Derm Flashcards
(85 cards)
How would you define acne?
common chronic disorder of the pilo-sebaceous unit, resulting in blockage of the follicle, formation of comedones and inflammation
how would you describe the appearance of acne?
- comedones can be open blackheads or closed whiteheads
- papules - small, raised, erythematous, inflammatory lesions that do not contain pus
- pustules - similar to papules but with pus
- nodules - large, painful, solid lesions deep within skin which can lead to scarring
- cysts - pus filled lesions that can lead to scarring, severe form
what are the classifications for acne?
- non-inflammatory: blackheads, whiteheads
- inflammatory: papules, pustules, nodules and cysts
- mild: non-inflammatory lesions
- moderate: inflammatory papules and pustules
- severe: codules, scarring, acne fulminans and conglobata
what is the pathophysiology of acne?
- follicular epidermal hyperproliferation resulting in formation of keratin plug
- this obstructs pilosebaceous follicle
- activity of sebaceous glands may be controlled by androgen
- leads to colonisation by anaerobic bacterium
- inflammation
what are some risk factors for acne?
- hormonal changes - puberty, menstrual cycle, PCOS
- increased sebum production
- blockage of hair follicles and sebaceous glands by keratin and sebum
- bacterial colonisation
- family history
- certain medications like steroids, hormonal tx
how might acne present?
- self confidence issues
- scarring
- post-inflammatory hyperpigmentation
- mental health
how is acne investigated?
- clinical
- swabs if uncertain
- pre-isotretinoin ix
- PCOS mx etc
how is acne managed?
12w course of management
- mild to moderate: topical benzyl peroxide, topical abx, topical retinoids
- moderate to severe: topical retinoids with topical benzoyl or abx, second line oral abx, COCP, isotretinoin
- referrals
how is acne complicated?
- Post-inflammatory erythema
- Post-inflammatory hyper- and hypo- pigmentation
- Psycho/social/sexual dysfunction
- Scars (atrophic, hypertrophic, keloid)
how would you describe psoriatic lesion?
clearly defined, dry, erythematous and scaly plaques, symmetrical distribution, scale silvery white and appears shiny on skin folds common on scalp, elbows, knees on extensor surfaces
what is the pathophysiology of psoriasis?
- systemic chronic relapsing inflammatory condition affecting skin, nails, joints and scalp with faster skin cell turnover
- hyperproliferative skin epidermis causes rapid regeneration of new skin cells, causing abnormal buildup and thickening of skin in those areas
- inflammatory cell infiltration
what are the various types of psoriasis?
plaque
guttate
pustular
erythrodermic
what are some triggers for psoriasis?
- Skin trauma (Koebner phenomenon)
- Infection: Streptococcus, HIV
- Drugs:B-blockers,Anti-malarials,Lithium,Indomethacin/NSAIDs (BALI)Withdrawal of steroids
- Stress
- Alcohol + smoking
- Cold/dry weather
how does psoriasis present?
- extensor surfaces
- itch, skin cracks, stress induced flare ups
- nail changes: pitting, thickening, discolouration, ridging
- joint involvement
- signs: auspitz (small points of bleeding where plaques scraped off), koebner (lesions affected by trauma), residual (skin after lesions)
how is psoriasis managed?
lifestyle - WL, stopping smoking, managing stress, topicals
- potent topical corticosteroid OD (eg Betnovate) + topical vitamin D OD (eg Dovonex)
- phototherapy
- systemic
- biologics
what are some complications of psoriasis?
- psychosocial
- CVS risk
- systemic tx side effects: pneumonitis, hepatotoxic, myelosuppression
what are the two types of contact dermatitis?
- Irritant - Eczema due to contact with an irritant. There may be burning, pain, and stinging. Eczematous rash appears localised to the direct area of contact
- Allergic - Presents as an itchy, eczematous rash (vesicles, fissures, erythema), typically 24-48 hours after exposure. The rash may extend beyond the boundaries of immediate contact
what is the pathophysiology of allergic contact dermatitis?
- delayed type 4 hypersensitivity reaction
- exposure to allergen sensitises immune system overtime
- Upon re-exposure (e.g. after repeated hair dyes), an immune response is triggered, leading to inflammation and the characteristic skin rash
what is the pathophysiology of irritant contact dermatitis?
natural barrier disrupted resulting in direct damage to skin cells and inflammation
how does contact dermatitis present?
- irritant: hairdressers, healthcare staff, builders and cleaners using irritants like bleach or detergents
- allergic: nickel, acrylates, fragrance, hair dye, henna
how is contact dermatitis investigated?
patch testing
skin biopsy
how is contact dermatitis managed?
- AVOIDANCE effective
- liberal emollient and soap substitutes to repair barrier
- topical steroids
- oral antihistamines
- occupational dermatitis, workplace modifications
- derm referral if - severe, recurring and persistent, no response to mx, associated with occupation
what are some complications of contact dermatitis?
- Secondary bacterial or fungal skin infections due to scratching
- Scarring or post-inflammatory hyperpigmentation
- Chronic or recurrent dermatitis
- Impact on quality of life, especially in individuals with severe or chronic forms
- Potential complications related to occupational dermatitis, such as work disability
what is the pathophysiology of eczema?
- chronic inflammatory disorder of the skin characterized by dermal inflammation leading to histological changes in the epidermis such as spongiotic change, acanthosis, hyperkeratosis
- as a result of abnormal barrier function of epidermis causing easy skin irritation