MSS Effects of Environment of Skin Flashcards
Why is the skin a vital organ?
Death may occur following extensive skin damage, e.g. severe burns or a rare drug reaction.
This is through one or more of:
- 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.
Describe the different types of environmental insults
Describe the basal features of intergument which protect the skin against various stresses
3 normal adaptations of skin to environmental stresses?
- Sweating and vasodilatation in heat; vasoconstriction in cold. quite fast (in minutes)
- Hyperkeratosis (callus) - thickening of stratus corneum with rubbing or pressure (e.g. feet, guitarist fingers), or (slighty) after UV exposure. slow (in weeks)
- Tanning (melanocyte response) - after UV exposure. quite slow (days)
Describe thermoregulation by skin’s blood supply
Thermo-receptors in skin control BF via symp nerves.
Vessel walls relax to increase arterial BF + heat loss (hot) or contract to decrease BF (cold) to the superficial (subpapillary) plexus below epidermis.
Hairless/glabrous skin (palms) also has AV shunts or anastomoses between arteries and a high-capacity venous plexus in the dermis. Shunts likewise open/close.
however if Reduce blood flow for too long –> frostbite to extremities.
Label this, what does it show?
Why do we get tanned upon sun exposure?
Melanocytes make more melanin y hay epidermal thickening to protect against more UV
DNA damage is the actual mechanism for sun-tanning, so tanning=you have significant DNA damage in your skin!
DNA damage signalling causes keratinocyte to make MSH - this activates MCR1 (melanocortin 1 receptor), stimulating melanocytes
Via their cAMP pathway, melanocytes increase melanin synthesis + transfer, and also cell division
More melanosomes goes to keratinocyte, arranged on top of nucleus–> increased protection against UV!
MCR1 gene is mutated in which types of ppl?
What does this show?
Differentiate between irritant and allergic contact dermatitis
Irritant contact dermatitis: common, upon too much
exposure to a substance. Reduce amount
Allergic contact dermatitis relatively uncommon
(e.g. nickel): immune mediated, tiny amount can be enough. Completley avoid amount
Sensitization first: Langerhans cells present Ag to lymphocytes. Delayed hypersensitivity (type IV) occurs at next exposure (memory T-cells)
Redness, itching, swelling, blistering, scaling or (weeping for allergic only) symptoms
These show examples of when mircobes infiltrate the skin. What do each of these show?
Microbes can enter a breach in the epidermis
e.g. streptococcus in cellulitis
Impetigo common in children, thinner skin
Also, impaired immunity predisposes to infection
- e.g. HIV and HPV viral warts
- eczema herpeticulum, which is herpes virus infecting eczema
Differentiate between 1st 2nd and 3rd degree burns
1st degree - superficial burn - affects just the epidermis
2nd degree affects some of the dermis, sebaceous glands still remaining, probs won’t scar
3rd degree is where most of dermis is lost including sense organs - loss of pinprick sensations
Give the types of UV radiation
UVA, UVB, UVC
- UVA has the longest UV wavelengths
- mainly UVA and some UVB reaches ground level
- ozone blocks some UVA and UVB/
Describe sunburn
A radiation burn
Inflammation can include blisters = epidermal cell death (severe DNA damage), or peeling (less severe damage)
‘Ever sunburnt’= increased skin cancer risk, so does ‘ever used a UV sun bed below 35’ - by 75%
Differentiate between naevi and freckles
Naevi: benign melanocyte proliferation. Many/large naevi = risk factor for melanoma
Freckles: aka ephelides, linked to red/fair hair
Often MC1R gene variants
Tend to be in sun exposed areas