Integumentary System Notebook 2024 PDF

Summary

This document is a notebook on the integumentary system. It covers the structure and function of the skin and its accessory structures. It also includes details about the epidermis, dermis, and subcutaneous layer. The notebook also discusses the functionalities of the integumentary system.

Full Transcript

Notebook – Integumentary System 2024-08-29 3:06 PM Unit 1: Integumentary System What is the Integumentary System? The integumentary system consists of the skin and various accessory structures...

Notebook – Integumentary System 2024-08-29 3:06 PM Unit 1: Integumentary System What is the Integumentary System? The integumentary system consists of the skin and various accessory structures Can referred to as skin or integument 12-16% of total body weight – largest organ in the body by weight Bodys first line of defence against environment Has 2 major components: 1. Cutaneous membrane 2. Accessory structures Functions of the Integumentary System Protect underlying tissues and organs against impact, abrasion, fluid loss, chemical attack Act as a blood reservoir (dermis) Maintain normal body temperature through either vasodilation, vasoconstriction, insulation or evaporative cooling, as needed Excrete salts, water, and organic wastes through integumentary gland Detect touch, pressure, pain, and temperature stimuli, and relay the info to the nervous system Synthesizes vitamin D3 Produce melanin, which protects underlying tissue from UV radiation – not its purpose (just what the skin does) Produce keratin, which protects against abrasion and serves as water repellent Stores lipids in adipocytes in the dermis and adipose tissue in the subcutaneous layer Integumentary System Components: 1. Cutaneous Membrane Epidermis (epi, above) Composed of stratified squamous epithelium Dermis 1. Papillary layer (areolar connective tissue) 2. Reticular layer (dense irregular connective tissue) **Subcutaneous layer** Not technically a layer of the skin Aka hypodermis or superficial fascia Separates integument from deep fascia 2. Accessory Structures Hairs Nails Exocrine glands Sebaceous glands Sweat glands Sensory receptors and nerve fibers Arrector pili muscles Cutaneous plexus Network of blood vessels Epidermis: Basic Structures of the Epidermis Superficial, thinner layer of the cutaneous membrane Epithelial tissue Multiple layers (strata) of tightly packed squamous cells - stratified squamous epithelium Avascular Epidermal Cell Types 4 major cell types in the epidermis: 1. Keratinocytes – the primary cell type in the epidermis 2. Melanocytes 3. Langerhans cells 4. Tactile epithelial cells – aka merkel cells Epidermal Cell Types: Keratinocytes 90-95% of epidermal cells Produce and accumulate keratin - a tough, fibrous protein protects skin and underlying tissue from mechanical stress, heat, microbes, and chemicals Also produce lamellar granules waterpoof sealant Melanocytes Produce melanin (pigment) Absorbs damaging ultraviolet (UV) light & contributes to skin colour Transfer melanin to keratinocytes via slender projections that extend b/w cells (dendrites) Inside keratinocytes, melanin covers/coats & protects nuclear material Langerhans cells Tissue-resident dendritic cell of the skin (APC – antigen presenting cell) Small fraction of epidermal cells Derived from bone marrow stem cells Notice if there are foreign bodies and will help the immune system Tactile epithelial cells Aka Merkel cells Least numerous of epidermal cells Contact a tactile disc – flattened neuron (sensory structure) Function in the sensation of touch Epidermal Layers: Epidermal Layers Overview Entire epidermis lacks blood vessels Cells get oxygen and nutrients from capillaries in the dermis Cells with highest metabolic demand are closest to the dermis Takes about 7 – 10 days for cells to move from the deepest stratum to the most superficial layer Cells in surface layer (stratum corneum) remain about 2 weeks before being shed or washed away Epidermal layers: 1. Stratum basale Deep – Superficial 2. Stratum spinosum 3. Stratum granulosum 4. Stratum lucidum (only in thick skin) 5. Stratum corneum Thick skin vs. Thin skin Thick skin Found on palms of hands and soles of feet Contains five strata (layers) No hair Thin skin Covers most of body surface Contains four strata (layers) Epidermal Layers: 1. Stratum basale 1 layer of cuboidal or columnar basal cells (basal keratinocytes) Attached to basement