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Questions and Answers
Reactive oxygen species are primarily responsible for eliminating bacteria.
Reactive oxygen species are primarily responsible for eliminating bacteria.
True (A)
Histamine promotes arteriolar contraction and venular dilation.
Histamine promotes arteriolar contraction and venular dilation.
False (B)
The classical pathway of the complement system requires antibodies to activate.
The classical pathway of the complement system requires antibodies to activate.
True (A)
Fever has harmful effects only and does not provide any benefits.
Fever has harmful effects only and does not provide any benefits.
Abscess formation is characterized by a walled-off collection of pus.
Abscess formation is characterized by a walled-off collection of pus.
Inflammation is a response intended to eliminate the initial cause of cell injury.
Inflammation is a response intended to eliminate the initial cause of cell injury.
Acute inflammation lasts for several weeks to years.
Acute inflammation lasts for several weeks to years.
Chronic inflammation is characterized by the presence of neutrophils.
Chronic inflammation is characterized by the presence of neutrophils.
The five classic signs of acute inflammation include calor and rubor.
The five classic signs of acute inflammation include calor and rubor.
Increased vascular permeability can be caused by endothelial cell changes.
Increased vascular permeability can be caused by endothelial cell changes.
Polymorphonuclear cells are primarily associated with chronic inflammation.
Polymorphonuclear cells are primarily associated with chronic inflammation.
Inflammation does not play any role in the healing process.
Inflammation does not play any role in the healing process.
Necrotic tissue can be a cause of inflammation.
Necrotic tissue can be a cause of inflammation.
Contraction causes cells to shrink and create gaps.
Contraction causes cells to shrink and create gaps.
Transudate is a thick fluid rich in proteins.
Transudate is a thick fluid rich in proteins.
Neutrophils roll along endothelial cells during the rolling phase mediated by selectins.
Neutrophils roll along endothelial cells during the rolling phase mediated by selectins.
The primary granules of neutrophils contain collagenase.
The primary granules of neutrophils contain collagenase.
Neutrophils identify pathogens through receptors that recognize PAMPs and DAMPs.
Neutrophils identify pathogens through receptors that recognize PAMPs and DAMPs.
Degranulation in neutrophils results in the ingestion of microorganisms.
Degranulation in neutrophils results in the ingestion of microorganisms.
Exudate forms during inflammation and is rich in proteins.
Exudate forms during inflammation and is rich in proteins.
Oxidative burst involves a sudden decrease in oxygen consumption.
Oxidative burst involves a sudden decrease in oxygen consumption.
Acute inflammation may last for several weeks to years.
Acute inflammation may last for several weeks to years.
Chronic inflammation is characterized by the presence of mononuclear cells.
Chronic inflammation is characterized by the presence of mononuclear cells.
The five classic signs of acute inflammation include dolor and function laesa.
The five classic signs of acute inflammation include dolor and function laesa.
The vascular response in acute inflammation involves immediate vasodilatation followed by vasoconstriction.
The vascular response in acute inflammation involves immediate vasodilatation followed by vasoconstriction.
A major event in acute inflammation is the extravasation of mononuclear cells.
A major event in acute inflammation is the extravasation of mononuclear cells.
Increased vascular permeability can result from decreased intravascular osmotic pressure.
Increased vascular permeability can result from decreased intravascular osmotic pressure.
Heat, also known as calor, is one of the classic signs of chronic inflammation.
Heat, also known as calor, is one of the classic signs of chronic inflammation.
Immune reactions can be a cause of inflammation.
Immune reactions can be a cause of inflammation.
Margination occurs when leukocytes move towards the center of the vessel as blood flow decreases.
Margination occurs when leukocytes move towards the center of the vessel as blood flow decreases.
Exudate is generally a thinner fluid with few immune cells that forms during inflammation.
Exudate is generally a thinner fluid with few immune cells that forms during inflammation.
