Effect of the Environment on Skin Flashcards

1
Q

what are three normal skin adaptations to environmental pressures?

A

sweating and vasodilation against heat, vasoconstriction against the cold

hyperkeratosis - thickening of the stratum corneum against constant rubbing/pressure at an area

tanning against UV rays - slow response form melanocytes after UV exposure, gives a tanned/pigmented appearance

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2
Q

list the potential types of environmental “insults” upon the skin.

A
  • severe burns and rare drug reactions causing extensive/severe damage
  • toxic epidermal necrolysis from a rare adverse drug reaction = epidermis detaches
  • irradiation and UV light = causes damage to skin cells, leading to skin cancers and premature ageing
  • physical trauma = causes tissue damage, scarring, may impair function
  • irritants, allergens, chemical agents = skin irritation, inflammation, triggering allergic reactions of varying severities
  • microbes or parasites = infections, infestations, skin damage
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3
Q

list protective features of the skin

A

waterproof epidermis and oil form sebaceous glands for drying

thick regenerating epidermis, wavy border anchoring the epidermis against shear forces, collagen dermal fibres providing tensile strength = protect against friction/impact

sweating and vasodilation against heat; subcutaneous fat in hypodermis and vasoconstriction against the cold

thick epidermis and melanin form melanocytes protects from UV damage

impervious epidermis, resident Langerhans cells protect against infections

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4
Q

what are the subpapillary plexus and the cutaneous plexus? how are they supplied?

A

subpapillary plexus - network of blood vessels close to the skin surface, under dermal papillae

cutaneous plexus - network of blood vessels at the dermal-hypodermal border

supplied by the subcutaneous arteries and veins

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5
Q

what are AV shunts?

A

arteriovenous shunts - anastomoses between arterioles and venules that allow blood to be shunted directly across

respond to thermoreceptors in the skin

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6
Q

describe thermoregulation when the environment is too HOT, involving skin plexus and AV shunts

A

increase in temperature is detected by thermoreceptors - blood needs to be supplied to the skin surface for skin to be lost

AV shunts are closed allowing continuous blood supply through subcutaneous arteries to the subpapillary plexus - heat is lost at the skin surface - deoxy. blood taken away by veins

the skin gets redder due to increased blood supply to the skin surface

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7
Q

describe thermoregulation when the environment is too COLD, involving skin plexus and AV shunts

A

decrease in temperature is detected by thermoreceptors - need to reduce blood supply to the skin to minimise heat loss

AV shunts open = blood is shunted directly from arterioles to venules, doesn’t reach the subpapillary plexus

skin gets bluer as blood is shunted away and doesn’t reach the skin surface

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8
Q

what is the danger of cutting off blood supply to the subpapillary plexus for too long?

A

blood supply to the subpapillary plexus is cut off as a thermoregulatory measure against the cold

for too long - can cause damage to the epidermal skin layers and risk frostbite

cells within the epidermal skin layers need blood supply to function, proliferate and differentiate

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9
Q

how does the skin adapt to protect against UV rays?

A

increases melanocyte activity to make and transmit more melanin from melanocytes to basal keratinocytes

more melanin = more protection against UV rays, DNA damage and skin cancer

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10
Q

summarise melanin production

A

melanin is produced in the epidermal layer by melanocytes

transmitted via melanosome granules through melanocytes dendrites to basal keratinocytes

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11
Q

describe the cellular mechanism of tanning in response to UV radiation

A

UV radiation causes DNA damage in basal keratinocytes

triggers DNA damage signalling = MSH is released from basal keratinocytes

MSH binds to MC1R receptors on melanocytes - triggers downstream signalling events involving cAMP

results in increased transcription of tyrosinase - this enzyme synthesises melanin

results in increased rate of production of melanin, but the same constitutive amount is produced in granules - also causes some skin thickening

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12
Q

how does melanin production differ between hair and nails?

A

initially melanin production is the same - tyrosine is hydroxylated to L-DOPA, which is oxidised to DOPA-quinone ; both processes catalysed by tyrosinase

in skin = eumelanin is produced

in hair = pheomelanin

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13
Q

what are Langerhans cells? how are they involved in protection of the skin?

A

Langerhans cells = small, dendritic antigen-presenting cells on the non-basal layer of the skin

work with the rest of the immune system and form a network in the epidermis as antigen-presenting cells

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14
Q

what is hyperkeratosis?

A

skin thickening in a particular area - result of excessive pressure, inflammation or irritation to the skin

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15
Q

what is Lichenification?

A

more extreme form of hyperkeratosis form excessive rubbing/scratching

gives skin an exaggerated wrinkled, leathery appearance

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16
Q

what are the types of UV radiation? which one is most dangerous?

A

types: UV-A,B and C

UV A and B = what we are exposed to, penetrate Earth’s surface and atmosphere

UV C = most dangerous, shortest wavelength. filtered out by atmosphere

UV B is implicated in skin cancer

17
Q

list conditions/ consequences associated with UV exposure

A

sunburn/ severe sunburn - form redness to blisters and burns from inflammation and cell death = increased risk of skin cancer

polymorphic light eruption = allergic reaction to UV light

wrinkles = loss of skin elasticity from overexposure to UV radiation

moles = benign proliferation of melanocytes, risk factor for melanoma

freckles = overactive melanocytes in small areas

solar keratoses = abnormal growth of keratinocytes

types of skin cancer:
- melanoma affecting melanocytes
- squamous cell carcinoma affecting the upper layer of skin
- basal cell carcinoma affecting the basal layer of epidermal cells

18
Q

positive aspects of UV exposure

A

vitamin D production

ultraviolet radiotherapy for treating skin conditions - vitiligo, psoriasis

19
Q

describe first, second and third degree burns

A

first = epidermal damage without extending beyond, heals without scaring

second = epidermal damage and upper dermal layer, scaring may occur but doesn’t reach sebaceous glands

third = full-thickness damage affecting the entire cutis, scarring is inevitable and loss of sensation may occur

20
Q

irritant contact dermatitis - cause? symptoms? management?

A

caused by excessive exposure to a substance - reactions and sensitivity may vary among individuals

symptoms: redness, itching, swelling, blistering, scaling

managed by using the substance in reduced amounts

21
Q

allergen contact dermatitis - cause? immune involvement? symptoms? management?

A

caused by an allergic reaction to a substance contacting the skin - e.g. latex allergy

involves the immune system - initial sensitisation, followed by delayed hypersensitivity upon re-exposure

symptoms: redness, itching, swelling, blistering, weeping

managed by avoiding the allergen in the future