membrane by hemidesmosomes & to other cells via desmosomes Most cells here are basal cells - stem cell keratinocytes, stem cells that divide to replace more superficial keratinocytes Also contains Merkel cells and melanocytes If this layer is damaged, new skin cannot be generated (skin graft necessary) 2. Statum spinosum "spiny layer" or "prickle layer" Composed of 8 – 10 layers of keratinocytes bound together by desmosomes Provides strength and flexibility Only looks spiny when on a prepared slide Contains Langerhans cells Melanin taken in by keratinocytes (endocytosis) from nearby melanocytes 3. Stratum granulosum "grainy layer" Composed of 3 – 5 layers of keratinocytes Most cells stopped dividing and started producing keratin and keratohyalin (waterproofing) Cells grow thinner and flatter Cell membranes thicken and become less permeable Marks the transition b/w the deeper, metabolically active strata and dead cells of superficial strata Contains lamellar granules that release water repellent lipid into cell spaces (of stratums granulosum, lucidum & corneum) 4. Stratum lucidum "clear layer" 3 – 5 layers of flat, dead cells that appear clear Found only in thick skin Flattened, densely packed dead cells filled with keratin and keratohyalin Adds additional layer of toughness to thick skin 5. Stratum corneum "cornu, horn" Outermost, protective region with 15 – 30 layers of keratinized cells (filled with keratin) Dead cells still tightly connected by desmosomes Water resistant, not waterproof - lose water through insensible perspiration (unable to see or feel) and sensible perspiration (sweat) Epidermal Keratinization Stem cells divide to produce keratinocytes As keratinocytes are pushed up towards the surface they accumulate keratin Keratinization Replacement of cell contents with keratin Occurs as cells move to the skin surface over 4 – 6 weeks They move further away from blood (O2) supply of dermis Gradually they die, are sloughed off, and replaced by cells moving up Epidermal growth factor (EGF) and other hormone-like proteins play a role in epidermal growth Epidermal Ridges Deeper layers of epidermis form epidermal ridges – just the bottom of the ridge Adjacent to dermal papillae (papilla, nipple-shaped mound) Increase surface area for better attachment Fingerprints Pattern of epidermal ridges on surface of fingertips Unique pattern that does not change during lifetime - prints of these patterns (fingerprints) used to identify individual Disorders of the Epidermis: Dandruff Excessive amount of keratinized cell shed from scalp Double the normal amount in larger clusters, becomes more visible Causes: Dry skin Irritated, oily skin Infection (fungal or bacterial infections) Psoriasis Chronic skin disorder with genetic link Cause poorly understood Rapidly dividing keratinocytes (producing too many keratinocytes) Cells shed in 3 – 5 days as flaky silvery scales Immature keratinocytes produce abnormal keratin Well-circumscribed erythematous plaques with silvery-white scales Commonly found at extensor surfaces (knees, elbows), trunk, and scalp Psoriasis Types: Plaque Psoriasis Most common type Described on previous slide Well-circumscribed erythematous plaques w/ silvery-white scales Commonly found at extensor surfaces (knees and elbows), trunk, and scalp Calluses and Corns Increased pressure or irritation of the skin leads to hyperkeratosis Increased keratinocytes in the stratum corneum leads to thickened skin Corns Smaller, deeper than calluses Have a hard centre surrounded by swollen skin May be painful when pressed Form on the top of the toes or the outer edge of the small toe Calluses Rarely painful Developed on pressure spot, such as the heels, the balls of the feet, the palms and the knees Dermis: Dermis Overview Layer between the epidermis and subcutaneous tissue (hypodermis) Connective tissue layer Highly vascular Components of the Dermis Fibers: Collagen fibers – most abundant protein in the body (tissue strength) Elastic fibers – allow for stretch Cells: Fibroblasts – king of connective tissue, creating all the connective tissue Macrophages Fat cells Hair follicles Glands Nerves Blood Vessels Fibers 1. Collagen Fibers Provide tensile strength (resist pushing and pulling) 2. Elastic Fibers Provide extensibility (ability to stretch) & elasticity (return to original shape) Cells 1. Fibroblasts Secrete ground substance & extracellular matrix most abundant protein in the body (tissue strength) 