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Questions and Answers
What is the first component of acute inflammation?
What is the first component of acute inflammation?
What characterizes microvascular changes during acute inflammation?
What characterizes microvascular changes during acute inflammation?
Which mediators of inflammation are derived from cell sources?
Which mediators of inflammation are derived from cell sources?
Which of the following is NOT a potential effect of inflammatory mediators?
Which of the following is NOT a potential effect of inflammatory mediators?
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What is the role of cytokines in inflammation?
What is the role of cytokines in inflammation?
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Which of these is an example of a plasma-derived mediator?
Which of these is an example of a plasma-derived mediator?
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What stimulates the release of other inflammatory mediators?
What stimulates the release of other inflammatory mediators?
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What is NOT a characteristic of active mediators of inflammation?
What is NOT a characteristic of active mediators of inflammation?
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What role does nitric oxide play in inflammation?
What role does nitric oxide play in inflammation?
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Which of the following are involved in plasma protein-derived mediators?
Which of the following are involved in plasma protein-derived mediators?
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What characterizes fibrinous inflammation?
What characterizes fibrinous inflammation?
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What is an example of serous inflammation?
What is an example of serous inflammation?
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Which type of inflammation is characterized by pus production?
Which type of inflammation is characterized by pus production?
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What leads to the formation of an abscess?
What leads to the formation of an abscess?
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How do plasma protein-derived mediators exist in circulation before activation?
How do plasma protein-derived mediators exist in circulation before activation?
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Which type of inflammation is associated with increased vascular permeability that allows larger molecules like fibrinogen to pass?
Which type of inflammation is associated with increased vascular permeability that allows larger molecules like fibrinogen to pass?
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What is the primary source of histamine in inflammation?
What is the primary source of histamine in inflammation?
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Which of the following mediates increased vascular permeability and chemotaxis?
Which of the following mediates increased vascular permeability and chemotaxis?
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Cytokines involved in inflammation are produced by which cells?
Cytokines involved in inflammation are produced by which cells?
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Which mediator is known for its role as a potent vasodilator?
Which mediator is known for its role as a potent vasodilator?
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What type of cytokines are produced exclusively by lymphocytes?
What type of cytokines are produced exclusively by lymphocytes?
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Which of the following is NOT a function of Platelet-Activating Factor?
Which of the following is NOT a function of Platelet-Activating Factor?
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Which mediator is mainly involved in acute inflammation and is released by activated macrophages?
Which mediator is mainly involved in acute inflammation and is released by activated macrophages?
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What is the primary role of prostaglandins during inflammation?
What is the primary role of prostaglandins during inflammation?
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Study Notes
Acute Inflammation
- Acute inflammation is a rapid response to tissue injury, characterized by four major components
- These components include vascular changes, microvascular changes, cellular events, and mediators.