Neutrophil activation can be mediated by cytokines such as IL-8.
Neutrophil activation can be mediated by cytokines such as IL-8.
Degranulation refers to the ingestion of microorganisms by neutrophils.
Degranulation refers to the ingestion of microorganisms by neutrophils.
Neutrophil extracellular traps (NETs) are primarily composed of DNA fibers and proteins.
Neutrophil extracellular traps (NETs) are primarily composed of DNA fibers and proteins.
Transmigration of leukocytes occurs through the process known as diapedesis.
Transmigration of leukocytes occurs through the process known as diapedesis.
Reactive oxygen species are only produced as a minor byproduct during the oxidative burst.
Reactive oxygen species are only produced as a minor byproduct during the oxidative burst.
The primary granules of neutrophils are primarily myeloperoxidases.
The primary granules of neutrophils are primarily myeloperoxidases.
Serotonin has vasoactive effects that are opposite to those of histamine.
Serotonin has vasoactive effects that are opposite to those of histamine.
The alternative pathway of the complement system requires antibodies for activation.
The alternative pathway of the complement system requires antibodies for activation.
Fever provides a hostile environment for bacterial and viral reproduction, which is considered a beneficial effect.
Fever provides a hostile environment for bacterial and viral reproduction, which is considered a beneficial effect.
Reactive oxygen species (ROS) primarily promote tissue healing and repair.
Reactive oxygen species (ROS) primarily promote tissue healing and repair.
Abscess formation is defined as the resolution of inflammation and complete healing of tissue.
Abscess formation is defined as the resolution of inflammation and complete healing of tissue.
Acute inflammation is characterized by the presence of mononuclear cells such as macrophages and lymphocytes.
Acute inflammation is characterized by the presence of mononuclear cells such as macrophages and lymphocytes.
The term 'itis' is used to indicate the presence of inflammatory lesions in tissues.
The term 'itis' is used to indicate the presence of inflammatory lesions in tissues.
Increased hydrostatic pressure during inflammation causes fluid to be retained within blood vessels.
Increased hydrostatic pressure during inflammation causes fluid to be retained within blood vessels.
The two major events in acute inflammation include a vascular response and a cellular response.
The two major events in acute inflammation include a vascular response and a cellular response.
The classic signs of acute inflammation include calor, dolor, and myelitis.
The classic signs of acute inflammation include calor, dolor, and myelitis.
Transudate is a fluid that is rich in proteins and forms during the inflammation process.
Transudate is a fluid that is rich in proteins and forms during the inflammation process.
Chronic inflammation can last from weeks to years and primarily features neutrophils.
Chronic inflammation can last from weeks to years and primarily features neutrophils.
Cytokines play a crucial role in mediating the activation of neutrophils during the inflammatory response.
Cytokines play a crucial role in mediating the activation of neutrophils during the inflammatory response.
Neutrophils primarily utilize degranulation as a mechanism to destroy pathogens.
Neutrophils primarily utilize degranulation as a mechanism to destroy pathogens.
Transudate is characterized by its high protein content and is primarily produced during inflammation.
Transudate is characterized by its high protein content and is primarily produced during inflammation.
Neutrophil rolling along endothelial cells is primarily facilitated by selectins that engage with their receptors.
Neutrophil rolling along endothelial cells is primarily facilitated by selectins that engage with their receptors.
Margination refers to leukocytes moving from the periphery of the blood vessel towards the center as blood flow decreases.
Margination refers to leukocytes moving from the periphery of the blood vessel towards the center as blood flow decreases.
Neutrophil extracellular traps (NETs) are mainly composed of histones and lipids.
Neutrophil extracellular traps (NETs) are mainly composed of histones and lipids.
Cytokines play a role in the activation of endothelial cells, leading to the expression of selectins on their surface.
Cytokines play a role in the activation of endothelial cells, leading to the expression of selectins on their surface.
