Skin Essential Function Flashcards
1
Q
What are the functions of the skin?
A
- Protection (UV, organisms, chamicals, water, mechanical).
- Sensation (pain, temperature, touch, pressure, vibration).
- Homeostasis and excretion of waste (water, electrolytes, macromolecules).
- Homeostasis - thermoregulation (vasodilation, sweating, hairs).
- Metabolic - fat store, vitamin D.
- Socio-cultural functions and self-expression.
2
Q
What are the components of the skin which are for protection?
A
- Oil/wax
- Water
- Melanin
3
Q
Describe the protection given to the skin by oil/wax.
A
-
Sebaceous glands in the skin secrete oily or waxy substance called sebum.
- Sebum lubricates and waterproofs the skin and hair.
- Occur all over body except the palms of the hands and soles of the feet.
- Large number on face and head.
- Excess sebum → acne and sebaceous cysts (and other pathologies).
- Too little sebum → ‘chapped’ skin.
4
Q
Describe the protection given to the skin by water.
A
- Skin hydration helps to maintain resistance against mechanical stress.
- Aged skin shows less hydration and has reduced elasticity.
- Normally skin controls of movement of water (as well as itself being hydrated) but some osmosis will occur - shrivelled fingers in the bath.
5
Q
Describe the protection given to the skin by melanin.
A
- Broad spectrum UV absorber. Protects deeper tissues from UV damage.
- Dark skinned people have more melanin than light skinned people.
6
Q
What is dermal sorption?
Use mercury as an example.
A
- The skin is protective but does not prevent absorption of everything.
- Mercury salts inhibit melanin formation by competing with copper in tyrosine reaction.
- Inorganic mercury is thought to be absorbed through the skin across the epidermis and via sweat glands, sebaceous glands and hair follicles.
- Mercury is neurotoxic.
7
Q
What are the defence components of skin?
A
- Melanocytes
- Keratinocytes
- SALT
8
Q
Describe the role of melanocytes in skin defence.
A
- Produce melanin which is dispersed to surrounding keratinocytes.
- Various pigments - black, brown, yellow, red.
- Sun exposure transiently increases melanin production to protect deeper tissues being damaged by UV.
9
Q
Describe the role of keratinocytes in skin defence.
A
- Produce keratin that eventually forms essential part of the tough outer layer.
- Probable role in T cell maturation.
10
Q
Describe the role of SALT in skin defence.
A
-
Langerhans cells
- Migrate from skin to bone marrow, initiate immune response in response to antigens.
-
Granstein cells
- May have a role in suppressing immune response.
- Transient T lymphocytes (scattered throughout epidermis and dermis).
11
Q
Describe the nociceptors found in the skin.
A
- Respond to pain.
- Free nerve endings (also found internally).
- Sensitive to tissue damage e.g. pinching, burning or distortion of tissue.
- Pain receptors don’t adapt to repetitive stimulation (survival).
- Typically have a high threshold for mechanical, chemical, and thermal stimuli (or a combination) or intensity sufficient to cause tissue destruction.
- But, they can be sensitised e.g. by prostaglandins released in response to injury (aspirin inhibits production of prostaglandins) (analgesic effect).
12
Q
Describe the thermoreceptors found in the skin.
A
- Sense temperature - separate receptors for hot and cold.
- Cooling or warming the skin opens ion channels in the receptor, initiating response.
- Density of temperature receptors differs at various places on the body surface.
- Lower density than cutaneous mechanoreceptors.
- Many more cold receptors than warm receptors.
- Receptors quickly adapt and we then ‘notice’ only a change.
- At very high skin temperatures (>45°C) → paradoxical cold, caused by nonspecific activation of some cold receptors.
13
Q
Describe the touch receptors found in the skin.
A
-
Meissner corpuscle - cutaneous touch receptor responds to light touch (also vibration).
- Concentrated in areas sensitive to light touch e.g. fingertips, lips, nipples.
-
Merkel disks - located in the lowest layer of the epidermis.
- Respond to steady pressure.
- Provide information about an object’s edges or curves.
-
Pacinian corpuscles - pressure / vibration.
- Receptors are nerve endings surounded by gel-like envelopes within capsules.
- When the capsule is deformed (by pressure), the underlying nerve ending is deformed and generates an electrical potential.
- Gel envelopes quickly equalise and remove local deformation so signal ceases.
- Deformation occurs again when pressure is released.
- So, pacinian corpuscle best detects the start and end of rapidly changing pressure.
14
Q
What are the different types of itch?
