Skin Flashcards

1
Q

Weight of skin

A

3.6kg

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2
Q

Surface area of skin

A

2m2

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3
Q

3 layers of skin

A

Epidermis
Dermis
Subcutis

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4
Q

Outermost layer of epidermis

A

stratum corneum

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5
Q

Epidermis is made up of

A

corneodesmosomes

desmosomes

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6
Q

Corneodesmosomes (known as…) are keep the — together

A

adhesion molecules

corneocytes

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7
Q

Increased numbers of corneodesmosomes are seen in diseases such as …

A

psoriasis, in which there is a thickening of the stratum corneum

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8
Q

Decreased number of corneodesomosomes are seen in diseases such as …

A

atopic eczema, where there is a thinning of the stratum corneum (= increased risk of inflammation)

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9
Q

Waterproof epidermis

A

Tight junctions between cells in the stratum granulosum,

epidermal lipids and keratin in stratum corneum form both an inside-out and outside-in barrier to water

Prevents transepidermal water loss

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10
Q

Epidermis

immune functions

A
  • Keratinocytes secrete cytokines and chemokines that maintain populations of leucocytes in skin
  • Langerhans cells are antigen-presenting cells and secrete cytokines
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11
Q

Dermis

immune

A
  • Regulatory T cells
  • Natural killer cells
  • Dendritic cells
  • Macrophages
  • Mast cells
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12
Q

Vitamin D synthesis (endocrine)

A
  • 7-dehydrocholesterol in plasma membranes of epidermal keratinocytes and dermal fibroblasts converted to previtamin D3 by UVB light
  • 15-25 minutes whole body exposure produces up to 10,000 IU Vitamin D
  • Serum concentrations peak 24-48 hours after exposure
  • Lipid soluble - can be stored in subcutis adipocytes
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13
Q

UV

A
  • Both UV-A and UV-B damage skin
    • burns
    • supress action of Langerhans cells
    • Photo-aging
    • DNA damage (skin cancers)
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14
Q

Skin colour depends on…

A
  • Melanin
  • Carotenoids
  • Oxy/deoxyhaemoglobin
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15
Q

Where is melanin synthesised

A

Synthesised in melaonsaomes within melaoncytes from tyrosine

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16
Q

Melanin transport

A

Transported via dendrites to adjacent keratinocytes

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17
Q

types of melanin

A
  • Pheomelanin (red/yellow)

- Eumelanin (brown/black)

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18
Q

All skin types contain more –melanin than —melanin.

A

All skin types contain more eumelanin than pheomelanin.

19
Q

Functions of the dermis

A
  • Thermoregulation
  • Vitamin D synthesis (endocrine)
  • Sensory organ
20
Q

Functions of the subcutis

A
  • Thermoregulation
  • Energy reserve
  • Vitamin D storage
  • Endocrine organ
  • Shock absorber
21
Q

Subcutis as endocrine organ

A

→ Site of hormone action

- Androgens act on follicles and sebaceous glands
- Thyroid hormones act on keratinocytes, follicles, dermal fibroblasts, sebaceous glands, eccrine glands
22
Q

The skin is an ENDOCRINE ORGAN

A
  • Vitamin D3 - unique site for cholecalciferol synthesis
  • 17β-hydroxysteroid dehydrogenase in sebocytes and 5α-reductase in dermal adipocytes convert dehydroepiandrosterone (DHEA) and androstenedione to 5α-dihydrotestosterone
  • Insulin-like growth factor (IGF) binding protein-3 (IGFBP-3) synthesised by dermal fibroblasts
23
Q

Hypothyroidism effect on skin

A
  • Epidermal changes
    • coarsened, thin scaly skin
  • Dermal changes
    • Myxoedema
  • Hair and nail changes
    • Dry, brittle coarse hair
    • Alopecia
    • Thin, brittle nails
  • Sweat gland changes
    • Dry skin
    • Decreased sweating
24
Q

How do we respond to sunlight? (3)

