Dermatology Flashcards
macule
a flat area of altered colour e.g. freckle or naevi
patch
a larger area of altered colour or texture compared to a macule
e.g. naevus flammeus/port wine stain - a congenital lesion consisting of small blood vessels in the skin that are open all the time
papule vs pustule
papule = solid raised lesion <0.5cm in diameter (some sources say <1cm)
e.g. xanthomata or some moles
pustule = similar to papule but have a white centre due to pus build up
nodule
solid raised lesion >0.5cm in diameter
e.g. pyogenic granuloma (a vascular lesion) or a wart
plaque
palpable scaling raised lesion >0.5cm
e.g. psoriasis
vesicle vs bulla
vesicle = <0.5cm
bulla = >0.5cm e.g. a burn blister
wheal
transient raised lesion due to dermal oedema
the fluid is within the dermis layer rather than higher up - like in a vesicle or bulla
are characteristically evanescent (i.e. lasting less than 24 hours)
e.g. urticaria
boil/furuncle vs carbuncle
boil/furuncle = staphylococcal infection around or within a hair follicle
carbuncle = staphylococcal infection of adjacent hair follicles as well (multiple boils/furuncles)
lichenification
Thickening (and hyperpigmentation) of the epidermis in response to excessive itching or rubbing of the skin (a secondary skin lesion)
crust
- Rough surface consisting of dried serum, blood, bacteria and cellular debris
- That has exuded through an eroded epidermis e.g. from a burst blister
- E.g. impetigo
types of scar
May be atrophic (thinning), hypertrophic (hyperproliferation within wound boundary), or keloidal (hyperproliferation beyond wound boundary)
hirsutism vs hypertrichosis
hirsutism - androgen-dependent hair growth in a female
hypertrichosis - non-androgen dependent pattern of excessive hair growth e.g. in pigmented naevi
onycholysis associations
associated with trauma, psoriasis, fungal nail infection, hyperthyroidism
pitting associations
psoraisis, eczema and alopecia acreata
medication risk factors for acne vulgaris
androgens, corticosteroids, antiepileptics, isoniazid, lithium, ACTH
pathophysiology of acne vulgaris
- abnormal follicular differentiation - in acne keratinocytes are retained and accumulate due to increased cohesiveness instead of being shed
- sebaceuous gland hyperplasia and excess sebum production (due to stimulation by androgens)
- propionibacterium acnes colonisation (gram positive non-motile rods)
- inflammation and immune response
open vs closed comedone
open = blackhead closed = whitehead
cysts in acne vulgaris
most severe type of acne spot
look similar to boils
carry the greatest risk of permanent scarring
acne vulgaris grading
mild
moderate
severe
depending on comedone count, number of inflammatory lesions and number of pseudocysts and scars
acne vulgaris treatment
PATIENT EDUCATION
- e.g. emphasise it doesn’t mean skin is dirty
CONSERVATIVE
- don’t over wash face, use fragrance free/paraben free products, SPF, role of diet is controversial (emerging data suggests high GI diets may exacerbate)
MEDICAL
- topical retinoid alone (adapalene, tretinoin) or in combination with benzoyl peroxide
- topical antibiotic (e.g. clindamycin 1%)
- azelaic acid
- cream or lotions preferable with dry/sensitive skin and less greasy gels in oily skin
- if not responding to topical then consider oral Abx
- COC
- refer to derm if all failed for consideration of oral isotretinoin
oral antibiotic for acne vulgaris
lymecycline or doxycycline for a max of 3 months
NB a topic retinoid or benzoyl peroxide should always be co-presrcibed with oral or topical ABx to reduce the risk of antibiotic resistance occuring
follow up in acne vulgaris
review each treatment step at 8-12 weeks
If acne has cleared or almost cleared — consider maintenance therapy with topical retinoids (first line, if not contraindicated) or azelaic acid
acne rosacea
chronic disorder of blood vessels and sebaceuos glands in central face regions
primarily affects the convexities of the face, cheeks, chin, nose and central forehead (but may also extend to the upper trunk)
symptoms; flushing, telangiectasia, erythema, rhinophyma, irritated eyes. episodes of remission and recurrence
management of acne rosacea
PATIENT EDUCATION
- avoid irritants and sun over-exposure, CBT proven to help avoid facial flushing
CONSERVATIVE
- don’t overwash face
- use fragrance free/paraben free products, SPF
- review medications as some drugs may aggrevate flushing symptoms (CCBs) and flares (topical steroids)
MEDICAL
- topical metronidazole or azelaic acid
- if with papules then prescribe an oral Abx
EXTREME MEDICAL
- isoretrinoin
- IPL (intense pulsed light) for erythema with telangiectasia
- prominent rhinophyma –> plastic surgeon
