13. Anatomy, Physiology, and Disorders of the Skin
Anatomy
Epidermis
The epidermis comprises the following cells:
Keratinocytes: 80% of epidermis
Melanocytes: Mostly within basal layer, pigment-producing cell, pigment provides UV protection
Merkel cells: Mostly within basal layer, mechanoreceptor, slow-adapting
Langerhans cells: Antigen-presenting/T-cell activating cells of the epidermis
The epidermis has five layers, each approximately 100 μm thick:
Stratum basale: Mitotically active layer providing cells for upper layer differentiation
Stratum spinosum: Spinelike appearance of cell margins from intercellular bridging
Stratum granulosum: Intracellular granules containing materials to create skin barrier
Stratum lucidum: Clear layer of dead cells devoid of nuclei, prominent in palms/soles
Stratum corneum: Cornified layer of cells following programmed cell death of the granular layer, providing skin barrier
Dermis
Makes up most of skin
Responsible for the strength, elasticity, and pliability of the skin
Composed of primarily collagen (type I/III ratio 4:1) and elastic fibers
Maintained by fibroblasts
Also inhabited by macrophages and mast cells
The dermis has two layers:
Papillary dermis: Superficial, similar thickness to epidermis, approximately 100 μm (thickness of all layers varies by location)
Reticular dermis: Deep, makes up most of dermis (2000–2500 μm). Collagen and elastic fibers are thicker and more organized in deeper dermis.
Vasculature
Small vessels penetrate from the subcutaneous tissue and form a horizontal vascular plexus within the deep reticular dermis.
Arterioles extend vertically from the plexus toward the epidermis, forming the subpapillary plexus at the interface of the papillary and reticular dermis.
Individual capillary loops then extend from these end arterioles up into each papilla of the papillary dermis.
Lymph
Lymph vessels are important to regulating interstitial fluid balance, collecting degraded substances, and sampling for immune function
Nerves
Nerves follow a distribution and pattern similar to those of the vasculature, with a deep reticular and subpapillary plexus.
Skin Appendages
Hair follicles, growth cycle variable by location
Anagen: Growth phase, 2 years
Catagen: Programmed cell death, hair loss, 2 weeks
Telogen: No hair, no growth, 2 months
Glands
Sebaceous glands, eccrine glands, apocrine glands
Maintain skin hydration and assist with thermal regulation
Provide source for epidermal regeneration–increased density on face allows resurfacing procedures, but below the jawline, reduced density delays epidermal regeneration, and can lead to scarring
Affected by retinoids (impaired by isotretinoin, which reduces sebaceous units)
Skin Physiology
Normal Skin Function
Thermal: Provides insulation and regulation through blood flow and eccrine secretions
Mechanical and chemical: Protection against injury, infection, and water loss
Metabolism: Vitamin D conversion
Sensation: Sensation, temperature, pressure, and vibration
Aesthetics
Histology
Thinning of epidermis
Flattening of the rete ridges
Thinning and degeneration of the dermis, collagen, and elastic fibers (solar elastosis)
Atrophy of subcutaneous tissue
Clinical Picture
Thinning skin
Lost elasticity
Facial laxity
Facial rhytids
Loss of facial volume
Wound Healing
Inflammation (days 1 to 6)
Vasoconstriction ➤ coagulation ➤ vasodilation/capillary leak ➤ chemotaxis ➤ cell migration
Neutrophils ➤ macrophages ➤ lymphocytes
Macrophage most important to regulate growth factors and wound healing
Proliferation (day 4 to week 3)
Fibroblasts predominate, increased collagen synthesis, and angiogenesis
Maturation (week 3 to 1 year)
Equilibrium between collagen deposition and breakdown
Increased collagen organization and stronger cross-links
Type I collagen replaces type III to restore 4:1 ratio
Healing strength begins to plateau at approximately 60 days at 80% original strength.
Reepithelialization
Mobilization: Loss of contact inhibition occurs for cells at edge of wound.
Migration: Cells migrate across wound until they meet cells from other side.
Mitosis: As edge cells migrate, cells farther back proliferate to support migration.
Contraction
Myofibroblasts (specialized fibroblasts) appear by day 3 and are maximal by day 10 to 21, with greater numbers and contraction in full thickness/deeper wounds.
Factors Affecting Wound Healing
Genetic Skin Disorders
Cutis laxa
Nonfunctioning elastase inhibitor leads to elastic fiber degeneration.
Skin has coarse texture, droops over all of body, and is diagnosed during neonatal or early childhood.
Congestive heart disease, emphysema, pneumothorax, aneurysms, and hernias may also occur.
It slowly worsens over time, but surgical correction can be beneficial.
Pseudoxanthoma elasticum
Similarities to cutis laxa, with loose skin secondary to elastic fiber degeneration
May also benefit from surgery
Ehlers-Danlos
Disorder of collagen cross-linking
Leads to fragile, hyperelastic skin, hypermobile joints, and aortic aneurysms
Surgery contraindicated because poor wound healing
Elastoderma
Poorly understood cause
Pendulous skin over trunk and extremities, eventually entire body
Surgery contraindicated
Progeria (also known as Hutchinson-Gilford syndrome)
Rapid progression and short lifespan, from childhood
Laxity and irregular skin contouring, craniofacial malformations, cardiac disease, ear abnormalities, and poor wound healing
Surgery contraindicated, poor wound healing
Comorbidities
Diabetes
Atherosclerotic disease
Renal failure
Immunodeficiency
Nutritional Deficiencies
Vitamins and minerals (vitamin C, zinc, iron)
Caloric
Protein (check albumin, prealbumin, transferrin, and haptoglobin)
Drugs
Smoking: Vasoconstriction and decreased oxygen delivery
Steroids: Impair wound healing
Antineoplastic agents: Impair fibroblast proliferation and wound contraction
Antiinflammatory medicine: Decreases collagen synthesis 45%
Lathyrogens: Prevent collagen cross-linking
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