Learning Objectives, Chapter 9, Inflammation, Tissue Repair,
and Wound Healing
After completing this section of the chapter, the learner will be able to
meet the following objectives:
1. Identify and state the physiologic reasons behind five cardinal signs of
acute inflammation.
Inflammation involves a wide variety of physiological and
pathological responses intended to eliminate the initial cause of cell
injury, remove the damaged tissue, and generate new tissue
It does this by: destroying, enzymatically digesting, walling off or
neutralizing the harmful agents (toxins, foreign agents or infectious
organisms)
Pathogeneses of multiple diseases that are linked to dysregulated
inflammatory response: bronchial asthma, plaques leading to a
heart attacks, diabetes, autoimmune and neurodivergent disorders
Inflammation is the reaction of vascularized tissues to injury
Inflammatory mediators:
Complement
Tumor Necrosis Factor-a
Vascular endothelia growth factor
Neutrophils
Serum amyloid
Movement of fluid (in cells or intracellular fluid)
Inflammation localizes and eliminates microbes, foreign particles
and abnormal cells and paves the way for the repair of injured
tissue
Inflammatory conditions use the suffix “itis” to the affected organ
or system
Cardinal signs of inflammation the local reaction of injury is known
as such
Signs:
Rubor (redness)
, Tumor (swelling)
Calor (heat)
Dolor (pain)
Functio laesa (loss of function)
In addition to cardinal signs that appear at the injury site , systemic
or constitutional manifestations may occur as chemical mediators
are produced at the site of inflammation and enter the circulatory
system
Acute-phase response: systemic manifestation that may occur
during acute inflammation
Degree of inflammation is impacted by the following:
Duration of insult
Type of foreign agent
Degree of injury
Microenvironment
2. Describe the vascular changes in an acute inflammatory response.
Endothelial cells:
Single cell-thick epithelia lining of the blood vessels
Selectively permeable membrane between circulating blood in
vessels and surrounding tissues
Produce:
Antiplatelet agents
Antithrombotic agents
Function:
Maintain patency of vasodilators and vasoconstrictors that regulate
blood flow
Key players in the inflammatory response
Functionally they provide a selectively permeable barrier to
exogenous and endogenous inflammatory stimuli
Regulate leukocyte extravasation by expression of cell adhesion
molecules and receptors
Regulates immune responses by synthesis and release of
inflammatory mediators
Regulate immune cell proliferation via secretion of hematopoietic
colony-stimulating factors
, Helps in the repair process of inflammation by producing growth
factors that stimulate angiogenesis and ECM synthesis
Used as an indicator for:
Vascular dysfunction in persons with systemic lupus erythematosus,
in the absence of cardiovascular disease
Vascular stage:
Changes due to inflammation occur in the arterioles, capillaries and
venules of microcirculation
Characteristics of changes:
Vasodilation
Changes in blood flow
Increased vascular permeability
Leakage of fluid into extravascular tissues
Vasodilation:
Earliest manifestations of inflammation
Follows a temporary constriction of arterioles
First involves the arterioles, then results in the capillary beds
opening in that area = erythema and warmth
Induced by the following mediators:
NO
Histamine
Following vasodilation:
Increased permeability of microvasculature, outpouring of protein
rich exudate into extravascular spaces
Loss of plasma proteins reduces the intracapillary osmotic pressure
and increases the osmotic pressure of interstitial fluid = fluid to
move into tissue and produces edema, pain, impaired function
Also causes dilution of the offending agent in the tissues
Results:
In an increased concentration of RBC, clotting factors and platelets
Stagnation of flow
Clotting of blood at the site of injury = localizes spread of infectious
microorganisms
Increased permeability characteristic of acute inflammation results
from:
and Wound Healing
After completing this section of the chapter, the learner will be able to
meet the following objectives:
1. Identify and state the physiologic reasons behind five cardinal signs of
acute inflammation.
Inflammation involves a wide variety of physiological and
pathological responses intended to eliminate the initial cause of cell
injury, remove the damaged tissue, and generate new tissue
It does this by: destroying, enzymatically digesting, walling off or
neutralizing the harmful agents (toxins, foreign agents or infectious
organisms)
Pathogeneses of multiple diseases that are linked to dysregulated
inflammatory response: bronchial asthma, plaques leading to a
heart attacks, diabetes, autoimmune and neurodivergent disorders
Inflammation is the reaction of vascularized tissues to injury
Inflammatory mediators:
Complement
Tumor Necrosis Factor-a
Vascular endothelia growth factor
Neutrophils
Serum amyloid
Movement of fluid (in cells or intracellular fluid)
Inflammation localizes and eliminates microbes, foreign particles
and abnormal cells and paves the way for the repair of injured
tissue
Inflammatory conditions use the suffix “itis” to the affected organ
or system
Cardinal signs of inflammation the local reaction of injury is known
as such
Signs:
Rubor (redness)
, Tumor (swelling)
Calor (heat)
Dolor (pain)
Functio laesa (loss of function)
In addition to cardinal signs that appear at the injury site , systemic
or constitutional manifestations may occur as chemical mediators
are produced at the site of inflammation and enter the circulatory
system
Acute-phase response: systemic manifestation that may occur
during acute inflammation
Degree of inflammation is impacted by the following:
Duration of insult
Type of foreign agent
Degree of injury
Microenvironment
2. Describe the vascular changes in an acute inflammatory response.
Endothelial cells:
Single cell-thick epithelia lining of the blood vessels
Selectively permeable membrane between circulating blood in
vessels and surrounding tissues
Produce:
Antiplatelet agents
Antithrombotic agents
Function:
Maintain patency of vasodilators and vasoconstrictors that regulate
blood flow
Key players in the inflammatory response
Functionally they provide a selectively permeable barrier to
exogenous and endogenous inflammatory stimuli
Regulate leukocyte extravasation by expression of cell adhesion
molecules and receptors
Regulates immune responses by synthesis and release of
inflammatory mediators
Regulate immune cell proliferation via secretion of hematopoietic
colony-stimulating factors
, Helps in the repair process of inflammation by producing growth
factors that stimulate angiogenesis and ECM synthesis
Used as an indicator for:
Vascular dysfunction in persons with systemic lupus erythematosus,
in the absence of cardiovascular disease
Vascular stage:
Changes due to inflammation occur in the arterioles, capillaries and
venules of microcirculation
Characteristics of changes:
Vasodilation
Changes in blood flow
Increased vascular permeability
Leakage of fluid into extravascular tissues
Vasodilation:
Earliest manifestations of inflammation
Follows a temporary constriction of arterioles
First involves the arterioles, then results in the capillary beds
opening in that area = erythema and warmth
Induced by the following mediators:
NO
Histamine
Following vasodilation:
Increased permeability of microvasculature, outpouring of protein
rich exudate into extravascular spaces
Loss of plasma proteins reduces the intracapillary osmotic pressure
and increases the osmotic pressure of interstitial fluid = fluid to
move into tissue and produces edema, pain, impaired function
Also causes dilution of the offending agent in the tissues
Results:
In an increased concentration of RBC, clotting factors and platelets
Stagnation of flow
Clotting of blood at the site of injury = localizes spread of infectious
microorganisms
Increased permeability characteristic of acute inflammation results
from:
