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Dermatology Flashcards

1
Q

how do you describe a rash?

A

DCM
Distribution
Configuration
Morphology

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2
Q

list some different terms you might use to describe the distribution of a rash

A
  • 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
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3
Q

list some different terms used in describing the configuration of a rash

A
  • discrete
  • confluent (lesions merging together)
  • target (concentric rings)
  • annular (circular/ring shaped)
  • discoid/nummular (coin shaped/round)
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4
Q

list some different terms used in describing morphology of a rash/lesion

A
  • macule
  • papule
  • nodule
  • plaque
  • vesicle
  • bulla
  • pustule
  • abscess
  • wheal
  • boil/furnuncle
  • carbuncle
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5
Q

define macule

A

flat area of altered colour

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6
Q

define papule

A

solid raised lesion <0.5cm in diameter

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7
Q

define nodule

A

solid raised lesion >0.5cm in diameter w/deeper component

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8
Q

define plaque

A

palpable scaling raised lesion >0.5cm in diameter

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9
Q

define vesicle

A

raised, clear fluid-filled lesion <0.5cm in diameter

like a small blister

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10
Q

define bulla

A

large blister - raised, clear fluid-filled lesion >0.5cm in diameter

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11
Q

define pustule

A

pus-containing lesion <0.5cm in diameter

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12
Q

define abscess

A

localised accumulation of pus in the dermis of subcutaneous tissues

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13
Q

define wheal

A

transient raised lesion due to dermal oedema - e.g. in urticaria

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14
Q

define a boil/furnuncle

A

staphylococcal infection around/within a hair follicle

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15
Q

define a carbuncle

A

staphylococcal infection of adjacent hair follicles - multiple boils/furnuncles

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16
Q

list the six functions of normal skin

A

1) protective barrier
2) temp. regulation
3) sensation
4) vit D synthesis
5) immunosurveillance
6) appearance/cosmesis

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17
Q

briefly explain the structure of normal skin

A

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.

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18
Q

what are the 4 major cell types of the epidermis? what is the key function of each?

A
  • 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
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19
Q

what are the 4 layers of the epidermis? how does the turnover time work?

A

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.

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20
Q

describe the composition of each layer of the epidermis

A

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.

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21
Q

describe the structure/composition of the dermis

A

mostly collagen. also elastin and glycosaminoglycans (made by fibroblasts) - provide dermis with strength/elasticity.

also contains - immune cells, nerves, skin appendages + lymphatic/blood vessels.

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22
Q

what are the four stages of wound healing?

A

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

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23
Q

outline the 4 essential principles of managing dermatological emergencies

A
  • supportive care (ABCDE, resuscitation)
  • withdrawal of precipitating agents
  • management of assoc. complications
  • specific treatments
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24
Q

what are the main dermatological emergencies to be aware of?

A 
skin reactions - urticaria, erythema nodosum, erythema multiforme
toxic epidermal necrolysis
Stevens-Johnson syndrome
acute meningococcaemia
erythroderma
eczema herpeticum
nec. fasc.
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25
Q

describe the pathology of urticaria

A

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

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26
Q

outline the presentation of: urticaria, angioedema, anaphylaxis

A

urticaria - itchy wheals
angioedema - swelling of tongue and lips

anaphylaxis - bronchospasm, facial + laryngeal oedenma, hypotension
anaphylaxis may initially present as urticaria + angioedema

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27
Q

briefly outline management of urticaria/angioedema/anaphylaxis

A

urticaria - antihistamines ± corticosteroids if severe
angioedema - corticosteroids
anaphylaxis - adrenaline, corticosteroids and antihistamines.

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28
Q

what is erythema nodosum? causes?

A
  • hypersensitivity response to variety of stimuli

- causes: group A beta-haemolytic strep, primary TB, pregnancy, malignancy, sarcoidosis, IBD, chlamydia + leprosy

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29
Q

describe the lesions seen in erythema nodosum

A
  • 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.
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30
Q

what is Stevens Johnson syndrome?

A

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.

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31
Q

what is toxic epidermal necrosis?

A

overlaps a bit with stevens johnson.
usually drug induced.
extensive skin and mucosal necrosis + systemic toxicity.
histology = full thickness epidermal necrosis + subepidermal detachment.

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32
Q

outline management/complications of erythema multiforme, Stevens-Johnson and toxic epidermal necrosis (TEN)

A

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.

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33
Q

describe the presentation of acute meningococcaemia - cause?

A 
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.
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34
Q

describe the presentation of acute meningococcaemia - cause?

A 
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.
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35
Q

what is erythroderma?

A

“red skin” - exfoliative dermatitis involving >90% of skin surface.
skin is inflamed, oedematus and scaly.
systemically unwell - lymphadenopathy + malaise.

