Inflammatory Response and Pharmacological Interventions Quiz

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.