2. Macrophages Phagocytize bacteria & cellular debris 3. Adipocytes Store triglycerides Layers of the Dermis: Papillary Region Superficial 20% of dermis Named for dermal papillae in this region Anchor to epidermis Composed of areolar tissue Thin collagen Elastic fibers Provides cushioning Contains: Capillary loops that feed epidermis Corpuscles of touch – sensory receptor Free nerve endings for sensation of heat, cold, pain, tickle and itch – sensory receptor Reticular Region Deep 80% of dermis Interwoven meshwork of dense irregular connective tissue w/ thick collagen and elastic fibers Contains: Blood and lymphatic vessels Nerve fibers Accessory organs - hair follicles, sebaceous and sudoriferous glands Adipocytes Disorders of the Dermis: Striae (stretch marks) Excessive or quick stretching of the skin leads to dermal scarring Dermis is torn, replaced with scar tissue Most fade with time although may always be there Causes: Weight gain, muscle gain, or rapid growth Pregnancy Excess cortisol (Cushing syndrome) Subcutaneous Layer: Subcutaneous Tissue Aka hypodermis or superficial fascia Fascia = sheet In the body, fascia attaches, wraps and/or separates deep structures There is superficial and deep fascia Subcutaneous layer (not part of skin) Connective tissue that separates skin from deeper structures Dominated by adipose tissue - protect and support - important energy storage site Where we hold our fat Burns: Burns are significant injuries Can damage large areas of skin compromising many essential functions Dehydration and electrolyte imbalance can lead to: - kidney impairment & circulatory shock Severity depends on: Depth of penetration Total area affected Severity is rated as: 1st degree 2nd degree 3rd degree Partial-thickness burns are either first or second degree burns Full thickness burns are considered third degree burns Partial thickness: First-degree Burns Only the surface of the epidermis affected Example – most sunburns Second-degree Burns Entire epidermis and maybe some of dermis damages Accessory structure not affected Blistering, pain, and swelling occur - infection can develop from ruptured blisters Healing takes 1 – 2 weeks Full Thickness: Third-degree Burns Destroy epidermis, dermis, and damage extends into subcutaneous layer Less painful than second-degree burns Extensive burns of this type cannot repair themselves - skin grafting usually necessary Evaluating burns in a clinical setting: 1. Depth of burn Assessed with a pin Absence of reaction to pin prick indicated third-degree burn (loss of sensation) 2. Percentage of skin that has been burned Rule of nines Method of estimating percentage of surface area affected by burns Modified for children (different body proportions) Emergency treatment for burns: 4 options for Treatment 1. Replacing lost fluids and electrolytes 2. Providing sufficient nutrients Increased metabolic demands for thermoregulation and healing 3. Prevent infection Cleaning and covering burn Administering antibiotics 4. Assisting tissue repair with skin grafts – autograft best Areas of intact skin are transplanted to cover the burn site Skin Grafts Split-thickness graft transfer of epidermis and superficial portions of dermis Full-thickness graft Transfer of epidermis and both layers of dermis Source of material: Autograft – patients own undamaged skin (best choice if possible – no rejection) Allograft – frozen skin from a cadaver Xenograft – animal skin What Determines Skin Colour: Factors Influencing Skin Colour Presence of 3 pigments: Melanin Carotene Hemoglobin Degree of dermal blood circulation Thickness and degree of keratinization Amount of exposure to ultraviolet (UV) radiation Can increase pigmentation even through skin colour genetically determined Melanin Produced by melanocytes in stratum basale Differences in skin pigmentation are from amount of melanin pigmentation are from amount of melanin produced, not from number of melanocytes Made from tyrosine Non-essential amino acid Function: Protect genetic material from UV radiation Two Types of Melanin 1. Eumelanin brown, yellow-brown, or black pigment 2. Pheomelanin Pink, red or yellow pigment Hair, freckles, lips, nipples Carotene Orange-yellow pigment Beta carotene is a precursor of vitamin A Also helps protect the skin Effects of blood supply on skin colour: Hemoglobin is red pigment found in red blood cells Blood flows to dermis through subpapillary plexus More blood flow to region results in redder