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Questions and Answers
What is the primary role of mast cells in the inflammatory response?
What is the primary role of mast cells in the inflammatory response?
What triggers the activation of the kinin system during inflammation?
What triggers the activation of the kinin system during inflammation?
What is a consequence of plasmin activity in inflammation?
What is a consequence of plasmin activity in inflammation?
Which mediator is primarily responsible for pain during inflammation?
Which mediator is primarily responsible for pain during inflammation?
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How does aspirin primarily affect the inflammatory response?
How does aspirin primarily affect the inflammatory response?
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What role do chemokines play in the inflammatory response?
What role do chemokines play in the inflammatory response?
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Which mediator is activated by immune complexes and leads to slow release during inflammation?
Which mediator is activated by immune complexes and leads to slow release during inflammation?
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What is the outcome of blocking leukotriene receptors with montelukast?
What is the outcome of blocking leukotriene receptors with montelukast?
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What effect does the activation of C3a and C5a have in the context of inflammation?
What effect does the activation of C3a and C5a have in the context of inflammation?
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What is the primary role of macrophages in inflammation?
What is the primary role of macrophages in inflammation?
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What role does plasmin play in tissue remodeling during inflammation?
What role does plasmin play in tissue remodeling during inflammation?
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Which of the following processes is NOT affected by corticosteroids in inflammation?
Which of the following processes is NOT affected by corticosteroids in inflammation?
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Which mediator is released in high concentrations to rapidly enhance vascular permeability and induce vasodilation?
Which mediator is released in high concentrations to rapidly enhance vascular permeability and induce vasodilation?
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What is the main role of chemokines during the inflammatory response?
What is the main role of chemokines during the inflammatory response?
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What is the primary effect of activated kinins in inflammation?
What is the primary effect of activated kinins in inflammation?
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Which of the following cell-derived mediators is activated through immune complexes?
Which of the following cell-derived mediators is activated through immune complexes?
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How do leukotrienes primarily affect the body during inflammation?
How do leukotrienes primarily affect the body during inflammation?
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Which component of the inflammatory response does not have an auxiliary cell-derived origin?
Which component of the inflammatory response does not have an auxiliary cell-derived origin?
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Which mediator is responsible for the delayed, slow release aspect of the inflammatory response?
Which mediator is responsible for the delayed, slow release aspect of the inflammatory response?
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What is the main consequence of inhibiting the COX pathway with ibuprofen?
What is the main consequence of inhibiting the COX pathway with ibuprofen?
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Study Notes
Inflammation
- Extravasation: Recruits immune cells to injury site; rapid process.
- Mast cells: Release histamine, increasing vascular permeability.
- Macrophages: Release IL-8, recruiting neutrophils.
- Monocytes: Turn into macrophages when leaving blood vessels.
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Plasma-derived mediators:
- Clotting system
- Kinin system
- Fibrinolytic system (plasmins)
- Complement system
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Cell-derived mediators:
- Auxiliary cells (basophils, mast cells, platelets)
- Lymphocytes
- Monocytes
- Kinins:
- Release nitric oxide (NO) for venous dilation and vascular permeability.
- Activated by Hageman factor (XIIa) during clotting, from damaged tissues and plasma enzymes.
- Produce bradykinin and lysyl-bradykinin.
- Plasmin:
- Converts plasminogen to plasmin.
- Activates matrix metalloproteinases (MMPs) for tissue remodeling.
- Promotes angiogenesis via cytokine release.
Cell-derived Mediators (cont'd)
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Cell-derived mediators:
- Mast cells, basophils, platelets: release histamine, serotonin, activating C3a and C5a (innate) and IgE adaptive immune responses.
- Rapid release via degranulation.
- Slow release of leukotrienes and prostaglandins.
- Activated by immune complexes.
- Platelet-activating factor (PAF) influences neutrophils, basophils, and macrophages.
- Type 1 and 2 hypersensitivity responses.
- Recruitment and activation of other immune cells.
- Chemokines (CCL3/MIP-1α and leukotriene B4) attract monocytes.
Pain
- Pain mediators: PAF, histamine, serotonin, prostaglandins, leukotrienes.
- Mechanism: Act on C-fibres causing poorly localized, dull, aching pain.
- Arachidonic acid pathway: Crucial in generating inflammatory mediators (prostaglandins and leukotrienes).
Anti-inflammatory Drugs
- Ibuprofen: Inhibits the COX pathway but can reduce blood flow to the stomach, leading to ulcers.
- Aspirin: Blood thinner, inhibits cyclooxygenase, affects TXA2 (vasodilation), mainly COX-2.
- Xylotol: Inhibits 5-lipoxygenase.
- Montelukast: Blocks leukotriene receptors.
- Leukotrienes: Cause airway tightening and vascular permeability; blocking them inhibits inflammation.
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Description
Test your knowledge on the key mechanisms of inflammation, including the roles of various immune cells and mediators. This quiz covers important concepts such as extravasation, mast cell functions, and the different systems involved in the inflammatory response.