Paediatric Dermatology Flashcards
Age range of eczema
Atopic eczema worse between ages 2-4
Worse pre-puberty (no sebum production to act as a barrier)
Tends to improve into teen years and beyond
Distribution of atopic eczema in different age groups
Infants: cheeks often first affected
Toddlers: Extensor aspects of joints and genitals
School age on: flexural pattern
Perioral dermatitis cause and treatment
typically occurs after beclamethasone, treatment is to stop using creams on the face +/- oral tetracyclines
Management of eczema
Bathing: lukewarm watern, soap-free cleanser
Dilute K+ permangenate compresses for acute severe patch
Avoid wool
Emolliients after bathing
Topical steroids
Pimecrolis/tacrolimus for severe refractory eczema
Antihistamines may help reduce irritation, e.g. at night
Systemic steroids
MTX, AZA, phototyherapy for severe cases
Steroid creams suitable for facial dermatitis
Hydrocortisone 0.5% or 1%
Suitable for face and other body parts with thin skin
Others are too strong
Common causes of nappy rash
Usually a form of irritant contact dermatitis (due to bile salts and ammonium hydroxide in waste)
Other causes: candida, impetigo, seborrhoeic dermatitis etc.
NOT due to dermatophyte fungal infections (tinea)
Management of nappy rash
Use disposable nappies over cloth
Gently clean with water and soft cloth
Pat dry gently, allow to air dry
Apply protective emollient ointment
give evening fluids early to reduce night time wetting
Observe if certain foods are related to rash (e.g. orange juice increasing stool acidity)
+/- mild topical steroid (e.g. hydrocortisone)
Definition of acne vulgaris
Cutaneous disorder affecting adolescents and young adults involving hyperkeratisation, increased sebum production, infection and inflammation of the pilosebaceous follicles
Predisposing and provoking factors of acne vulgaris
Family history Stress high BMI (in females) PCOS Meds: steroids, hormones, AEDs, EGFR inhibitors Application of occlusive cosmetics (e.g. make up) High environmental humidity Diet high in dairy and high GI foods
pathophysiology of acne vulgaris
increased proliferation and reduced desquamation of keratinocytes lining follicle - partial obstruction of follicle with sebum and keratin- inflammatory cells + sebum acts as growth medium for PROPIONIBACTERIUM ACNES - enzymes produced by bacterium promote degradation and rupture of follicular wall
Sebaceous glands are enlarged and sebum production increased by prepubertal levels of DHEA (androgens)
Pathogen responsible for acne vulgaris
Propionibacterium acnes
Management of acne
Investigate for hyperandrogenism in females (PCOS)
if Mild:
topical benxoyl peroxide (clearasil)
Low dose COCP
Antiseptic washes with salicylic acid
Light/laser therapy
MODERATE: as above plus
tetracycliness for 6 months (or erythromycin or trimethoprim if allergic)
Antiandrogen therapy: COCP, cyproterone acetate + ethinylesrtadiol and/or spironolactone
Isotretinoin (reduces sebum production, only use for 6-12m at a time)
SEVERE:
higher dose antibiotics, oral isotretinoin, referral to derm
Bacteria responsible for impetigo
Strep pyogenes
Bullous impetigo: Staph aureus
Common sites of impetigo
Exposed areas (hands and face) or in skin folds (esp. armpits)
Appearance of impetigo
Round oozing patches of pustules enlarging every day
Clear blisters = bullous impetigo
May be golden yellow crusts