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What is the primary purpose of inflammation?
Which component is NOT part of the inflammatory response?
What suffix is commonly used to denote inflammation?
Which sequence of events is the first step in the inflammatory response?
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Which of the following is a potentially harmful consequence of inflammation?
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Which factor is involved in the regulation of the inflammatory response?
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Which type of inflammation is characterized by prolonged response and may involve tissue damage?
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Which of the following can induce chronic inflammation?
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What primarily induces vasodilation during a vascular reaction?
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What role do Toll-like receptors (TLRs) play in the inflammatory response?
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What consequence occurs shortly after the increase in blood flow due to vasodilation?
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What is the primary function of NOD-like receptors (NLRs)?
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Which mediators can cause vascular leakage through contraction of endothelial cells?
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Which of the following statements accurately describes exudate?
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What is the primary function of lymphatic vessels during acute inflammation?
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What happens to leukocytes during the process of emigration in acute inflammation?
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What is the main distinction between exudate and transudate?
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What condition indicates inflammation of lymphatic vessels?
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What causes the enlargement of inflamed lymph nodes during inflammatory lymphadenitis?
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What is the significance of opsonization in the immune response?
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What is a likely consequence of neutrophils adhering to endothelial cells?
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Which cytokine is produced as a result of inflammasome activation?
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Plasma proteins exiting the circulation during inflammation primarily contribute to which process?
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What is indicated by red streaks near a skin wound?
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Study Notes
Inflammation Overview
- A response of vascularized tissues that delivers leukocytes and host defense molecules from circulation to sites of infection and cell damage
- Purpose: Elimination of offending agents
- Protective response: Essential for survival
- Mediators: Phagocytic leukocytes, antibodies, complement proteins
- Resident cells: Immediate response
- Circulating cells: Recruited as needed
- Inflammation: Delivery of circulating cells and proteins to tissues and activation of resident and recruited cells and soluble molecules
- "Itis": Denotes inflammation
- Steps: Recognition of noxious agent, recruitment of leukocytes and plasma proteins, removal of stimulus, regulation of response, repair
Fundamental Properties of Inflammatory Response
- Components: Blood vessels and leukocytes
- Harmful consequences: Protection against infections accompanied by local tissue damage (pain and functional impairment)
- Self-limited: Inflammation resolves with little or no permanent damage
- Disease: In many diseases, inflammation is misdirected or inadequately controlled
- Local and systemic: Primarily local reactions but may have systemic effects causing widespread pathologies (sepsis, systemic inflammatory response syndrome)
Fundamental Properties of Inflammatory Response
- Mediators: Vascular and cellular reactions triggered by soluble factors produced by various cells or derived from plasma proteins
- Mediators: Activated or generated in response to inflammatory stimulus
- Mediators: Initiate and amplify response, determine pattern, severity, clinical and pathological manifestations
- Acute and Chronic: Difference NOT just duration, but several features
Causes of Inflammation
- Infections (bacterial, fungal, viral, parasitic)
- Tissue necrosis (ischemia, trauma, physical or chemical injury)
- Foreign bodies (splinters, dirt, sutures)
- Immune reactions (hypersensitivity): Autoimmune reactions to self-antigens or environmental antigens associated with chronic inflammation induced largely by cytokines produced by T lymphocytes and other cells of the immune system
Recognition of Microbes and Damaged Cells
- Initiating step: Cellular receptors and circulating proteins recognize the noxious agent and trigger inflammation
- Cellular receptors for microbes: Receptors in plasma membrane, endosomes, and cytosol
- Toll-like receptors (TLRs): Trigger production of inflammation-inducing molecules (adhesion molecules, cytokines, and mediators)
Recognition of Microbes and Damaged Cells
- Sensors of cell damage: Cytosolic receptors (NOD-like receptors, NLRs), recognizing various molecules released or altered due to cell damage
- Inflammasome: A multiprotein cytosolic complex activated by receptors, inducing production of cytokine IL-1 and recruiting leukocytes leading to inflammation
Recognition of Microbes and Damaged Cells
- Other cellular receptors: Leukocytes express receptors for Fc tails of antibodies and complement proteins
- Opsonization: Coating of microbes promotes ingestion and activation of the complement system
- Collectins: Bind and combat microbes
ACUTE INFLAMMATION
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3 Major components:
- Dilation of small vessels (increased blood flow)
- Increased permeability of microvasculature (plasma proteins and leukocytes leave the circulation)
- Emigration of leukocytes (accumulation at the site of injury)
Vascular Reaction
- Exudation: Movement of proteins and leukocytes out of circulation into the site of infection or injury
- Exudate: High protein, cellular debris, increased permeability
- Transudate: Low protein content, no cellular material, low specific gravity, no increase in vascular permeability
- Edema: Excess fluid in interstitial tissue or serous cavities
- Pus: Purulent exudate (neutrophil rich)
Vascular Reaction
- Vasodilation: Induced by histamine action on vascular smooth muscle
- Result: Increased blood flow
- Increased permeability: Loss of fluid, increased vessel diameter, slower blood flow, RBCs concentrate, increasing viscosity
- Stasis: Slow moving RBCs, vascular congestion, localized redness
- Adhesion: Endothelial cells activated by mediators, express increased levels of adhesion molecules, leukocytes adhere to endothelium
Vascular Leakage
- Contraction of EC: Elicited by histamine, bradykinin, leukotrienes, and other mediators
- Delayed prolonged leakage: 2-12 hours; due to contraction or mild EC damage
- Endothelial injury: EC necrosis and detachment
Principal Mechanisms of Increased Vascular Permeability
Responses of Lymphatic Vessels and Lymph Nodes
- Lymphatics: Participate in acute inflammation
- Lymph nodes: Filter and police extravascular fluids
- Increased lymph flow: Helps drain edema fluid
- Lymphangitis: Secondary inflammation of lymphatic vessels
- Lymphadenitis: Inflammation of draining lymph nodes
Responses of Lymphatic Vessels and Lymph Nodes
- Enlarged lymph nodes: Due to hyperplasia of lymphoid follicles and increased numbers of lymphocytes and macrophages
- Reactive or inflammatory lymphadenitis: Red streaks near skin wounds are diagnostic of lymphangitis, accompanied by painful enlargement of draining lymph nodes
Cellular Response: Leukocyte Recruitment
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Description
This quiz covers the basic concepts of inflammation, including its purpose, protective responses, mediators, and fundamental properties. Understand how the body responds to infection and tissue damage through the inflammatory process, recognizing its critical role in survival and healing.
