Podcast
Questions and Answers
The word "inflammation" is derived from the Latin word "______" which means "to set on fire"
The word "inflammation" is derived from the Latin word "______" which means "to set on fire"
inflammare
What are the four cardinal signs of inflammation?
What are the four cardinal signs of inflammation?
What is exudation?
What is exudation?
The escape of fluid, proteins, and blood cells from the vascular system into the interstitial tissue or body cavities.
Transudate is a fluid with high protein content and cellular material.
Transudate is a fluid with high protein content and cellular material.
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What is the role of leukocytes in inflammation?
What is the role of leukocytes in inflammation?
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Which of the following accurately describes the steps involved in leukocytic recruitment during inflammation?
Which of the following accurately describes the steps involved in leukocytic recruitment during 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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Which of the following is NOT a trigger of acute inflammation?
Which of the following is NOT a trigger of acute inflammation?
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Which of these factors contributes to increased vascular permeability during inflammation?
Which of these factors contributes to increased vascular permeability during inflammation?
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What are the three major steps involved in phagocytosis?
What are the three major steps involved in phagocytosis?
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What is the main characteristic feature of suppurative inflammation?
What is the main characteristic feature of suppurative inflammation?
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Fibrinous inflammation is typically associated with the formation of a blister.
Fibrinous inflammation is typically associated with the formation of a blister.
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What is the primary function of macrophages during the resolution of inflammation?
What is the primary function of macrophages during the resolution of inflammation?
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Study Notes
Course Information
- Course Code: 301
- Instructor: Dr. Ayesha Ilyas
- Semester: Spring 2020
- Reference Text: Robbins Pathology by Vinay Kumar, Abul K. Abbas, Jon C. Aster-Robbins, and Cotran (2015)
Overview
- The course material involves an overview of the topic
- It covers intracellular accumulations
Intracellular Accumulations
- Accumulations of normal cell metabolites (e.g., fats, proteins, carbohydrates)
- Accumulations of abnormal substances (e.g., storage diseases, inborn errors of metabolism)
- Accumulations of pigments (e.g., endogenous pigments, exogenous pigments)
Acute Inflammation: Vascular and Cellular Events
- The study material covers the topic of acute inflammation, focusing on vascular and cellular events.
- Images of inflammation (e.g., swollen ankles, hands, burns) are presented.
Introduction to Inflammation
- Survival of organisms depends on eliminating foreign invaders, like pathogens and damaged tissues.
- This function is mediated by a complex host immune response called inflammation
- Inflammation is a protective mechanism that removes harmful stimuli and initiates the healing process.
- Without inflammation, injuries and infections would not heal.
Definition of Inflammation
- The word inflammation is derived from Latin "inflammare," meaning "to set on fire."
- Inflammation is a response of vascularized tissues to infection or injury.
- It brings cells and molecules of host defense from the circulation to the affected site to eliminate the offending agent.
- Inflammation is a protective response, not harmful
Mediators of Defense
- Phagocytic leukocytes
- Antibodies
- Complement proteins
- The inflammatory process delivers these elements to damaged/necrotic tissues & foreign invaders (e.g., microbes)
- These elements activate recruited cells/molecules to eliminate harmful substances
Historical Background
- Celsus (30 BC – 45 AD), a Roman physician, identified the four cardinal signs of inflammation: rubor (redness), tumor (swelling), calor (heat), and dolor (pain).
- Virchow (1871) added a fifth sign: loss of function (functio laesa).
- Cohnheim (1873) described diapedesis (movement of cells out of blood vessels).
- Lewis (1927) described inflammation as "triple response" to injury.
Cardinal Signs of Inflammation
- Rubor (Redness): Increased blood flow
- Tumor (Swelling): Exudation of fluid
- Calor (Heat): Increased blood flow, exudation of fluid, release of inflammatory mediators
- Dolor (Pain): Stretching of pain receptors & nerves, inflammatory exudates, chemical mediators
- Functio Laesa (Loss of Function): Pain, disruption of tissue structure, fibroplasia, and metaplasia
Steps of Inflammation (5R's)
- Recognition of injurious agent
- Recruitment of leukocytes
- Removal of agent
- Regulation of the response
- Resolution
Types of Inflammation
- Acute inflammation
- Chronic inflammation
Acute Inflammation
- Rapid response to microbes or injury
- Designed to deliver leukocytes and plasma proteins to injury sites
- Stimuli for inflammation include: Infections, trauma, physical/chemical agents, foreign bodies, immune reactions.
Components of Acute Inflammation
- Vascular changes
- Cellular events
Vascular Changes
- Changes in vascular caliber and flow
- Increased vascular permeability
Changes in Vascular Caliber and Flow
- Changes in blood vessels start rapidly after infection or injury.
- Development rate varies based on the severity and nature of the stimulus.
Increased Vascular Permeability
- Endothelial cell contraction increases interendothelial spaces.
- This is primarily triggered by histamine, leukotrienes, and bradykinin.
- Endothelial injury - resulting in endothelial necrosis and detachment
- Endothelial damage is caused by direct damage, microbes, microbial toxins and neutrophils.
Responses of Lymphatic Vessels and Lymph Nodes
- Lymphatic vessels proliferate to handle increased load.
- Lymphatics become inflammed (lymphangitis/lymphadenitis)
- This inflammation leads to redness/swelling
Pathophysiology of Inflammation
- Inflammation causes vasodilation, increasing blood flow (manifested as rubor).
- Increased permeability lets protein-rich fluid enter the extravascular tissues.
- Red blood cells (RBCs) concentration increases, leading to blood viscosity and stasis.
- Leukocytes accumulate along vessels' endothelium.
Cellular Events
- Leukocytes delivery to injury site is crucial for inflammation.
- Leukocytes activation following transmigration, chemotaxis, phagocytosis.
- Phagocytosis involves: recognition & attachment, engulfment (phagocytic vacuole), killing/degradation (ingested material).
Resolution of Inflammation
- Phagocytes clear dead tissue and leukocytes during inflammation.
- Lymphatic drainage and macrophages remove fluid/proteins.
- Macrophages release growth factors for new blood vessels and fibroblasts, aiding fibrosis & scarring.
Patterns of Acute Inflammation
- Morphologic manifestations of acute inflammation (e.g., serous, purulent, fibrinous).
- Key features differentiate these patterns.
Different Morphological Patterns
- Serous inflammation
- Purulent inflammation (pus)
- Fibrinous inflammation
- Ulcer
Serous, Fibrinous, and Purulent Inflammation
- These are morphologic classifications of acute inflammation
- Serous inflammation: Characterized by a watery, low protein fluid. This fluid can appear as a blister
- Fibrinous inflammation: Occurs as a consequence of significant injury. This type of inflammation results in high vascular permeability, allowing large molecules (fibrin) to leak out into the tissues.
- Purulent inflammation (suppurative inflammation): Characterized by a large amount of purulent exudate or pus. This fluid consists mainly of neutrophils, necrotic cells and edema fluid.
Home Task
- Study the principle mediators of inflammation.
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