6. EFFECT OF ENVIRONMENT ON SKIN Flashcards

1
Q

Define the integument in terms of the environment

A
  • The integument acts as the border or interface between the body & the environment. It can be subject to stresses which is anything causing harm or damage
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2
Q

What are the 5 potential types of environmental insults to the skin?

A
  1. PHYSICAL TRAUMA (Friction, burns, scratching)
  2. UV IRRADIATION
  3. IRRITANTS
  4. ALLERGENS
  5. MICROBES
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3
Q

**What are the protective features of the skin against these insults?

A
  1. FRICTION/IMPACT :
    - Thick regenerating epidermis
    - Dermal - epidermal border protects against shear forces
    - Collagen in the dermis provides tensile strength
    - Nails
  2. BURNS
    - Thick regenerating epidermis
  3. UV LIGHT
    - Thick epidermis, melanin
  4. INFECTION
    - Langerhans cells resident in epidermis & epidermis is impervious
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4
Q

What are some consequences of skin damage that can lead to death?

A
  1. DEHYDRATION/SHOCK - loss of haemostatic function
  2. INFECTION - can spread to the lymph nodes
  3. *HEAT LOSS & HYPOTHERMIA - Impaired thermoregulation
    • HIGH OUTPUT CARDIAC FAILURE - Extensive damage to the skin, means that more blood supply to the skin surface is needed, but there’s less venous return. The heart is therefore unable to cope with the demands of the skin
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5
Q

**Describe the structure of the vasculature of the dermis?

A
  • The dermis is involved in thermoregulation, it also contains thermoreceptors
  • It has an ARTERIOVENOUS SHUNT, which is an anastomoses between the venules & arterioles. The AV shunt can be shut or open depending on the temperature. The AV shunts respond to signals from thermoreceptors
  • There’s a SUB-PAPILLARY PLEXUS located beneath the dermal papillae
  • The CUTANEOUS PLEXUS is found on the border of the dermis & the hypodermis. - Sub- cutaneous arteries supply blood to the cutaneous plexus, the venules then pick up this blood and take it to the surface of the skin & back. This pathway can be bypassed with AV shunts
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6
Q

How does the skin adapt to heat?

A
  • HEAT = VASODILATION & SWEATING
  • Thermoreceptors detect heat & the AV shunts close in response.
  • Closing the AV shunts, closes the shortcut for blood. The blood will be taken to the surface of the skin when AV shunts are closed
  • Continuous delivery of blood to the skin surface will allow the loss of energy, allowing the body to cool down
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7
Q

How does the skin adapt to the cold?

A
  • COLD = VASOCONSTRICTION
  • Thermoreceptors detect the cold & the AV shunts open in response
  • The AV shunts allow the blood to be taken back by the venules to reduce surface blood flow. The blood will be shunted straight to the venules to minimise heat loss by surface blood flow
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8
Q

How is tanning an adaptation to UV light?

A
  • TANNING is a melanocyte response that occurs after UV light exposure, as an adaptation
  • Tanning is a slow process that can take a few days
  • Melanocytes protect against DNA damage. During tanning, there’s more melanocyte activity, transmitting more melanin to the basal keratinocytes
  • Thickening of the skin can also occur which is an additional protection
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9
Q

Describe the process of melanin synthesis involving MSH

A
  1. UV light causes DNA damage in the basal keratinocytes
  2. DNA damage triggers a signaling pathway
  3. The signaling pathway results in the synthesis & secretion of MSH (Melanocyte stimulating hormone)
  4. MSH binds to MC1R (melanocortin receptor) on melanocytes causing cAMP signalling
  5. cAMP signalling leads to the transcription of enzymes involved in melanin synthesis such as tyrosinase
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10
Q

How is tyrosinase involved in melanin synthesis & when is it produced?

A
  • When MSH binds to MC1R receptors on melanocytes, it triggers cAMP signaling. The cAMP signalling leads to the transcription of enzymes such as TYROSINASE & TYROSINASE RELATED PROTEIN
  • TYROSINASE converts Tyrosine -> L-DOPA -> Dopaquinone
  • Tyrosinase related proteins act on the Dopaquinone to produce two types of melanin, depending on where the melanocytes are located: eumelanin or pheomelanin
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11
Q

What are the two types of melanin produced by tyrosinase related protein?

A
  • TYROSIANSE RELATED PROTEIN acts on Dopaquinone to produce:
    1. EUMELANIN - Found in skin (Brown -> Black)
    2. PHEOMELANIN - Found in hair, responsible for producing naturally brighter hair colours (Yellow -> Red)
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12
Q

What is hyperkeratosis?

A
  • HYPERKERATOSI is the thickening of he upper layer of skin (stratum cornuem) with rubbing, pressure or UV exposure
  • E.g feet
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13
Q

What is Lichenification?

A
  • LICHENIFICATION is a more extreme form of hyperkeratosis, it occurs due to excessive rubbing or scratching
  • Its characterized by a tree bark like appearance
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14
Q

What type of sun rays are we exposed to?

