Dermatology Flashcards
how do you describe a rash?
DCM
Distribution
Configuration
Morphology
list some different terms you might use to describe the distribution of a rash
- generalised/widespread/localised
- flexural
- extensor (knees, elbows, shins)
- pressure areas
- dermatomal
- photosensitive (e.g. face, neck, back of hands)
- Koebner phenomoen = linear eruption at sigh of trauma, occurs in e.g. psoriasis
list some different terms used in describing the configuration of a rash
- discrete
- confluent (lesions merging together)
- target (concentric rings)
- annular (circular/ring shaped)
- discoid/nummular (coin shaped/round)
list some different terms used in describing morphology of a rash/lesion
- macule
- papule
- nodule
- plaque
- vesicle
- bulla
- pustule
- abscess
- wheal
- boil/furnuncle
- carbuncle
define macule
flat area of altered colour
define papule
solid raised lesion <0.5cm in diameter
define nodule
solid raised lesion >0.5cm in diameter w/deeper component
define plaque
palpable scaling raised lesion >0.5cm in diameter
define vesicle
raised, clear fluid-filled lesion <0.5cm in diameter
like a small blister
define bulla
large blister - raised, clear fluid-filled lesion >0.5cm in diameter
define pustule
pus-containing lesion <0.5cm in diameter
define abscess
localised accumulation of pus in the dermis of subcutaneous tissues
define wheal
transient raised lesion due to dermal oedema - e.g. in urticaria
define a boil/furnuncle
staphylococcal infection around/within a hair follicle
define a carbuncle
staphylococcal infection of adjacent hair follicles - multiple boils/furnuncles
list the six functions of normal skin
1) protective barrier
2) temp. regulation
3) sensation
4) vit D synthesis
5) immunosurveillance
6) appearance/cosmesis
briefly explain the structure of normal skin
made up of the epidermis + dermis overlying subcutaneous tissue.
skin appendages = hair, nails, sebaceous glands + sweat glands. these are structures formed by skin-derived cells.
what are the 4 major cell types of the epidermis? what is the key function of each?
- keratinocytes = produce keratin for protective barrier
- Langerhans cells = present antigens + active T cells for immune function
- Melanocytes = produce melanin - pigment for skin, protects from UV damage
- Merkel cells = specialised nerve endings for sensation
what are the 4 layers of the epidermis? how does the turnover time work?
each layer = different stage of maturation of keratinocytes.
turnover time is c.30 days.
stratum basale = basal cell layer
stratum spinosum = prickle cell layer
stratum granulosum = granular cell layer
stratum corneum = horny layer
*in areas of thickened skin (e.g. sole of foot) there’s 5th layer = stratum lucidum. sits beneath stratum corneum, made up of paler, compact keratin.
describe the composition of each layer of the epidermis
stratum basale = deepest layer, actively dividing cells
stratum spinosum = differentiating cells
stratum granulosum = cells lose their nuclei + contain granules of keratohyaline. secrete lipid into intercellular spaces.
stratum corneum = layer of keratin, most superficial layer.
describe the structure/composition of the dermis
mostly collagen. also elastin and glycosaminoglycans (made by fibroblasts) - provide dermis with strength/elasticity.
also contains - immune cells, nerves, skin appendages + lymphatic/blood vessels.
what are the four stages of wound healing?
1) haemostasis - vasoconstriction + platelet aggregation –> clot formation
2) inflammation - vasodilation, migration of neutrophils and macrophages, phagocytosis of cellular debris + invading bacteria
3) proliferation - granulation tissue formation + angiogenesis, re-epithelialisation
4) remodelling - collagen fibre reorganisation, scar maturation
outline the 4 essential principles of managing dermatological emergencies
- supportive care (ABCDE, resuscitation)
- withdrawal of precipitating agents
- management of assoc. complications
- specific treatments
what are the main dermatological emergencies to be aware of?
skin reactions - urticaria, erythema nodosum, erythema multiforme toxic epidermal necrolysis Stevens-Johnson syndrome acute meningococcaemia erythroderma eczema herpeticum nec. fasc.
describe the pathology of urticaria
local increase in permeability of capillaries and small venules.
loads of inflammatory mediators (prostaglandins, leukotrienes, chemotactic factors) get involve but histamine main culprit (derived from skin mast cells).
causes - idiopathic, food/drug/insect/contact allergy, viral or parasitic infections, autoimmune
outline the presentation of: urticaria, angioedema, anaphylaxis
urticaria - itchy wheals
angioedema - swelling of tongue and lips
anaphylaxis - bronchospasm, facial + laryngeal oedenma, hypotension
anaphylaxis may initially present as urticaria + angioedema
briefly outline management of urticaria/angioedema/anaphylaxis
urticaria - antihistamines ± corticosteroids if severe
angioedema - corticosteroids
anaphylaxis - adrenaline, corticosteroids and antihistamines.
what is erythema nodosum? causes?
