Effects of the Environment on the Skin Flashcards
How could epidermal damage lead to death?
Dehydration and shock
Infection
Heat loss ad hypothermia (or sometimes hyperthermia due to impaired thermoregulation)
Others: protein loss, electrolyte imbalance, high-output cardiac failure
With high output cardiac failure- as a result of the burn, the demand for blood and oxygen in affected areas is unusually high and as a result the heart can not keep up even though it is functioning normally
Poor venous return caused by the burn contributes to this
What is toxic epidermal necrolysis?
Often as a result of adverse drug reaction
Detachment of the epidermis
List some environmental insults?
Irraditation and UV light
Physical trauma such as burns, friction, pressure etc.
Irritants
Allergens- substances that can trigger allergic reaction
Microbes and ectoparasites
What are the protective features of the skin?
Drying: Waterproof epidermis + oil from sebaceous glands
Friction, impact:
- Thick, regenerating epidermis; keratin
- Nails
- Basement membrane anchoring epidermis to dermis, wavy border against shear forces
- Collagen fibres in dermis (strong, running in all directions)
Heat: Sweating; vasodilatation
Cold: Subcutaneous fat, adaptable blood supply, hair (head)
Burns, injury: Thick, regenerating epidermis
Radiation/sunlight: thick epidermis; melanin
Infections: Impervious epidermis; resident cells of immune system
What are normal skin adaptations to environmental pressures?
Sweating and vasodilation in heat; vasoconstriction in cold
Quite fast (minutes)
Hyperkeratosis (callus); thickening of stratum corneum with rubbing or pressure or (slightly) after ultraviolet exposure (weeks)
Tanning; melanocyte response after ultraviolet exposure (quite slow- days)
How does the blood supply regulate thermoregulation?
Arteriovenous (AV) shunts are anastomoses between arterioles and venules that supply blood to the subpapillary plexus.
Numerous in dermis.
Respond to thermoreceptors in skin – hot/cold.
Shunts open or close respectively to decrease (when cold) or increase (when hot) blood flow to the superficial vascular plexus in the papillary dermis (just below epidermis).
Hence skin goes redder (more heat loss) or bluer.
In face: can also respond to emotion/ sympathetic nervous system – blushing.
If the blood supply is shut off for too long – danger of damage (frostbite).
Subpapillary plexus = beneath the dermal papillae
↑Temp = Homeostatic response is more blood flow to the skin surface with the aim of heat loss via skin surface
↓ Temp =Homeostatic response is reduced blood flow to the skin surface with the aim of retaining as much core heat and preventing any further heat loss.
How is epidermal melanin used for UV protection?
The colour of the human skin is due to mainly to melanin (dark skin) and haemoglobin (light skin)
Much normal genetic variation in the amount of melanin (>12 genes known)
Melanin protects against DNA damage and thus skin cancer, especially in dark (black and asiatic) skin; incidence is only 8-10% that of white people
UV protection; tanning
Melanocytes increase activity- make and transmit more melanin
Gives some protection against UV
Additional protection by skin thickening in response to UV
How does tanning work?
MSH- melanocyte-stimulating hormone
MC1R- melanocortin 1 receptor, has genetic variation
MC1R is located on the melanocyte
You are always gonna have a constitutive melanin being produced
In response to a UV ray hitting a basal keratinocyte, you have DNA damage.
This triggers signalling resulting in the release of MSH which binds to the MC1R on the melanocyte
This then triggers signalling events, cAMP signalling which results in transcription of enzymes that will go on to synthesise melanin
As a result you have more melanin being produced and supplied to the basal keratinocyte
Why does hair turn lighter in the sun?
Increased tyrosinase (tyr) transcription in response to MC1R activation and downstream signaling.
Tyrosinase hydroxylates tyrosine
Tyrosine is hydroxylated to L-DOPA
Tyrosinase also hydroxylates L-DOPA
L-DOPA is oxidized to DOPAquinone
Tyrosinase related proteins are involved in the reactions after
In the skin you have eumelanins being produced , more in individuals with darker skin
In hair we have pheomelanins that result in brighter hair
How does the skin protect against microorganisms?
Langerhans cells (& rest of immune system)
Small cells in non-basal layers of skin- dendritic cells
Function- antigen-presenting cells (like macrophages
Form a network in the epidermis as part of immune system
What is lichenification?
More extreme form of hyperkeratosis
Reaction to excessive rubbing or scratching/skin conditions
What is a sunburn?
Is a radiation burn
Blisters, inflammation and cell death (severe DNA damage)
“Ever sunburnt” associates with increased risk of cancer
So does “ever used a UV sunbed below age 35”- by 75%
Sun cream has to be applied everywhere for a reason
Wrinkles- solar elastosis
Loss of elasticity
What are naevi?
Naevi (moles)
Singular- naevus
Benign proliferation of melanocytes
Many or large naevi; risk factor for melanoma skin cancer
Freckles (ephelides)
Involve a genetic component
Also linked to red/fair hair, often MC1R gene variants
Sun-exposed areas
What is the good side of UV?
UV needed for vitamin D3 production in skin- 15 minute summer sun on fae and arms every day is enough for white skin, longer needed for dark skin
Or take tablets
Ultraviolet radiotherapy for skin conditions e.g. vitiligo, psoriasis
What are the different types of burns?
A burn that only damages the epidermis it is a first degree burn
When it reaches the dermis but hasn’t reached the sebaceous glands it is a second degree burn
When you have a full thickness burn with the entire epidermis and dermis it is a 3rd degree burn, which will scar and the victim may lose sensation
