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Questions and Answers
What is the primary purpose of inflammation?
What is the primary purpose of inflammation?
Which of the following is NOT a cardinal sign of inflammation?
Which of the following is NOT a cardinal sign of inflammation?
What causes the redness associated with inflammation?
What causes the redness associated with inflammation?
Which mediator is responsible for the pain experienced during inflammation?
Which mediator is responsible for the pain experienced during inflammation?
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What does tumor refer to in the context of inflammation?
What does tumor refer to in the context of inflammation?
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What is a potential consequence if inflammation does not occur?
What is a potential consequence if inflammation does not occur?
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Which type of inflammation is caused by physical injury?
Which type of inflammation is caused by physical injury?
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What role do prostaglandins play in inflammation?
What role do prostaglandins play in inflammation?
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What is the first step in the process of phagocytosis?
What is the first step in the process of phagocytosis?
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Which component enhances the recognition and attachment of microorganisms by phagocytic cells?
Which component enhances the recognition and attachment of microorganisms by phagocytic cells?
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What forms when the plasma membrane of a phagocyte pinches off during engulfment?
What forms when the plasma membrane of a phagocyte pinches off during engulfment?
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Which of the following is NOT involved in oxygen-independent killing mechanisms during phagocytosis?
Which of the following is NOT involved in oxygen-independent killing mechanisms during phagocytosis?
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What role do acid hydrolases play in the phagocytosis process?
What role do acid hydrolases play in the phagocytosis process?
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What is the first major event in acute inflammation?
What is the first major event in acute inflammation?
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Which of the following best describes edema?
Which of the following best describes edema?
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What triggers vasodilation during the acute inflammatory response?
What triggers vasodilation during the acute inflammatory response?
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Which component is NOT part of the cellular events in acute inflammation?
Which component is NOT part of the cellular events in acute inflammation?
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What is the purpose of pattern recognition receptors in immune response?
What is the purpose of pattern recognition receptors in immune response?
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What causes the increased permeability of microvasculature in acute inflammation?
What causes the increased permeability of microvasculature in acute inflammation?
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Which of these is a consequence of the recruitment of leukocytes during acute inflammation?
Which of these is a consequence of the recruitment of leukocytes during acute inflammation?
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What phase follows the removal of the offending agent in the inflammatory response?
What phase follows the removal of the offending agent in the inflammatory response?
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What is the first step in the process of leukocyte extravasation?
What is the first step in the process of leukocyte extravasation?
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Which type of cell is involved in the Rolling step of extravasation?
Which type of cell is involved in the Rolling step of extravasation?
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What mediates the adhesion of leukocytes to endothelial cells during extravasation?
What mediates the adhesion of leukocytes to endothelial cells during extravasation?
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What is the role of chemotactic agents in leukocyte activation?
What is the role of chemotactic agents in leukocyte activation?
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What is the primary type of leukocyte that emigrates within the first 6-24 hours of an inflammatory response?
What is the primary type of leukocyte that emigrates within the first 6-24 hours of an inflammatory response?
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What facilitates the transmigration of leukocytes across the endothelium?
What facilitates the transmigration of leukocytes across the endothelium?
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Which of the following can act as a chemotactic agent?
Which of the following can act as a chemotactic agent?
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What is a common result of leukocyte activation during the inflammatory process?
What is a common result of leukocyte activation during the inflammatory process?
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Study Notes
Lecture 7: Inflammation: Introduction & Acute Inflammation
- Learning Outcomes: Students will be able to define inflammation and discuss the events and components of an acute inflammatory response.
What is Inflammation?
- Inflammation is an inflammatory response to tissue injury.
- Types of inflammation resulting in inflammation include: appendicitis (appendix inflammation), gastritis (stomach inflammation), and arthritis (joint inflammation).
Inflammation: Overview
- Inflammation is a protective response.
- Its goals are to eliminate the initial cause of injury (e.g., bacteria, toxins), the consequences of cell injury (e.g., necrotic cells), and initiate the repair process.
- Without inflammation, infections would not be controlled, wounds would never heal, and injured tissue would remain open sores.
Cardinal Signs of Inflammation
- Calor (Heat): Due to vasodilation (increased blood flow) from histamine, prostaglandins, and bradykinin.
- Rubor (Redness): Increased blood flow.
- Tumor (Swelling/Edema): Fluid accumulation due to increased permeability and tissue damage, especially from histamine, tissue damage.
