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Questions and Answers
What is inflammation?
What is inflammation?
A complex biological response of vascularized living tissues to local injury or harmful stimuli.
Inflammatory conditions are termed by adding the suffix '______' to the affected organ or tissue.
Inflammatory conditions are termed by adding the suffix '______' to the affected organ or tissue.
-itis
Which of the following is a sign of inflammation?
Which of the following is a sign of inflammation?
Acute inflammation has a longer duration than chronic inflammation.
Acute inflammation has a longer duration than chronic inflammation.
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What are the two major components of acute inflammation?
What are the two major components of acute inflammation?
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What is the cause of swelling in inflammation?
What is the cause of swelling in inflammation?
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A transudate is formed when fluid leaks out due to increased ______ pressure.
A transudate is formed when fluid leaks out due to increased ______ pressure.
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Which of the following are components of inflammation?
Which of the following are components of inflammation?
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What is purulent exudate?
What is purulent exudate?
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Which process contributes to the heat and redness observed during inflammation?
Which process contributes to the heat and redness observed during inflammation?
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What primary effect results from increased vascular permeability in acute inflammation?
What primary effect results from increased vascular permeability in acute inflammation?
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Which inflammatory mediator is most commonly associated with endothelial cell contraction leading to vascular leakage?
Which inflammatory mediator is most commonly associated with endothelial cell contraction leading to vascular leakage?
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Which of the following signs is typically more prominent in acute inflammation than in chronic inflammation?
Which of the following signs is typically more prominent in acute inflammation than in chronic inflammation?
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What initiates the active anti-inflammatory mechanisms during the inflammatory response?
What initiates the active anti-inflammatory mechanisms during the inflammatory response?
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What is the primary characteristic of transudate?
What is the primary characteristic of transudate?
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Which process describes the movement of leukocytes through blood vessels during inflammation?
Which process describes the movement of leukocytes through blood vessels during inflammation?
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Which molecule is primarily responsible for the rolling of leukocytes along the endothelium?
Which molecule is primarily responsible for the rolling of leukocytes along the endothelium?
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What triggers the activation of leukocytes once they reach the site of infection?
What triggers the activation of leukocytes once they reach the site of infection?
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Which step is NOT part of the phagocytosis process performed by leukocytes?
Which step is NOT part of the phagocytosis process performed by leukocytes?
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Study Notes
Inflammation
- Inflammation is a complex biological response to injury or harmful stimuli, initiated by chemical mediators from host cells.
- Terminology: Inflammatory conditions are named by adding "-itis" to the affected organ or tissue (e.g., pulpitis, gingivitis, hepatitis, appendicitis).
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Significance:
- Can cause life-threatening hypersensitivity reactions.
- Can lead to progressive organ damage from chronic inflammation and fibrosis (e.g., rheumatoid arthritis, atherosclerosis).
Components of Inflammation
- Circulating Cells & Proteins: Neutrophils, monocytes, eosinophils, lymphocytes, basophils, platelets, and plasma fluid proteins.
- Blood Vessels: Endothelial cells and smooth muscle cells.
- Connective Tissue Cells: Mast cells, fibroblasts, macrophages, and lymphocytes.
- Extracellular Matrix: Collagen, elastin, fibronectin, laminin, and proteoglycans.
Types of Inflammation
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Acute:
- Early onset (seconds to minutes).
- Short duration (minutes to days).
- Fluid exudation (edema).
- Neutrophil emigration.
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Chronic:
- Later onset (days).
- Longer duration (weeks to years).
- Blood vessel proliferation and scarring.
- Lymphocyte and macrophage infiltration.
Cardinal Signs of Inflammation
- Redness: Caused by vasodilation increasing blood flow.
- Swelling: Caused by increased vascular permeability leading to exudate accumulation.
- Heat: Also due to increased blood flow.
- Pain: Caused by pressure on nerve endings from edema and chemical mediators (e.g., bradykinin, prostaglandins).
- Loss of Function: Resulting from pain, edema, and tissue damage.
General Characteristics of Inflammation
- Vascular Wall Response: Includes vasodilation and increased vascular permeability.
- Inflammatory Cell Response: Involves leukocyte recruitment and activation.
- Mediators: Inflammatory mediators (e.g., plasma proteins, locally produced factors) trigger and control inflammatory responses.
- Termination: Active anti-inflammatory mechanisms begin when the causative agent is removed and secreted mediators are cleared.
Acute Inflammation: Vascular Changes
- Vasodilation: Increases blood flow, causing heat and redness.
- Increased Vascular Permeability: Allows protein-rich fluid (exudate) to escape into the interstitial tissue, leading to edema (swelling).
Mechanisms of Vascular Leakage
- Endothelial Cell Contraction: Caused by histamine, bradykinin, leukotrienes, and other chemical mediators, results in gaps in venules.
- Direct Endothelial Injury: Caused by burns or infections.
Edema
- Exudate: High protein, cellular debris, and often microbes. Indicates increased vascular permeability.