colour (erythema) Less blood flow to region initially results in pale color - sustained reduction of blood flow decreases available oxygen - from surface view, skin has bluish color (cyanosis) - most apparent in very thin skin (lips, beneath nails) Skin Colour Pathologies: Erythema Redness of skin due to enlargement of capillaries in dermis During inflammation, infection, allergy or burns Cyanosis Bluish colour to nail beds and skin Hemoglobin depleted of oxygen look purple-blue Pallor Paleness may be due to shock or anemia Jaundice Yellowing of the skin due to increased bilirubin Effects the liver Due to prehapatic, hepatic, or extrahepatic causes Albinism Inherited inability to produce melanin due to mutation in one of the genes involved with melanin production Eg. Melanocytes inability to produce tyrosinase Melanin not present in hair, eyes or skin Affects vision and sunburn easily Vitiligo A chronic, usually progressive disorder causing depigmentation Complete or partial loss of melanocytes causing light coloured patches Autoimmune condition in which antibodies attack melanocytes Freckles (ephelides) Local increased in concentration of melanin (no extra melanocytes) Genetic component Darken due to sun exposure Lighten in the winter Age Spots Accumulations of melanin over time due to long term sunlight exposure and age (liver spots or solar lentigo) Flat blemishes, light brown to black (darker than freckles) Don’t fade in winter, common in adults over 40 Moles (melanocytic nevi) Benign over-growth of melanocytes Can be congenital or acquired Acquires moles are due to a combination of genetics and exposure to UV radiation, but it is poorly understood May be flat or raised Atypical or dysplastic nevi may indicate melanoma The ABCDEs of moles A = asymmetry B = borders C = colour D = diameter E = evolving Malignant melanoma Main cause is UV light exposure Extremely dangerous Cancerous melanocytes grow rapidly and metastasize through lymphatic system If detected early and removed surgically, the 5 year survival rate is 99% If not detected until after metastasis, the 5 year survival rate drops to 14 % Basal cell carcinoma (BCC) Most common form of skin cancer Originates in stratum basale due to mutations caused by overexposure to UV radiation Appears as transparent or pearly while nodule - although there is a variety of appearance Virtually no metastasis and most people survive - 100% 5 year survival rate Squamous cell carcinoma (SCC) Second most common form of skin cancer Originates in squamous cells of the surface layers of the skin Caused by overexposure to UV radiation More likely to metastasize than BCC, but still very rare - 5 year survival rate is 99% especially if detected early Accessory Structures of the Skin: Accessory Structures Hair follicles Produce hairs that protect skull Produce hairs that provide delicate touch sensations Exocrine glands Sweat glands (assist in thermoregulation and excrete wastes) Sebaceous glands (lubricate epidermis) Nails Protect and support tips of fingers and toes Hair: Hair overview Hair is composed of dead, keratinized cells produced in a specialized hair follicle Found almost everywhere on the body except... palms of hands sides and soles of feet sides of fingers and toes Lips parts of external genitalia Each hair produced by a hair follicle Complex structure composed of epithelial and connective tissue that forms a single hair Functions of Hair Senses light touch Hair root plexus Protection Head hair: protects scalp from injury & UV light Eyelashes & eyebrows: protect eyes from foreign particles Body: prevent abrasions Prevents heat loss Insulating layer Hair Regions Hair shaft Begins deep within hair follicle, but can be seen on the surface Hair root Anchors the hair into the skin Extends from base of follicle to point where hair shaft loses connection with follicle walls Hair Follicle Found in the dermis Site of hair growth The hair follicle regulates hair growth Hair Follicle Structure Hair matrix Actively dividing basal cells in contact with hair papilla (WHAT MAKES HAIR GROW) Hair growth is just like skin growth Hair Follicle Associated Structures Root hair plexus Collection of sensory nerves surrounding the base of the follicle Arrector pili Smooth muscle attached to hair follicle; contraction pulls hair erect Sebaceous gland Produces secretions to coat hair and skin surface Hair Growth: Hair grow and shed in hair growth cycle in 4 stages: 1. Anagen