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36
Q

what causes erythroderma? management?

A
  • 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.

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37
Q

what is eczema herpeticum?

A

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.

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38
Q

how do you treat eczema herpeticum? complications?

A

antivirals (aciclovir)
abx if secondary bacterial infection.

complications - herpes hepatitis, encephalitis, DIC, death (rare)

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39
Q

what is necrotising fasciitis?

A

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!

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40
Q

how does nec fasc present?

A 
severe pain
erythematous, blistering + necrotic skin
fever + tachycardia
crepitus due to subcutaneous emphysema
really rapidly progressing rash.
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41
Q

management of nec fasc?

A

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%

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42
Q

what is erysipelas? and cellulitis?

A

both spreading bacterial infections of skin
cellulitis = deep subcutaneous tissue
erysipelas = acute, superficial form of cellulitis - dermis and upper subcut tissue

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43
Q

what causes erysipelas/cellulitis?

A

strep. pyogenes and staph aureus

RFs - immunosuppression, wounds, leg ulcers, minor skin injury, poor hygiene (toewebs), poor vascularisation (E.g. DM)

44
Q

how does erysipelas/cellulitis present?

A

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.

45
Q

how is erysipelas/cellulitis managed?

A

abx (e.g. fluclox, benpen)
supportive care - rest, leg elevation, sterile dressings, analgesia

complications - local necrosis, abscess and septicaemia.

46
Q

what is staphylococcal scalded skin syndrome?

A

seen in babies/early childhood.

due to production of epidermolytic toxin from phage group II, benpen-resistant (coagulase positive) staph.

47
Q

how does staphylococcal scalded skin syndrome present?

A
  • 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
48
Q

how do you manage staphylococcal scalded skin syndrome?

A

abx e.g. penicillinase-resistant penicillin, fusidic acid, erythromycin. IV then oral.
fluid resus.
analgesia.

49
Q

what are the three main groups of fungal infections?

A

dermatophytes - tinea, ringword
yeasts - candidiasis
moulds - aspergillus.

usually superficial and itchy.

50
Q

how does tinea corporis present?

A

tinea infection of trunk + limbs

itchy, circular/annular lesions. clearly defined, raised and scaly edge.

51
Q

how does tinea cruiris present?

A

tinea infection of groin and natal cleft.

very itchy, similar appearance to tinea corporis.

52
Q

how does tinea pedis present?

A

athlete’s foot

moist scaling and fissuring in toewebs, spreading to sole and dorsal aspect of foot.

53
Q

how does tinea manuum present?

A

tinea infection of hand

scaling and dryness in palmar creases

54
Q

how does tinea capitis present?

A

scalp ringworm

patches of broken hair, scaling and inflammation

55
Q

how does tinea unguium present?

A

tinea infection of nail

yellow discolouration, thickened and crumbly nail

56
Q

how does tinea incognito present?

A

inappropriate treatment of tinea infection with topical or systemic corticosteroids
ill-defined and less scaly lesions

57
Q

how does candidiasis present?

A

white plaques on mucosal areas, erythema with satellite lesions in flexures

58
Q

how does pityriasis/tinea versicolor present?

A

scaly pale brown patches on upper trunk that fail to tan on sun exposure, usually asymptomatic.

59
Q

outline general management of fungal skin infections

A
  • 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
60
Q

what are the main types of skin cancer?

A

basal cell carcinoma and squamous cell carcinoma (non-melanomas)
malignant melanoma - the worst one.

61
Q

what is basal cell carcinoma?

A

slow-growing, locally invasive malignant tumour of epidermal keratinocytes - normally older people, rarely mets.
most common malignant skin tumour.

62
Q

list some risk factors for basal cell carcinoma

A 
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
63
Q

describe the appearance of basal cell carcinomas

A

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

64
Q

briefly outline management of BCCs

A
  • 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
65
Q

what is Mohs micrographic surgery?

A

lesion is excised, then tissue borders progressively excised until specimens are microscopically free of tumour.
used in high risk/recurrent tumours.

66
Q

what is squamous cell carcinoma?

A

locally invasive malignant tumour of the epidermal keratinocytes/appendages
has the potential to metastasise

67
Q

give some RFs for SCC

A
  • excessive UV exposure
  • pre-malignant skin conditions (e.g. actinic keratoses)
  • chronic inflammation (e.g. leg ulcers, wound scars)
  • immunosuppression
  • genetic predisposition
68
Q

describe the appearance of an SCC

A

keratotic (e.g. scaly, crusty), ill-defined nodule which may ulcerate

69
Q

outline the management options for SCC

A
  • surgical excision
  • Mohs micrographic surgery
  • radiotherapy - for large, non-respectable tumours
70
Q

what is malignant melanoma?

