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
