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Questions and Answers
What is a primary purpose of acute inflammation?
What is a primary purpose of acute inflammation?
Which of the following is NOT a characteristic of acute inflammation?
Which of the following is NOT a characteristic of acute inflammation?
Which chemical mediators are primarily involved in controlling acute inflammation?
Which chemical mediators are primarily involved in controlling acute inflammation?
What is the initial response of living tissues to injury called?
What is the initial response of living tissues to injury called?
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Which type of infection is commonly associated with acute inflammation?
Which type of infection is commonly associated with acute inflammation?
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Which of the following is a potential complication of acute inflammation?
Which of the following is a potential complication of acute inflammation?
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What happens to neutrophils during the acute inflammatory response?
What happens to neutrophils during the acute inflammatory response?
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Which type of acute inflammation is associated with hypersensitivity reactions?
Which type of acute inflammation is associated with hypersensitivity reactions?
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Which adhesion molecule is primarily expressed on endothelial cells?
Which adhesion molecule is primarily expressed on endothelial cells?
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What process allows leukocytes to migrate through the vessel wall?
What process allows leukocytes to migrate through the vessel wall?
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Which of the following substances can act as a chemotactic factor for leukocytes?
Which of the following substances can act as a chemotactic factor for leukocytes?
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What is the primary role of neutrophils during inflammation?
What is the primary role of neutrophils during inflammation?
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How does vasodilation contribute to the inflammatory response?
How does vasodilation contribute to the inflammatory response?
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What is NOT a purpose of the exudation of fluid during acute inflammation?
What is NOT a purpose of the exudation of fluid during acute inflammation?
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Which of the following changes is characteristic of acute inflammation?
Which of the following changes is characteristic of acute inflammation?
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What effect does pain and loss of function have during acute inflammation?
What effect does pain and loss of function have during acute inflammation?
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Which clinical sign is associated with redness during acute inflammation?
Which clinical sign is associated with redness during acute inflammation?
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What happens to arterioles at the onset of acute inflammation?
What happens to arterioles at the onset of acute inflammation?
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What is the result of increased vascular permeability during acute inflammation?
What is the result of increased vascular permeability during acute inflammation?
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How does Starling's Law relate to fluid movement in acute inflammation?
How does Starling's Law relate to fluid movement in acute inflammation?
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What type of fluid loss occurs during inflammation, exudate or transudate?
What type of fluid loss occurs during inflammation, exudate or transudate?
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What effect does vasodilatation have in the context of acute inflammation?
What effect does vasodilatation have in the context of acute inflammation?
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What characterizes stasis during acute inflammation?
What characterizes stasis during acute inflammation?
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Which of the following components is NOT a characteristic microscopic feature of acute inflammation?
Which of the following components is NOT a characteristic microscopic feature of acute inflammation?
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What is the primary characteristic of transudate?
What is the primary characteristic of transudate?
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Which mechanism is NOT associated with increased vascular permeability during acute inflammatory responses?
Which mechanism is NOT associated with increased vascular permeability during acute inflammatory responses?
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During neutrophil recruitment, which step follows the rolling of neutrophils along the endothelium?
During neutrophil recruitment, which step follows the rolling of neutrophils along the endothelium?
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What is a purulent exudate primarily characterized by?
What is a purulent exudate primarily characterized by?
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What leads to margination of leukocytes during inflammation?
What leads to margination of leukocytes during inflammation?
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What occurs during the process of emigration of neutrophils?
What occurs during the process of emigration of neutrophils?
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Which factor is not related to the mechanisms that increase vascular permeability?
Which factor is not related to the mechanisms that increase vascular permeability?
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Which event occurs last in the sequence of leukocyte recruitment to the site of injury?
Which event occurs last in the sequence of leukocyte recruitment to the site of injury?
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Study Notes
Acute Inflammation - Overview
- Acute inflammation is the body's local response to injury caused by any agent.
- It's a protective mechanism to eliminate or limit the spread of injurious agents, and remove necrosed cells and tissues.
- Acute inflammation is innate, immediate, and early, typically lasting minutes to hours or a few days.
- Key objectives include understanding the causes and purposes of acute inflammation, its macroscopic and microscopic features (edema, vasodilation, neutrophil margination/migration), and the relationship between microscopic and macroscopic changes.
