Inflammation and Its Purposes

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Questions and Answers

What is one of the functions of histamine in inflammation?

Promotes arteriolar dilation and increases vascular permeability (correct)

Promotes blood coagulation

Activates the complement system

Inhibits immune responses

Which system is activated by inflammation through Factor XII?

Blood coagulation system (correct)

Arachidonic acid pathway

Kallikrein-bradykinin system

Complement system

What beneficial effect does fever provide during inflammation?

Shift the oxygen-dissociation curve to the right (correct)

Decrease oxygen availability

Enhance bacterial and viral reproduction

Shift the oxygen-dissociation curve to the left

Which pathway of the complement system requires antibodies for activation?

Classical pathway Signup and view all the answers

What is one harmful effect of inflammation?

Impaired flow, as seen in acute meningitis Signup and view all the answers

What is the process called when connections between cells pull back, creating spaces?

Junctional retraction Signup and view all the answers

Which fluid forms during inflammation and is rich in proteins and immune cells?

Exudate Signup and view all the answers

What is the term for neutrophils moving towards the site of injury, mediated by chemokines?

Chemotaxis Signup and view all the answers

Which cells are primarily involved in the early response to infection and contain myeloperoxidases?

Neutrophils Signup and view all the answers

What process describes the ingestion of microorganisms into a phagocytic vacuole by neutrophils?

Phagocytosis Signup and view all the answers

Which type of granules in neutrophils is known to contain collagenase?

Secondary granules Signup and view all the answers

What are neutrophil extracellular traps (NETs) primarily composed of?

DNA fibers and histones Signup and view all the answers

Which mechanism destroys microorganisms during phagocytosis through increased oxygen consumption?

Oxidative burst Signup and view all the answers

What is the primary purpose of inflammation?

To eliminate cell injury causes and begin healing Signup and view all the answers

Which type of cells primarily characterize acute inflammation?

Neutrophils Signup and view all the answers

What are the five classic signs of acute inflammation?

Calor, rubor, tumor, dolor, function laesa Signup and view all the answers

What triggers increased vascular permeability during acute inflammation?

Endothelial cell changes Signup and view all the answers

Which of the following is NOT a cause of inflammation?

Excessive hydration Signup and view all the answers

What phase follows transient vasoconstriction during the vascular response of acute inflammation?

Vasodilation Signup and view all the answers

What is a common outcome of inflammation that can be both beneficial and harmful?

Formation of scar tissue Signup and view all the answers

Which of the following correctly describes chronic inflammation?

It lasts from weeks to years and involves mononuclear cells Signup and view all the answers

What is the role of the membrane attack complex in inflammation?

It punches a hole in the cell membrane of pathogens. Signup and view all the answers

Which of the following describes a harmful effect of inflammation?

Impaired function leading to loss of tissue integrity. Signup and view all the answers

What is a primary function of reactive oxygen species in inflammation?

To eliminate bacteria. Signup and view all the answers

Which statement about the kinin system is accurate?

It involves the activation of factor XII. Signup and view all the answers

Which outcome of acute inflammation involves the formation of a walled-off collection of pus?

Abscess formation. Signup and view all the answers

What is the primary purpose of inflammation?

To localize and eliminate the causative agent Signup and view all the answers

Which types of cells are predominantly involved in acute inflammation?

Polymorphonuclear cells (neutrophils) Signup and view all the answers

What are the two major events that occur in acute inflammation?

Vascular response and cellular response Signup and view all the answers

Which of the following causes increased vascular permeability during acute inflammation?

Decreased osmotic pressure inside blood vessels Signup and view all the answers

Which of the following is NOT one of the five classic signs of acute inflammation?

Contraction Signup and view all the answers

What is the typical duration of acute inflammation?

Minutes to days Signup and view all the answers

Which of the following is a common cause of inflammation?

Infectious agents Signup and view all the answers

What suffix is commonly associated with inflammatory lesions?

ITIS Signup and view all the answers

What is the main characteristic of transudate fluid?

It is a watery fluid with few proteins. Signup and view all the answers

What is the primary role of neutrophil rolling in the inflammatory response?

To transiently adhere to endothelial cells. Signup and view all the answers

Which of the following describes the process of chemotaxis in neutrophils?

