|What are the three main layers of skin? ||The epidermis, The Dermis and subcutis/Hypodermis|
|What are the four main layers of the epidermis? ||Stratum Basale, Stratum Spinosum, Stratum Granulosum, Stratum Corneum|
|What is the extra layer of the epidermis that could be present in THICK skin? ||Stratum Lucideum (between Stratum Granulosum and Stratum Corneum)|
|Features of the Stratum Basale? ||Innermost layer lies adjacent to the dermis compromises mainly dividing and non dividing keratinocytes.
1 in 10 of the basal cell population is melanocytes.
Merkel cells are also found in this layer, provide touch receptors|
|Features of the Stratum Basale (2) cont? ||Basal cells are anchored to the basement membrane by hemidesmosomes.
Site of mitotic division responisible for regeneration of other layers
Some cells are stem cells|
|Histological arrangement of cells in the stratum Basale? ||Cells are arranged as a regimented single layer of cuboidal or low collumnar cells|
|Features of the Stratum Spinosum? ||Daughter cells migrate upwards to form this layer of polyhedral cells which are held together by desmosomes.
Name comes from Spikey appearance of intracellular bridges (desmosomes)
Langerhan cells mainly found in this layer.|
|Features of the stratum Spinosum (2) cont? ||Keratinocytes have large, pale nuclei due to their function of protein synthesis. They synthesize a fibrilllar protein, cytokeratin, which accummulates in cells in the form of aggregates called tonofibrils, bundles of tonofibrils form desmosomes.|
|Features of the stratum granulosum? ||Cells become flattened and lose their polyhedral shape nearer the surface.
Cells contain dense basophilic and electron dense granules called Keratinohyaline granules.|
|What are keratinohyaline granules ||Are distinct from cytokeratin tonofibrils and contain proteins rich in sulphur-containing amino acids such as cytenine and other proteins which interact with the cytokeratin tonofibrils.|
|A combination of tonofibrils with keratinohyaline produces? ||Keratin|
|Features of Stratum Corneum? ||End result of keratinocyte maturation.
Made up of sheets of overlapping polyhedral cornified cells with no nuclei, called corneocytes.
Palms/ soles have the thickest layer.|
|Features of Straum Corneum (2) cont..? ||Each corneocyte is surrounded by protein envelope and is filled with water retaining keratin protein.|
|What does the term Basophilic mean? ||Describes any cell that stains well with basic dyes.|
|In histological terms describe the appearance of Keratinocytes in the basal membrane? ||Are low collumnar with prominent nuclei, and perinuclear zone containing ribosomes and mitochondria|
|In histological terms describe the appearance of keratinocytes in the prickle cell layer? ||have abundant electron dense tonofibrils which extend into desmosomes.|
|In histological terms describe the appearance of keratinocytes in the granular layer? ||Are degenerate with an ill-definied remnant of the nucleus. Cytoplasm contains both linear cytokeratin tonofibrills and ovid keratohyaline granules and keratinosomes.|
|How long approximately does the epidermis take to turn over? ||1 month|
|How long does it take from granular layer -> stratum corneum? ||2 weeks|
|How long does it take for corneocyte -> surface of stratum corneum? ||2 weeks|
|De-arrangement in epidermal turnover process are responsible for which examples of skin conditions? ||Psoriasis, icthyosis, keratoderma|
|Which is the main cell that makes up the dermis? ||Keratinocyte|
|What do these cells form? ||Stratified keratinized squamous epithelium|
|Why is the epithelium described as "Stratified keratinized squamous epithelium"? ||Stratified because there are many layers of cells, squamous because the upper layers of cells are flattened. Keratinized because the upper most cells have lost their nuclei and become converted into flakes of keratin.|
|Where are melanocytes found in the epidermis? ||basal layer|
|What is the number of melanocytes found in the epidermis? ||1 in 10 of the basal cells|
|Where is the highest concentration of melanocytes found? ||Face and male genitilia, lowest on trunk|
|Is there a difference in the number of melanocytes between different racial groups? ||NO difference in number of melanocytes in racial-groups but in dark skin- larger and more processes|
|What is the role of melanocytes? ||Are responsible for manufacturing melanin, the pigment that gives skin its colour. Melanin accumulates in melanosomes that are transferred to adjacent keratinocytes where they remain as granules.|
|What is the function of Langerhan cells? ||Intra-epidermal antigen recognition/ immune surveillance cells|
|Where are Langerhan cells found? ||present in all layers of the epidermis but most easily recognized in prickle cell layer. 2-4% of epidermal population|
|What do Langerhan cells look like on an H+E section? ||A tennis racket|
|Are Langerhan cell numbers affected by UV? ||Numbers not affected by UV but increase in allergic reactions|
|What is the function of Merkel Cells ||Intra-epidermal touch receptors and contain neuroendocrine type membrane bound vesicles in cytoplasm|
|Where are merkel cells found? ||Found near base where they make synaptic junctins with myelinated sensory nerve twigs in the upper dermis.|
|Dermo-Epidermal junction? ||Complex region holding epidermis to dermis. Consists of Keratinocytes and fibroblasts. Congenital lack of some of the elements leads to fragile skin e.g EB. Zone is the target of multiple diseases.|
|Dermis ||Responsible for bulk of skin.
