Biology Chapter 3: Inflammation and Repair

Podcast Beta

Play an AI-generated podcast conversation about this lesson

Questions and Answers

What is phagocytosis?

Phagocytosis is the process of engulfing and disposing of offending agents by leukocytes.

Which type of cells produce vasoactive amines and AA metabolites as chemical mediators?

Mast cells (correct)

Macrophages

Dendritic cells

Neutrophils

Histamine is primarily stored in platelets and neuroendocrine cells.

False

Leukotrienes are produced by leukocytes and mast cells through the _________ pathway.

lipoxygenase Signup and view all the answers

What are the cardinal signs of acute inflammation?

Rubor, Tumor, Calor, Dolor Signup and view all the answers

What is the primary goal of inflammation after an injury?

Get rid of damaged or necrotic tissues and foreign invaders Signup and view all the answers

In acute inflammation, what is the term used to describe the increased vascular permeability resulting in fluid accumulation in the extracellular space? Edema and/or _______

Exudate Signup and view all the answers

Match the major components of acute inflammation with their descriptions:

Increase blood flow to site of injury (vascular response) = Cardinal Signs Permit plasma protein and leukocytes to leave the circulation (vascular response) = Recognition of the offending agent Leukocytes emigration and accumulation in the site of injury (cellular response) = Tissue repair Signup and view all the answers

What are two consequences of defective inflammation?

Increased susceptibility to infections and Delayed wound healing Signup and view all the answers

What are the two types of reactions in tissue healing?

Regeneration Signup and view all the answers

Repair involves restoration of tissue architecture and function after an ____.

injury Signup and view all the answers

Tissue repair can only occur with an effective inflammatory response.

True Signup and view all the answers

What drives the regeneration of injured cells and tissues?

Cell proliferation and growth factors Signup and view all the answers

Match the growth factors with their functions:

Epidermal growth factor (EGF) = Mitogenic for keratinocytes and fibroblasts; stimulates keratinocyte migration and granulation tissue formation Transforming growth factor alpha (TGF-α) = Similar to EGF; stimulates replication of hepatocytes and most epithelial cells Hepatocyte growth factor (HGF) = Enhances proliferation of hepatocytes, epithelial cells, and endothelial cells; increases cell motility and keratinocyte replication Vascular endothelial growth factor (VEGF) = Increases vascular permeability; mitogenic for endothelial cells; promotes angiogenesis Signup and view all the answers

Which factor converts XII to XIIa (active form) in the clotting system?

Activated platelets Signup and view all the answers

What is the function of bradykinin in inflammation?

Increase vascular permeability, non-vascular smooth muscle contraction, arteriolar dilation, causes pain Signup and view all the answers

Fever is an acute-phase response in inflammation.

True Signup and view all the answers

______ inflammation is characterized by watery fluid with small amounts of proteins and cells.

Serous Signup and view all the answers

Match the following mediators with their roles in inflammation:

Prostaglandins, Nitric oxide, Histamine = Vasodilation Histamine and serotonin, C3a and C5a, Bradykinin = Increased vascular permeability TNF, IL-1, Chemokines = Chemotaxis, leukocyte recruitment, and activation IL-1, TNF, Prostaglandin = Fever Prostaglandin, Bradykinin = Pain Signup and view all the answers

What are the steps of scar formation after repair by connective tissue deposition?

Angiogenesis, Formation of granulation tissue, Remodeling of connective tissue Signup and view all the answers

Which phase involves clot formation, chemotaxis, and angiogenesis in wound healing?

Inflammatory phase Signup and view all the answers

In healing by second intention, wound contraction only occurs when healing by primary intention is not achievable.

False Signup and view all the answers

Formation of granulation tissue is a hallmark of __________ repair.

tissue Signup and view all the answers

Match the steps of angiogenesis with their descriptions:

Vasodilation and increased permeability induced by VEGF = Step 1 of angiogenesis Migration of endothelial cells from the original capillary toward an angiogenetic stimulus = Step 3 of angiogenesis Recruitment of periendothelial cells to form the mature vessel = Step 5 of angiogenesis Signup and view all the answers

What are some local factors that influence wound healing?