References
- Robbins basic pathology
- Muir's Textbook of pathology
Objectives
- Major causes and biological purposes of acute inflammation
- Macroscopic features of acute inflammation
- Microscopic features of acute inflammation, including edema and vasodilation
- Neutrophil margination and migration
- Relationship between microscopic and macroscopic changes
Causes of Acute Inflammation
- Microbial infections (bacterial, viral, fungal, parasitic) are common causes
- Hypersensitivity reactions (acute phase) against environmental substances or "self" tissues
- Physical and chemical agents (burns, frostbite, radiation, toxins) causing host cell injury
- Tissue necrosis (ischemia, physical/chemical injury)
Clinical Features of Acute Inflammation
- Main clinical signs include:
- RUBOR (redness)
- TUMOR (swelling)
- CALOR (heat)
- DOLOR (pain)
- Loss of function
Acute Inflammation - Major Characteristics
- Vascular Reaction: Accumulation of fluid exudate and neutrophils in tissues
- Controlled by chemical mediators derived from plasma or cells
- It's a protective mechanism but can lead to local and systemic complications, usually followed by repair.
Vascular Changes
- Transient vasoconstriction of arterioles (few seconds)
- Vasodilation of arterioles and capillaries, leading to increased blood flow (heat and redness)
- Increased permeability of blood vessels, causing exudation of protein-rich fluid into tissues, and slowing of circulation.
- Concentration of red blood cells (RBCs) in small vessels, increasing blood viscosity (stasis)
Increased Vascular Permeability
- Increased vascular permeability leads to movement of protein-rich fluid and blood cells into the extravascular tissues.
- This causes increased osmotic pressure of interstitial fluid and more fluid outflow from the blood into the tissues.
Starling's Law and Fluid Loss
- Fluid flow across vessel walls depends on the balance of hydrostatic pressure within the vessels and the difference in colloid osmotic pressure between plasma and interstitial fluid.
- Increased hydrostatic pressure leads to increased fluid flow out of the vessels.
- Increased colloid osmotic pressure of the interstitial fluid pulls fluid into the vessels, and/or prevents fluid from leaving.
Exudate vs. Transudate
- Exudate: High protein content, specific gravity above 1.02, characteristic of inflammation
- Transudate: Low protein content, specific gravity less than 1.012, caused by hydrostatic pressure imbalance (e.g., venous obstruction)
Edema
- Edema is excess fluid in the interstitium, and can be transudate or exudate.
- Edema leads to increased lymphatic drainage.
- Pus is a purulent exudate, rich in neutrophils and cell debris.
Lymphatic Drainage in Inflammation
- Lymph flow increases during inflammation to drain edema fluid, leukocytes, and cell debris from extravascular space
- In severe inflammatory reactions, especially to microbes, lymphatics may transport the offending agent, contributing to dissemination.
Mechanisms of Increased Vascular Permeability
- Endothelial cell contraction (intercellular gaps in postcapillary venules)
- Endothelial injury (e.g., burns, infections)
- Increased transcytosis (proteins through intracellular vesicles)
- Leakage from new blood vessels (angiogenesis)
Cellular Events in Acute Inflammation (Leukocyte Recruitment)
- Stasis slows blood flow, leading to margination of neutrophils at vessel walls.
- Neutrophils roll along endothelium (rolling).
- Neutrophils adhere firmly to endothelium (adhesion).
- Neutrophils migrate through the vessel wall (emigration).
- Neutrophils migrate in interstitial tissues toward a chemotactic stimulus (chemotaxis).
Chemotaxis & Phagocytosis
- Leukocytes move towards sites of infection/injury along a chemical gradient (chemotaxis).
- Exogenous and endogenous substances are chemotactic, including bacterial products, cytokines, complement system components, and products of the lipoxygenase pathway.
Phagocytosis
- Neutrophils phagocytose microorganisms.
- Activated neutrophils release toxic metabolites/enzymes harming host tissue.
How Do These Changes Combat Injury?
- Exudation of Fluid: Delivers plasma proteins (immunoglobulins, inflammatory mediators, fibrinogen) to the injured area, diluting toxins. Increases lymphatic drainage, delivering microbes/antigens to phagocytes and the immune system.
- Infiltration of Cells: Removes pathogenic organisms/necrotic debris.
- Vasodilation: Increases blood flow/delivery to the injured area (increases temperature).
- Pain and Loss of Function: Enforces rest, reduces further trauma.
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Description
Test your knowledge on the fundamentals of acute inflammation. This quiz covers the characteristics, chemical mediators, and physiological responses involved in this critical aspect of the immune response. Explore the initial reactions and complications associated with acute inflammation.