Movement toward the site of injury mediated by chemokines. Signup and view all the answers

What is a key feature of neutrophil degranulation?

Release of granule contents into the tissue. Signup and view all the answers

Which of the following describes the function of myeloperoxidases (MPO) in neutrophils?

They play a role in the oxidative burst mechanism. Signup and view all the answers

Which molecule mediates the firm adhesion of neutrophils during inflammation?

ICAM-1-LFA-1 Signup and view all the answers

What is the role of neutrophil extracellular traps (NETs) in the immune response?

To capture and kill pathogens extracellularly. Signup and view all the answers

What triggers endothelial cell activation during the inflammatory response?

Cytokine signaling. Signup and view all the answers

What is a result of the vasoactive effects of serotonin during inflammation?

Promotion of arteriolar dilation Signup and view all the answers

Which statement accurately describes the alternative pathway of the complement system?

It does not require antibodies for activation. Signup and view all the answers

Which role of reactive oxygen species during inflammation is typically detrimental?

Induction of tissue damage Signup and view all the answers

What denotes the process of abscess formation during acute inflammation?

A collection of pus walled off from surrounding tissues Signup and view all the answers

What is a characteristic feature of the kinin-bradykinin system in relation to inflammation?

It modulates blood pressure during the inflammatory response. Signup and view all the answers

What type of cells primarily characterize chronic inflammation?

Mononuclear cells Signup and view all the answers

What is the primary purpose of the vascular response during acute inflammation?

Promote extravasation of leukocytes Signup and view all the answers

Which event follows vasodilatation within the vascular response during acute inflammation?

Increased vascular permeability Signup and view all the answers

Which factor contributes to the loss of function observed during acute inflammation?

Swelling and pain in the affected area Signup and view all the answers

What are the two main cellular responses in acute inflammation?

Extravasation and chemotaxis Signup and view all the answers

What suffix is commonly associated with inflammatory lesions, indicating inflammation?

-itis Signup and view all the answers

Which of the following describes a beneficial effect of inflammation?

Elimination of pathogens and initiation of repair Signup and view all the answers

What causes increased hydrostatic pressure during acute inflammation?

Increased blood volume and flow Signup and view all the answers

Which factor is primarily responsible for the firm adhesion of neutrophils to the endothelial cells during inflammation?

ICAM-1-LFA-1 Signup and view all the answers

What is the main difference between transudate and exudate in the context of vascular permeability?

Transudate forms due to imbalances in pressure, while exudate forms during inflammation. Signup and view all the answers

Which of the following mechanisms involves the ingestion of microorganisms into a phagocytic vacuole by neutrophils?

Phagocytosis Signup and view all the answers

Which component released during the oxidative burst is primarily responsible for producing reactive oxygen species?

Myeloperoxidases (MPO) Signup and view all the answers

What is the process called when neutrophils roll along endothelial cells and adhere transiently?

Rolling Signup and view all the answers

What type of granules do neutrophils release that contain proteolytic enzymes such as collagenase?

Secondary granules Signup and view all the answers

Which term describes the movement of leukocytes from the center of a blood vessel towards its periphery?

Margination Signup and view all the answers

Which mechanism involves neutrophils forming structures made of DNA fibers to trap pathogens?

Neutrophil extracellular traps (NETs) Signup and view all the answers

Study Notes

Inflammation

A localized response to injury in vascularized living tissue.
A protective response triggered by injury to eliminate the cause of injury and necrotic cells/tissues.
Can be harmful.
Intimately associated with repair processes.
Inflammatory lesions are often indicated by the suffix, "itis."

Inflammation Purpose

Localize and eliminate the causative agent.
Limit tissue injury.
Begin the process of healing.

Inflammation Causes

Infectious agents (bacterial, viral, parasitic, fungal).
Physical agents (trauma, burns, radiation, extreme temperatures).
Chemical agents (acids, alkalis, toxins).
Immune reactions (allergies, autoimmune diseases, hypersensitivity).
Necrotic tissue.

Types of Inflammation

Acute inflammation: Minutes to days. Characterized by fluid and protein, dominated by neutrophils.
Chronic inflammation: Weeks to years. Characterized by mononuclear cells (macrophages, lymphocytes, plasma cells).