Infection, type/size/location of wound, movement, foreign bodies Signup and view all the answers

What can delay wound healing and lead to more granulation tissue and scarring?

Infection Signup and view all the answers

Wounds over joints heal well due to traction. (True/False)

False Signup and view all the answers

Excessive scar formation primarily composed of type III collagen is known as ___.

keloids Signup and view all the answers

Match the abnormalities in tissue repair with their descriptions:

Defective granulation tissue or scar formation = Usually due to wound infection (common); malnutrition (rare); hypoxia with ulceration, usually due to inadequate vascularity in a skin flap (common) Excessive scar formation (keloid) = Result of over-exuberant production of scar tissue, primarily composed of type III collagen; thought to be due to genetic factors, perhaps due to lack of the proper metalloproteinases to degrade type III collagen Contraction = Excessive contraction of a wound; known as a contracture; special problem in the treatment of extensive burns Signup and view all the answers

Study Notes

Inflammation and Repair

Inflammation as a Defense Mechanism

Inflammation is the second line of defense and a nonspecific defense mechanism
It is a host response that aims to:
- Get rid of damaged or necrotic tissues and foreign invaders
- Repair tissue damage

Types of Inflammation

Acute inflammation:
- An expected body response to injury
- Aims to eliminate the offending agent and initiate tissue repair
Chronic inflammation:
- An altered inflammatory response due to unrelenting injury
- Can lead to tissue damage and disease

Sequential Steps of Inflammation

Recognition of the offending agent
Recruitment of leukocytes and plasma proteins
Activation of leukocytes and plasma proteins and elimination of the offending substances
Reaction is controlled and terminated
Tissue repair

Causes of Inflammation

Infections
Tissue necrosis
Ischemia
Trauma
Physical and chemical injury
Foreign bodies
Immune reactions

Features of Acute Inflammation

Cardinal signs:
- Rubor (redness)
- Tumor (swelling)
- Calor (heat)
- Dolor (pain)
- Functio laesa (loss of function)
Manifestation:
- Redness due to vasodilation and increased blood flow
- Heat due to vasodilation and increased blood flow
- Pain due to chemical mediators and edema
- Edema and/or exudate due to increased vascular permeability
- Loss of function due to tissue damage and pain

Cellular Response

Three major components:
1. Increase blood flow to the site of injury (vascular response)
2. Permit plasma protein and leukocytes to leave the circulation (vascular response)
3. Leukocyte emigration and accumulation in the site of injury (cellular response)
Vascular response:
- Vascular dilation and increased blood flow
- Increase of permeability of the blood vessel
Cellular response:
- Leukocyte recruitment and activation
- Phagocytosis and clearance of the offending agent

Phagocytosis and Clearance

Recognition and activation of leukocytes
Phagocytosis: removal of the offending agents
Clearance: removal of ingested particles by lysosomal enzymes and reactive oxygen and nitrogen species

Termination of Acute Inflammation

Inflammation declines after the offending agents are removed
Mediators are produced in rapid bursts and have short half-lives
Neutrophils have short half-lives
Inflammation process triggers a variety of stop signals

Chemical Mediators

Substances that initiate and regulate inflammatory reactions
Come from cells or plasma
Produced in response to various stimuli
One mediator can stimulate the release of another
Mediators vary in their range of cellular targets
Short-lived: quickly decay, are inactivated enzymatically, or are scavenged

Cell-Derived Chemical Mediators

Vasoactive amines
Arachidonic acid metabolites
Cytokines and chemokines
Produced by macrophages, dendritic cells, and mast cells

Vasoactive Amines

Histamine and serotonin
Stored in cells and released in response to various stimuli
Histamine:
- Causes dilation of arterioles and increases the permeability of venules
- Released from mast cells
Serotonin:
- Vasodilator and vasoconstrictor
- Released from platelets and neuroendocrine cells

Arachidonic Acid Metabolites

Lipid mediators produced from AA
Prostaglandins and leukotrienes
Stimulate vascular and cellular reactions in acute inflammation### Inflammation
Inflammation is a response to tissue damage or infection, characterized by increased blood flow, swelling, heat, redness, and pain.
Acute inflammation is a short-term response, whereas chronic inflammation is a long-term response that can last for weeks or months.

