The integumentary system Flashcards
where is thick skin found
only on plantar and palmar surfaces, around 4mm thick, thin skin covers the rest of the body
three main layers of the skin
epidermis, dermis and hypodermis
there are also sweat glands and hairs which have sebaceous glands and a smooth muscle called the erector pili muscle
epidermis
thin outer portion that is the keratinised stratified squamous epithelium of skin (keratin threadlike protein, protective role)
epidermis has an important protective function of skin
the basal layers of this epithelium are folded to form dermal papillae
what are the epidermis layers
stratum corneum stratum lucidium (only thick skin) stratum granulosum stratum spinosum stratum basale
stratum corneum
protection- keratinised stratified squamous epithelium( layers of flattened keratinised (dead) cells), no blood supply relies on blood supply from dermis
cells are completely filled with keratin filaments embedded in a dense matrix of proteins
space between cells is full of lipids that cement the cells together, closer to the surface has looser appearance
cells are constantly lost from this layer
stratum lucidium
highly reflective only seen in thick skin
stratum granulosum
in thick skin, a few layers kf flattened cells eith cytoplasmic granules
in thin skin, only one layer may be visible
nuclei begin to degenerate
cytoplasm contains many fine grains of keratohyalin granules which release their lipid components into the interstitial space, this acts as a protective barrier
stratum spinosum
keratinocytes attached to each other by desmosomes on spiny processes, several layers of polyhedral cells
stratum basale
single layer of germinal cells resting on the basement membrane which is attached to the dermis- low columnar or cuboidal cells at the base of the epidermis
these are the stem cells of the epidermis
renewal of epidermis takes about 3-4 weeks
keratinocytes0
90% of epidermal cells, ectodermally derived. waterproof protection- keratinised, stratified, squamous epithelium.
synthetic phase- build up cytoplasmic supply of keratin, arranged in an alpha-helical coil pattern of the cells cytoskeleton. bundles of keratin filaments converge on and terminate at the plasma membrane forming the intracellular attachment plates know as desmosomes
degradative phase- cellular organelles lost, contents of cell consolidated into mixture of keratin filaments and amorphous cell envelopes, cell finally known as corneocyte. process of maturation resulting in cell death is known as terminal differentiation
melanocytes
8% of epidermal cell
dendritic, pigment-synthesising cell derived from the neural crest and confined in the skin predominantly to the basal layer un-pigmented do not store melanin which is transferred to other keratinocytes in membrane bound organelles
langerhan cells
collectively form a defensive network in the epidermis
primarily located k stratus spinosum, phagocytic cells that engulf foreign materials that invade the epidermis
contact with an antigen they migrate out of epidermis and skin to lymph nodes
merkel cells
granular basal epidermal cells, attached to a free nerve ending
mostly found in thick skin
oval shaped, slow adapting, type one mechanoreceptors located in sites of high tactile sensitivity that are attached to basal keratinocytes by desmosomal junctions
sebaceous glands
produce lipid rich sebum released into hair follicle
size and activity increase in response to increasing leveks kf androgens
if gland blocked, sebum can be forced out into dermis, elicits an inflammatory response, can cause acne
sudoriferous or sweat glands
eccrine- secrete a watery fluid, evaporation important for thermoregulation
apocrine- produce cloudy secretion which smells if bacteria react with it, production of pheromones
ceruminous glands
external auditory canal, combines with sebum to produce earwax
dermis
fundamentally composed of fibrillary structural protein collagen. dense irregular connective tissue that supports the epidermis important for sensation, protection and thermoregulation. lies on the subcutaneous tissue which contain lipocytes small lobes of fat dells
papillary layer- papillae that project into dermis
dermal papillae increase adhesion between epidermis and dermis, papillary capillaries bring nutrients to epidermis
reticular layer- dense irregular connective tissue
encapsulated nerve endings in the dermis
mechanoreceptors- sensory receptors that responds to mechanical pressure or distortion.