Five Classic Signs of Acute Inflammation

Heat (Calor): Caused by increased blood flow.
Redness (Rubor): Caused by increased blood flow.
Swelling (Tumor): Caused by fluid accumulation.
Pain (Dolor): Caused by chemical mediators, pressure from swelling.
Loss of function (Functio laesa): Caused by swelling, pain, tissue destruction.

Two Major Events in Acute Inflammation

Vascular response: Transient vasoconstriction followed by vasodilation, and increased vascular permeability.
Cellular response: Extravasation of neutrophils.

Reasons for Increased Vascular Permeability

Increased hydrostatic pressure: "Pushing pressure" forces fluid out of blood vessels.
Decreased intravascular osmotic pressure: Less "pulling power" inside blood vessels retains fluid.
Endothelial cell changes: Cells become leaky.

Outcomes of Increased Vascular Permeability

Transudate: Watery fluid with low protein content. Forms due to imbalances in pressure.
Exudate: Thicker fluid, rich in proteins and immune cells (neutrophils). Forms during inflammation.

Cellular Response - Key Points

Margination: As blood slows, leukocytes move to the periphery of the vessel.
Endothelial cell activation: Cytokines activate endothelium, causing selectins and other mediators to move to the surface.
Rolling: Neutrophils roll and transiently adhere to endothelial cells, mediated by selectins.
Neutrophil activation: Mediated by interleukin-8 (IL-8) and other chemokines.
Firm adhesion (pavementing): Mediated by intercellular adhesion molecule-1 (ICAM-1) and leukocyte function-associated antigen-1 (LFA-1).
Transmigration (diapedesis): Mediated by platelet endothelial cell adhesion molecule-1 (PECAM-1). Cells crawl through vessel walls.
Chemotaxis: Movement toward the site of injury mediated by chemokines (chemical attractants for cells ).

Neutrophil Functions

Primary granules: Contain myeloperoxidase (MPO) and other enzymes.
Secondary granules: Contain collagenase and chitinase 3-like 1 (CHI3L1).
Tertiary granules: Contain matrix metalloproteinases (MMPs) and other enzymes.
Neutrophils express receptors: Recognize pathogen-associated molecular patterns (PAMPs) from pathogens and damage-associated molecular patterns (DAMPs) from injured cells.

Antimicrobial Mechanisms of Neutrophils

Phagocytosis: Ingestion of microorganisms into a phagocytotic vacuole, which fuses with lysosomes to destroy the microbe.
Oxidative burst: Release of reactive oxygen species (ROS) such as superoxide ion (O2-), hydrogen peroxide (H2O2), hypochlorous acid (HOCl), hydroxyl radical (OH), and nitric oxide (NO).
Degranulation: Release of granule contents into the environment.
Neutrophil extracellular traps (NETs): Form by releasing net like structures of DNA, histones, etc., to trap pathogens.

Reactive Oxygen Species

Eliminate bacteria.
Can damage tissues.

Chemical Mediators of Inflammation

Most bind to cell surface receptors, while some act directly through enzymatic or toxic activity.
Tightly regulated.

Vasoactive Amines:

Histamine: Found in mast cells, basophils, and platelets. Promotes arteriolar dilation and venular endothelial contraction, increasing vascular permeability.
Serotonin (5-HT): Similar vasoactive effects to histamine. Found in platelets, released during platelet aggregation.

Complement System

Classical pathway: Antibody-dependent activation (antigen-antibody complex) to activate C1.
Alternative pathway: Antibody-independent activation.

Membrane Attack Complex (MAC)

Forms pores in cell membranes.

Role of C3a and C5a in Inflammation

C3a and C5a: Anaphylatoxins that cause mast cell degranulation, smooth muscle contraction, and increased vascular permeability.

Blood Coagulation System

Factor XII (Hageman factor): Activated during inflammation, triggering the coagulation cascade.

Kallikrein-Bradykinin System

Bradykinin: A potent vasodilator and pain mediator.