Vascular Changes
- Alteration in vascular caliber results in increased blood flow, known as vasodilation
- The increased blood flow enables the movement of more cells and proteins to the affected area
Microvascular Changes
- Increased permeability of the microvasculature allows plasma proteins and white blood cells (WBCs) to leak into the injured tissue
- This leakage is crucial for the inflammatory response
Cellular Events
- Involves the recruitment, accumulation, and activation of white blood cells (WBCs) at the site of injury
- WBCs migrate to the site of injury driven by chemical signals
Mediators
- Chemical substances derived from plasma proteins and cells that trigger different processes in the inflammatory response
- The mediators are categorized into cell-derived and plasma-derived mediators
Cell-Derived Mediators
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Cell-derived mediators are differentiated according to their origin
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Some mediators are preformed and stored in granules, while other mediators are synthesized as needed
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Mediators and Sources:*
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Histamine: Mast cells, basophils, platelets
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Serotonin: Platelets
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Lysosomal enzymes: Neutrophils, macrophages
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Prostaglandins: All leukocytes, platelets, endothelial cells (ECs)
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Leukotrienes: All leukocytes
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Platelet-activating factors (PAFs): All leukocytes, ECs
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Activated oxygen species: All leukocytes
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Nitric oxide: Macrophages
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Cytokines: Lymphocytes, macrophages, ECs
Principles of Mediators
- Initially bind to specific receptors and act
- Initiate the release of other mediators
- Affect one or a few specific target cell types
- Have short lifespans
- Can be harmful (in certain contexts)
Active Mediators
- Produced in reaction to injurious stimuli, like microbial products or necrotic cells
- Include proteins from the complement, kinin, and coagulation systems activated by microbes and injured tissues
- Ensures the inflammation response is localized and triggered only when and where needed
Roles of Mediators
- Affect blood vessels
- Affect inflammatory cells
- Affect other cells within the body
- Have diverse effects on the body (vasodilation, vasoconstriction, altered permeability, activation of inflammatory cells and cells within the body)
Effects of Mediators
- Vasodilation: widening of blood vessels
- Vasoconstriction: narrowing of blood vessels
- Altered vascular permeability: increased leakage of fluid from blood vessels to affected tissue
- Activation of inflammatory cells: stimulation of white blood cells to migrate into injured tissue
- Chemotaxis: recruitment of inflammatory cells to the affected area
- Cytotoxicity: destruction of cells
- Degradation of tissue: breakdown of tissue
- Pain: sensation of pain
- Fever: elevation of body temperature
(A) Cell-Derived Mediators
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Vasoactive amines (Histamine): Most notable example; originating in mast cells, basophils, and platelets. Effects: (1) vasodilation, (2) increased venular permeability, (3) endothelial activation
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Arachidonic Acid (AA) Metabolites (Prostaglandins & Leukotrienes): Prostaglandins (PGI2, PGD2, PGE2): mediate vasodilation, pain, and fever. Leukotrienes (LTB4, LTC4, LTD4, LTE4): mediate increased vascular permeability, chemotaxis, and leukocyte adhesion and activation. Originating in mast cells and leukocytes (mainly neutrophils). Involved in all stages of inflammation
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Platelet-Activating Factors (PAFs): Produced by mast cells and other leukocytes (mainly neutrophils). Effects: vasodilation, increased vascular permeability, leukocyte adhesion, oxidative burst, chemotaxis, and induced platelet degranulation.
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Cytokines: Proteins produced by many cell types that modulate the functions of other cells. Produced by activated lymphocytes and macrophages to modulate other cell types. Involved in both acute and chronic inflammation
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Nitric Oxide (NO): A potent vasodilator. Source: Soluble gas produced by endothelial cells and macrophages. Acts as a regulator of inflammation, actively reducing the effects of other pro-inflammatory mediators.
(B) Plasma protein-derived mediators
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Circulate in an inactive form
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Require activation from an activator
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Numerous, both specific and non-specific activators
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Include natural in-activators to maintain an inflammatory balance
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Three Interrelated Protein Systems:*
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Complement: Derived from plasma
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**Bradykinin:**Derived from plasma
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Factor XII: Derived from plasma
Morphological Patterns of Acute Inflammation
- Serous: Outpouring of thin fluid from plasma or mesothelial cells; examples include skin blisters
- Fibrinous : Deposition of fibrin in extra-cellular spaces occurs with sever injuries; examples include fibrinous exudate
- Purulent (Suppurative Inflammation): Production of pus encompassing neutrophils, liquefactive necrosis, and edema fluid; caused by pyogenic bacteria like staphylococci. Often seen as localized collections (abscesses)
- Haemorrhagic: presence of blood
- Ulcers: a local defect or excavation on an organ or tissue surface; occurs when tissue necrosis and inflammation exist on, or near, a surface
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Description
This quiz explores the key aspects of acute inflammation, including vascular changes, microvascular changes, cellular events, and mediators. Understand how these components work together to respond to tissue injury and foster healing. Test your knowledge on the rapid response mechanisms involved in the inflammatory process.
