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Questions and Answers
What is the purpose of the inflammatory response?
Which cardinal sign of inflammation is due to increased capillary permeability and fluid accumulation in the affected area?
What is the cardinal sign of inflammation characterized by redness due to increased blood flow to the affected area?
What is the term for altered or impaired function of the affected area in inflammation?
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What is the first step in protection from infection provided by tissue macrophages?
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Which step is not involved in the inflammatory response?
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What causes the increased temperature (heat) in the affected area during inflammation?
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What is the main reason for the swelling in the affected area during inflammation?
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What is the role of tissue macrophages in the inflammatory response?
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What is the purpose of walling-off the inflamed area during the inflammatory response?
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Which of the following is responsible for the increased delivery of phagocytes and plasma proteins to the affected area during the inflammatory response?
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Where are mast cells primarily found in the body?
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What is the main effect of histamine and bradykinin during the inflammatory response?
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What is the result of plasma proteins escaping into tissue spaces during the inflammatory response?
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What is the role of active fibrin during the inflammatory response?
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Which process is facilitated by the increased concentration of complement protein C3b in the injured area during the inflammatory response?
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What is the main outcome of phagocytosis during the inflammatory response?
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Which enzyme do nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin inhibit?
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What is the main effect of glucocorticoids in response to various stimuli including mechanical, chemical, infectious, and immunological factors?
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In what instances can an exaggerated or prolonged inflammatory response cause serious tissue injury or impair tissue function?
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Which enzyme do aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit?
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What is the main effect of corticosteroids in inhibiting the formation of eicosanoid inflammatory mediators?
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What is the role of nitric oxide in inflammation?
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Which of the following is a potent inflammatory mediator that stimulates the release of cytokines, eicosanoids, and chemokines?
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What is the main mechanism of action of glucocorticoids in addressing allergic reactions and arthritis-related inflammation?
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What is the main effect of mast cell release of histamine during inflammation?
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What is the main role of prostaglandins and leukotrienes in inflammation?
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What is the main effect of cytokines in the inflammatory response?
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What is the main function of chemokines during the inflammatory response?
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What is the main effect of T cell activation and antibody production in the context of glucocorticoid use?
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Study Notes
Inflammatory Response and Pharmaceutics
- Vasodilation of arterioles increases blood flow to the affected area, primarily caused by histamine released from activated mast cells and activated bradykinin, resulting in increased delivery of phagocytes and plasma proteins.
- Mast cells are found in connective tissues, particularly in areas of potential microbial entry such as the lungs, skin, and gastrointestinal tract.
- Histamine and bradykinin cause an increase in capillary permeability, allowing movement of plasma proteins into tissue spaces, leading to localized edema.
- Vasodilation and increased capillary permeability also result in redness, heat, and swelling in the inflamed area.
- Plasma proteins escaping into tissue spaces convert inactive fibrinogen into active fibrin, effectively walling off the injured area and preventing the spread of infection.
- Increased blood flow and capillary permeability facilitate infiltration of phagocytes, including neutrophils and monocytes that mature into macrophages.
- Opsonization, involving the marking of bacteria for phagocytosis, is facilitated by the increased concentration of complement protein C3b in the injured area.
- Phagocytosis involves ingestion and digestion of bacteria, foreign particles, and tissue debris by phagocytes, ultimately leading to their death.
- Nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin inhibit cyclooxygenase, the enzyme involved in prostaglandin synthesis, contributing to the inflammatory response.
- Selective COX-2 inhibitors, once effective and causing fewer gastric side effects, have been associated with an increased risk of serious cardiovascular events and have been removed from the market.
- Glucocorticoids can prevent or reduce inflammation in response to various stimuli including mechanical, chemical, infectious, and immunological factors.
- In some instances, an exaggerated or prolonged inflammatory response may cause serious tissue injury or impair tissue function, which can be addressed by anti-inflammatory drugs.
Inflammatory Mediators and Glucocorticoids
- Glucocorticoids are used to treat allergic reactions, asthma, and arthritis-related inflammation by addressing symptoms, not the underlying cause.
- Mechanism of action involves decreasing release of inflammatory substances like histamine, prostaglandins, cytokines, and ELAM-1, reducing vasodilation, leukocyte extravasation, and chemotaxis.
- T cell activation and antibody production are decreased, leading to an increased risk of infection due to immunosuppression.
- Mast cells release histamine, causing vasodilation, increased vascular permeability, and bronchial smooth muscle constriction.
- Mast cells also release chemotactic factors to attract leukocytes and other inflammatory mediators like cytokines, prostaglandins, leukotrienes, and platelet-activating factor.
- Prostaglandins and leukotrienes are inflammatory mediators derived from arachidonic acid and play roles in inflammation, smooth muscle contraction, capillary permeability, and vasodilation.
- Aspirin and nonsteroidal anti-inflammatories inhibit prostaglandin and thromboxane production by inhibiting cyclooxygenase.
- Corticosteroids inhibit the release of arachidonic acid, thus inhibiting the formation of eicosanoid inflammatory mediators.
- Cytokines, including interleukins, interferons, and TNF-α, are small proteins with proinflammatory effects, causing fever, leukocyte attraction, and immune cell proliferation.
- TNF-α is a potent inflammatory mediator that stimulates the release of cytokines, eicosanoids, and chemokines.
- Chemokines are small peptides that function as chemotactic substances for immune cells, produced in response to proinflammatory cytokines.
- Nitric oxide causes vasodilation and inhibits leukocyte aggregation, platelet adhesion, and cytokine release, playing a role in inflammation.
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Description
Test your knowledge of inflammatory response and pharmacological interventions with this quiz. Explore the mechanisms of vasodilation, capillary permeability, and phagocytosis, as well as the role of inflammatory mediators such as histamine, prostaglandins, and cytokines. Understand the effects of glucocorticoids and nonsteroidal anti-inflammatory drugs on the inflammatory process.