A
- Neurogenic and systemic
- Psychogenic
- Neuropathic
- Pruritoceptive
15
Q
What causes neurogenic and systemic itch?
A
Results from disorders that affect organ systems other than the skin (e.g. renal, liver disease).
16
Q
What is a psychogenic itch?
A
Itching associated with psychological abnormalities (e.g. depression, OCD).
17
Q
What is a neuropathic itch?
A
Itching which results from damage to central or peripheral sensory neurons.
18
Q
Describe pruritoceptive itch.
A
- Pruritoceptive itch is generated in the skin, usually by inflammation or other visible pathological processes involving the skin.
- Physiology is poorly unerstod:
- Historically thought to be a low-intensity pain response but recent studies suggest not.
- Itch receptors may be on keratinocytes and / or free nerve fibres (may be communication between the two).
- May be a subpopulation of nociceptors.
- May be that pain and itch signals are transmitted via different nerves.
- There are various mediators (signallers) for itch: e.g. histamine, tryptase, dust mite protease allergens, IL-31 plus others.
19
Q
Which layer of the skin prevents water loss?
A
Stratum corneum
20
Q
Why can people with burns often lose a massive fluid volume very quickly?
A
- Because the stratum is lost in burns and the stratum corneum layer usually prevents water loss.
- Physiological mechanisms to return homeostasis are often overwhelmed (e.g. renal compensation) and hypovolaemic shock is a risk.
21
Q
Describe the role of skin in thermoregulation.
A
- Sweat glands located over the majority of the body.
- Release dilute salt solution onto the surface of the body.
- Evaporation helps to reduce temperature of the skin and helps to cool the body temperature.
- Amount of sweating depends on:
- Internal temperature
- External temperature
- Muscular activity
- Other factors such as nervousness, fear
- Most sweat contains compounds toxic to bacteria
- Sweat from armpits and pubic region produce protein-rich sweat whic does support bacteria = smell.
22
Q
How is blood flow to the skin regulated?
A
- Blood flow to the skin is regulated mostly via CNS through sympathetic NS but also by local effects of temperature on dilation / constriction of blood vessels.
23
Q
Desribe the blood flow through the skin.
A
- Skin is highly vascularised.
- Nutrient requirements are quite low so blood flow doesn’t have a primarily metabolic support role.
- Main purpose is to regulate body temperature.
-
Venous plexus supplied by inflow from skin capillary loops and from small arteries through the muscular arteriovenous (AV) anastomoses.
- Venous plexus contains most of cutaneous blood.
- Especially prominent feature in extremities (nose, ears, fingers, toes).
- Venous plexus blood contributes to skin colour in those with light skin pigmentation.
24
Q
Describe the role of blood flow to the skin in the regulation of body temperature.
A
- Diameter of blood vessels controlled (mostly) by sympathetic nerves governed by hypothalamus but also sensitive to circulating substances.
- E.g. catecholamines, bradykinin and nitric oxide (in sweating), histamine and bradykinin (local changes e.g. mechanical trauma, heat) (possibly other unidentified substances).
- Blood flow to venous plexus varies between ~zero and 30% of CO.
- At normal body temp, there is a high degree of sympathetic tone.
- As body temp rises, sympathetic discharge to skin decreases → vasodilation, increased blood flow → more blood near body surface so more potential for heat exchange with environment and cooling of the body.
- As body temp decreases, sympathetic discharge increases, blood flow to skin decreases; less heat lost to environment.
25
What are the effects of local changes to skin temperature on blood flow?
* Extreme cold → cold-induced vasodilation.
* Initial vasoconstriction, followed by dilation.
* Makes light skin go pink / red (rosy cheeks / nose in cold weather).
* Continued exposure results in alternating dilation and constriction.
* Mechanism not clear but probably due to local axon reflexes and impaired ability to vasoconstriction due to hypothermia.
26
Describe the effect of external temperature on heat conductance through the skin.
* **Increased sympathetic stimulation constricts** arteriovenous (AV) anastomoses and restricts flow.
* As external temperature decreases, vasoconstriction occurs, minimising heat loss.
* As external temperature increases, vasodilation increases and heat loss can increase 8-fold.
27
Heat moves according to physics. Describe how this is relevant to heat loss from the skin.
* **Radiation -** net loss or gain depends on temperature gradient.
* **Conduction -** through direct contact with an object or with air.
* **Convection -** heat lost through conduction then moved away due to convection.
* Breeze removes hot air next to skin and convction increases.
* Water can 'remove' absorb more heat than air, hence danger of hypothermia in cold water.