Thicker than epidermis.
Dermis of animals is converted to leather.
Composed of bundles of collagen fibres and elastic fibres embedded in "ground substance", fibroblasts synthesize collagen.
Complex blood vessel supply|
|Dermis (2) cont.. ||Diseases may affect collagen/elastin: overproduction/ underproduction/
|What are the two layers of the dermis? ||Papillary Dermis and Reticular Dermis|
|Papillary Dermis ||Top 1/5th, upper layer of epidermis.
Composed of loosley interwoven collagen, areolar connective tissue, elastic fibres, dermal papillae that house capillaries, corpsucles of touch and nerve endings.|
|Reticular Dermis ||Bottom 4/5ths, contains dense, coarser and horizontally running bundles of collagen and elastin, free nerve endings + skin appendages.|
|Disorder of collagen in DERMIS? ||Ehlers Danlos syndrome|
|Compostion of subcutaneous tissue/hypodermis? ||Fat/adipose tissue amd cartilage|
|What is the function of fat/adipose tissue in subcutaneous tissue in skin? ||Energy reservoir, padding and site of inflammation.|
|What is the function of cartilage in subcutaneous tissues in skin? ||subcutaenous support|
|What are the three types of sweat glands? ||Ecrine glands, Apocrine glands and sebacous glands.|
|Ecrine glands ||Temperature control glands that excrete sweat. Everywhere on human skin apart from nail beds.
Most Abundant on palms/soles and axillae|
|Apocrine Glands ||Scent glands. Role unclear in humans. Found in axillae and genitals|
|Sebaceous glands ||Present everwhere apart from palms/soles.
Greatly enlarged at puberty in response to androgens.
Main function is to provide lipids which lubricate hair shafts.|
|Disorder of apocrine glands ||Hidradenitis suppurativia|
|Disorder of sebaceous glands ||Acne Vulgaris|
|What are the three main functions of skin? ||Protection, regulation and sensation.|
|Protectory role of the skin ||Protection from:
Mechanical impacts, pressure, variations in temperature, micro-organisms and radiation/chemicals|
|Regulatory role of the skin ||regulates:
Body temperature, changes in peripheral circulation, fluid balance via sweat and synthesis of Vitamin D.|
|Sensatory role of the skin ||Provides sensation through: Network of nerve cells that detect and realy changes in the environment.|
|Which embrological part is the epidermis dervived from? ||Ectoderm|
|What happens during the 5th week of embryological development to the skin of an embryo? ||Skin of embryo is covered by simple cuboidal epithelium|
|What happens during the 7th week of embryological development to the skin of an embryo? ||Skin of embryo is covered by single squamous layer (periderm), and a basal layer.|
|What happens in the 4th month of embryological development? ||an intermediate layer, containing several cell layers, is interposed between the basal cells and the periderm.|
|What are the damaging effects of ultraviolet radiation on skin? ||Direct cellular damage and alteration in immunologic function|
|What are the direct effects of ultraviolet radiation ||Photoaging, DNA damage and carcinogenesis|
|What tumour suppressor gene is mutated by DNA damage? and what is the effect of this? ||p53 tumour suppressor gene, implicated in development of melanoma and non melanoma skin cancers|
|What cell types work together to protect cells from UV DNA damage? ||keratinocytes and melanocytes|
|Chronic UV exposure in humans leads to? ||Loss of skin elasticity/fragility.