The oxidative burst in neutrophils involves a rapid decrease in the production of reactive oxygen species.
The oxidative burst in neutrophils involves a rapid decrease in the production of reactive oxygen species.
Diapedesis describes the process where leukocytes pass through the endothelial wall, also known as transmigration.
Diapedesis describes the process where leukocytes pass through the endothelial wall, also known as transmigration.
The membrane attack complex functions by puncturing the bacterial membrane.
The membrane attack complex functions by puncturing the bacterial membrane.
Serotonin, found in mast cells, elevates blood pressure by inducing venular dilation.
Serotonin, found in mast cells, elevates blood pressure by inducing venular dilation.
The kinin system plays a role in the production of reactive oxygen species.
The kinin system plays a role in the production of reactive oxygen species.
The alternative pathway of the complement system requires antibody binding to activate.
The alternative pathway of the complement system requires antibody binding to activate.
Fever is an adaptive response that enhances the availability of oxygen during inflammation.
Fever is an adaptive response that enhances the availability of oxygen during inflammation.
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Study Notes
Inflammation
- Inflammation is the reaction of vascularized living tissue to local injury.
- A protective response intended to eliminate the initial cause of cell injury and the necrotic cells and tissues arising from the injury.
- May be harmful.
- Intimately associated with the repair process.
- Inflammatory lesions designated by the suffix "(ITIS)".
Inflammation Purpose
- Localise 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 - minutes to days.
- Immediate and early response to injury.
- Characterized by fluid and protein.
- Polymorphonuclear cells (neutrophils).
- Chronic - weeks to years.
- 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).
Increased Vascular Permeability
- Increased hydrostatic pressure (increased "pushing pressure" inside blood vessels that forces fluid out).
- Decreased intravascular osmotic pressure (less "pulling power" inside the blood vessels to retain the fluid).
- Endothelial cell changes.
- Contraction.
- Junctional retraction.
- Injury.
Outcomes of Increased Vascular Permeability
- Transudate: Watery fluid with few proteins (imbalance in pushing and pulling pressures).
- Exudate: Thicker fluid rich in proteins and often with immune cells like neutrophils (during inflammation).
Cellular Response - Key Points
- 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 roll along and transiently adhere to the endothelial cells, mediated by selectin molecules (transiently bind to their receptors).
- Neutrophil activation: Mediated e.g., by IL-8.
- Firm adhesion (pavementing): Mediated by ICAM-1-LFA-1.
- Transmigration: mediated by PECAM-1…diapedesis (cells crawling).
- Chemotaxis: Movement toward the site of injury mediated by chemokines.
Functions of Neutrophils
- Primary granules: Myeloperoxidases (MPO) and others.
- Secondary granules: Collagenase and CHI3L1 (also known as chitinase 3-like 1).
- Tertiary granules: MMPs and others.
- Neutrophils express cell surface receptors that recognize pathogen-associated molecular patterns (PAMPs) produced by infectious agents and damage-associated molecular patterns (DAMPs) from injured and dead cells.
Antimocrobial Mechanisms of Neutrophils
- Phagocytosis: Ingestion of the microorganism into a phagocytic vacuole, fuses with lysosome to form phagolysosome. Microorganism is destroyed by oxidative burst with a sudden increase in oxygen consumption and glycogenolysis. Reactive oxygen species are released - superoxide ion O2-, hydrogen peroxide (H2O2), hypochlorous acid (HOCL), hydroxyl radical (OH), nitric oxide (NO).
- Degranulation: Release of granule contents to the environment (tissue damage).
- Neutrophil extracellular traps (NETs): Formed by DNA fibers, histones, etc.
Reactive Oxygen Species
- Elimination of bacteria
- Tissue damage.
Chemical Mediators of Inflammation
- Most bind to cell surface receptors, but some have direct enzymatic or toxic activity.
- All are tightly regulated.
