Anatomy Epidermis function protection, temperature regulation, moisture retention major cell types keratinized squamous epithelial cells, melanocytes layers (top to bottom): stratum Corneum stratum Lucidum stratum Granulosum stratum Spinosum stratum Basale (contains pluripotent stem cells) "CaliforniansLike Girls inString Bikinis" from basale to corneum, cells mature, lose their organelles, become keratinized Dermis function structure, sensation, wound healing contains hair follicles, sebaceous glands, specialized nerve endings, vasculature compression of vasculature can lead to pressure ulcers neoplasm of glomus apparatus can lead to glomus tumors mostly made up of extracellular matrix collagen, glycosaminoglycans, proteoglycans, glycoproteins major cell types fibroblasts, Langerhans cells, pluripotent stem cells (in hair follicles), endothelial cells layers (top to bottom) papillary dermis reticular dermis Subcutaneous tissues consist of fat, muscle, tendon, ligament, bone, etc. Exocrine glands glands that retain ducts to body surfaces 3 types, based on the manner in which they secrete substances merocrine cells form membrane-bound secretory vesicles internal to the cell and move to the apical surface of the cell to release contents most glands apocrine cells in which the apical portions of cells are pinched off and lost during the secretory process, resulting in secretory products that contain a variety of molecular components including those of the membrane i.e., mammary glands holocrine: involves death of the cell secretory cell is released, and as it breaks apart, the contents of the cell become the secretory product. i.e. sebaceous glands, sweat glands located in the axillae, pubic areas, around the areoli of the breasts Normal Wound Healing Phases: not discrete, but rather overlapping hemostasis (1 - 24h) endothelial damage leads to exposure of the basement membrane, activation of intrinsic and extrinsic coagulation cascade, and ultimately deposition of fibrin with creation of a platelet plug platelets are integral to initiating wound healing they release cytokines that cause leukocyte migration and chemotaxis into the wound inflammation (1 - 5d) mast cells native cells initiate the inflammatory phase secrete cytokines that cause vasodilation and increase vascular permeability allows influx of neutrophils and macrophages to the wound bed neutrophils present early in inflammatory phase clear intralesional pathogens prepare the wound bed by removing damaged cells secrete cytokines that stimulate infux of macrophages macrophages present late in inflammatory phase early on act in coordination with neutrophils to phagocytose bacteria and dead cells secrete cytokines and growth factors that drive fibroblast proliferation and angiogenesis act to downregulate the initial infammatory response proliferation (4 - 21d) fibroblasts lay down type III collagen myofibroblasts (fibroblasts with contractile filaments) initiate wound contraction angiogenesis and vasculogenesis lay down new blood vessels granulation tissue (newly laid collagen with neovascularization) forms epithelialization occurs from surrounding basal keratinocytes and hair follicle basal cells maturation (21d to up to 1 year) type III collagen remodeled to type I collagen vessels mature and excess vasculature involutes erythema and raised appearance of wound resolves Types of Wound Healing Primary intention wound edges are approximated grafts and flaps are considered primary closure Secondary intention wound edges are left open and allowed to fill in Tertiary intention wound edges are left open and allowed to granulate and are approximated and closed at a later time aka delayed closure