- Transudate: Low protein content. Results from increased hydrostatic pressure or decreased osmotic pressure. Accumulates in non-inflammatory conditions.
- Purulent Exudate: Rich in leukocytes (mostly neutrophils), cell debris, and often microbes.
Transudate vs. Exudate Formation
- Transudate: Fluid leaks out due to increased hydrostatic pressure or decreased osmotic pressure.
- Exudate: Fluid leaks out due to increased vascular permeability.
Inflammation
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Inflammation is a protective response to injury or infection, aiming to eliminate the cause and repair damaged tissue.
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Cardinal signs of inflammation:
- Redness (rubor): Caused by increased blood flow due to vasodilation.
- Swelling (tumor): Due to fluid accumulation (edema) in the interstitial space.
- Heat (calor): Resulting from increased blood flow.
- Pain (dolor): Caused by chemical mediators and pressure from swelling.
- Loss of Function (functio laesa): Occurs when inflammation is severe enough to impair tissue function.
Mechanisms of Inflammation
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Two main components:
- Vascular response: Changes in blood vessel caliber and permeability.
- Cellular response: Involving leukocyte recruitment and activation.
Vascular Response
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Vasodilation: Increased blood flow to the area of injury, resulting in redness and heat.
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Increased Vascular Permeability: Allows fluid and proteins to escape from the blood into the interstitial space, causing swelling.
- Common mechanism: Endothelial cell contraction leading to gaps in venules, elicited by mediators like histamine, bradykinin, and leukotrienes.
- Direct endothelial injury: Can occur from burns or infections.
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Edema: Excessive fluid in the interstitial tissue or body cavities.
- Exudate: Protein-rich inflammatory fluid, indicating increased vascular permeability.
- Transudate: Fluid with low protein content, caused by increased hydrostatic pressure or decreased osmotic pressure, usually in non-inflammatory conditions.
Cellular Response
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Leukocyte recruitment and activation:
- Margination and rolling: Leukocytes slow down and interact with the endothelium.
- Adhesion: Leukocytes bind tightly to the endothelium.
- Transmigration: Leukocytes cross the endothelium into the interstitial tissue.
- Leukocyte activation: Stimulated by microbes, necrotic cell products, and inflammatory mediators.
Phagocytosis
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Process: Involves engulfment and degradation of bacteria and cellular debris by neutrophils and macrophages.
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Three steps:
- Recognition and attachment: Leukocytes recognize and bind to particles via surface receptors.
- Engulfment: Extension of cytoplasm wraps around the particle and forms a phagocytic vacuole (phagosome).
- Killing and degradation: Phagosome fuses with lysosomes, releasing enzymes and reactive oxygen species to kill the engulfed material.
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Three steps:
Outcomes of Acute Inflammation
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Resolution: Return to normal tissue structure and function.
- Factors favoring resolution: Limited injury, minimal tissue damage, and good tissue regenerative capacity.
- Progression to chronic inflammation: If the offending agent is not removed, there is continuing tissue injury, or the tissue has limited regenerative ability.
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Suppuration (pus formation): Characterized by a purulent exudate rich in neutrophils, dead cells, and bacterial debris.
- Abscess: Focal collection of pus.
- Scarring and fibrosis: Replacement of damaged tissue with fibrous connective tissue, often following severe injury or inflammation in tissues with poor regenerative potential.
Morphology of Acute Inflammation
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Types:
- Serous inflammation: Outpouring of thin fluid (plasma or mesothelial secretions), often occurring in body cavities like the pleura, pericardium, and peritoneum.
- Fibrinous inflammation: Characterized by the deposition of fibrin in the extracellular space, often seen in the meninges, pericardium, and pleura, indicating more severe injury.
- Suppurative (purulent) inflammation: Formation of pus, a creamy yellow or blood-stained exudate, associated with pyogenic bacteria.
- Pseudomembranous inflammation: Extensive epithelial necrosis and sloughing on mucous membranes, forming a pseudomembrane composed of fibrin, dead cells, and inflammatory cells. Seen in diphtheria.
Ulcers
- Definition: Local defects or excavations on the surface of an organ caused by inflammatory necrosis.
- Common locations: Mucous membranes (mouth, larynx, stomach), subcutaneous tissues (especially in elderly with vascular disease).
Effects of Acute Inflammation
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Beneficial:
- Dilution of toxins: Edema fluid dilutes toxins.
- Production of antibodies: Antibodies are produced by the immune response.
- Fibrin network: Provides a scaffold for inflammatory cells and limits the spread of infection.
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Harmful:
- Swelling and edema: Can cause pressure-induced tissue necrosis.
- Increased tissue pressure: May lead to tissue necrosis.
- Digestion of viable tissue: Can cause collateral damage to healthy tissue.
- Severe damage in allergic reactions: Can lead to extensive tissue injury.
- Generalized increased vascular permeability: May lead to shock.
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Description
Explore the complex biological process of inflammation, including its terminology, components, and types. Understand the significance of inflammatory conditions and how they can affect the body. This quiz is ideal for those studying biology or medicine.