- hypersensitivity response to variety of stimuli
- causes: group A beta-haemolytic strep, primary TB, pregnancy, malignancy, sarcoidosis, IBD, chlamydia + leprosy
describe the lesions seen in erythema nodosum
- discrete tender nodules, may become confluent. usually on shins.
- will continue to appear for 1-2 weeks + leave bruise-like discolouration as they resolve. don’t ulcerate, don’t scar.
what is Stevens Johnson syndrome?
mucocutaneous necrosis with 2+ mucosal sites involved. skin involvement limited or extensive.
associated with drugs or combinations of infections + drugs.
histopathology = epithelial necrosis + few inflammatory cells.
extensive necrosis differentiates it from erythema multiforme.
what is toxic epidermal necrosis?
overlaps a bit with stevens johnson.
usually drug induced.
extensive skin and mucosal necrosis + systemic toxicity.
histology = full thickness epidermal necrosis + subepidermal detachment.
outline management/complications of erythema multiforme, Stevens-Johnson and toxic epidermal necrosis (TEN)
early recognition and call for help important.
supportive care to maintain haemodynamic equilibrium.
mortality rates: 5-15% SJS, >30% TEN.
death is due to sepsis, electrolyte imbalance or multi-system organ failure.
describe the presentation of acute meningococcaemia - cause?
meningitic features (headache, fever, neck stiffness etc) ± septicaemia. non-blanching purpuric rash on trunk and extremities. might get a blanching maculopapular rash before. can progress to ecchymoses, haemorrhagic bullae, tissue necrosis.
describe the presentation of acute meningococcaemia - cause?
meningitic features (headache, fever, neck stiffness etc) ± septicaemia. non-blanching purpuric rash on trunk and extremities. might get a blanching maculopapular rash before. can progress to ecchymoses, haemorrhagic bullae, tissue necrosis.
what is erythroderma?
“red skin” - exfoliative dermatitis involving >90% of skin surface.
skin is inflamed, oedematus and scaly.
systemically unwell - lymphadenopathy + malaise.
what causes erythroderma? management?
- causes: prev. skin disease (e.g. eczema, psoriasis), lymphoma, drugs (sulphonamides, gold, sulphonyureas, penicillin, allopurinol, captopril) and idiopathic
- management: treat underlying causes. emollients + wet-wraps. topical steroids.
mortality can be 20-40%! depends on underlying cause.
risk of secondary infection, fluid loss/electrolyte imbalance, hypothermia, high-output cardiac failure.
what is eczema herpeticum?
complication of atopic eczema (or other rarer skin conditions) due to HSV.
widespread eruption of extensive crusted papules, blisters and erosions.
systemically unwell - fever and malaise.
how do you treat eczema herpeticum? complications?
antivirals (aciclovir)
abx if secondary bacterial infection.
complications - herpes hepatitis, encephalitis, DIC, death (rare)
what is necrotising fasciitis?
rapidly spready infection of deep fascia with secondary tissue necrosis.
caused by group A haemolytic strep, or mix of aerobic+anaerobic bacteria.
RFs - abdo surgery, medical co-morbidities (diabetes, malignancy)
but 50% occur in prev. healthy people!
how does nec fasc present?
severe pain erythematous, blistering + necrotic skin fever + tachycardia crepitus due to subcutaneous emphysema really rapidly progressing rash.
management of nec fasc?
might do an XR for soft tissue gas, but absence of this doesn’t exclude.