- Dolor (Pain): Release of chemicals (e.g., bradykinin and PGE2) which stimulate nerve endings.
- Functio Laesa (Loss of Function): Increased pain and swelling.
Causes and Types of Inflammation
- Infections: Bacterial, viral, fungal, parasitic.
- Tissue Necrosis: Ischemia (lack of blood supply), physical/chemical injury, trauma.
- Foreign Bodies: Sutures, splinters, dirt.
- Immune Reactions: Hypersensitivity, autoimmune diseases.
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Types:
- Acute inflammation (initial response)
- Chronic inflammation (long-term response)
- Granulomatous inflammation (a type of chronic inflammation)
The Steps of Inflammatory Response
- Recognition: Host cells recognize the offending agent.
- Recruitment: Leukocytes and plasma proteins move to the site of injury.
- Removal: Activated leukocytes eliminate the offending agent.
- Regulation: Termination of the response.
- Repair: Damaged tissue is repaired.
Acute Inflammation
- Vascular Changes: Vasodilation (increased blood flow).
- Microvascular Changes: Increased vascular permeability (plasma proteins and white blood cell leakage).
- Cellular Events: WBC emigration, accumulation, and activation at the site of injury.
- Chemical Mediators: Derived from plasma proteins and cells.
Recognition of Microbes, Necrotic Cells, and Foreign Substances
- Danger signals are triggered from microbes and dead cells.
- Phagocytes, dendritic cells, and epithelial cells express pattern recognition receptors that recognize infectious agents.
- Examples include: toll-like receptors (TLRs), inflammasomes, Fc receptors, and the complement system (lectin).
I. Vascular Changes: Alteration in Vascular Flow and Caliber
- Earliest manifestation is vasodilation, which is induced by histamine and nitric oxide.
- Vasodilation leads to increased blood flow resulting in redness (rubor) and heat (color).
II. Microvascular Changes: Increased Permeability of Microvasculature
- A hallmark of acute inflammation.
- Caused by histamine, kinins, and other mediators.
- Increased gaps between endothelial cells lead to increased vascular permeability, allowing plasma proteins and leukocytes to escape and enter sites of infection/injury.
- Fluid leak results in edema (swelling).
What is Edema?
- Edema is the accumulation of excess fluid in interstitial tissues or serous cavities.
- It's classified into transudate (low protein) and exudate (high protein).
Differences between Transudate and Exudate
- Transudate: Low protein content, low specific gravity (<1.020), result from hydrostatic imbalance, light straw color.
- Exudate: High protein content, high specific gravity (>1.020), result from inflammation/injury, yellowish-white colored.
III. Cellular Events: WBC Extravasation and Phagocytosis
- WBCs migrate to the site of injury and exit blood vessels, a process called extravasation.
- Extravasation steps include margination, rolling, adhesion, transmigration, and chemotaxis.
Step 5: Chemotaxis and WBC Activation
- Transmigrated leukocytes migrate to sites of injury along chemotactic gradients.
- Chemotactic agents can be exogenous or endogenous.
- Examples include soluble bacterial products, components of the complement system (e.g. C5a), and cytokines (e.g IL-8, leukotrienes).
- Leukocyte type varies depending on the stimulus and age of the inflammatory response (e.g., neutrophils in early stages, macrophages later).
Leukocyte Activation
- Activated by microbes, necrotic cells, antigen-antibody complexes, and chemotactic factors.
- Activation results in production of arachidonic acid metabolites, secretion of lysosomal enzymes, degranulation, cytokine secretion, and modulation of cell adhesion molecules (CAMs).
Phagocytosis
- Process of engulfing and eliminating solid particles (e.g., bacteria, necrotic tissue, foreign material) by phagocytic cells (e.g., neutrophils, macrophages).
- Three stages: Recognition/attachment, engulfment (phagosome formation), killing/degradation (phagolysosome formation).
- Killing/degradation uses both oxygen-dependent and oxygen-independent mechanisms.
References
- Robbins and Cotran Pathologic Basis of Disease, 10th ed. (2021)
- Harsh Mohan Textbook of Pathology, 7th ed.
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Description
This quiz focuses on the introduction and acute inflammation as discussed in Lecture 7. Students will explore the definition of inflammation, its types, and the cardinal signs that characterize the inflammatory response. Understanding these concepts is crucial for comprehending how the body reacts to injury and infection.