Arachidonic Acid Pathway

Arachidonic acid: A fatty acid released from cell membranes during inflammation.
Cyclooxygenase (COX) pathway: Leads to the production of prostaglandins and thromboxane A2.
Lipoxygenase pathway: Leads to the production of leukotrienes and lipoxins.

Fever

Beneficial effects:
- Shifts the oxygen-dissociation curve to the right, increasing oxygen availability for cells.
- Provides a hostile environment for bacterial and viral reproduction.

Effects of Inflammation

Beneficial:
- Dilution of toxins.
- Stimulation of adaptive immunity, arrival of antibodies.
- Delivery of nutrients and oxygen, drug transport.
- Formation of fibrin (delays bacterial spread).
- Destruction of microbial agents.
- Removal of tissue debris.
Harmful:
- Mechanical effects (e.g., epiglottitis).
- Impaired flow (e.g., acute meningitis).
- Impaired function.
- Tissue destruction.

Outcomes of Acute Inflammation

Resolution: Healing and repair.
Abscess formation: Walled-off collection of pus.
Progression to chronic inflammation.

Inflammation Definition

Inflammation is a localised reaction to injury in vascularised living tissues
It is a protective response that aims to eliminate the cause of the injury and its byproducts (necrotic cells and tissues)
Inflammation can be beneficial in the short term
Inflammation is closely linked to the repair process
Many inflammatory lesions are identified by the suffix "-itis"

Inflammation Purpose

Localise and eliminate the causative agent
Limit tissue injury
Initiate the healing process

Inflammation Causes

Infectious agents
Physical agents
Chemical agents
Immune reactions
Necrotic tissue

Types of Inflammation

Acute inflammation occurs within minutes to days
- Characterized by fluid and protein exudation
- Polymorphonuclear cells (neutrophils) are the primary inflammatory cells
Chronic inflammation persists for weeks to years
- Dominated by mononuclear cells (macrophages, lymphocytes, and plasma cells)

Classic Signs of Acute Inflammation

Heat: Calor
Redness: Rubor
Swelling: Tumor
Pain: Dolor
Loss of function: Function laesa

Major Events in Acute Inflammation

Vascular response:
- Transient vasoconstriction, followed by vasodilatation
- Increased vascular permeability
Cellular response:
- Extravasation of neutrophils (polymorphonuclear leukocytes)

Increased Vascular Permeability Mechanisms

Increased hydrostatic pressure: Increased pressure inside blood vessels forces fluid out
Decreased intravascular osmotic pressure: Lower pressure inside vessels reduces fluid retention
Endothelial cell changes: Damaged or altered endothelial cells allow fluid leakage
Contraction: Cells shrink, creating gaps between them
Junctional retraction: Connections between cells loosen, forming spaces
Injury: Direct damage to endothelial cells leads to gaps

Outcomes of Increased Vascular Permeability

Transudate: Watery fluid with few proteins, primarily due to pressure imbalances
Exudate: Thick fluid rich in proteins and inflammatory cells like neutrophils, characteristic of inflammation

Cellular Response Key Points

Margination: As blood flow slows, leukocytes move to the periphery of blood vessels.
Endothelial cell activation: Cytokines activate endothelial cells, causing selectins and other mediators to surface.
Rolling: Neutrophils transiently adhere to endothelial cells, facilitated by selectins.
Neutrophil activation: Triggered by chemokines, like IL-8, preparing neutrophils for firm adhesion.
Firm adhesion (pavementing): Through ICAM-1-LFA-1 binding neutrophils firmly adhere to endothelium.
Transmigration: Mediated by PECAM-1, neutrophils crawl through endothelial gaps (diapedesis).
Chemotaxis: Movement towards the injury site guided by chemokines.

Neutrophil Functions

Primary granules: Contain myeloperoxidase (MPO) and other enzymes.
Secondary granules: Include collagenase and CHI3L1 (chitinase 3-like 1).
Tertiary granules: Contain MMPs and other enzymes.
Cell surface receptors: Recognize pathogen-associated molecular patterns (PAMPs) from pathogens and damage-associated molecular patterns (DAMPs) from damaged cells.