URGENT REFERRAL TO DERM AND PLASTICS.
needs extensive, urgent debridement + IV abx.
mortality is up to 76%
what is erysipelas? and cellulitis?
both spreading bacterial infections of skin
cellulitis = deep subcutaneous tissue
erysipelas = acute, superficial form of cellulitis - dermis and upper subcut tissue
what causes erysipelas/cellulitis?
strep. pyogenes and staph aureus
RFs - immunosuppression, wounds, leg ulcers, minor skin injury, poor hygiene (toewebs), poor vascularisation (E.g. DM)
how does erysipelas/cellulitis present?
usually lower limb. inflamed - swelling, erythema, warmth, pain.
systemically unwell with fever, malaise or rigors (esp. with erysipelas).
distinguish erysipelas from cellulitis by well-defined raised red border.
how is erysipelas/cellulitis managed?
abx (e.g. fluclox, benpen)
supportive care - rest, leg elevation, sterile dressings, analgesia
complications - local necrosis, abscess and septicaemia.
what is staphylococcal scalded skin syndrome?
seen in babies/early childhood.
due to production of epidermolytic toxin from phage group II, benpen-resistant (coagulase positive) staph.
how does staphylococcal scalded skin syndrome present?
- few hrs to days, worse over face, neck, axillae, groin
- scalded skin appearance followed by large flaccide bulla
- perioral crusting
- intraepidermal blistering
- very painful
- recovery is withint 5-7 days but beware dehydration
how do you manage staphylococcal scalded skin syndrome?
abx e.g. penicillinase-resistant penicillin, fusidic acid, erythromycin. IV then oral.
fluid resus.
analgesia.
what are the three main groups of fungal infections?
dermatophytes - tinea, ringword
yeasts - candidiasis
moulds - aspergillus.
usually superficial and itchy.
how does tinea corporis present?
tinea infection of trunk + limbs
itchy, circular/annular lesions. clearly defined, raised and scaly edge.
how does tinea cruiris present?
tinea infection of groin and natal cleft.
very itchy, similar appearance to tinea corporis.
how does tinea pedis present?
athlete’s foot
moist scaling and fissuring in toewebs, spreading to sole and dorsal aspect of foot.
how does tinea manuum present?
tinea infection of hand
scaling and dryness in palmar creases
how does tinea capitis present?
scalp ringworm
patches of broken hair, scaling and inflammation
how does tinea unguium present?
tinea infection of nail
yellow discolouration, thickened and crumbly nail
how does tinea incognito present?
inappropriate treatment of tinea infection with topical or systemic corticosteroids
ill-defined and less scaly lesions
how does candidiasis present?
white plaques on mucosal areas, erythema with satellite lesions in flexures
how does pityriasis/tinea versicolor present?
scaly pale brown patches on upper trunk that fail to tan on sun exposure, usually asymptomatic.
outline general management of fungal skin infections
- treat any known precipitating factors (e.g. immunosuppression, moist environment)
- topical antifungal agents e.g. terbinafine cream
- oral antifungals (itraconazole) if severe, widespread or nail infection
AVOID topical steroids
what are the main types of skin cancer?
basal cell carcinoma and squamous cell carcinoma (non-melanomas)
malignant melanoma - the worst one.
what is basal cell carcinoma?
slow-growing, locally invasive malignant tumour of epidermal keratinocytes - normally older people, rarely mets.
most common malignant skin tumour.
list some risk factors for basal cell carcinoma
UV exposure freq./severe sunburn in childhood skin type I (always burns, never tans) increasing age male sex immunosuppression prev. hx of skin cancer genetic predisposition
describe the appearance of basal cell carcinomas
different types:
- nodular - most common, a small skin-coloured papule/nodule with surface telangiectasia and pearly rolled edge. may have necrotic/ulcerated centre (rodent ulcer)
- superficial (plaque-like)
- cystic
- morphoeic (sclerosing)
- keratotic
- pigmented
most common over head and neck
briefly outline management of BCCs
- surgical excision (+ histology)
- Mohs micrographic surgery if high risk/recurrent
- radiotherapy if surgery not possible
- others e.g. cryo, curettage + cautery, topical photodynamic therapy, imiquimod cream - all only if small/low-risk
what is Mohs micrographic surgery?
lesion is excised, then tissue borders progressively excised until specimens are microscopically free of tumour.
used in high risk/recurrent tumours.
what is squamous cell carcinoma?
locally invasive malignant tumour of the epidermal keratinocytes/appendages
has the potential to metastasise
give some RFs for SCC
- excessive UV exposure
- pre-malignant skin conditions (e.g. actinic keratoses)
- chronic inflammation (e.g. leg ulcers, wound scars)
- immunosuppression
- genetic predisposition
describe the appearance of an SCC
keratotic (e.g. scaly, crusty), ill-defined nodule which may ulcerate
outline the management options for SCC
- surgical excision
- Mohs micrographic surgery
- radiotherapy - for large, non-respectable tumours
what is malignant melanoma?
invasive malignant tumour of epidermal melanocytes
has potential to metastasise
this is the bad one - affects young people, can progress rapidly.
list some RFs for malignant melanoma
- excessive UV exposure
- type I skin
- hx of multiple moles/atypical moles
- family/prev. hx of melanoma
outline the key features to look for when assessing a mole for malignant melanoma
"ABCDE Symptoms" * Asymmetrical shape Border irregularity * Colour irregularity Diameter > 6mm * Evolution of lesions (change of size, shape etc) Symptoms e.g. bleeding, itching
- major suspicious features
more common on legs in women, trunk in men
what are the different types of melanoma?