Phase (Active or Growth Phase) 2. Catagen Phase (Regression Phase) 3. Telogen Phase (Resting Phase) 4. Exogen Phase Variations in growth rate and duration of cycle result in different lengths of uncut hair Shed about 50-100 hairs per day Rate of growth & replacement cycle dependent on: Genetics Nutrition Gender (hormones) Can be affected by: Illness Radiation/chemo, surgery, medications Blood loss Severe emotional stress 1. Anagen Phase (Active Phase) Hair matrix cells actively dividing to produce length Lasts 2-6 years Hair grows at rate of 0.33 mm/day (0.5 inches per month) 2. Catagen Phase (Regression Phase) Hair matrix cells stop dividing Hair follicle atrophies 2 – 3 weeks in head hair 3. Telogen Phase (Resting Phase) Last 3 – 4 months Hair loses attachment to follicle Becomes club hair Club hair is shed when follicle is reactivated and new hair formation begins 4. Exogen Phase Club hair falls out of follicle Two types of hair: 1. Terminal Hairs Large, coarse, darkly pigmented Hairs found on scalp, armpit, eyebrows, eyelashes, facial hair, chest, pubic regions 2. Vellus hairs Smaller, shorter, delicate Found on general body surface At puberty vellus hair replaced by terminal hair in response to androgens produced in testes & adrenal cortex Ratios Adult males 95% terminal hair 5% vellus hair Adult females 35% terminal hair 65% vellus hair Hair Colour Due to melanin produced by melanocytes Melanocytes scattered into matrix of hair bulb Melanin passed into keratinized cortex & medulla cells of hair Dark hair: eumelanin Blonde/red hair: pheomelanin Gray hair: decreased melanin production due to progressive decline in tyrosinase Hair Conditions: Alopecia Partial or complete loss of hair May be caused by genes, aging, endocrine disorders, chemotherapy, skin disease Chemotherapy: Drugs kill rapidly dividing cells such as hair matrix cells The 15% of hairs in resting stage are not affected Androgenic Alopecia Male pattern baldness Genetically predetermined disorder due to an excessive response to androgens Hirsutism Excessive body hair or body hair in uncommon areas in females or prepubertal males Causes: PCOS Cushing syndrome (excess cortisol) Congenital adrenal hyperplasia Functional tumours of the ovaries or adrenal glands (androgen secreting) Medication Sebaceous glands Holocrine exocrine glands that discharge an oily lipid secretion into skin Located in the dermis Associated with hair (so absent on palms and soles of feet) Contractions of arrector pili muscle cause release of sebum onto follicle and skin surface Sebum Mixture of triglycerides, cholesterol, proteins, and electrolytes Lubricates and moisten hair shaft and is antimicrobial Sudoriferous glands Located in the dermis Produce watery secretion Myoepithelial cells (myo-, muscle) Squeeze gland to discharge secretion Two types: 1. Eccrine sweat glands 2. Apocrine sweat glands 1. Eccrine sweat glands Secrete directly onto surface of the skin Highest number found on palms and soles Present at birth Produce watery secretions with electrolytes Important in thermoregulation and excretion of wastes Helps you with grip Stimulated during emotional stress (cold sweat) 2. Apocrine sweat glands Found in axillae, groin, around nipples, and in pubic region Ducts open into hair follicle Active after puberty – play a role in "body odour" Body odour – feeding the bacteria that lives there Produce sticky, cloudy, odorous secretion with complex composition Include ceruminous glands & mammary glands Strongly influenced by hormones Stimulated during emotional stress & sexual excitement Ceruminous glands Modified sudoriferous glands in external auditory meatus (EAM) - ear wax Duct opens into external auditory meatus or into ducts of sebaceous glands there Secretory portion in subcutaneous layer Begins to function soon after birth Produces cerumen Waxy/lubricating Waterproofs canal Barrier to foreign bodies Conditions of Glands of the Skin: Pimples (comedones) Increased sebum blocks sebaceous duct and hair follicle Acne Numerous pimples caused by excessive sebum production or bacterial inflammation of sebaceous glands Hormonal connection Impacted Cerumen Abnormal amount of cerumen in EAM can prevent sound from reaching ear drum May be structural Accessory structures: Nails Nails Thick sheets of tightly packed keratinized epidermal cells Functions: Protect exposed dorsal surfaces of tips of fingers and toes Help limit distortion of digits under physical