Acneiform Eruptions Flashcards
What is the pathophysiological mechanism of inflammation in acne?
- Hyperkeratosis occurs due to hyperproliferation of ductal keratinocytes or reduced separation of ductal corneocytes which leads to blockage of pilosebaceous duct
- Sebum excretion increases via androgen stimulation and builds up
- Propionibacterium acnes overpopulates duct along with shed keratin and sebum
- Stimulates inflammatory mediators
How does sebum excretion rate change in acne?
Increases (androgen stimulates it)
increases in puberty
What are the 2 types of comedones?
Open (blackheads)
Closed (whiteheads)
What are blackheads?
Dilated keratin filled follicles which appear as black papules due to keratin debris
What are whiteheads?
Accumulation of sebum and keratin deeper in the pilosebaceous ducts
What is the most common peak age for acne vulgaris?
15-18yrs (90% of teens)
What happens to the squamous epithelium in acne?
Hypercornification/hyperkeratinisation - develops into tough protective layers
What are the 3 variants of acne?
Mild
Moderate
Severe
How is mild acne described?
Non-inflammatory
Open + closed comedones
Lesions <30; <15 inflammatory
How is moderate acne described?
Inflammatory (papules, pustules, nodules, cysts)
20-100 comedones
Lesions 30-125; inflammatory 15-50
What can early treatment of moderate acne prevent?
Scarring
How is severe acne described?
> 5 pseudocysts
Comedones >100
Lesions >125; Inflammatory >50
Severe acne is difficult to treat, may need lasers, but what is left once it is treated?
Permanent scarring and post-inflammatory pigmentation
Give 3 acne variants
Acne Fulminans
Drug induced acne
Acne excoriee
How is acne fulminans characterised?
Most severe form of cystic acne
Abrupt onset of nodular and suppurative acne with systemic manifestations