glands? Eccrine glands release a clear odourless substance comprised mainly of what? Involved in what? Location of apocrine glands? These can be broken down by what producing what? Layer that’s a major body store of adipose tissue?
Eccrine and apocrine
NaCl + water- thermoregulation
Axillary and genital regions
Cutaneous microbes–> body odour
Hypodermis
Cellulitis preferentially involves what area? Aetiology? RFs?
Lower extremities
Group A Beta-haemolytic strep e.g. s.pyogenes= most common, s.aureus, sometimes MRSA
Lymphoedema, leg ulcers, immunosuppression, traumatic wounds, athletes, leg oedema, obesity
PP and presentation of cellulitis? DDx?
Lower leg/ arm and spreads proximally, also abdomen, perianal and periorbital areas- can affect just one side of face
Local inflammation- proximally spreading, hot erythema in affected area, poorly demarcated margins, swelling, warmth and tenderness, occasionally will blister if oedema is prominent, systemically unwell with pyrexia
DVT, septic arthritis, acute gout, ruptured Baker’s cyst
Ix and tx of cellulitis?
Clinical, skin swabs= negative unless from broken skin, serological testing to confirm a strep infection e.g. antistreptolysin O titre(ASOT)
ABx: oral phenoxymethylpenicillin/ oral flucloxacillin, oral erythromycin if penicillin allergic
If widespread- then IV for 3-5 days followed by at least 2 weeks of oral therapy
Recurrent–> prophylaxis low-dose ABx e.g. oral phenoxymethylpenicillin x2 daily
What is necrotising fasciitis? 2 forms? RFs?
Deep-seated infection of SC tissue–> fulminant and spreading destruction of fascia and fat- initially spares the skin, high mortality
Type 1: caused by mixture of aerobic and anaerobic bacteria following abdominal surgery/ diabetics
Type 2: from group A beta-haemolytic strep e.g. s.pyogenes- most common cause, arises in previously healthy patients
Abdominal surgery, immunosuppression
Presentation of necrotising fasciitis?
Severe pain out of proportion to skin findings at initial site of infection rapidly followed by tissue necrosis, infection track rapidly along the tissue planes causing spreading erythema, pain and sometimes crepitus
Suspect in those with fever, toxicity and pain out of proportion to the skin findings
Multi-organ failure= common, mortality= high
Ix and tx of necrotising fasciitis?
Soft tissue gas on XR, raised CRP, very raised white cell count, treat aggressively and promptly
For confirmed group A strep: Type 2= IV benzylpenicillin + clindamycin
Unknown aetiology e.g. Type 1= broad spec IV ABx with inclusion of IV metronidazole
Urgent surgical exploration with extensive debridement/ amputation if necessary
Eron classification for cellulitis: class 1, 2, 3, 4? Admit for IV ABx if what class or what?
No systemic toxicity/ comorbidity, systemic toxicity/ comorbidity, significant systemic toxicity/ significant comorbidity, sepsis/ life-threatening
Class 3 or 4, frail, very young or immunocompromised
Example of diffuse non-scarring hair loss? Responds to what orally, but what happens? Other causes? Causes of localised non-scarring hair loss? Scarring?
Male pattern baldness- topical minoxidil and 1mg finasteride orally- returns as soon as it’s stopped(not available on NHS prescription)
Hypothyroidism; iron deficiency; malnutrition; hypopituitarism; hypoadrenalism; drug-induced
Alopecia areata; ringworm, traumatic, hair pulling, traction; SLE; secondary syphilis
Burns; radiation; shingles; tertiary syphilis; lupus erythematosus; morphoea; lichen planus
Example of diffuse non-scarring hair loss? Responds to what orally, but what happens? Other causes? Causes of localised non-scarring hair loss? Scarring?
Male pattern baldness- topical minoxidil and 1mg finasteride orally- returns as soon as it’s stopped(not available on NHS prescription)
Hypothyroidism; iron deficiency; malnutrition; hypopituitarism; hypoadrenalism; drug-induced
Alopecia areata; ringworm, traumatic, hair pulling, traction; SLE; secondary syphilis
Burns; radiation; shingles; tertiary syphilis; lupus erythematosus; morphoea; lichen planus
What is alopecia areata? % with a family hx? Alternative diagnosis of what if scales/ erythema are present? Tx?
Chronic inflammatory disease affecting the hair follicles +/- nails, patches of hair loss usually on the scalp
20%
Tinea capitis
Reassure and monitor hair loss; refer more severe cases, topical/ locally injected/ systemic steroids +/- contact immunotherapy
If skin lesions are present with itch, search for what? Exceptions are patch testing for what and skin biopsy for what? Causes when skin lesions are present?
Unexcoriated lesions, contact dermatitis and dermatitis herpetiformis
Urticaria, infections, contact dermatitis and allergies, prickly heat, skin infestations e.g. scabies, pediculosis, insect bites, dermatitis herpetiformis, lichen planus, senile atrophy, psychological causes