A
  • We are exposed to UVA & UVB sun rays
  • The sun also produces UVC rays, but these don’t penetrate the ozone layer. The ozone layer also blocks some UVA & UVB rays but not all
  • UVB rays are thought to be the most implicated in skin cancer
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15
Q

What are 7 consequences of UV irradiation?

A
  1. Sun burn
  2. Polymorphic light eruption
  3. Solar elastosis
  4. Naevi/moles
  5. Freckles/ Ephelides
  6. Solar lentigos
  7. Solar keratoses
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16
Q

What is sun burn?

A
  • Prolonged sun exposure can lead to sun burn

- It’s a radiation burn characterised by blisters, inflammation & cell death due to severe DNA damage

17
Q

What is polymorphic light eruption?

A
  • Polymorphic light eruption is sensitivity to sunlight which manifest as a red, itchy or burning rash
18
Q

What is solar elastosis?

A
  • Solar elastosis refers to the degeneration of elastic tissue (elastin) in the skin due to prolonged sun exposure
  • The skin loses it’s elasticity, becoming coarse & wrinkly
19
Q

What are naevi or moles?

A
  • Benign proliferation of melanocytes which aren’t always skin cancer causing
20
Q

What causes freckles?

A
  • Melanocytes are over-active & produce melanin at faster rates in these areas compared to others
  • Freckles tend to appear in sun-exposed areas such as the face. It’s thought be associated with a mutation of MC1R gene coding for the melanocortin receptor on melanocytes
21
Q

What’s solar lentigos & solar keratoses?

A
  • Solar lentigos - darkened spots of skin that tend to be due to ageing, also known as sun or liver spots
  • Solar keratoses involves abnormal or dysplastic growth of keratinocytes
22
Q

What are the two main types of skin cancer & their characteristics?

A
  1. MELANOMA CANCER
    - Affects the melanocytes & is the most dangerous
    - Spreads rapidly & can spread to the lymph nodes
  2. NON-MELANOMA CANCER
    - Non-melanoma cancer affects the keratinocytes & is the most common
    - Non-melanoma cancer can be further sub-divided into two categories: Basal cell carcinoma & squamous cell carcinoma
23
Q

What are the two types of non-melanoma cancer?

A
  1. BASAL CELL CARCINOMA
    - Affects the basal keratinocytes of the basal layer of the epidermis
    - Most common of the two non-melanoma cancer types
    - Can eat into the skin if left untreated leading to a rodent ulcer
  2. SQUAMOUS CELL CARINOMA
    - affects the flattened squamous cells of the upper epidermis (cornified layer)
24
Q

What are the three categories for burns?

A
  1. FIRST DEGREE BURN
  2. SECOND DEGREE BURN
  3. THIRD DEGREE BURN
25
Q

What is a first degree burn?

A
  • A first degree burn affect the epidermis (superficial burn)
  • The epidermis is destroyed but it doesn’t reach the dermal -epidermal border
26
Q

What is a second degree burn?

A
  • A second degree burn affect the epidermis and the upper dermis
  • However, the burn doesn’t reach the sebaceous glands
  • There may be some scarring
27
Q

What is a third degree burn?

A
  • A third degree burn affect the epidermis & the dermis

- This is a deep burn that can lead to the loss of sensation & scarring

28
Q

What is irritant contact dermatitis?

A
  • IRRITANT CONTACT DERMATITIS occurs due to too much exposure to a substance or irritant
  • Can still use it but amount should be reduced
  • Manifests as redness, itching, swelling or scaling
  • People can vary in sensitivity
29
Q

What is allergen contact dermatitis?

A
  • ALLERGEN CONATCT DERMATITIS occurs when an allergen comes into contact with the skin & involves the immune system, where there’s an initial period of sensitisation
  • The allergen should be avoided
  • Allergen contact dermatitis can occur after short term or long term exposure
  • Manifests as swelling, itching, redness & scaling
30
Q

What are the two phases of allergen contact dermatitis?

A
  1. SENSITISTAION - first exposure to allergen, allergen antigen is processed by Langerhans. Langerhans present antigens to lymphocytes
  2. DELAYED HYPERSENSITIVITY - next exposure leads to allergy repsonse due to memory T cells
31
Q

How can microbes cause an infection & what can cause a pre-disposition to infection?

A
  • Microbes ca enter the skin through breaches in the epidermis & cause infection
  • Individuals with impaired immunity are more susceptible to infection e.g HIV as the immune system is already compromised so it’s less likely to be able to deal with infectious microbes
32
Q

What is paronychia?

A
  • Paronychia is a bacterial/fungal infection of the nail fold
33
Q

What is tinea capitis?

A
  • A scalp ringworm caused by fungus leading to hair loss
34
Q

What is bacterial impetigo & bacterial cellulitis?

A
  • Bacterial impetigo - lesions characterised by breaking of the skin
  • Bacterial cellulitis - caused by streptococcus bacteria, inflammation of the skin leading to redness