Vasoactive Amines
- Histamine: Found in mast cells, basophils, and platelets. Promotes arteriolar dilation and venular endothelial contraction resulting in widening of inter-endothelial cell junctions with increased vascular permeability.
- Serotonin: Vasoactive effects similar to histamine. Found in platelets. Released when platelets aggregate.
Complement System
- 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)
- Punches a hole in the membrane.
Role in Inflammation (C3A and C5A)
- C3a & C5a are anaphylatoxins:
- Induce degranulation of mast cells (release histamine).
- Increase vascular permeability.
- Attract leucocytes.
- C5a also:
- Activates neutrophils, macrophages, and endothelial cells.
- Can be chemotactic for neutrophils.
- Increase phagocytosis.
Blood Coagulation System
- Factor XII is activated by inflammation.
Kallikrein-Bradykinin System
- Prekallikrein: Activates to kallikrein by exposure to negatively charged surfaces (e.g., collagen, activated platelets, bacterial cell walls).
- Kallikrein: Activated by Factor XII.
- Bradykinin: Increases vascular permeability. Induces pain.
Arachidonic Acid Pathway
- Cyclooxygenase (COX) pathway: Produces prostaglandins (PGI2, PGE2, TXA2). Involved in vasodilation, increased vascular permeability, pain, and fever.
- Lipoxygenase (LOX) pathway: Produces leukotrienes (LTB4, LTC4, LTD4, LTE4). Important in chemotaxis, vasoconstriction, bronchospasm, and increased vascular permeability.
Fever
- Beneficial effects of fever:
- Oxygen-dissociation curve is shifted right.
- More oxygen is available.
- 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 agent.
- Removal of tissue debris.
- Harmful:
- Mechanical effect e.g., epiglottitis.
- Impaired flow e.g., acute meningitis.
- Impaired function.
- Tissue destruction.
Outcomes of Acute Inflammation
- Resolution: Healing and repair.
- Abscess formation: Abscess is a walled-off collection of pus.
- Progression to chronic inflammation.
Inflammation Definition
- A reaction of a vascularised living tissue to local injury.
- A protective response intending to eliminate the cause of injury and necrotic cells and tissues.
- May be harmful.
- Inflammation is closely linked to the repair process.
- Inflammatory lesions are usually indicated by the suffix "itis".
- The purpose of inflammation is to localise and eliminate the causative agent, limit tissue injury, and begin the process of healing.
Causes of Inflammation
- Infectious agents
- Physical agents
- Chemical agents
- Immune reactions
- Necrotic tissue
Types of Inflammation
- Acute inflammation:
- Occurs within minutes to days.
- An immediate and early response to injury.
- Characterized by fluid and protein.
- Dominant cell type is the polymorphonuclear cell (neutrophil).
- Chronic inflammation:
- Lasts for 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 of Acute Inflammation
- Vascular response:
- Transient vasoconstriction followed by vasodilatation.
- Increased vascular permeability.
- Cellular response:
- Extravasation of neutrophils (polymorphonuclear leucocytes).
Increased Vascular Permeability
- Increased hydrostatic pressure: Increased "pushing pressure" inside blood vessels, forcing fluid out.
- Decreased intravascular osmotic pressure: Reduced "pulling power" inside blood vessels to retain fluid.
- Endothelial cell changes: Vessel walls become leaky due to changes in endothelial cells.
- Contraction: Cells shrink, creating gaps.
- Junctional retraction: Connections between cells pull back, creating spaces.
- Injury: Damage to endothelial cells can lead to gaps.
Increased Vascular Permeability Outcomes
- Transudate: Watery fluid with few proteins. Forms when there's an imbalance in pushing and pulling pressures.
- Exudate: Thicker fluid, rich in proteins and immune cells (like neutrophils). Forms during inflammation.
Cellular Response: Key Points
- Margination: As blood slows down, leucocytes move from the center of the vessel towards the periphery.