A

invasive malignant tumour of epidermal melanocytes
has potential to metastasise

this is the bad one - affects young people, can progress rapidly.

71
Q

list some RFs for malignant melanoma

A
  • excessive UV exposure
  • type I skin
  • hx of multiple moles/atypical moles
  • family/prev. hx of melanoma
72
Q

outline the key features to look for when assessing a mole for malignant melanoma

A 
"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
73
Q

what are the different types of melanoma?

A
  • superficial spreading melanoma
  • nodular melanoma
  • lentigo maligna melanoma
  • accral lentiginous melanoma
74
Q

what is superficial spreading melanoma?

A

common on lower limbs, in young/middle-age adults.

related to intermittent high-intensity UV exposure

75
Q

what is nodular melanoma?

A

common on trunk, in young/middle age adults.

related to intermittent high-intensity UV exposure.

76
Q

what is lentigo maligna melanoma?

A

common on face and in elderly population.

related to long-term cumulative UV exposure.

77
Q

what is acral lentiginous melanoma?

A

common on palms, soles and nailbeds; in elderly.

no clear relation to UV exposure.

78
Q

how is malignant melanoma managed? prognosis?

A

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.

79
Q

what is atopic eczema? what causes it?

A 
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.

80
Q

how does atopic eczema present?

A

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.

81
Q

outline some general advice to give patients for the management of atopic eczema

A

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.

82
Q

briefly describe management options for atopic eczema

A
  • 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
83
Q

what is acne vulgaris? causes?

A

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.

84
Q

describe the different lesions seen in acne

A
  • 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.

85
Q

outline management options for acne

A

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.
86
Q

what is psoriasis? types?

A

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

87
Q

what causes psoriasis?

A
  • complex - genetic, immunological, environmental.

- precipitating factors - trauma (Koebner phenomenon), infection, drugs, stress, alcohol

88
Q

how does psoriasis present?

A
  • 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
89
Q

outline management of psoriasis?

A
  • 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
90
Q

what are the different types of blistering skin disorders?

A
  • 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

91
Q

how are leg ulcers classified?

A

main types = venus, arterial, neuropathic.

others = vasculitic (punched out lesions), infected, malignancy (e.g. SCC)

92
Q

describe the typical lesion and common sites of venous ulcers

A
  • 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
93
Q

what associated features might you see with a venous ulcer?

A
  • warm skin
  • normal peripheral pulses
  • leg oedema, brown pigment (haemosiderin + melanin deposition), lipodermatosclerosis
94
Q

what Ix/Rx might you do for a venous ulcer?

A

Ix - will have normal ABPI (0.8-1)

Rx - compression bandaging (excl arterial insufficiency first)

95
Q

describe the typical lesion and common sites of arterial ulcers

A
  • 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
96
Q

what associated features might you see with an arterial ulcer?

A
  • cold skin
  • weak or absent peripheral pulses
  • shiny pale skin
  • loss of hair
97
Q

what Ix/Rx might you do for an arterial ulcer?

A

Ix - ABPI <0.8 (arterial insufficiency); doppler studies + angiography
Rx - vascular reconstruction. compression bandages CI!!

98
Q

describe the typical lesion and common sites of neuropathic ulcers

A
  • 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)
99
Q

what associated features might you see with a neuropathic ulcer?

A
  • warm skin
  • normal peripheral pulses (cold/weak/absent if neuroischaemic ulcer)
  • peripheral neuropathy
100
Q

what Ix/Rx might you do for a neuropathic ulcer?

A

Ix - ABPI <0.8 => neuroischaemic ulcer; XR to excl osteomyelitis
Rx - wound debridement, regular reposition, appropriate footwear, good nutrition

101
Q

give some brief info on topical treatments

A

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)

102
Q

what is a “finger tip unit”?

A

from crease to tip of finger = 0.5g of topical treatment. used when calculating amount to prescribe and for instructing patients.

103
Q

give some basic info on emollients

A

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.

104
Q

how are topical corticosteroids classified? give examples of each

A

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.

105
Q

list some possible side effects of topical corticosteroids

A

skin atrophy
telangiectasia
striae
can mask/cause/exacerbate skin infections/acne/contact dermatitis etc

106
Q

give some examples of topical antibiotics, and possible side effects

A

e.g. fusidic acid, mupirocin, neomycin
side effects:
- local (irritation, allergy)
- systemic: GI upset, rash, anaphylaxis, candidiasis, abx associated infections

107
Q

give some basic info on oral retinoids

A

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)

► Med Notes (62 decks)

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