meissners corpuscle- nerve endings in skin responsible form sensitivity to light touch
pacinian corpuscle- nerve endings in skin responsible for sensitivity to vibration and pressure
which pigments contribute to skin colour
melanin, carotene, haemoglobin
functions of the skin
protection, sensation, thermoregulation, metabolic functions
skin levels of protection
epidermis is largely responsible for providing the protective barrier between the body and external environment
dermis contains collagen fibres that provide a structural framework that hosts a dynamic immunologic environment
epidermis hosts 2 key players in immune function of skin: keratinocytes and resident dendritic cells called langerhan cells
dendritic cells found in dermis differ from langerhan cells, having different surface cell markers and functions
langerhan cells are antigen presenting cells in the epidermis that cluster around hair follicles, process antigens and migrate to regional lymph nodes where they play an important role during infection and tolerance induction
vitamin D conversion
vit D synthesised in epidermis through action of solar or artificial UVB, radiation on a steroid precursor 7-dehydrocholesterol
1,25-dihydroxyvitamin D is thr biologically active natural vitamin D metabolite
formed from vitamin D by consecutive hydroxylations at position 25 in the liver and at position 1 in the kidneys and in many other tissues
low levels of vitamin D produce rickets and skeletal malformations that can result in death during childbirth
too much results in kidney stones and calcification of soft tissue
an important role of vitamin D - stimulates the body to absorb calcium and phosphorus from foods in intestine and has some other calcium retention effects
most cells of immune system have vitamin D receptors, vitamin D is activated in response to an infection particularly a respiratory one such as influenza
also believed to enhance phagocytic activity, increase production of antimicrobial substances in phagocytes, regulate immune function and help reduce inflammation
thermoregulation
homeostatic regulation of body temperature, the skin contributes in 2 ways: liberating sweat from its surface, adjusting the flow of blood in dermis.
exercise or high environmental temp; sweat production increases, evaporation from the skins surface helps to lower body temp. blood vessels in dermis dilate so increased blood flow through dermis which increases heat loss from body
low environmental temperature: production of sweat from eccrine glands decreased which helps conserve heat, blood vessels constrict to reduce heat loss
what does the skin act as
blood reservoir (carry 8-10%of total blood flow)
absorption and secretion
despite the stratum cornea, around 400ml of water evaporates through the skin daily an additional 200ml lost as sweat lost by sedentary individual more jf physically active
excretion of salts and small amounts of wastes (ammonia and urea) occurs with the production of sweat
absorption of water soluble substance negligible
lipid soluble compounds do penetrate including vit A,D,E and K, toxic compounds, drugs and gases
accessory structures of the skin
hair- found on most skin surfaces, made of fused keratinised cells, consists of shaft and root, surrounded by hair follicle
nerves- hair root plexus
muscle-erector pili
nails-plates of packed hard dead keratinised cells
nail body is majorly visible portion
free edge- part extending past finger or toe
toot- part not visible
phases of wound healing (epidermal)
epidermal-may extend to dermis
edges of wound usually only involve slight damage to superficial epidermal cells. wound healing- when a minor burn or abrasion occurs basal cells of the epidermis break away from the basement membrane and migrate across the wound. they migrate as a sheet, when the slides meet the growth stops and this is called contact inhibition
as the basal epidermal cells migrate, EGF stimulates basal cells to divide and replace the ones that have moved into the wound
the relocated basal epidermal cells divide to build new strata-thickening the new epidermis i.e. abrasions, minor burns
phases of wound healing (deep)
when the injury extends to dermis and subcutaneous layer
in deep wound healing, a clot forms in the wound, blood flow increases and many cells move to the wound. the clot becomes a scab, granulation tissue fills the wound and intense growth of epithelial cells beneath the scab. the scab falls off and the skin returns to normal thickness
usually occurs in 4 phases: inflammatory, migratory, proliferative, maturation
haemostasis
arrest of bleeding- normal physiological response of the body following wounding. volume of blood lost depends on the severity injury and blood vessels involved
cut blood vessels surfaces expose connective tissue which attracts platelets to the site of injury. platelets enter the area aggregate with collagen in the walls of the damaged blood vessels. aggregation activates the platelets to release a number of agents that trigger clotting cascade
results in initial vasoconstriction reducing blood flow through the damaged vessels so area surrounding the wound may appear pale
platelet aggregation and the release of bradykinin and histamine result in a build up of pressure within the capillary, causing the vessel to dilate
increase in blood flow helps to flush debris and bacteria from the wound
vessel dilation promotes the movement of fluid into the tissues
this response is observed at the wound site as redness, heat and swelling
inflammation
inflammation ‘normal’ vascular and cellular response to any kind of injury, not only a wound. healing will not progress if this response does not occur. lasts approx 3-5 days in acute wounds (can be longer for chronic wounds). stage begins as spoon as injury is obtained
the release of PDGF and proteases assist in attracting chemical agents and cells to the area. this phase of wound healing is recognised by visible erythema, oedema and increased heat .
