13.4 Wound healing and skin disorders

Wound healing is a complex process involving four stages: hemostasis, inflammation, proliferation, and remodeling. These stages work together to repair damaged skin, with each phase playing a crucial role in restoring the skin's protective barrier.

Skin disorders can be classified by their causes: infectious, inflammatory, neoplastic, or congenital. Understanding these disorders and their treatments is essential for maintaining healthy skin and addressing various skin conditions effectively.

Wound Healing Stages and Processes

Hemostasis and Inflammation

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• Wound healing is a complex process that involves four overlapping stages: hemostasis, inflammation, proliferation, and remodeling
• Hemostasis occurs immediately after injury and involves vasoconstriction, platelet aggregation, and formation of a fibrin clot to stop bleeding
• The inflammatory phase begins within hours of injury and is characterized by vasodilation, increased vascular permeability, and the recruitment of neutrophils and macrophages to the wound site
  • Neutrophils remove debris and bacteria (dead cells, foreign particles)
  • Macrophages secrete growth factors (PDGF, TGF-β) and cytokines (IL-1, TNF-α) to stimulate the proliferative phase

Proliferation and Remodeling

• The proliferative phase begins within days of injury and involves the formation of granulation tissue, angiogenesis, and re-epithelialization
  • Fibroblasts migrate into the wound and produce collagen and other extracellular matrix components (glycosaminoglycans, proteoglycans) to form granulation tissue
  • Endothelial cells form new blood vessels (angiogenesis) to supply the granulation tissue with oxygen and nutrients
  • Keratinocytes migrate from the wound edges to re-epithelialize the wound surface
• The remodeling phase begins weeks to months after injury and involves the reorganization of collagen fibers, contraction of the wound, and maturation of the scar tissue
  • Collagen fibers align along lines of tension to increase wound strength
  • Myofibroblasts contract the wound to reduce its size
  • Scar tissue becomes less cellular and vascular over time

Factors Affecting Wound Healing

Factors Impairing Wound Healing

• Factors that can impair wound healing include age, nutritional deficiencies (protein, vitamin C, zinc), smoking, diabetes, obesity, and certain medications (corticosteroids, chemotherapy)
• Chronic diseases such as diabetes and peripheral vascular disease can impair blood flow and oxygenation to the wound, leading to delayed healing and increased risk of infection
• Immunocompromised states, such as those caused by HIV/AIDS or immunosuppressive medications, can impair the inflammatory response and increase the risk of infection
  • Impaired neutrophil and macrophage function reduces the ability to clear bacteria and debris
  • Reduced growth factor and cytokine production delays the proliferative phase

Factors Promoting Wound Healing

• Factors that can promote wound healing include proper nutrition, adequate hydration, and maintaining a moist wound environment
  • Adequate protein intake is necessary for collagen synthesis and tissue repair
  • Vitamin C is essential for collagen cross-linking and enhances immune function
  • Zinc plays a role in collagen synthesis, immune function, and epithelialization
• Wound dressings that maintain a moist environment, such as hydrocolloids and hydrogels, can promote re-epithelialization and reduce scarring
  • Moist environments prevent cell desiccation and promote migration
  • Occlusive dressings (film, foam) maintain moisture and protect the wound from contaminants
• Growth factors, such as platelet-derived growth factor (PDGF) and epidermal growth factor (EGF), can stimulate cell proliferation and migration to promote wound healing
  • PDGF attracts and activates macrophages and fibroblasts
  • EGF stimulates keratinocyte migration and proliferation

Skin Disorder Classification

Etiology-based Classification

• Skin disorders can be classified based on their etiology into four main categories: infectious, inflammatory, neoplastic, and congenital
• Infectious skin disorders are caused by bacteria (cellulitis, impetigo), viruses (herpes simplex), fungi (tinea), or parasites (scabies)
• Inflammatory skin disorders are characterized by an abnormal immune response and include conditions such as acne, eczema, psoriasis, and contact dermatitis
• Neoplastic skin disorders involve the abnormal growth of skin cells and include benign conditions (seborrheic keratosis) and malignant conditions (basal cell carcinoma, melanoma)
• Congenital skin disorders are present at birth and include conditions such as epidermolysis bullosa and ichthyosis

Clinical Presentation

• Clinical presentation of skin disorders can vary widely and may include symptoms such as erythema, edema, vesicles, bullae, scales, plaques, and ulcers
  • Erythema is redness of the skin caused by dilation of blood vessels (cellulitis, eczema)
  • Edema is swelling caused by fluid accumulation in the skin (angioedema, contact dermatitis)
  • Vesicles are small, fluid-filled blisters (herpes simplex, chickenpox)
  • Bullae are large, fluid-filled blisters (pemphigus, bullous pemphigoid)
  • Scales are flakes of dead skin cells (psoriasis, seborrheic dermatitis)
  • Plaques are raised, flat-topped lesions (psoriasis, lichen planus)
  • Ulcers are open sores that extend into the dermis (venous ulcers, pressure ulcers)

Pathophysiology and Treatment of Skin Disorders

Acne and Eczema

• Acne is a chronic inflammatory disorder of the pilosebaceous unit characterized by the formation of comedones, papules, pustules, and nodules
  • The pathophysiology of acne involves increased sebum production, abnormal keratinization of the follicular epithelium, colonization by Propionibacterium acnes, and inflammation
  • Treatment options for acne include topical retinoids (tretinoin, adapalene), benzoyl peroxide, antibiotics (clindamycin, erythromycin), and oral medications (isotretinoin)
• Eczema, also known as atopic dermatitis, is a chronic inflammatory skin disorder characterized by pruritic, erythematous, and scaly lesions
  • The pathophysiology of eczema involves a complex interplay between genetic susceptibility, immune dysregulation, and environmental triggers
  • Treatment options for eczema include emollients, topical corticosteroids (hydrocortisone, triamcinolone), topical calcineurin inhibitors (tacrolimus, pimecrolimus), and systemic immunosuppressants (cyclosporine, methotrexate)

Psoriasis

• Psoriasis is a chronic autoimmune disorder characterized by the formation of well-demarcated, erythematous plaques with silvery scales
  • The pathophysiology of psoriasis involves hyperproliferation and abnormal differentiation of keratinocytes, as well as infiltration of inflammatory cells (T cells, dendritic cells) into the skin
  • Treatment options for psoriasis include topical corticosteroids, vitamin D analogs (calcipotriol), phototherapy (UVB, PUVA), and systemic medications (methotrexate, cyclosporine, biologic agents)
    • Biologic agents target specific cytokines (TNF-α, IL-17, IL-23) involved in the inflammatory cascade of psoriasis
    • Examples of biologic agents include etanercept, adalimumab, ustekinumab, and secukinumab