- Endothelial cell activation: Cytokines activate the endothelium, causing selectins and other mediators to appear on the surface.
- Rolling: Neutrophils roll along and transiently adhere to endothelial cells, mediated by selectin molecules (transiently bind to their receptors).
- Neutrophil activation: Mediated by IL-8.
- Firm adhesion (pavementing): Mediated by ICAM-1-LFA-1.
- Transmigration: Mediated by PECAM-1 (diapedesis, cells crawling).
- Chemotaxis: Movement toward the site of injury mediated by chemokines.
Neutrophil Functions
- Primary granules: Myeloperoxidases (MPO) and other enzymes.
- Secondary granules: Collagenase and CHI3L1 (chitinase 3-like 1).
- Tertiary granules: MMPs and others.
- Neutrophils express cell surface receptors that recognize pathogen-associated molecular patterns (PAMPs) produced by infectious agents and damage-associated molecular patterns (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. The microorganism is destroyed by the oxidative burst, with a sudden increase in oxygen consumption and glycogenolysis; reactive oxygen species are released:
- Superoxide ion (O2-)
- Hydrogen peroxide (H2O2)
- Hypochlorous acid (HOCL)
- Hydroxyl radical (OH)
- Nitric oxide (NO)
- Degranulation: Release of granule contents to the environment (tissue damage).
- Neutrophil extracellular traps (NETs): Formed by DNA fibers, histones, etc.
Reactive Oxygen Species
- Involved in the elimination of bacteria.
- Can cause tissue damage.
###Chemical Mediators of Inflammation
- Most bind to cell surface receptors, but some have direct enzymatic or toxic activity.
- All are tightly regulated.
Vasoactive Amines
- Histamine: Found in mast cells, basophils, and platelets. Promotes arteriolar dilation and venular endothelial contraction, resulting in a widening of inter-endothelial cell junctions with increased vascular permeability.
- Serotonin: Vasoactive effects similar to histamine; found in platelets; released when platelets aggregate.
- Complement system:
- 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)
- Punches a hole in the membrane of target cells.
Role in Inflammation (C3A and C5A)
- C3A and C5A: Anaphylatoxins; induce mast cell degranulation, histamine release, and increased vascular permeability.
Blood Coagulation System
- Factor XII is activated by inflammation.
Kallikrein-Bradykinin System
- Bradykinin: Causes vasodilation; increases vascular permeability; induces pain.
Arachidonic Acid Pathway
- Involved in the production of prostaglandins, leukotrienes, and thromboxanes: Inflammatory mediators.
Fever (Beneficial Effects)
- Oxygen-dissociation curve is shifted right, making more oxygen available.
- Creates 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 effect (e.g., epiglottitis).
- Impaired flow (e.g., acute meningitis).
- Impaired function.
- Tissue destruction.
Outcomes of Acute Inflammation
- Resolution: Healing and repair.
- Abscess formation: A walled-off collection of pus.
- Progression to chronic inflammation
Inflammation
- A reaction of a vascularized living tissue to local injury.
- A protective response to eliminate the cause of cell injury, necrotic cells and tissues.
- May be harmful.
- Intimately associated with the repair process.
- Inflammatory lesions are usually indicated by the suffix (ITIS).
Purpose 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: Minutes to days.
- Immediate and early response to injury.
- Characterized by fluid and protein.
- Polymorphonuclear cells (neutrophils).
- Chronic: Weeks to years.
- 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 of Acute Inflammation
- Vascular response: Transient vasoconstriction followed by vasodilatation. Increased vascular permeability.
- Cellular response: Extravasation of neutrophils (polymorphonuclear leukocytes).
Increased Vascular Permeability
- Increased hydrostatic pressure: Increased "pushing pressure" inside blood vessels that forces fluid out.
- Decreased intravascular osmotic pressure: Less "pulling power" inside the blood vessels to retain fluid.
- Endothelial cell changes: Make the vessel walls leaky.