Haemorrhage of blood vessels.
Wrinkles in premature ageing.|
|During exposure to sunlight, UVB photons are absorbed by? and converted to? ||UVB photons are absorbed by 7-dehydrocholesterol in the skin and converted to previtamin D(3)|
|Previtamin D (3) undergoes? ||Transofrmation within the plasma membrane of cells to activate vitamin D(3)|
|What happens during the winter to vitamin d production? ||There is minimal previtamin D(3) production in the skin.|
|What are the associations with Vitamin D deficiency? ||Increase risk of commom cancers.
|What is a wound? ||A wound is the breakdown in the protective function of the skin; the loss of continutity of epithelium, with or without loss of underlying connective tissue, following injury to the skin caused by surgery, a blow, cut, cehmicals, heat/cold or friction etc|
|What two ways to wounds heal? ||Primary Intention or Secondary Intention|
|Primary Intention ||When healing can start immediately because there is no gap to close and no infection to overcome|
|Secondary intention ||If the margins are spearated and/or infected, and/or bruised, the wounds must correct these three actions before it can close.|
|erosion ||Only epidermis lost|
|Ulceration ||Structures deep to epidermis|
|Partial thickness ||Epidermis + varying parts of dermis. Adnexal structures serve as a resevoir of epithelial cells to repopulate the wound + cells from wound edge|
|Full Thickness ||Epidermis + all of dermis + deeper structures. Wound edge cells only|
|What is the sophisticated mechanism of wound healing ||To prevent infection/dehydration/bleeding by pluggin any gap in the skin integrity quickly, re-epitheliaze over the defect and rapidly replace the lost dermis with new matrix. Final producti is in the form of a scar, which is visable on skin surface.|
|Heling involves three phases which overlap what are they? ||Inflammation (Platelet + WBC into wound)
Tissue proliferation = epithelialisation +granulation tissue.
|Inflammation ||Platelets are the first cell to appear after wounding. They initiate haemostasis but also the healing cascade by releasing growth factors. GFs attract other cells to the wound to fight infection (WBC/neutrophils etc).|
|Inflammation cont.. ||All new cells migrating to the area give the characteristic signs of inflammation: red/swelling. Acute inflammation lasts 24-48 hours. Neutrophils and macrophages kill micro-organisms and secrete GFs|
|What is the influence of GFs on wound healing ||GFs produced by cells involved in wound healing communicate with other cells.|
|Step 2 Proliferative phase/ Tissue formation ||Initial response to injury provide a framework for the production of a new barrier: Re-epithelilastion and neovascularisation|
|Re-epithelilasation ||Within 1-2 days of wounding, keratinocytes move from skin appendages and near the edge of the wound. The keratinocytes adapt: Loose cell-cell adhesion properties, become flatter.|
|Re-epithelialisation of the wound may occur in several ways what are they? ||- Classic "leapfrog model": cells move 2-3 lengths from their original position and roll over other cells previosuly implanted in the wound. They then fix and other cells leap frog over them.
- "train" method: cells migrate in order.|
|What happens once the wound is covered in a single layer of ketainocytes by re-epithelisation? ||Keratinocytes start to proliferate|
|Neovascularisation ||Same idea as Re-epithelilastion. Chemotactic factors signal for endothelial cells to migrate and proliferate. Multiplication fo fibroblasts occurs and causes fibroblasts to produce collagen.|
|Neo-vascularisation cont.. ||Collagen fibres are deposited in a haphazardous way and from a fibrous network that supports the new capillary loops. The tissue formed is called granulation tissue: moist translucent red appearance.|
|Neo-vascularisation cont... ||Signs of inflammation disappear: fibroblasts contract pulling wound edges together. Wound contraction is important as means less granulation tissue required to fill wound cavity.|
|Step 3 Tissue Remodelling ||Collagen is organised into thick bundles and extensively cross-linked to from the mature scar.|
|Factors affecting wound healing ||Speed of wound healing depends upon many factors: size of the wound, blood supply to the area, presence of foreign antibodies/ micro-organisms, age and health of the patient, nutritional status of patient, drugs the patient may be taking, diabetes.|