Anatomy, Biology and Function of the Skin Flashcards
1
Q
What is the embryological development of the skin?
A
- Epidermis derived from ectoderm
- Skin of embryo is covered by simple cuboidal epithelium in 5th week
- Single squamous layer (periderm) and a basal later by 7th week
- Intermediate layer interposed between basal cells and periderm in 5th month
- Early foetal period epidermis invaded by melanoblasts
2
Q
What are the layers of the epidermis?
A
- Strarum corneum
- Stratum lucidum
- Stratum granulosum
- Stratum spinosum
- Stratum basale
3
Q
What do Merkel cells (base of epidermis) do?
A
- Respond to sustained gentle and localised pressure
4
Q
What do Meissner corpuscles (just below epidermis) do?
A
- Sensitive to light touch
5
Q
What do Ruffini’s corpuscules (in dermis) do?
A
- Receptors sensitive to deep pressure and stretching
6
Q
What do Pacinian corpuscules (deep in dermis) do?
A
- Sensitive to deep touch, rapid deformation and around joints for position/proprioception
7
Q
What are free nerve endings for?
A
- Pain and temperature sensing
8
Q
What are Langerhan’s cells?
A
- Members of the dendritic cells family
- Residing in basal layers
- Specialise in antigen presentation
9
Q
What is a macule?
A
- Flat patch of skin
10
Q
What is a papule?
A
- Raised patch of skin
11
Q
What is a pustule?
A
- Collection of inflammatory cells giving a yellow discolouration under the skin
12
Q
What is a plaque?
A
- A palpable macule
13
Q
What is a vesicle?
A
- A small blister
14
Q
What is a bulla?
A
- A large blister
15
Q
What does erythematous mean?
A
- Something that’s red, hot and fiery to touch
16
Q
What does ulceration mean?
A
- Top layers of skin have been removed
17
Q
What is the pathophysiology of acne vulgaris?
A
- Skin disease affecting the pilosebaceous unit characterised by comodones, papules, pustules, nodules, cysts and/or scarring.
- Keratin and thick sebum blockage of sebaceous gland
- Androgenic increased sebum production and viscosity
- Proprioni bacterium inflammation
- Cutibacterium acnes colonisation
- First microcomedo form when follicular keratinocytes that exhibit cohesiveness do not shed normally leading to retention and accumulation. Androgens stimulate enlargement of sebaceous glands and increased sebum production and the material collect in the microcomedo. This leads to a build up of pressure and whorled lamellar concretions develop. C. acnes can then proliferate and metabolise triglycerides producing pro-inflammatory mediators and ultimately causing inflammation.
18
Q
What are the clinical features of acne?
A
- Papules
- Pustules
- Erythema
- Comedones (blackheads)
- Whiteheads
- Nodules
- Cysts
- Scarring
- Risk factors include age 12-24 years, genetic predispositions, greasy skin and some medications (i.e. androgens).
19
Q
How is acne treated?
A
- Reduce plugging (topical retinoid, topical benzoyl peroxide)
- Reduce bacteria (antibiotics)
- Reduce sebum production (hormones - anti-androgen)
- Oral isotretinoin
- Oral retinoid for severe acne vulgaris
- Concentrated vitamin A
- Reduces sebum, plugging and bacteria
- Standard course for 16-week 1mg/kg
- Multiple side effects including dry lips, nose bleeds, dry skin, myalgia, deranged liver function, raised lipids, mood disturbance and teratogenicity
- Pregnancy Prevention Program
- Expensive and consumes a lot of clinical time
- Side effects
- Topical agents – irritant, burning, peeling and bleaching
- Oral antibiotics – gastro upset
- OCP – possible DVT risk
20
Q
How is oral isotretinoin used in acne vulgaris?
A
- Oral retinoid
- Concentrated vitamin A
- Reduces sebum, plugging and bacteria
- Standard course is 16 weeks 1mg/kg
- Side effects include dry lips, nose bleeds, dry skin, myalgia, deragned liver function, raised lipids, mood disturbance and teratogenicity
- Pregnancy Prevention Program
