W8 - Effect of environment on skin Flashcards

1
Q

What is the integument?

A

Interface between body and environment. Thus
subject to a wide range of insults (stresses).

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2
Q

Why is skin a vital organ?

A

On extensive epidermal (or epidermal + dermal) damage, e.g. with severe burns
or a rare drug reaction, death may occur, owing to one or more of:
* Dehydration and shock
* Infection
* Heat loss and hypothermia (or sometimes hyperthermia due to impaired
thermoregulation).
* Others: protein loss, electrolyte imbalance, high-output cardiac failure, renal
failure.

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3
Q

What is Toxic epidermal necrolysis?

A

(rare adverse drug reaction)
Detachment of epidermis. Often fatal.

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4
Q

What is an environmental ‘insults’?

A
  • Irradiation & UV light
  • Physical trauma (burns, friction, pressure
    etc)
  • Allergens
  • Irritant
  • Microbes

These upset the homeostasis, thermoregulation etc…

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5
Q

What are the Protective features of the skin?

A
  • 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
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6
Q

What are the Normal skin adaptations to environmental pressures?

A
  • Sweating & vasodilatation in heat;
    vasoconstriction in cold. Quite fast
    (minutes).
  • Hyperkeratosis (callus): thickening of
    stratum corneum with rubbing or pressure
    (e.g. feet, guitarist fingers), or (slightly) after
    ultraviolet exposure. Slow (weeks).
  • Tanning: (melanocyte response) after
    ultraviolet exposure. Quite slow (days).
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7
Q

How does thermoregulation by blood supply help?

A

Arteriovenous (AV) shunts are anastomoses
between arterioles and venules. Numerous in
dermis.
Respond to thermoreceptors in skin – hot/cold.
Shunts open or close respectively to decrease or
increase 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.
Shut off for too long – danger of damage (frostbite).

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8
Q

How does UV protection through epidermal melanin work?

A
  • The colour of human skin is due 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 & Asiatic)
    skin: incidence only 8-10% that of white people

Transfer of melanosomes (pigment granules) mainly to basal keratinocytes

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9
Q

How is tanning a form of protection?

A

Melanocytes increase activity - make &
transmit more melanin.

Gives some protection against UV.

Additional protection by skin thickening in
response to UV.

MSH: melanocyte-stimulating hormone
MC1R: melanocortin 1 receptor

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10
Q

What is UV protection? Basics of suntanning?

A

MSH - melanocyte-stimulating hormone
MCIR - melanocartin I receptor

From UVR damage, there would be DNA damage signalling the release of MSH from the basal keratinocyte to the MCIR receptor in the melanocyte. This result in the transcriptional increase of melanin synthesis and transfer and increase in cell division.

The thing being transcribed in Tyrosinase (TYR).
Tyrosine-related proteins (TRPs)
Tyrosine - (TYP) -> L-DOPA - (TYR) -> DOPAquinone - (TRPs)–> Eumelanins( Brown/black) or Pheomelanins (Yellow to Red)

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11
Q

How does skin protect against microorganisms?

A

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 – part of immune system.

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12
Q

What are examples of environmental insults?

A

 Friction/ scratching
 Ultraviolet irradiation
 Burns
 Irritants
 Allergens
 Microbes (bacteria, viruses, fungi)

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13
Q

What is Lichenification?

A

More extreme form of hyperkeratosis.
Reaction to excessive rubbing or scratching/skin conditions. Leathery/tree bark appearance from addition to wrinkles etc.

This is a reaction to friction/scratching

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14
Q

How does sunburning work?

A

Solar UV Radiation in relation to the Earth and ozone layer.
* Is a radiation burn
* Blisters, inflammation and cell death
(severe DNA damage)
* “Ever sunburnt” associates with
increased risk of skin cancer
* So does “ever used a UV sunbed
below age 35” – by 75%

When we are out in the sun, we are exposed to both UVA and UVB. UVB is most associated to skin cancer - suncream.

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15
Q

What is Polymorphic light eruption?

A

Manifestation in the form of a rash - several types of sun allergies.

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16
Q

How do wrinkles form?

A

Solar elastosis (loss of elasticity)

17
Q

What are naevi (moles)?

A

(Singular, naevus. USA: nevus)
Benign proliferation of melanocytes
Many or large naevi: risk factor for melanoma skin cancer

18
Q

How do freckles (ephelides) form?

A
  • Involve a genetic component. Also linked to
    red/fair hair. Often MC1R gene variants.
  • Sun-exposed areas

Melanocytes in these areas are over active producing melanin at an abnormal rate. Though not fully understood.

19
Q

What are Solar lentigos [liver spots, age spots]?

A

Age related.

20
Q

What is solar keratoses?

A

Dysplastic growth of keratinocytes

21
Q

What is skin cancer?

A

Melanoma / Non-melanoma
(melanocytes) / (mostly keratinocytes)
Most dangerous

mk:
Common Squamous cell
carcinoma
Basal cell
carcinoma
Commonest

22
Q

What is Basal cell carcinoma [‘rodent ulcer’]?

A

It eats into the skin if left untreated.
Often curable by surgery
- especially if reported early!

23
Q

What is Melanoma?

A

Can be thin, but still dangerous – rapid spread

Noonan et al. (2012): UVA as well as UVB can
cause melanoma, in pigmented mice. Relevant to sunscreen design and tanning

Later, if untreated:
If untreated, it would almost certainly spread to lymphatics etc.

24
Q

What is the good side of UV?

A
  • UV needed for vitamin D3 production in skin.
    15-min summer sun on face & arms per day
    enough for white skin, longer for dark skin. Or
    take tablets.
  • Ultraviolet radiotherapy for skin conditions, e.g.
    vitiligo, psoriasis
25
Q

How do burns work?

A

1st degree = does not go beyond the epidermis
2nd degree = epidermis and upper layers of dermis - does not read sebaceous glands (may or may not scar)
3rd degree = Full thickness upto the fatty layer. These will lose the pinprick sensation when presented acutely.

26
Q

How does irritant contact dermatitis work?

A
  • Occurs when too much exposure to a
    substance.
  • Can still use it, but reduce amount.
  • People vary in sensitivity
  • Any of: Redness, itching, swelling, blistering
    and/or scaling
27
Q

How does allergen contact dermatitis work?

A
  • Allergy to something that contacts skin
  • immune system involved.
  • Tiny amount may be sufficient.
  • Varies greatly between people. May
    develop after long or short use.
  • Any of: Redness, itching, swelling,
    blistering and/or weeping.
  • Avoid allergen in future
  • popular are metal like nickle in jewellery etc
  • Latex is another one - can cause nasty blistering in severe cases.
28
Q

What are some further comments on allergins?

A
  • Irritant contact dermatitis is common
  • Allergic contact dermatitis relatively uncommon (e.g. nickel)
  • Sensitization first: Langerhans cells process antigen and ‘present’ to lymphocytes
  • Delayed hypersensitivity occurs at next exposure (memory T-cells)
29
Q

What are microbes (fungi, viruses, bacteria) induced disease?

A

Paronychia(nail fold infection-fungal or bacterial)
Fungal : Tinea capitis (scalp ringworm)
Bacterial : Impetigo
Bacterial : Cellulitis streptococcus
Viral: Human papilloma virus (HPV) (Warts)

  • Portal of entry: microbes can enter breach in epidermis (e.g. Streptococcus in cellulitis)
  • Impaired immunity predisposes to infection,
  • e.g. HIV and viral warts;
  • eczema herpeticum, which is herpes (cold sore) virus infecting eczema