for ocular - eyelid hygeine measures, ocular lubricants for dry eye
oral antibiotic for acne rosacea
lymecycline, erythromycin, doxycycline or tetracycline
follow up on those on isotretinoin
depression screen LFTs lipids - pancreatitis risk photosensitivity (SE) dry mucus membranes PPP - double contraception - condom + OCP
solar keratosis (actinic keratosis)
small scaly macules or plaques localised in sun-exposed areas of the body - ill-defined
typically in middle-aged men with fair skin
what can solar keratosis (actinic keratosis) progress into
sqaumous cell carcinoma (SCC)
removal of actinic keratosis
o Can be with cryotherapy
o 5-FU (5-flurouracil – a chemotherapy drug) creams where the lesions are widespread
o imiquimod cream
(Diclofenac and retinoic acid are other drugs in cream or ointment form that are helpful when applied to milder actinic keratoses)
o excision as an alternative to cryotherapy for large lesions
o chemical peels
o photodynamic therapy
o curettage and cautery (where the affected skin is scraped away under LA)
another name for Bowen’s disease
squamous cell carcinoma in situ
1 in 20 – 1 in 30 will progress to cancer in untreated Bowen’s disease
appearance of Bowen’s disease vs actinic keratosis
bowen’s disease = red or pink, scaly or crusty, flat or raised, possibly itchy area
actinic keratosis = skin coloured, yellowish or erythematous ill defined small scaly macules or papules
ABCDE
asymmetry border irregulatiry colour variation diameter >6mm evolution of the lesion
name for melanoma in situ
lentigo maligna
lentigo maligna
consists of malignant cells but does not show invasive growth - is confined to the epidermis
unlike other types of melanoma, it is related to chronic sun exposure rather then infrequent intense exposure
management of lentigo maligna
excision biopsy with a 2mm margin followed by WLE oe Mohs surgery to remove all the cells
the other option is to watch the lesion carefully and biopsy if it becomes more suspicious
seborrheic keratosis
benign skin tumour frequently found on the torso
75% of those aged 70 are affected - often arise in middle age
cause unknown but HPV and sunlight are risk factors
stuck on, brown/black appearance, painless but can cause itching
management of seborrheic keratosis
diagnosed by clinical appearance (can use dermoscopy) or biopsy if unsure (e.g. isolated dark SK)
manage - usually none required
- Corticosteroids (topical betamethasone) can be used on irritated and itching seborrhoeic keratosis
- They can also be removed if there are unsightly or rubbing against clothing with cryotherapy, curettage and cautery, cryotherapy, and laser therapy
treatment of viral warts
watchful waiting
debridement + salicyclic acid (an adjunct to this is duct tape occlusion)
cryotherapy
silver nitrate solution - applied every other day for 3-6 weeks
curretage and cautery can be used for larger warts under LA
dermatofibroma
nodules of the dermis that can develop in reaction to insect bites or trauma but exact cause is not clear
ranges from pink to brown
more common in women - often on the LL of young or middle ages adults
treat if causing problemss (e.g. if unsightly)
epidermoid cyst management
can safely be left alone
- Can have Abx if become infected
- Both epidermoid and pilar cysts can be removed under LA – but will leave a scar
- Reasons for removal
o If the cyst is unsightly and easily seen by others
o If it interferes with everyday life, for example by catching on your comb
o If the cyst becomes infected
pyogenic granuloma
Vascular lesion that occurs on both mucosa and skin
Rapidly developing bright-red or blood -crusted, pedunculated nodule
Are an acquired form of haemangioma
typically present at the site of localised trauma and are prone to bleeding
usually managed with curettage and cautery, followed by histological examination to exclude melanoma
recurrence is common
layers split with a blisters
intra-epidermal split - causes blisters to rupture easily
sub-epidermal split (between the epidermis and dermis) - blisters are less fragile
epidermolysis bullosa
includes >30 inherited (usually dominant) conditions characterised by mechanical fragility of the skin and epithelial lined tissues like the mouth
results from mutations within genes encoding for any of at least 20 structural skin proteins that hold the skin cells together
diagnostic factors for epidermolysis bullosa
FHx mechanical fragility of the skin recurrent blisters and erosions poorly healing wounds onset of cutaneous signs at birth or early infancy
diagnosis of epidermolysis bullosa
can be made on history alone if other family members are affected
or take a skin biopsy and perform immunofluorescene antigenic mapping or just transmission electron microscopy
