Module 1 – Integumentary, Musculoskeletal, and Cancer
Chapter 3 – Inflammation and Tissue Repair
Acute Inflammation
• The acute inflammatory response has three major goals:
o Vascular response – to increase blood flow to site of injury
o Cellular response – to alert the products of healing to attend to the site of injury
o To remove injured tissue and prepare the site for repair and healing
• Vascular Response
o Goal – to attract sufficient products of clotting and healing to the site of injury and to prevent infection
▪ Facilitated by chemical mediators
▪ Causes vasodilation
▪ Increases blood vessel permeability
• Tissue injury
o Production and release of inflammatory mediators
▪ Vasoactive mediators – histamines, leukotrienes, and prostaglandins
▫ Actions:
o Vasodilation via histamines
o Increased capillary permeability
▫ Manifestations:
o Localized redness
o Heat
o Swelling
o Pain
o Loss of function
▪ Chemotactic mediators/chemokines - stimulate a cellular response
▫ Actions
o Chemotaxis
o Adherence
o Migration
o Phagocytosis
▫ Manifestations
→ Acute inflammation
▪ PMNs
▪ Platelets
▪ Mast Cells release histamines → vasodilation
→ Chronic inflammation
▪ Macrophages
▪ Lymphocytes
• Inflammatory Mediators
o Within cells
▪ White blood cells
▪ Platelets
▪ Endothelial cells
, o Within plasma
▪ Complement system
▫ Role: to destroy and remove microorganisms to prevent infection through opsonization
and cell lysis
▫ Produced in liver
▫ 10-15% of plasma
▫ Activates a cascade of inflammatory mediators
▪ Clotting
▫ Promotes coagulation through a cascade of clotting factors
▫ Suppresses coagulation when clotting is complete
▫ Various clotting factors produce and release inflammatory mediators
▪ Kinin
▫ Source of highly potent vasoactive inflammatory mediators
▫ Amplifies the inflammatory response by triggering other inflammatory mediators
• Clinical manifestations
o Local
▪ Erythema
▪ Heat
▪ Edema
▪ Pain
▪ Incapacitation
o Systemic
▪ Fever
▪ Leukocytosis
▪ Pyrexia
▪ Incr plasma
Healing and Tissue Repair
• Inflammatory phase
o Active inflammatory response
o Cover the wound
▪ Hemostasis
• Platelets released
• Vasoconstriction
▪ Thrombus forms
• Proliferative phase
o Clean the debris
▪ Polymorphonuclear neutrophils
▪ Macrophages
▪ Remove necrotic tissue
o Restore structure integrity
▪ Provisional matrix
• Granulation tissue
▪ Rebuild extracellular matrix
• Basement membrane
, • Connective tissue
• Remodeling phase
o Restore function integrity
▪ Resolution
▪ Repair
▪ Regeneration
o Remodeling
▪ Maturation of cells
▪ Degradation of provisional matrix
Skin and Burn Injuries
• Pathophysiology
o Thermal injury
o Electrical injury
o Caustic chemical injury
o Radiation exposure
o Inhalation of noxious fumes
• Clinical manifestations
o Superficial partial-thickness burns
▪ Damages only epidermis
▪ Mild sunburns
▪ Erythema
▪ Warmth
▪ Pain
▪ Edema
▪ Loss of function of affected areas
▪ No blisters!!!!
o Deep partial-thickness burns
▪ Damages epidermis and dermis
▪ Severe sunburn, hot liquids, mild-moderate chemical burns, flash flame exposure
▪ Erythema
▪ Warmth
▪ Pain
▪ Edema
▪ Serous exudate
▪ BLISTERS!!