- Contraction: Cells shrink, creating gaps.
- Junctional retraction: The connections between cells pull back, creating spaces.
- Injury: Damage to these cells can lead to gaps.
Outcomes of Increased Vascular Permeability
- Transudate: Watery fluid with few proteins. Forms when there is mainly an imbalance in pushing and pulling pressures.
- Exudate: Thicker fluid, rich in proteins and often with immune cells like neutrophils. Forms during inflammation.
Cellular Response: Key Points
- Margination: As blood slows, leukocytes 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 roll along and transiently adhere to endothelial cells, mediated by selectins molecules (transiently bind to their receptors).
- Neutrophil activation: Mediated by IL-8.
- Firm adhesion (pavementing): Mediated by ICAM-1-LFA-1.
- Transmigration: Mediated by PECAM-1…diapedesis (cells crawling).
- Chemotaxis: Movement toward the site of injury mediated by chemokines.
Functions of Neutrophils
- Primary granules: Myeloperoxidases (MPO), and others.
- Secondary granules: Collagenase and CHI3L1, also known as chitinase 3-like 1.
- Tertiary granules: MMPs and others.
- Neutrophils express cell surface receptors that recognize pathogen-associated molecular patterns (PAMPs) produced by infectious agents and damage-associated molecular patterns (DAMPs) from injured and dead cells.
Antimicrobial Mechanisms of Neutrophils
- Phagocytosis: Ingestion of the microorganism into a phagocytic vacuole, fuses with lysosome to form phagolysosome. Microorganism is destroyed by oxidative burst with a sudden increase in oxygen consumption and glycogenolysis reactive oxygen species are released - superoxide ion O2-, hydrogen peroxide (H2O2), hypochlorous acid (HOCL), hydroxyl radical (OH), nitric oxide (NO).
- Degranulation: Release of granule contents to the environment (tissue damage).
- Neutrophil extracellular traps (NETs): Formed by DNA fibres, histones, etc.
Reactive Oxygen Species
- Elimination of bacteria.
- Tissue damage.
Chemical Mediators of Inflammation
- Most bind to cell surface receptors, but some have direct enzymatic or toxic activity. All are tightly regulated.
Vasoactive Amines
- Histamine: Found in mast cells, basophils, and platelets. Promotes arteriolar dilation and venular endothelial contraction. Results in widening of inter-endothelial cell junctions with increased vascular permeability.
- Serotonin: Vasoactive effects similar to histamine. Found in platelets. Released when platelets aggregate.
Complement System
- 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
- Punches a hole in the membrane.
Role in Inflammation: C3a and C5a
- C3a and C5a: Increase vascular permeability and contraction of smooth muscle.
Blood Coagulation System
- Factor XII is activated by inflammation.
Kallikrein-Bradykinin System
- Kallikrein: Converts kininogen to bradykinin.
- Bradykinin: Increases vascular permeability, pain, and smooth muscle contraction.
Arachidonic Acid Pathway
- Cyclooxygenase (COX) pathway: Produces prostaglandins and thromboxanes.
- Lipoxygenase pathway: Produces leukotrienes and lipoxins.
- Prostaglandins: Vasodilation, pain, fever.
- Thromboxanes: Platelet aggregation and vasoconstriction.
- Leukotrienes: Bronchoconstriction, increased vascular permeability, chemotaxis.
- Lipoxins: Inhibit neutrophil chemotaxis and inflammation.
Fever
- Beneficial effects of fever:
- Oxygen-dissociation curve is shifted right. More oxygen is available.
- 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 agent.
- Removal of tissue debris.
- Harmful:
- Mechanical effect e.g., epiglottitis.
- Impaired flow e.g., acute meningitis.
- Impaired function.
- Tissue destruction
Outcomes of Acute Inflammation
- Resolution: Healing and repair.
- Abscess formation: Abscess is a walled-off collection of pus.
- Progression to chronic inflammation.
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