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MSS & Skin > Skin: Effect of Environment > Flashcards

Skin: Effect of Environment Flashcards

1
Q

What is integument?

A

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

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2
Q

Explain the significance of skin as a vital organ

A

On extensive epidermal (or epidermal + dermal) damage, e.g. with severe burns or a rare drug reaction, death may occur

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3
Q

What may occur to cause severe skin damage resulting in death?

A
  • Dehydration and shock
  • Infection
  • Heat loss and hypothermia (or hyperthermia due to
    impaired thermoregulation)

Others: protein loss; electrolyte imbalance; high-output cardiac failure; renal failure

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4
Q

What is toxic epidermal necrolysis?

A

(rare adverse drug reaction)

Detachment of epidermis. Often fatal

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5
Q

Give examples of environmental insult to skin

A
  • Irradiation and UV light
  • Physical trauma (burns, friction, pressure)
  • Irritants
  • Allergens
  • Microbes, ectoparasites etc.
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6
Q

How does the skins ability to dry aid protection?

A

Drying: Waterproof epidermis + oil from sebaceous glands

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7
Q

What factors aid skins ability to protect against friction and impact?

A

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)

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8
Q

How does thermoregulation of skin maintain homeostasis?

A

Heat: Sweating; vasodilatation
Cold: Subcutaneous fat, adaptable blood supply, hair (head)

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9
Q

How is the skin adapted to deal with burns?

A

Thick, regenerating epidermis

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10
Q

How does skin react to sunlight and radiation?

A

thick epidermis; melanin

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11
Q

How does skin fight infection?

A

Impervious epidermis; resident cells of immune system

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12
Q

Outline a fast response from the skin?

A 
Sweating & vasodilatation in heat; vasoconstriction in cold.
Quite fast (minutes)
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13
Q

What are the slower ways skin adapts to the environment?

A

Hyperkeratosis: thickening of stratum corneum with rubbing or pressure (e.g. feet, guitarist fingers), or (slightly) after ultraviolet exposure. Slow (weeks)

Melanocytes: tanning after ultraviolet exposure. Quite slow (days).

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14
Q

What are arteriovenous shunts?

A

Arteriovenous (AV) shunts found across the dermis, are anastomoses between arterioles and venules

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15
Q

What is the role of AV shunts?

A

Respond to thermoreceptors in skin – hot/cold

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16
Q

Explain why the skin turns red/blue in extreme temperatures?

A

Av shunts open and close to increase/decrease blood flow to superficial vascular plexus in the papillary dermis (just below epidermis)
Hence skin goes redder (more heat loss) or bluer

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17
Q

What other factors contribute to redness/bluish colour of skin?

A

In face: can also respond to emotion/ sympathetic nervous system – blushing.
Shut off for too long – danger of damage (frostbite)

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18
Q

What 2 molecules mainly contribute to the colour of skin?

A

The colour of human skin is due mainly to melanin (dark skin) and haemoglobin (light skin)

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19
Q

What is the normal range of melanin in the body?

A

Much normal genetic variation in the amount of melanin (>12 genes known)

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20
Q

Apart from pigmentation what is the role of melanin?

A

Melanin protects against DNA damage and thus skin cancer, especially in dark (black & Asiatic) skin: incidence only 8-10% that of white people

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21
Q

How does melanin contribute to skin colour?

A

Melanocytes transfer melanosomes (pigment granules) mainly to the basal keratinocytes

22
Q

What effect does tanning have on the skin?

A

Melanocytes increase activity - make & transmit more melanin.
Gives some protection against UV.
Additional protection by skin thickening in response to UV.

23
Q

Outline the protective mechanism of skin against suntanning

A

Basal level of melanin constantly present in keratinocyte

  1. UVR causes DNA damage in the keratinocyte
  2. The DNA damage creates signalling molecules resulting
    in MSH production
  3. MSH binds to its MC1R receptor stimulating melanocyte
    activity
  4. Causes stimulation of MSH and melanocyte production => produces more melanin
24
Q

At what level is suntanning safe?

A

Sun tanning is never safe - any sun tan causes DNA damage

25
Q

What are the main cells within the skin responsible for the protection against microorganisms?

A

Langerhans cells and 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

26
Q

What is lichenification?

A

More extreme form of hyperkeratosis.

Reaction to excessive rubbing or scratching/ skin conditions

27
Q

What are the 3 types of UV radiation?

A

UVA>UVB>UVC

UVA is the longest wavelengths of UV spectrum

28
Q

What is the relationship between UV radiation and the Earth and ozone layer

A

UVC is blocked by the ozone layer (some UVA and UVB is blocked as well but some still reacehs ground level)

29
Q

What is sunburn?

A

Is a radiation burn causing blisters, inflammation and cell death in keratinocytes (severe DNA damage)

30
Q

What is the long term effect of sunburn?

A

Associated with increased risk of skin cancer

Using a UV sunbed below age 35 increases skin cancer chances by 75%

31
Q

What is Polymorphic Light Eruption?

A

One of many types of sun allergies

Causes rash when exposed to sun

32
Q

What causes wrinkles?

A

Prolonged sun exposure can cause solar elastosis (loss of elasticity) due to loss of elastic fibres

33
Q

What are naevi?

A

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

34
Q

What are ephelides?

A

Freckles
Occurrence involves a genetic component - linked to red/fair hair
Often MC1R gene variants
Sun-exposed areas more prone to freckles

35
Q

What are solar lentigos?

A

Liver spots, age spots, Age related

36
Q

What is solar keratoses?

A

The dysplastic growth of keratinocytes

37
Q

What are the 2 types of skin cancer?

A

Melanoma (melanocytes) - most dangerous

Non-melanoma (mostly keratinocytes) - common

38
Q

What are the 2 types of non-melanoma skin cancer?

A
  • squamous cell carcinoma

- basal cell carcinoma (common)

39
Q

What are the treatments for basal cell carcinoma?

A

Rodent ulcer
Often curable by surgery
- especially if reported early!

40
Q

Describe a melanoma

A

(can be thin, but still dangerous – rapid spread)

41
Q

What (if any) are the benefits of UV radiation?

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, eg vitiligo, psoriasis

42
Q

How are burns differentiated?

A

Burns categorised by how deep into the skin they are

1st degree - 3rd (worst v.deep)

43
Q

What causes irritant contact dermatitis?

A

Occurs when too much exposure to a substance.
Can still use substance but reduce amount
People vary in sensitivity

44
Q

What are the symptoms associated with irritant contact dermatitis?

A

Any of: Redness, itching, swelling, blistering and/or scaling

45
Q

What is allergic contact dermatitis?

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

46
Q

What are the symptoms of allergic contact dermatitis?

A

Any of: Redness, itching, swelling, blistering and/or weeping.
Avoid allergen in future

47
Q

Compare the two formsofocntact dermatitis

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)

48
Q

What microbes could potentially cause skin disorders?

A

Fungi
Bacteria
Viruses

49
Q

What is Paronychia?

A

nail fold infection-fungal or bacterial

50
Q

Give an example of each of the microbes causing disease

A

> fungal example: Tinea capitis scalp ringworm
bacterial example: Impetigo, Cellulitis: streptococcus
viral example: Human Papillomavirus (HPV) warts

51
Q

How may the skin cause re-infection?

A

Portal of entry: microbes can enter breach in epidermis

e.g. Streptococcus in cellulitis

52
Q

How may the immune system contribute to re-infection?

A

Impaired immunity predisposes to infection,
e.g. HIV and viral warts;
eczema herpeticum, which is herpes (cold sore) virus infecting eczema

MSS & Skin (6 decks)

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