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.