A
  1. Immediate pigment darkening
    • photo-oxidation of existing melanin
    • redistribution of melanosomes
    • occurs within minutes and lasts hours/days
  2. Persistent pigment darkening (tanning)
    • UVA&raquo_space; UVB
    • Oxidation of melanin
    • Occurs within hours
    • Lasts 3-5 days
  3. Delayed tanning
    • Increased melanin synthesis
    • Occurs 2-3 days after UV exposure, maximal at 10-28 days
25
The skin is a SENSORY organ
Merkle cells - basal epidermis - light touch Encapsulated mechanoreceptors in dermis - Pacinian corpuscles (pressure/vibration) = Meissner corpuscles (touch) - Myelinated and unmyelinated sensory nerve endings in dermis (pain, itch, temperature)
26
Heat loss
- Cutaneous blood flow - Deep vascular plexus (lower reticular dermis) - Superficial vascular plexus (upper reticular dermis) - Loops of blood vessels from superficial plexus extend to reticular dermis
27
Pilorection
- Arrector pili muscles innervated by sympathetic α1-adrenergic fibres - Contraction raises cutaenous hairs - Likely little significant impact on heat conservation
28
Layers of epidermis
stratum corneum granular layer spinous layer basal layer
29
Dermis layers
Glands | tough connective tissue
30
Subcutaneous tissue components
fats | connective tissue
31
Skin barrier
Lipid lamellae – water barrier, allows cells to swell Natural moisturising factor (NMF) – maintains pH Corneocytes – cells of the skin filled with NMF Cornified envelope – surrounds corneocytes Corneodesmosomes – link corneocytes
32
Emollients
trap moisture in the skin and allow it to rebuild
33
Humectants
trap moisture and maintain low pH
34
NMF
Natural moisturising factor
35
What does NMF contain
acids, which make the pH of normal skin low (around 5)
36
What is NMF produced by
the breakdown of filaggrin
37
How are skin cells shed from the surface of skin?
by breaking down the corneodesmosomes that link the skin cells together IMPORTANT: They are only broken down near the surface and not further down, otherwise the skin would fall apart and allergens would fall through
38
Why is low pH significant? (healthy skin barrier)
it switches off proteases and prevents the breakdown of corneodesmosomes It is also optimum for lipid processing enzymes, so they form a robust 'mortar' for lipid lamellae
39
ATOPIC DERMATITIS
1) Mutations in the filaggrin gene means theres less filaggrin in AD and so less NMF. Therefore there's less acid so the pH of the skin goes up to 7 and beyond. 2) High skin pH switches on the proteases, so they break down the desmosomes all across the skin barrier. 3) High pH switches off the lipid processing enzymes so the 'mortar' breaks up like crumbling mortal in an old brick wall.
40
Negative environment interaction
1. Environmental factors interact w gene susceptibility and cause the skin barrier to break down and cause sub-clinical inflammation 2. This then causes mild atopic dermatitis without allergic antibodies 3. Allergens then penetrate through this defective barrier and cause 'sensitisation' → **type 1 allergic response** and produce high levels of IgE to the allergens 4. Inflammation then feeds back and down-regulated filaggrin and so makes the skin barrier defect worse → vicious cycle
41
vitamin D is essential in ...
producing the anti-microbial peptides necessary to defend the skin from bacteria and viruses
42
Effect of increased pH on the skin
If profilaggrin and thus filaggrin are not present for any reason, there will be a lack of NMF meaning there will be less water retention in the corneocytes. This means that pH will increase, resulting in damage to the skin barrier since the corneodesmosomes become damaged by the increased pH resulting in breakdown of the skin barrier and thus increasing the risk of infection.
43
ACNE
Hypercornification of skin, this blocks the hair follicle entrance Sebum released from sebaceous glands Trapped in narrow hair follicle No oxygen provides anaerobic conditions This allows propionic bacteria to multiply These bacteria breakdown triglycerides into fatty acids Result Increased irritation Increased inflammation Attraction of neutrophils This leads to pus and further inflammation