- superficial spreading melanoma
- nodular melanoma
- lentigo maligna melanoma
- accral lentiginous melanoma
what is superficial spreading melanoma?
common on lower limbs, in young/middle-age adults.
related to intermittent high-intensity UV exposure
what is nodular melanoma?
common on trunk, in young/middle age adults.
related to intermittent high-intensity UV exposure.
what is lentigo maligna melanoma?
common on face and in elderly population.
related to long-term cumulative UV exposure.
what is acral lentiginous melanoma?
common on palms, soles and nailbeds; in elderly.
no clear relation to UV exposure.
how is malignant melanoma managed? prognosis?
surgical excision is definitive.
radiotherapy + chemo both have a role. chemo esp for metastatic disease.
recurrence risk based on Breslow thickness scoring.
survival depends on TNM staging.
what is atopic eczema? what causes it?
eczema = papules and vesicles on erythematous base atopic = most common type. usually develops by early childhood and resolves during teenage years - but may recur.
causes - not 100% known. family hx of atopy. primary genetic defect in skin barrier function - loss of function of filaggrin protein.
exacerbating factors = infections, allergens, sweating, heat, severe stress.
how does atopic eczema present?
itchy, erythematous dry scaly patches.
common on face + extensor surfaces in infants, on flexor surfaces in children/adults.
acute lesions = erythematous, vesicular + exudative.
chronic scratching can lead to excoriations, lichenification.
can get nail pitting/ridging of nails.
outline some general advice to give patients for the management of atopic eczema
avoid known exacerbators
emollient use needs to be frequent and liberal - prescribe the greasiest that they’ll actually use (no point going greasier if they’re not gonna comply)
may need to use bandages over the emollients if severe.
bath/soap substitutes.
briefly describe management options for atopic eczema
- general/lifestyle measure
- topical: emollients, steroids for flare-ups, immunomodulators (tacrolimus, pimecrolimus)
- oral: antihistamines stop itching (helps break itch/scratch cycle), abx (fluclox) for secondary infections.
- phototherapy + immunosuppressants in severely non-responsive cases
what is acne vulgaris? causes?
inflammatory disease of the pilosebaceous follicle.
affects 80% of teenagers.
causes - hormonal (androgen).
contributing factors = increased sebum production, abnormal follicular keratinization, bacterial colonization and inflammation.
describe the different lesions seen in acne
- non-inflammatory = mild acne. open and closed comedones (black + white heads)
- inflammatory = mod-severe acne. papules, pustules, nodules and cysts.
commonly affects face, chest, upper back.
outline management options for acne
treatments must last 6+ weeks to work.
- topical (for mild acne): benzoyl peroxide, abx, retinoids
- oral (mod-severe): abx, anti-androgens (in females)
- retinoids - severe acne only.
what is psoriasis? types?
chronic inflammatory skin disease due to hyperproliferation of keratinocytes and inflammatory cell infiltration.
Types:
- chronic plaque psoriasis = most common
- guttate = raindrop lesions
- seborrhoeic = naso-labial and retro-auricular
- flexural
- pustular = palmar/planatr
what causes psoriasis?
- complex - genetic, immunological, environmental.
- precipitating factors - trauma (Koebner phenomenon), infection, drugs, stress, alcohol
how does psoriasis present?
- well demarcated erythematous scaly plaques
- may be itchy, burning, painful
- extensor surfaces of body/scalp
- Auspitz sign = scratch/removal of scales causes capillary bleeds
- nail changes (pitting, oncyolysis) in 50%
- 5% have psoriatic arthropathy associated
outline management of psoriasis?
- avoid precipitating, emollients
- topical (for localised/mild): vit D analogues, corticosteroids, coal tar preparations, dithranol, topical retinoids, keratinolytics, scalp preparations
- phototherapy (extensive disease)
- oral (extensive + severe, or w/systemic involvement): methotrexate, retinoids, ciclosporin, antibiologics etc
what are the different types of blistering skin disorders?