Neutrophil Antimicrobial Mechanisms

Phagocytosis: Engulfing microorganisms into a phagosome that fuses with a lysosome to form a phagolysosome for degradation.
Microorganism destruction: Reactive oxygen species (ROS) are produced, including superoxide ion (O2-), hydrogen peroxide (H2O2), hypochlorous acid (HOCL), hydroxyl radical (OH), and nitric oxide (NO).
Degranulation: Release of granule contents into the environment, potentially leading to tissue damage.
Neutrophil extracellular traps (NETs): DNA fibers, histones, and other components form traps to capture pathogens.

Reactive Oxygen Species (ROS)

Eliminate bacteria
Cause tissue damage

Chemical Mediators of Inflammation

Bind to cell surface receptors, although some have direct enzymatic or toxic activity.
All mediators are tightly regulated.

Vasoactive Amines

Histamine:
- Found in mast cells, basophils, and platelets.
- Causes arteriolar dilation and venular endothelial contraction, increasing vascular permeability.
Serotonin:
- Vasoactive effects similar to histamine.
- Found in platelets.
- Released during platelet aggregation.

Complement System

Classical pathway: Requires antibodies for activation (Ag-Ab complex)
- C1 binds to IgG or IgM bound to antigens
Alternative pathway: Does not require antibodies for activation

Membrane Attack Complex (MAC)

Complements system component that forms pores in cell membranes, leading to cell lysis.

Complement Role in Inflammation

C3a and C5a: Act as anaphylatoxins, triggering mast cell degranulation, histamine release, and other inflammatory responses.

Blood Coagulation System

Factor XII: Activated by inflammation, initiating the coagulation cascade.

Kallikrein-Bradykinin System

Bradykinin:
- Causes vasodilation, increased vascular permeability, and pain.
- Plays a role in the inflammatory response.

Arachidonic Acid Pathway

Cyclooxygenase (COX) pathway: Produces prostaglandins, thromboxanes, and prostacyclins.
Lipoxygenase pathway: Generates leukotrienes and lipoxins.
Prostaglandins: Involved in vasodilation, pain, and fever.
Leukotrienes: Attract neutrophils and cause bronchoconstriction.
Lipoxins: Anti-inflammatory mediators.

Fever

Beneficial effects:
- Shifts the oxygen-dissociation curve to the right, increasing oxygen availability.
- Creates an unfavorable environment for bacterial and viral reproduction.

Effects of Inflammation

Beneficial:
- Dilution of toxins
- Stimulation of adaptive immunity, antibody delivery
- Nutrient and oxygen supply, drug transport
- Fibrin formation, delaying bacterial spread
- Destruction of microbial agents
- Removal of tissue debris
Harmful:
- Mechanical effects (e.g., epiglottitis)
- Impaired flow (e.g., acute meningitis)
- Impaired function
- Tissue destruction

Outcomes of Acute Inflammation

Resolution: Healing and repair
Abscess formation: Walled-off collection of pus
** Progression to chronic inflammation:** Persistent inflammation with a shift in cell types.

Inflammation

A reaction of a vascularized living tissue to injury
Protective response to eliminate the source of injury and infected cells
Plays a role in tissue repair
Inflammatory lesions often indicated by the suffix "itis"

Aims of inflammation

Localize and eliminate the causative agent
Limit tissue injury
Begin the process of healing

Causes of inflammation

Infectious agents
Physical agents
Chemical agents
Immune reactions
Necrotic tissue

Types of Inflammation

Acute
- Immediate and early response to injury
- Characterized by fluid and protein
- Predominantly involves Polymorphonuclear cells (neutrophils)
Chronic
- Onset takes weeks to years
- Characterized by Mononuclear cells (macrophages, lymphocytes and plasma cells)

Five classic signs of acute inflammation

Heat (Calor)
Redness (Rubor)
Swelling (Tumor)
Pain (Dolor)
Loss of function (Function laesa)

Two major events in acute inflammation

Vascular response
- Transient vasoconstriction, followed by vasodilatation
- Increased vascular permeability
Cellular response
- Extravasation of neutrophils (polymorphonuclear leucocytes)

Reasons for increased vascular permeability

Increased hydrostatic pressure (pushing fluid out of blood vessels)
Decreased intravascular osmotic pressure (less pulling power inside blood vessels)
Endothelial cell changes (vessel walls become leaky)
Contraction (cells shrink, creating gaps)
Junctional retraction (connections between cells pull back)
Injury (damage to cells creates gaps)