Lipoxins

Produced by leukocytes through the lipoxygenase pathway
Suppress inflammation by inhibiting the recruitment of WBCs

Eicosanoids

Metabolites of arachidonic acid (AA)
Mediate various inflammatory responses, including:
- Vasodilation: PGI2, PGE1, PGE2, PGD2
- Vasoconstriction: Thromboxane A2, leukotrienes C4, D4, E4
- Increased vascular permeability: Leukotrienes C4, D4, E4
- Chemotaxis and leukocyte adhesion: Leukotrienes B4, HETE

Cytokines and Chemokines

Cytokines:
- Proteins produced by many cell types, including activated lymphocytes, macrophages, and dendritic cells
- Act as messengers to other cells, telling them how to behave
- Mediate and regulate immune and inflammatory reactions
- Examples: Tumor necrosis factor (TNF), interleukin-1 (IL-1)
Chemokines:
- Small proteins that act as chemoattractants for specific types of WBCs
- Play a crucial role in recruiting immune cells to sites of inflammation

Plasma Protein-Derived Mediators

Complement system:
- Functions in host defense against microbes and in pathologic inflammatory reactions
- Activated complement proteins can stimulate histamine release, chemotaxis, and opsonization
Clotting system:
- Inflammation and blood clotting are intertwined, with each promoting the other
- Hageman factor (factor XII) converts to XIIa, initiating the clotting cascade
Kinins:
- Vasoactive peptides derived from plasma proteins
- Functions: increase vascular permeability, non-vascular smooth muscle contraction, arteriolar dilation, and pain

Morphologic Patterns of Acute Inflammation

Serous inflammation:
- Characterized by a watery fluid with small amounts of proteins and cells
- Causes: allergic chemicals, burns
Fibrinous inflammation:
- Characterized by a thick, sticky fluid with increased cell and fibrin content
- Increase risk of scar tissue
Purulent inflammation:
- Characterized by a thick, yellow-green fluid with increased leukocytes, cell debris, and microbes
- Indicates bacterial infection
Ulcers:
- Circumscribed, open, crater-like lesions of the skin or mucous membranes

Systemic Effects of Inflammation

Acute-phase responses:
- Cytokine-induced systemic reactions that occur in response to inflammation
- Clinical and pathologic changes: fever, leukocytosis, acute-phase proteins
Possible outcomes of acute inflammation:
- Complete resolution
- Scarring or fibrosis
- Chronic inflammation

Chronic Inflammation

Recurrent or persistent inflammation lasting several weeks or months
Causes: persistent injury or infection, prolonged toxic agent exposure, autoimmune disease states
Morphologic features:
- Mononuclear cell infiltration
- Tissue destruction
- Attempts at repair with fibrosis and angiogenesis
Cells and mediators:
- Macrophages: dominant cells in most chronic inflammatory reactions
- T cells: involved in the regulation of chronic inflammation
- Cytokines and chemokines: mediate chronic inflammation

Tissue Repair

Restoration of tissue architecture and function after an injury
Two types of reactions:
- Regeneration: restores normal tissue
- Connective tissue deposition (scar formation): repair by laying down of connective tissue
Cell and tissue regeneration:
- Dependent on the integrity of the extracellular matrix (ECM)
- Driven by growth factors and stem cells### Classification of Cells by Proliferative Potential
Labile cells: continuous dividing, found in epithelium of skin, respiratory tract, gastrointestinal tract, and urinary tract, as well as hematopoietic cells.
Stable cells: quiescent, found in parenchymal cells of liver, kidney, pancreas, and salivary gland.
Permanent cells: non-dividing, found in myocardium, skeletal muscle, and neurons.