stress Counter-pressure to palmar surfaces of fingers - enhance touch perception and manipulations Allow grasping & manipulation of small objects Scratch & groom the body Nail body Bulk of the visual part of the nail – finger nail Pink underneath due to capillaries in dermis Nail bed Skin beneath the nail – underneath the finger nail Nail matrix Proximal portion of the epithelium deep to the nail root – where the nail grows from Cells divide mitotically to produce new nail cells Growth influenced by age, health, nutritional status, season, time of day and environmental temperature Age-related Changes to the Integumentary System: Fewer melanocytes In light-skinned people, skin becomes very pale Increased sensitivity to sun exposure, more likely to sunburn Drier epidermis Decreased sebaceous gland activity Thinning epidermis – declining basal cell activity Connections b/w epidermis and dermis weaken More prone to injury, skin tears, and skin infection Reduced vitamin D3 production - causes muscle weakness and brittle bones Diminished immune response Declining number of dendritic cells (to about ½ of levels at age 21) Increased change of skin damage and infection Thinning dermis Fewer elastic fibers Sagging and wrinkling are the results Decreased perspiration Sweat glands are less active Greater risk of overheating Reduced blood supply Cools skin and stimulates thermoreceptors Make person feel cold even in warm room Slower skin repair Example: blister repair 3 – 4 weeks in young adults, takes 6 – 8 weeks in 65 to 75 year old Fewer active follicles Thinner, finer hairs (grey or white from decreased melanocyte activity) Altered hair and fat distribution Decreased sex hormone levels Vitamin D3: Vitamin D3 production Sunlight UV radiation causes epidermal cells of stratum spinosum and stratum basale to convert steroid to cholecalciferol (vitamin D3) Liver creates intermediate product; then converted to calcitriol by kidneys – calcitriol is the active form of vit D Calcitriol allows calcium and phosphate absorption in small intestine Diet Naturally from fish, fish oils, and shellfish Egg yolks From fortified food products Vitamin D3 deficiency Inadequate supply of calcitriol leads to impaired bone growth and maintenance Rickets (In children) Flexible, poorly mineralized bones From not enough sunlight or not enough dietary cholecalciferol (vitamin D3) Bone matrix has insufficient calcium and phosphate Uncommon in united states In adults, leads to decreased bone density Partially from insufficient dietary intake Additionally, skin production of cholecalciferol decreases by 75% Increases risk for fractures Slows healing process Wound Healing: 1. Epidermal Wound Healing Abrasion or minor burn Basal cells migrate across the wound Contact inhibition with other cells stops migration Epidermal growth factor (EGF) stimulates basal cells to divide Full thickness of epidermis results from further cell divisions 2. Deep Wound Healing Injury extends to dermis Complex repair process & scar formation Four stages of wound healing: 1. Inflammatory 2. Migratory 3. Proliferative 4. Maturation Four stages of Wound Healing: Inflammatory phase Blood clot unites the wound edge Inflammation Vasodilation and increased permeability of blood vessels deliver: 1. Neutrophils (phagocytic WBC) 2. Macrophages (to clean up debris & microbes) 3. Fibroblasts (to produce scar) Migratory phase Wound repair Clot becomes scab Epithelial cells migrate beneath scab to bridge wound Fibroblasts begin forming scar tissue Damage blood vessels begin to regrow Tissue filling wound here is called granulation tissue – normal regrowing of healing tissue Granulation tissue grows best when its wet Proliferative phase Growth of epithelial cells beneath scab Fibroblasts lay down collagen randomly Blood vessel growth Maturation phase Scab sloughs off when epidermis is restored to normal thickness Collagen fibers become more organized Fibroblasts begin to disappear Blood vessels restored to normal Scar Tissue Formation: Fibrosis Scar Tissue Formation = Fibrosis Scar tissue is different from normal skin Collagen fibers more densely arranged Decreased elasticity Fewer blood vessels – pale Fewer hairs, glands and/or sensory structures Excess scar tissue is raised above epidermal surface Hypertrophic scar – stays w/in boundaries of original wound Keloid scar – extends beyond wound boundaries into normal tissue

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