Dermatology Flashcards
what organism causes acne and what type of organism is it?
propionibacterium acnes - gram -ve anaerobic bacteria
list the 4 processes involved in development of acne
follicular epidermal hyperproliferation
blockage of pilosebaceous units with surrounding inflammation
increased sebum production
infection with P. acne
give 3 cardinal features of acne
blackheads/whiteheads (open/closed comedones), inflammatory papules and pustules
where does acne most commonly develop?
face, back and sternal area
name 2 clinical variants of acne
infantile acne, oil acne (occupational oil exposure), acne fulminans
what are the different treatment options for acne?
1st line - topical keratolytics (benzoyl peroxide), retinoids (tretinoin) or abx (erythromycin).
2nd line - low dose oral abx (tetracycline, trimethoprim).
3rd line - retinoid drug (tretinoin) but only in severe cases
what are retinoids and what must be monitored in a patient using them?
synthetic vitamin A analogues.
highly teratogenic - monitor bloods/do pregnancy tests
explain the pathophysiology underlying atopic eczema
abnormal epithelial barrier function allows antigenic/irritant agents to reach immune cells
(mutations in filaggrin).
Th2 activation initially, then Th0 and Th1 drive chronic phase.
high serum IgE.
list some possible exacerbating factors of atopic eczema
strong detergents and chemicals, cat and dog fur, some dietary allergens, infection, woolen clothes, anxiety/stress
when taking a history for a possible diagnosis of atopic eczema, would the family history be more significant if the patient’s mother or father has atopic eczema?
mother - strong maternal predominance in family histories
describe the rash that eczema produces
itchy erythematous scaly patches, especially in flexures.
skin thickening.
can weep/exudate - infection.
give 3 features associated with atopic eczema apart from the rash
pitting and ridging of nails, prominent skin creases, dry scaling of skin, follicular hyperkeratosis
give a complication of atopic eczema
infections - usually S aureus, appear as yellow lesions.
cutaneous viral infections - HSV (can lead to Kaposi’s sarcoma).
cataracts, conjunctival irritation.
give 3 investigations you might perform to confirm eczema as a diagnosis, or to confirm atopy
skin-prick testing.
RAST tests.
bloods - raised serum IgE or eosinophilia.
what is the triple combination treatment of eczema?
topical steroid (hydrocortisone = mild, betamethasone = potent). frequent emollient (e.g. aqueous cream). bath oil/soap subsitutes.
for severe cases of atopic eczema, in which triple combination therapy has failed, what could you prescribe?
topical immunomodulators - tacrolimus ointment.
what causes contact dermatitis?
substance in contact with the skin - either a chemical irritant or a type IV hypersensitivity reaction.
how would you identify contact dermatitis?
rash with clear demarcation/odd-shaped areas - patch test to identify allergen
how would you treat contact dermatitis?
remove cause(s) steroids, antipuritic agents
explain the underlying pathology of psoriasis
T lymphocyte driven.
increased cell turnover - epidermal rete ridges appear elongated and clubbed, capillary dilatation, mixed neutophil and lymphohistiocytic infiltration
give 4 clinical features of chronic plaque psoriasis
well demarcated, red scaly plaques with silver scale.
found on extensor surfaces, lower back, ears and scalp.
Kobner phenomenon - new plaques arise if there’s skin trauma.
can be itchy and sore.
name 3 triggers of psoriasis
infection (Strep group A), drugs (lithium), UV light, alcohol, stress
name 4 features associated with psoriasis
nail pitting, distal separation of nail plate, yellow brown dicolouration, damaged nail matrix and lost nail plate.
psoriatic arthritis.
how would you manage psoriasis?
emollients to hydrate skin.
moderate - use topical steroids, vit D analogues and purified coal tar.
tazaroten - a retinoid.
salicylic acid, phototherapy.
severe (ulceration, pyrexia) - methotrexate.
what are the two peaks in age of onset of psoriasis?
16-22yrs and 55-60yrs
how would flexural psoriasis present?
red glazed, non-scaly plaques in flexures - groin, natal cleft, sub-mammary
how would guttate or “raindrop psoriasis” present?
explosive eruption of small circular/oval plaques appear on trunk 2wks after strep throat
how do venous ulcers develop?
sustained venous hypertension in superficial veins due to incompetent valves in deeper veins - this increased pressure causes extravasation of fibrinogen through capillary walls, giving rise to perivascular fibrin deposition leading to poor oxygenation of the skin
give 3 clinical features of a venous ulcer
oedema, venous eczema, brown pigmentation, varicose veins, lipodermatosclerosis, scarring white atrophy with telangiectasia
how would you manage a venous ulcer?
high compression bandaging with leg elevation.
Doppler to exclude arterial disease.
diuretics for oedema, analgesia if painful, compression stockings to reduce recurrence.
give 4 clinical features of arterial ulcers
punched-out painful ulcers, higher up the leg or on feet, cold and pale, absent peripheral pulses, arterial bruits.
Doppler US to confirm.
Hx of claudication, angina, hypertension and smoking.
what treatment must NEVER be given to arterial ulcers?
compression stockings.
in what group of people do neuropathic ulcers develop most commonly?
diabetics with peripheral neuropathy
how does a patient with cellulitis normally present?
hot, tender area of erythema of skin due to infection of deep subcutaneous layer - poor margins.
upward spread with blistering and oedema.
px is unwell with fever.
prefers lower limb.
what is the usual causative organism of cellulitis?
strep pyogenes.
give 2 risk factors for cellulitis
lymphoedema, venous insuffiency, leg oedema, obesity.
site of entry - leg ulcer, trauma, tinea pedis (athletes foot).
what is the main differential of cellulitis?
DVT
how would you treat cellulitis?
phenoxymethylpenicillin and flucloxacillin.
erythromycin if penicillin allergy.
how would you confirm a diagnosis of cellulitis due to strep pyogenes?
serological streptococcal titres
what is the likely causative organism of necrotising fasciitis? how does it present?
group A beta haemolytic strep.
arises spontaneously with intense pain of affected skin and muscle.
how would you treat necrotising fasciitis?
radial debridement ± amputation.
IV - benzylpenicillin and clindamycin
which skin cancer is most associated with excessive sunlight exposure?
basal cell carcinoma
what does a basal cell carcinoma look like?
pearly nodule with rolled telangiectasia edge, erodes and ulcerates
what does a squamous cell carcinoma look like?
ulcerated lesion with hard raised edges
which types of skin cancer metastasise, and which one is the most serious?
squamous cell and melanoma metastasise.
melanoma is most serious - early mets.
how are all skin cancers treated?
surgical excision ± radiotherapy
what are the components of the ABCDE criteria for moles?
Asymmetry of mole Border irregularity Colour - non-unifrom Diameter >6mm Elevation
what are the components of the Glasgow 7 point mole checklist?
Major - change in colour/size/shape (2pts).
Minor - diameter >6mm, inflammation/crusting/bleeding, sensory change (e.g. itch).
need 3+ to refer.