treatment of epidermolysis bullosa
dressings, sterile drainage of large blisters, topical antibacterial agents, nutritional supplementatoin
bullous pemphigoid
a chronic acquired autoimmune blistering disease characterised by autoantibodies against hemidesmosomal antigens (BP180 and BP230)
presentation of bullous pemphigoid
may be preceded by a non-specific itchy rash
presents with tense blisters on the skin - usually affecting the trunk and limbs
investigations for bullous pemphigoid
usually clinical but can skin biopsy a blister
look at with light micrscopy or direct immunofluorescne testing
treatment of bullous pemphigoid (v similar to pemphigus vulagris)
wound dressings to prevent infection
topical steroids or topical tacrolimus
oral steroids + Abx for widespread disease
sedating antihistamines for itch
3 categories of pemphigus
pemphigus vulgaris
pemphigus foliaceus
paraneoplastic pemphigus
pemphigus vs pemphigoid
pemphigus e.g. pemphigus vulgaris
pemphigoid - bullous pemphigoid
pemphigoid affects a lower layer of skin between the epidermis and dermis –> TENSE blisters that do not break easily
pemphigus affects the epidermis –> easily rupture
pemphigus vulgaris is more common
pemphigus vulgaris presentation
easily ruptured blistering of the skin, mucosa or both (mucosal involvement can preceded skin involvement)
Nikolsky’s sign - The skin is very fragile, and the top layer is often easily removed with lateral pressure
Pruritic scalp, Bloody nose, Painful skin
pemphigus foliaceus
blisters are more superficial than in pemphigus vulgaris - the antibody targets a desmoglein which links keratinocytes at a higher level
confined to SKIN - does not affect mucus membranes like pemphigus vulgaris
causes scaly, crusty lesions (blisters themselves are rarely seen)
Dermatitis herpetiformis
blistering skin condition related to coeliac disease - IgA antibodies against gliadin
presentation and diagnosis of dermatitis herpetiformis
intensely itchy
blisters are distributed symmetrically on extensor surfaces
come and go
often misdiagnosed - need a skin biopsy and blood test for anti-tTG (tissue transglutaminase)
treatment for dermatitis herpetiformis
strict gluten-free diet
steroid creams
dapsone (oral) - an antibiotic that alleviates the rash and itching
erythroderma define
intense and widespread reddening of the skin (at least 90%) due to inflammatory skin disease
often preceded with exfoliation of the skin (peeling off)
another word for idiopathic erythroderma
red man syndrome
causes of erythroderma
30% idiopathic drug eruption dermatitis, especially atopic dermatitis psoriasis (especially after the withdrawal of systemic steroids) pityriasis rubra pilaris eczema lymphoma
systemic diseases: haematological malignancies, GvHD, HIV
presentation of erythroderma
warm skin
itchiness
eyelid swelling may result in ectropion
scaling that may lead to hair loss
complications of erythroderma
heat loss
dehydration and electrolyte abdnormalities
secondary skin infection - impetigo or cellulitis
hypoalbuminaemia from protein loss and increased metabolic rate causes oedeam
high-output HF
urticaria vs angiodema
urticaria (hives) = red, blanching, oedematous 9confined to DERMAL layer), pruritic lesions
approximately 40% of urticaria is associated with angiodema
angiodema = swelling involving the deeper layers of the subdermis (subcutaneous tissue)
acute vs chronic angiodema
acute = <6 weeks
causes - allergic (drug, foods), insect bites
chronic = >6 weeks
causes - more difficult to tell - approx 40% are thought to be autoimmune in nature - while many cases are thought to be idiopathic
pathophysiology of urticaria
mast cells activation –> release vasoactive mediators that lead to vasodilation and increased permability
–> pruritus and oedema
NB angiodema due to same response but may also involve the kinin system
investigations for urticaria
FBC - infection, anaemic, or findings of chronic illness and establishes a baseline for monitoring
CRP
anti-IgE receptor antibody
skin biopsy - may show urticarial vasculitis in setting of atypical urticarial lesions
complement levels - low C4 suggests hereditary or acquired angiodema. C1 esterase inhibitor level decreased in hereditary. C1q is normal in hereditary but low in acquired
treatment of acute urticaria without airway involvement
trigger identification and avoidance
plus H1 receptor antagonist (antihistamine) e.g. loratadine, desloratadine
plus systemic steroids for severe acute urticaria and angiodema
SE of oral steroids
adrenal suppression, weight gain, osteoporosis, hyperglycaemia, acne, easy bruising, hypertension, swollen puffy face, difficulty sleeping
