Acne vulgaris
- definition
- etiopathogenesis
- polymorphic chronic inflammatory skin disease
- comedones and inflammatory lesions
- androgen-mediated - enhances sebaceous glands activity and seborrhea
- follicular hyper-keratinisation - increased cornification + abnormal follicular differentiation
- Propionibacterium acnes - hypercolonization due to low oxygen level and accumulation of sebum
- inflammation
Acne vulgaris
-factors aggravating acne (9)
genetic endocrinal factors stress overuse of cosmetics local/systemic GCS environment diet drugs manipulation of lesion
Acne vulgaris
-classification
Non-inflammatory - comedones, closed (white) or open (black)
-black due to oxidized lipids, melanin causes darkened color
Inflammatory - nodules, pustules, cysts
Acne vulgaris
-clinical forms (5)
- Acne comedonia - children
- Acne papulopustulosa - teenager
- Acne nodulocystica - develops quickly - adults
- Acne conglobata
- Acne tarda - smokers acne
Acne vulgaris
- diagnosis
- treatment
-clinical examination
- sebo-suppression, anti-comedogenic, anti-bacterial, anti-inflammatory
- systemic - oral retinoids - isotretinoin (Roaccutane)
- phototherapy
Rosacea
- definition
- factors aggravating it
- effects of the triggers (4)
- chronic inflammatory skin disease
- causes facial erythema - capillary vasomotor lability
- environment, emotion (stress), physiological, exogenous
- increased blood flow to blood vessels (erythema), damage of cutaneous blood vessels and dermal CT (papillary dermis atrophy), perivascular inflammation, edema
Rosacea
-classification
- Diathesis/ Pre-rosacea
- Erythematous-telangiectatic
- Papulo-pustular
- Phymatous/ Hyperplastic
- Ocular
Rosacea
-clinical features
Primary
-flushing (transient erythema), persistent erythema, papules and pustules and telangiectasia
Secondary
- burning or stinging sensation
- plaques, dry appearance, edema
- eye damage
- peripheral localization
- rhinophyma
NO COMEDOMES - main difference between acne
Rosacea
- diagnosis
- treatment
- erythema, inflammatory papules and pustules, telangiectasia, ocular manifestations
- antibiotics, good skin care, anti-parasitic (ivermectin)
Pemphigus vulgaris
- definition
- etiopathogenesis
-severe, acquired, potentially fatal disease with intraepidermal blister formation
- auto-antibodies against desmogleins 3 and 1 –> proteases cause damage –> intraepidermal acantholysis
- genetic, drugs
Pemphigus vulgaris
-clinical features (5)
- sites: oral mucosal, scalp, face, mechanically stressed areas, nail, intertriginous areas
- non-erythematous, non-swelling –> blisters are not stable –> fast rupture
- extremely painful
- poorly healing crusted erosions and ulcers surrounded by epidermal splits –> bleeding –> blisters hard to find
- pruritus is uncommon
Pemphigus vulgaris
- staging
- diagnosis
- treatment
-1. oral involvement, 2. localized disease, 3. generalized disease
- Nikolsky sign - POSITIVE!!!
- ELISA, direct or indirect immunofluorescence, cytology (acantholytic cells), CBC
- SGCS: prednisolone
- immunosuppression in very aggressive cases
- topical: wound treatment, local anesthetic, antiseptics and anticandida
Bullous pemphigoid
- definition
- etiopathogenesis
-acquired autoimmune sub-epidermal blistering disease caused by auto-abs to components of the hemidesmosomes in the b.m
- auto-abs against hemidesmosome –> attraction of inflammatory cells –> release of proteases –> separation between dermis and epidermis
- less common causes: drugs, sunlight, ionizing radiation
Bullous pemphigoid
-clinical features
Non-blistering phase - polymorphous rash, not specific, prodromal symptoms (urticaria, eczematous rash, pruritus)
Blistering phase - blisters appear on normal or erythematous skin, urticarial, papular rash come together
- blister is very stable
- symmetrical manifestation
Bullous pemphigoid
- diagnosis
- treatment
- Nikolsky’s sign - NEGATIVE!!!
- Lab, direct or indirect immunofluorescence, ELISA, histology
-systemic corticosteroids, combination therapy with methotrexate, local wound treatment
Ichthyoses vulgaris
- definition
- etiopathogenesis
-inherited disorder characterized by excessive scaling
- autosomal dominant, genetic mutation that causes the keratinocytes to behave differently
- abnormal formation of keratohyalin granules –> delayed destruction of desmosomes because of defective/absent profilaggrin –> hyperkeratosis
Ichthyoses vulgaris
-clinical features (6)
- usually starts in the first year of life –> progresses until puberty and lasts all lifetime
- white fine scales
- on extensor surfaces (shins), trunk and lateral aspects of face
- no mucosal involvement
- dry skin, itchy
- hyperlinear palms
Ichthyoses vulgaris
- diagnosis
- treatment
-family history, clinical diagnosis
- lubrification of the skin with emollients
- keratolytic substances
- topical corticosteroids are not useful!!!
