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What is inflammation?
A reaction of a tissue and its microcirculation to a pathologic insult characterized by the generation of inflammatory mediators and movement of fluid and leucocytes.
Which of the following are clinical signs of inflammation? (Select all that apply)
Who described that inflammation is a reaction to prior tissue injury?
Rudolf Virchow
What are the three possible outcomes of the inflammatory process?
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Match the terms related to inflammation with their descriptions:
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Which of the following are hallmarks of acute inflammation? (Select all that apply)
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What is the primary action of bradykinin in the inflammatory response?
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The kinin system is primarily responsible for clotting mechanisms.
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Which of the following are actions of leukotrienes? (Select all that apply)
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Which of the following are clinical signs of inflammation? (Select all that apply)
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John Hunter contributed to the modern understanding of the vascular basis of inflammation.
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What is the primary purpose of the inflammatory response?
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The stages in the inflammatory process include initiation, ____, and termination.
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What are the three possible outcomes of inflammation?
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What is a hallmark of acute inflammation?
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What triggers the process of acute inflammation?
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Increased vascular permeability during inflammation results in ____.
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What is bradykinin?
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Which of the following are eicosanoids derived from arachidonic acid?
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Study Notes
General Considerations
- Inflammation is the tissue and microcirculation's response to pathologic insults, involving inflammatory mediators and fluid movement.
- Five clinical signs of inflammation: Rubor (redness), Calor (heat), Tumor (swelling), Dolor (pain), and Loss of function (functio laesa).
- John Hunter contributed to the understanding of inflammation's vascular basis.
- Rudolf Virchow emphasized that inflammation follows tissue injury.
- Thomas Lewis highlighted the role of chemical mediators in inflammation.
- The primary goal of inflammation is to eliminate pathologic insults and clear injured tissue.
- Outcomes of inflammation: regeneration of normal tissue and formation of scar tissue if repair is not possible.
Stages in Inflammatory Process
- Initiation occurs when injury triggers localization and clearance mechanisms.
- Amplification involves activation of soluble mediators and cellular systems.
- Termination is mediated through specific inhibitors of inflammatory mediators.
Sequence of Events
- Begins with normal histology, followed by vasodilatation and increased vascular permeability.
- Results in exudate leakage, margination, rolling, adhesion, and transmigration of white blood cells (WBCs).
- Neutrophil activation leads to phagocytosis: recognition, attachment, engulfment, and degradation.
- Outcomes can be 100% resolution, scar formation, or chronic inflammation.
Acute Inflammation
- The initial response to tissue injury occurs in microvasculature.
- Key changes include loss of endothelial integrity, fluid leakage, and emigration of blood cells.
- Characterized as a protective, non-specific response.
- Hallmarks include fluid accumulation, platelet activation, and presence of polymorphonuclear leukocytes.
Major Events in Acute Inflammation
- Changes in vascular flow and caliber.
- Increased vascular permeability.
- Exudation of leucocytes.
Stimuli for Acute Inflammation
- Infectious agents, physical agents, chemical agents, tissue necrosis, foreign bodies, and immune responses.
Vascular Changes
- Acute inflammation leads to alterations in vascular flow and increased permeability.
Increased Vascular Permeability
- Edema occurs when fluid accumulates in the extravascular space exceeding lymphatic clearance.
- Inflammatory edema arises from microvascular alterations.
- Post-capillary venules are key sites for vasoactive mediator effects on endothelial cells.
Definitions
- Edema: Excess fluid in interstitial tissues.
- Effusion: Excess body fluid in cavities like the peritoneum or pleura.
- Transudate: Low protein fluid accumulation due to systemic factors.
Kinin System
- Bradykinin is a crucial component, inducing increased permeability, smooth muscle contraction, and pain.
Clotting Factors
- Involved in coagulation and production of fibrin, leading to fibrinolysis.
Eicosanoids
- Derived from arachidonic acid in cell membranes, includes prostaglandins, leukotrienes, and lipoxins.
- Prostaglandins (including thromboxanes): Pain, fever, and contribute to clotting.
- Leukotrienes: Facilitate chemotaxis, vasoconstriction, and increased permeability.
- Lipoxins: Inhibit chemotaxis, promote vasodilation, and counteract leukotriene effects.
Platelet-Activating Factor (PAF)
- A phospholipid with diverse actions, involved in inflammatory and hemostatic processes.
General Considerations of Inflammation
- Inflammation is a tissue and microcirculation reaction to pathological insults, marked by inflammatory mediators and fluid and leukocyte movement.
- Clinical signs include rubor (redness), calor (heat), tumor (swelling), dolor (pain), and loss of function (functio laesa).
- John Hunter contributed to the vascular basis of inflammation; Rudolf Virchow emphasized inflammation's response to tissue injury; Thomas Lewis highlighted chemical mediators' role.
- Main goals of inflammation: eliminate insults and clean injured tissue.
- Outcomes of inflammation include regeneration of normal tissue architecture or scar tissue formation for irreparable tissues.
- The inflammatory process has three stages: initiation, amplification, and termination.
Sequence of Events in Inflammation
- Normal histology progresses to vasodilation.
- Increased vascular permeability leads to exudate leakage.
- White blood cells (WBCs) undergo margination, rolling, adhesion, and transmigration (diapedesis) into tissue.
- Chemotaxis guides inflammatory cells to injury sites.
- PMN (neutrophil) activation involves phagocytosis: recognition, attachment, engulfment, and degradation.
- Final outcomes can be 100% resolution, scar formation, or chronic inflammation.
Characteristics of Acute Inflammation
- Acute inflammation is a protective and non-specific response.
- Hallmarks include fluid and plasma accumulation in tissues, vascular stimulation of platelets, and presence of polymorphonuclear leukocytes (PMNs).
- Major events encompass changes in vascular flow and caliber, increased permeability, and leukocyte exudation.
Stimuli for Acute Inflammation
- Triggers include infectious agents, physical agents, chemical agents, tissue necrosis, foreign bodies, and immune responses.
Vascular Changes in Acute Inflammation
- Changes include alterations in vascular flow and increased permeability.
- Increased vascular permeability leads to edema, causing swelling as fluid moves into the extravascular space, exceeding lymphatic clearance.
Key Definitions
- Edema: fluid accumulation in interstitial tissues.
- Effusion: excess fluid in body cavities (e.g., pleura).
- Transudate: fluid with low protein content.
Inflammatory Mediators
- Kinin System: Bradykinin plays a key role, increasing permeability, promoting smooth muscle contraction, and causing pain.
- Clotting Factors: Involved in coagulation and production of fibrin.
- Eicosanoids: Derivatives of arachidonic acid include prostaglandins, leukotrienes, and lipoxins, each with multiple biological actions.
Effects of Eicosanoids
- Prostaglandins (including thromboxanes): contribute to pain, fever, and clotting mechanisms.
- Leukotrienes: promote chemotaxis, vasoconstriction, and increased permeability.
- Lipoxins: inhibit chemotaxis and induce vasodilation, counteracting leukotriene effects.
Platelet-Activating Factor (PAF)
- A phospholipid derived from numerous cellular sources involved in inflammatory responses.
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Description
Explore the key concepts of inflammation, including its definition, clinical signs, and the roles of inflammatory mediators and leucocytes. This quiz delves into the pathological reactions of tissues to insults and the modern understanding of inflammation as defined by key figures in the field. Test your knowledge on the fundamental aspects of anatomic and clinical pathology related to inflammation.