- immunobullous diseases (e.g. bullous pemphigoin, pemphigus vulgaris)
- blistering skin infections (e.g. herpes simplex)
- other e.g. porphyria cutanea tarda
bullous pemphigoid and pemphis vulgaris = uncommon conditions due to immune reaction within skin.
most common causes of blisters = impetigo, insect bites, HSV, HZV, acute contact dermatitis, pompholyx, burns
how are leg ulcers classified?
main types = venus, arterial, neuropathic.
others = vasculitic (punched out lesions), infected, malignancy (e.g. SCC)
describe the typical lesion and common sites of venous ulcers
- painful, worse on standing
- hx of venous disease (e.g. varicose veins, DVT)
- large, shallow, irregular ulcer
- exudative and granulating base
- site = malleolar area, medial > lateral
what associated features might you see with a venous ulcer?
- warm skin
- normal peripheral pulses
- leg oedema, brown pigment (haemosiderin + melanin deposition), lipodermatosclerosis
what Ix/Rx might you do for a venous ulcer?
Ix - will have normal ABPI (0.8-1)
Rx - compression bandaging (excl arterial insufficiency first)
describe the typical lesion and common sites of arterial ulcers
- painful especially at night + when legs are elevated
- hx of arterial disease
- small, sharply defined deep ulcer
- necrotic base
- site = pressure and trauma sites, e.g. pretibial, supramalleolar (lateral), at distal points e.g. toes
what associated features might you see with an arterial ulcer?
- cold skin
- weak or absent peripheral pulses
- shiny pale skin
- loss of hair
what Ix/Rx might you do for an arterial ulcer?
Ix - ABPI <0.8 (arterial insufficiency); doppler studies + angiography
Rx - vascular reconstruction. compression bandages CI!!
describe the typical lesion and common sites of neuropathic ulcers
- often painless
- abnormal sensation
- hx of diabetes or neurological disease
- lesion: variable size/depth, granulating bases, surrounded by/underneath hyperkeratotic lesion (e.g. callus)
- site = pressure sites (soles, heels, toes, metatarsal heads)
what associated features might you see with a neuropathic ulcer?
- warm skin
- normal peripheral pulses (cold/weak/absent if neuroischaemic ulcer)
- peripheral neuropathy
what Ix/Rx might you do for a neuropathic ulcer?
Ix - ABPI <0.8 => neuroischaemic ulcer; XR to excl osteomyelitis
Rx - wound debridement, regular reposition, appropriate footwear, good nutrition
give some brief info on topical treatments
Deliver Rx to affected area and reduces SE side effects.
Suitable for local + less severe disease.
Active constituent transported to skin by base.
Types:
- Lotion - liquid
- Cream (oil in water)
- Gel (polymers in liquid)
- Ointment (oil with little water)
- Paste (powder in ointment)
what is a “finger tip unit”?
from crease to tip of finger = 0.5g of topical treatment. used when calculating amount to prescribe and for instructing patients.
give some basic info on emollients
used to rehydrate skin + re-establish surface lipid layer.
used for dry, scaling conditions and as soap substitutes.
all 500g/tub.
e.g. diprobase, double base.
how are topical corticosteroids classified? give examples of each
mildly potent = hydrocortisone
moderately potent = eumovate (clobetasone butyrate)
potent = betnovate (betamethasone valerate)
very potent = dermovate (clobetasol propionate)
aim to use weakest effect strength - especially in sensitive areas/children.
come in 30g tubes.
list some possible side effects of topical corticosteroids
skin atrophy
telangiectasia
striae
can mask/cause/exacerbate skin infections/acne/contact dermatitis etc
give some examples of topical antibiotics, and possible side effects
e.g. fusidic acid, mupirocin, neomycin
side effects:
- local (irritation, allergy)
- systemic: GI upset, rash, anaphylaxis, candidiasis, abx associated infections
give some basic info on oral retinoids
e.g. isotretinoin, acitretin
indications - acne, psoriasis, disorders of keratinisation
side effects:
- Mucocutaneous reactions: dry skin, lips, eyes
- Disordered liver function (LFT)
- Hypercholesterolaemia (Blood test)
- Myalgia, arthralgia, depression
- Teratogenicity (effective contraception one month before, during and after isotretinoin, 2 years after acitretin)