the rise in extracellular fluid as it passes through the vessel walls gives rise to oedema
the increase in blood flow brings with it a rise in local temperature, and the increase in pressure from the volume of extracellular fluid leads to pain. the extra blood flow resulting from vasodilation leads to extra white cells at the site, which cleanse the wound area of bacteria and devitalised tissue
monocytes are also attracted to the area by PDGF. monocytes transform into macrophages which continue with the cleansing activity and are essential id healing is to progress
macrophages secrete the proteases collagenase and elastase. these break down damaged tissue that is not required
inflammatory exudate in a healthy wound contains vital ingredients to assist the healing process
two agents that are important for wound bed preparation include the proteases and neutrophils. although the presence of exudate is vital for cell activity, it can also damage intact skin, so exudate needs to be managed to prevent further breakdown in the wounded area
complement system is activated and stimulates the release of histamine and the attack destruction of microbes
proliferative phase
proliferative phase vascular endothelial growth factor VEGF released by macrophages stimulates formation of new blood vessels
the newly formed blood vessels deliver oxygen and nutrients to the healing tissues, fibroblasts will start to divide and produce collagen which builds elasticity and strength in the wound. together with glycosaminoglycans and proteoglycans, they form an extracellular matrix ECM. ECM supports the new and developing blood vessels and fills the intracellular spaces with collagen fibres. the deposition of the extracellular matrix, together with angiogenesis, comprises the granulation tissue.
healthy granulation tissue- moist and bright red, unhealthy may be dark and bleed easily.
maturation
may take up to 18 months to complete
this phase is sometimes known as the remodelling phase of healing and, during this time, the wound is strengthened and the scar will change colour significantly
collagen bundles within the wound which were once laid down in an irregular fashion, mature to form a stronger, more organised layer. in addition the vascular network will decrease which may leave the scar looking less red and, in many cases the scar appears silver or white in colour
the scar itself is relatively avascular and will not support hair follicles, sweat glands or sebaceous glands
skin lesions
grouped into primary and secondary
primary- variations in colour or texture that may be present at birth such as moles or birthmarks or scars
secondary- changes in the skin that result from primary skin lesions, either as natural progression or from a person manipulating a primary lesion
bed sores
caused by a constant deficiency of blood to tissues overlying a bony projection that has been subjected to prolonged pressure
typically occur between bony projection and hard object such as bed, cast or splint. deficiency of blood flow results in tissue ulceration
in stages 3 and 4 there may be little or no pain due to significant tissue damage
infections can occur if sores progress
eczema
can effect all age groups, effects around 1in 12 adults and one in 5 children in the UK
. different types: atopic, contact and varicose
symptoms of atopic; red inflamed skin, dry cracked skin, itchy skin. small eater blisters on the skin particularly hands and feet- or skin can become wet and weepy if affected. thickened areas of skin in places that are scratched frequently
scratching damages skin causing it to bleed which can lead to infection
acne
most common skin disorder, sebum and epithelial cells clog glands, produces whiteheads and blackheads, anaerobic bacteria trigger inflammation, largely hormonally induced
treatments; antibiotics, topical creams, birth control pills
paronychia
infection that develops along edge of fingernail and toenail is called paronychia. most common infection and can progress to more severe infection of entire finger or toe if left untreated. most commonly caused by bacteria entering the skin around the nail that has been damaged by trauma such as nail biting, finger sucking, dishwashing or chemical irritants. fungus can also cause paronychia especially in people with recurrent infection
