Summary
Summary Acne Vulgaris
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Background, presentation, classification and treatment of Acne Vulgaris
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18/10/2022, 17:47 OneNoteDerm: Acne Vulgaris
Monday, 19 September 2022 12:42
Background
Acne is caused by chronic inflammation, with or without localised infection, in pockets within the skin known
as the pilosebaceous unit.
• Hair follicles get blocked by dead skin cells or oils
• Form small raised red bumps
• Common among skin changes due to the skin changes during puberty
• Types
Mild - white heads and black heads
Moderate - pustules
Severe - cysts and nodules
• Layers of skin
Epidermis - thin outer layer with 5 sub-layers
Dermis
• Connective tissue
• Nerve endings
• Hair follicles - each contains a strand of hair aka pilosebaceous unit
• Epidermal tissue that dips down into to the dermis
• Associated with:
• Arrector pill muscle - surround sebaceous glands so when they contract sebum
is pushed out
• Apocrine sweat glands
• Nerve receptors
• Sebaceous glands
• Sebaceous glands - secretes oily substance into hair follicle or through pours named
sebum:
• Helps transport nutrients
• Lubricate skin
• Softens hair shaft - prevents brittle
• Prevents moisture loss
• Acidic - deters pathogens
• Lymphatic vending
• Blood vessels
Hypodermis - fat and connective tissue that anchors skin to underlying muscle
Causes of acne - not fully understood
• Keratin plugs
Made of dead keratinocytes+ keratin + melanin
Hyperkeratosis from alive keratinocytes = more keratin plugs
Block opening of hair follicle
• Sebum
Androgen e.g. testosterone stimulates S glands to produce it
During puberty = more androgen production = more sebum secreted
Clogs up the follicles and causes blockage
• Bacterial overgrowth
Propionibacterium = part of normal skin flora
• It is an anaerobic rod
• Traditional beta-lactam antibiotics are ineffective in treating infections caused by this
• SO tetracyclines, macrolides or trimethoprim must be used in managing acne.
If hair follicle become fully closed up = closed comdeodme
Bacteria have nowhere to go so duplicate/grow feasting on keratin plug and sebum
This attracts the immune cells
Immune cells + bacteria cells = white pus with red inflammation
Genetic and environmental factors
• Hyperkeratosis can be due to
Genetics - runs in families
Hormones
• More androgen production during puberty
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• More androgen with PCOS
Psychological stress = increased cortisol = increased sebum production
Products and behaviours
• Creams can block pores
• Wearing headband = contact acne = acne venenata
• Excessive face washing irritates the skin
• Consuming dairy and chocolate
• Open comedome
Sebum or keratin plugs don't pull block the hair follicle pore so are still open to the
environment
Looks black due to oxidised melanin
Aka black heads
• Closed comedome
Hair follicles are fully plugged up with keratin plugs and sebum
Pustule-like lesion
Aka white heads
Types of Acne/ symptoms/presentation
Found on face, shoulders, chest or back - red inflamed sore spots (
• Type 1 - mild
No scarring
Few small comodones
• Type 2 - moderate
No scarring
Large closed comodones (papules - sometimes break and leak pus)
• Type 3 - moderately severe
Some scarring
Papular and pustular acne (comodomes containing necrotic tissue)
• Type 4 - severe acne
Severe scarring
Nodulocystic acne (nodules & cysts)
Invades deeper into the dermis creating interconnecting abscesses
Pick ice scars - small indentensions in the skin after acne heals
Hypertrophic scars - small lumps in skin after acne heals
Rolling scars
Treatment
Main aims:
The aim of treatment is to reduce the symptoms of acne, reduce the risk of scarring and minimise the
psychosocial impact of the condition. Always explore the psychosocial burden and any potential anxiety
and depression that may be associated with the condition.
Type 1 acne - mild
• Topical treatments
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