Regulation of Cell Proliferation

Growth factors: polypeptide molecules that stimulate cell proliferation, including an increase in cell size, mitotic activity, and protection from apoptosis.
Growth factors induce synthesis or activity of transcription factors, promoting cellular migration, differentiation, and contractility.
Examples of growth factors include EGF, TGF-α, HGF, VEGF, PDGF, FGF, and TGF-β.

Regulation of Cell Proliferation (continued)

The extracellular matrix (ECM) plays a crucial role in regulating cell proliferation, providing mechanical support, determining cell orientation, controlling cell growth, maintaining cell differentiation, and scaffolding for tissue renewal.
The ECM is composed of three types of macromolecules: fibrous structural proteins (collagens and elastin), adhesive proteins (immunoglobulin family CAM, cadherins, integrins, and selectins), and proteoglycans and hyaluronan.

Cell-Matrix Interactions

Cell growth and differentiation involve both soluble and insoluble signals, including growth factors and ECM interactions.
Cell-matrix interactions involve integrins, which connect the matrix elements to one another and to cells.

Repair by Connective Tissue Deposition

If repair cannot be accomplished by regeneration alone, it occurs by replacement of injured cells with connective tissues, leading to scar formation.
Steps of scar formation include angiogenesis, formation of granulation tissue, and remodeling of connective tissue.

Cutaneous Wound Healing

Wound healing can occur by either first intention (primary closure) or second intention (secondary closure).
First intention involves a clean wound with well-apposed edges, minimal clot formation, and a small scar.
Second intention involves a wound with separated edges, abundant clot formation, and a large scar.

Stages of Wound Healing

Inflammatory phase: clot formation, chemotaxis, and removal of debris and bacteria.
Proliferative phase: angiogenesis, granulation tissue formation, and epithelialization of the wound.
Maturational phase: ECM deposition, tissue remodeling, and wound contraction.

Formation of Blood Clot

The coagulation pathway is activated, and a blood clot forms to cover the wound, stop bleeding, and serve as a scaffold for migrating cells.

Formation of Granulation Tissue

Granulation tissue forms 24-72 hours after injury, composed of proliferating fibroblasts, newly formed thin capillaries, and loose ECM.
The amount of granulation tissue depends on the size of the tissue deficit and the intensity of inflammation.

Angiogenesis

Angiogenesis is the process of new blood vessel development from existing vessels.
Steps of angiogenesis include vasodilation, proteolytic degradation of the parent vessel basement membrane, migration of endothelial cells, proliferation of endothelial cells, and maturation of endothelial cells.

Roles of Granulation Tissue in Fibrous Repair

Granulation tissue grows into the necrotic tissue, replacing it with a scar.
Granulation tissue supports the integrity of the body and protects the wound from infection.

Cell Proliferation and Collagen Deposition

Macrophages replace neutrophils, cleaning extracellular debris, and promoting angiogenesis and ECM deposition.
Fibroblasts proliferate and deposit collagen fibers, leading to scar formation.

Scar Formation

During the second week, the granulation tissue becomes a scar composed of inactive spindle-shaped fibroblasts, dense collagen, and fragments of elastic tissue.
By the end of the first month, the scar is made up of acellular connective tissue devoid of inflammatory infiltrate, covered by intact epidermis.

Connective Tissue Remodeling

The balance between ECM synthesis and degradation results in remodeling of the connective tissue framework.
A scar after surgical operation or trauma will become softer and smaller due to degradation of collagens and other ECM elements.

Factors that Influence Wound Healing

Systemic factors: overall nutrition, metabolic status, circulatory status, hormones, and age.
Local factors: wound size, depth, and location, as well as the presence of infection or foreign bodies.

Studying That Suits You

Use AI to generate personalized quizzes and flashcards to suit your learning preferences.

Description

This quiz covers the basics of inflammation and repair, including the concept of defense mechanisms and lines of defense.