* **Evaporation**
* ****Insensible water 600-700ml/day → heat loss of 16-19kCal/day.
* NOT used in thermoregulation as not controlled.
* **Sweat -** used in thermoregulation.
* If external temp exceeds skin temp, the body gains heat by conduction and radiation and heat loss must be by evaporation.
* Anything preventing evaporation will cause body temp to increase (e.g. lack of sweat glands).
* Clothing traps air and decreases convection. Wet clothes transmit heat.
28
Describe sweat production in the skin.
* Initiated by cholinergic sympathetic nerve fibres ending on / near glandular cells.
* Primary secretion produced by epithelial cells in subdermal gland.
* Simiar composition to plasma (but no plasma proteins).
* Sweat is **modified in the duct.**
* Flow rate determines concentration of sweat.
29
Describe sweat flow (low flow, high flow).
* **Low flow**
* ****Most of Na+ and Cl- is absorbed, water follows, urea, lactic acid and K+ become very concentrated in sweat compared with primary secretion.
* **High flow**
* ****Some Na+ and Cl- is absorbed, a small amount of water follows, other constituents are only slightly more concentrated than primary solution.
* **Long term, acclimatisation** to heat
* Sweat gland cells adapt to increase production, aldosterone decreases NaCl in plasma and reduces salt loss through sweat.
30
What is the function of hair follicles and arrector pili?
* Sympathetic NS / stress response / high emotion e.g. adrenaline causes arrector pili to contract.
* Hair stands on end.
* In other mammals this mechanism has a large role in defence and thermoregulation.
31
Describe the metabolic role of skin.
* **Storage of fat - main reserve.**
* Skin is anchored to underlying tissue (muscle or bone) by hypodermis (subcutaneous tissue).
* Most of the body's fat cells are housed in the hypodermis.
* Collectively referred to as adipose tissue.
* Also a very good insulator - see thermoregulation.
* **Vitamin D**
* ****Not really a vitamin - it is a fat-soluble prohormone steroid.
* Main role is to control levels of calcium found in the bloodstream by enabling balancing of calcium and phosphate absorption from the gut with liberation from bone.
32
Describe the skin's role in vitamin D3 activation.
* 7-dehydrocholesterol found in the skin.
* UVB radiation converts it to vitamin D.
* 'Effective radiation' is 255 to 330nm UVB.
* Relatively small 'dose' of OVB required to generate a store of vitamin D.
* D3 is also available from diet.
33
What are the factors which affect the availability of UV-activated vitamin D?
* Availability of sunlight due to weather (cloud / sun / pollution).
* Geographic latitude.
* Time of year - season, 'strength' of UV.
* Exposure of skin - covering with clothes, indoor lifestyle, protection of skin.
* Skin pigmentation
* Melanin is a broad UV radiation absorber and reduces UVB available for 7-dehydrocholesterol.
* Darker skin reported to have the same capacity for vitamin D synthesis but higher absolute UV doses are required.
* Higher prevalence of rickets due to lack of vitamin D in northern countries (colder / more covered up / less sunlight) as well as countries whose culture is to cover up skin (rickets due to lack of vit C can be overlapping).
* Age, obesity
34
What are the different agents which can cause rash?
* Increased sensitivity due to loss of barrier function
* Bacterial / viral infection
* Insect bite / stings / infestations
* Heat
* Adverse reaction to drugs
* Allergic reaction
35
Describe the pathophysiology of acne vulgaris.
* **Blockage and inflammation of the hair follicle, hair shaft and sebaceous gland.**
* Acne may result in scarring - formed when the dermis is damaged, some scars have sunken / pitted appearance when subcutaneous muscle / fat is damaged.
* Fibroblasts produce large amounts of 'permanent' collagen fibres.
* This skin is often less well-organised and lacks features (e.g. hairs) or normal skin.
* May have issues of lack of function as well as form.
* May impact on socio-cultural functions, communication and self-expression.
36
Describe the process of scar formation.
* Blood fills the damaged area of skin and starts to clot.
* Fibrin mesh forms and dries into a scab, giving temporary protection.
* Fibroblasts are activated and replace the clot with collagen and pull the sides of the wound together.
* Epidermal cells divide and migrate to cover the healing dermis (within about 48 hours).
* New tissue forms over about a week (called granulation tissue because new, tiny blood vessels form, giving it a grainy, red appearance).
* Tiny blood vessels disappear (weeks / months) and skin becomes less red.
* Collagen is gradually remodelled and organised skin is formed.