heat rash
(prickly heat, milairia)develops when sweat ducts become blocked and perspiration is trapped under your skin
symptoms range from superficial blisters to deep red lumps
3 types; miliaria crystallina- develops on top layer (stratum corneum)
miliaria rubra- develops deeper in epidermis
miliaria profunda- develops much deeper in dermis can cause dizziness and nausea
burns
burn deaths - leading cause if accidental deaths- result primarily from fluid loss, infection and toxic effects of burned tissue
loss of plasma circulatory and kidney problems
the most immediate threat ti burn patient is dehydration and electrolyte imbalance due to fluid loss, and then infection
3 components to extent of burn injury; temp, concentration of heat injury, length of contact
first degree burn
sun burn
UVA- long wave 95% reaches earth, absorbed by melanocytes stimulate to produce melanin, depress immune system
UVB- short wave, sunburn, produce oxygen free radicals disrupt collagen, responsible for wrinkling ageing cataracts
sunburn is burn from UV radiation, consequence is inflammation, injury can start within 30 mins of exposure
first degree burns are mildest- redness pain minor swelling
3-6 days to heal, skin may peel off in 1-2 days
second degree burns
involve epidermis and part of dermis but leave some of dermis intact
may be red, tan or white and is blistered and very painful
may take 2 weeks to several months to heal and may leave scars
the dermis regenerates by division of epithelial cells in the hair follicles and swear glands and those around the edge of the lesion
some sunburns and many scalds are second degree burns
third degree burns
epidermis dermis and often some of the deeper tissues are completely destroyed. usually result of immersion scalds, flame burns, chemical and high voltage electrical injuries
since no dermis remains, the skin can only regenerate from edges of wound. deep second and third degree burns will likely meed to be treated with skin grafts, in which healthy skin is taken from another part of the body and surgically placed over the burn wound to help the area heal
when are burns considered critical
over 25% has second degree burns
over 10% has third degree burns
there are third degree burns on face hands or feet
developmental aspects of integument
epidermis develops from ectodermal germ layer
dermis develops from mesodermal germ layer
during infancy and childhood the skin thickens and more subcutaneous fat is deposited
during adolescence, the skin and hair become oilier as sebaceous glands are activated
photosensitivity
UV radiation- natural sunlight or artificial
characterised by redness, itching, peeling. hives and even shock
heightened sensitivity
medications of contact certain substances
antibiotics
NSAIDs
herbal supplements
some artificial sweeteners, perfumes etc
homeostatic imbalance skin cancer
induced by UV rays of the sun
most common in fair skinned and elderly
one of most common cancers but easiest to treat, highest survilval rate when treated early
causes of skin cancer
most skin tumours are benign and do not metastasise, skin cancers form because of an interplay between genes and environment. sun exposure appears to be lead cause of skin cancer, more common in sunny areas of the world. also tends to be genetic and occurs very frequently in ethnic groups.
3 types of skin cancer
basal cell carcinoma
squamous cell carcinoma
malignant melanoma
basal cell carcinoma
most common, least dangerous
arises from cells of the stratum basale and eventually invades the dermis
appears as a shiny bump and develops a central depression and a beaded pearly edge, usually occurs on face
squamous cell carcinoma
arises from keratinocytes of the stratus spinosum. lesions usually appear on the scalp, ears or lower lip or bsck of hand
have a raised reddened scaly appearance layer forming a concave ulcer with raised edges
malignant melanoma
arises from melanocytes in pre existing mole. metastasises quickly fatal if not treated immediately. risk in severe sun burns
if mole becomes malignant, forms a large flat spreading lesion with a scalloped edge
highly metastatic
resistant to chemo
treating skin cancer
surgery, laser therapy, grafting, clinical trials, biological therapy
types of drug delievery
topical, transdermal, subcutaneous iv injection