o Full-thickness burns
▪ Damages epidermis, dermis, and subcutaneous layers
▪ Extremely hot objects, flame exposure, caustic chemicals
▪ Destruction of blood vessels, nerves, sweat glands, and hair follicles
▪ Erythema
▪ Eschar
▪ Exudate
▪ Contractures
Rheumatoid Arthritis
Chapter 3 – Inflammation and Tissue Repair
Acute Inflammation
• The acute inflammatory response has three major goals:
o Vascular response – to increase blood flow to site of injury
o Cellular response – to alert the products of healing to attend to the site of injury
o To remove injured tissue and prepare the site for repair and healing
• Vascular Response
o Goal – to attract sufficient products of clotting and healing to the site of injury and to prevent infection
▪ Facilitated by chemical mediators
▪ Causes vasodilation
▪ Increases blood vessel permeability
• Tissue injury
o Production and release of inflammatory mediators
▪ Vasoactive mediators – histamines, leukotrienes, and prostaglandins
▫ Actions:
o Vasodilation via histamines
o Increased capillary permeability
▫ Manifestations:
o Localized redness
o Heat
o Swelling
o Pain
o Loss of function
▪ Chemotactic mediators/chemokines - stimulate a cellular response
▫ Actions
o Chemotaxis
o Adherence
o Migration
o Phagocytosis
▫ Manifestations
→ Acute inflammation
▪ PMNs
▪ Platelets
▪ Mast Cells release histamines → vasodilation
→ Chronic inflammation
▪ Macrophages
▪ Lymphocytes
• Inflammatory Mediators
o Within cells
▪ White blood cells
▪ Platelets
▪ Endothelial cells
, o Within plasma
▪ Complement system
▫ Role: to destroy and remove microorganisms to prevent infection through opsonization
and cell lysis
▫ Produced in liver
▫ 10-15% of plasma
▫ Activates a cascade of inflammatory mediators
▪ Clotting
▫ Promotes coagulation through a cascade of clotting factors
▫ Suppresses coagulation when clotting is complete
▫ Various clotting factors produce and release inflammatory mediators
▪ Kinin
▫ Source of highly potent vasoactive inflammatory mediators
▫ Amplifies the inflammatory response by triggering other inflammatory mediators
• Clinical manifestations
o Local
▪ Erythema
▪ Heat
▪ Edema
▪ Pain
▪ Incapacitation
o Systemic
▪ Fever
▪ Leukocytosis
▪ Pyrexia
▪ Incr plasma
Healing and Tissue Repair
• Inflammatory phase
o Active inflammatory response
o Cover the wound
▪ Hemostasis
• Platelets released
• Vasoconstriction
▪ Thrombus forms
• Proliferative phase
o Clean the debris
▪ Polymorphonuclear neutrophils
▪ Macrophages
▪ Remove necrotic tissue
o Restore structure integrity
▪ Provisional matrix
• Granulation tissue
▪ Rebuild extracellular matrix
• Basement membrane
, • Connective tissue
• Remodeling phase
o Restore function integrity
▪ Resolution
▪ Repair
▪ Regeneration
o Remodeling
▪ Maturation of cells
▪ Degradation of provisional matrix
Skin and Burn Injuries
• Pathophysiology
o Thermal injury
o Electrical injury
o Caustic chemical injury
o Radiation exposure
o Inhalation of noxious fumes
• Clinical manifestations
o Superficial partial-thickness burns
▪ Damages only epidermis
▪ Mild sunburns
▪ Erythema
▪ Warmth
▪ Pain
▪ Edema
▪ Loss of function of affected areas
▪ No blisters!!!!
o Deep partial-thickness burns
▪ Damages epidermis and dermis
▪ Severe sunburn, hot liquids, mild-moderate chemical burns, flash flame exposure
▪ Erythema
▪ Warmth
▪ Pain
▪ Edema
▪ Serous exudate
▪ BLISTERS!!
o Full-thickness burns
▪ Damages epidermis, dermis, and subcutaneous layers
▪ Extremely hot objects, flame exposure, caustic chemicals
▪ Destruction of blood vessels, nerves, sweat glands, and hair follicles
▪ Erythema
▪ Eschar
▪ Exudate
▪ Contractures
Rheumatoid Arthritis