Outcomes of increased vascular permeability

Transudate
- Watery fluid with few proteins
- Occurs due to imbalances in pushing and pulling pressures
Exudate
- Thicker fluid, rich in proteins and often with immune cells (neutrophils)
- Forms during inflammation

Key points of cellular response

Margination: As blood slows, leucocytes move from the center of the vessel towards the periphery
Endothelial cell activation: Cytokines activate the endothelium causing selectins and other mediators to move to the surface
Rolling: Neutrophils transiently adhere to endothelial cells, facilitated by selectins molecules
Neutrophil activation: Mediated by chemokines, for example IL-8
Firm adhesion (pavementing): Mediated by ICAM-1-LFA-1 (integrin molecules)
Transmigration: Mediated by PECAM-1 ... diapedesis (cells crawling through endothelial gaps)
Chemotaxis: Movement towards the site of injury, mediated by chemokines

Functions of neutrophils

Primary granules: contain myeloperoxidases (MPO) and other enzymes
Secondary granules: contain collagenase and CHI3L1 (chitinase 3-like 1)
Tertiary granules: contain MMPs (matrix metalloproteinases) and other enzymes
Neutrophils express cell surface receptors that recognize PAMPs (produced by infectious agents) and DAMPs (from injured and dead cells)

Antimicrobial mechanisms of neutrophils

Phagocytosis: Ingestion of microorganisms into a phagocytic vacuole, which fuses with a lysosome to form a phagolysosome. Microorganisms are destroyed by oxidative burst, with oxygen consumption and glycogenolysis
Degranulation: Release of granule contents to the environment (which can damage tissue)
Neutrophil extracellular traps (NETs): Formed by DNA fibres, histones, etc.

Reactive oxygen species (ROS)

Generated by neutrophils
Eliminate bacteria
Contribute to tissue damage

Chemical mediators of inflammation

Most bind to cell surface receptors, some have direct enzymatic or toxic activity
Tightly regulated

Vasoactive Amines

Histamine
- Found in mast cells, basophils and platelets
- Promotes arteriolar dilation and venular endothelial contraction, increasing vascular permeability
Serotonin
- Vasoactive effects similar to histamine
- Found in platelets
- Released when platelets aggregate

Complement system

Essential part of innate immunity
Classical Pathway: Requires antibodies to activate (Ag-Ab complex) C1 binds to IgG or IgM that is bound to antigen)
Alternative Pathway: Does not require antibody to activate

Membrane attack complex (MAC)

Forms pores in cell membranes, leading to cell lysis

Role of C3a and C5a in inflammation

Act as anaphylatoxins by inducing mast cell degranulation and histamine release
C5a also acts as a chemoattractant for neutrophils

Blood coagulation system

Plays a role in inflammation via factor XII activation

Kallikrein-Bradykinin system

Activated by Factor XII
Bradykinin causes vasodilation, increased vascular permeability and pain

Arachidonic Acid pathway

Produces inflammatory mediators:
- Prostaglandins: Vasodilation, pain, fever
- Leukotrienes: Vasoconstriction, bronchospasm, increased vascular permeability
- Lipoxins: Anti-inflammatory effects

Fever

Beneficial effects:
- Shifts oxygen-dissociation curve right, increasing oxygen availability
- Creates a hostile environment for bacterial and viral reproduction

Effects of inflammation

Beneficial:
- Dilution of toxins
- Stimulation of adaptive immunity
- Delivery of nutrients and oxygen
- Formation of fibrin (delays bacterial spread)
- Destruction of microbial agents
- Removal of tissue debris
Harmful:
- Mechanical effects (e.g., epiglottitis)
- Impaired flow (e.g., acute meningitis)
- Impaired function
- Tissue destruction

Outcomes of acute inflammation

Resolution: Healing and repair
Abscess formation: Walled-off collection of pus
Progression to chronic inflammation

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Description

This quiz explores the various aspects of inflammation, including its causes, types, and purposes in the body. You will learn about the body's protective response to injury and the mechanisms involved in healing. Test your knowledge on acute and chronic inflammation and their implications.