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Questions and Answers
What is the primary role of leukocytes in an inflammatory reaction?
What is the process called when fluid, proteins, and blood cells escape from the vascular system into surrounding tissues?
Which of the following is NOT a major component of acute inflammation?
What role do plasma proteins play during acute inflammation?
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Which cells are responsible for the dilation of small blood vessels during an inflammatory response?
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Which of the following circulating cells is NOT involved in the inflammatory process?
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Which mediators primarily induce vasodilation during acute inflammation?
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What is the purpose of increasing the permeability of the microvasculature during an inflammatory response?
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What initial physiological change occurs during acute inflammation?
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What causes the localized redness observed at an inflamed site?
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Which mediator is least likely to contribute to vascular leakage?
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Which type of response occurs quickly after exposure to chemical mediators during inflammation?
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What is the term for the slowed blood flow and concentration of red cells in small vessels during inflammation?
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How does endothelial injury typically occur in severe cases of inflammation?
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What role does transcytosis play in the inflammatory response?
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What is the consequence of decreased fluid movement from the vascular space during inflammation?
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What is the primary purpose of inflammation in the body?
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Which of the following is NOT one of the four cardinal signs of inflammation?
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Who first described the four cardinal signs of inflammation?
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Which chemical substance is known to mediate vascular changes during inflammation?
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What type of agents can cause inflammation as a result of immune reactions?
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What discovery did Elie Metchnikoff contribute to our understanding of inflammation?
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Which of the following is considered a physical agent that can trigger inflammation?
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Excess deposition of urate crystals can lead to which type of inflammation?
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Study Notes
Inflammation Introduction
- Inflammation is a protective response to injury, designed to eliminate the cause of injury, dead cells, and damaged tissue.
- Inflammation initiates healing and tissue repair.
- Inflammation is a response of vascularized tissues to infection and tissue damage, bringing cells and molecules from the circulatory system to the site of injury.
Inflammation History
- Inflammation was described in an Egyptian papyrus around 3000 BC.
- Celsus, a Roman writer in the first century AD, described the four cardinal signs of inflammation: rubor (redness), tumor (swelling), calor (heat), and dolor (pain).
- A fifth sign, loss of function (functio laesa) was added by Rudolf Virchow in the 19th century.
- John Hunter, a Scottish surgeon, noted that inflammation is a response to injury and not a disease in 1793.
- Elie Metchnikoff discovered phagocytosis in the 1880s.
- Sir Thomas Lewis, studying the inflammatory response in skin, identified the role of chemical mediators like histamine in vascular changes.
Causes of Inflammation
- Infective agents: bacteria, viruses, toxins, fungi, parasites.
- Immune reactions: autoimmune diseases, allergies.
- Physical agents: heat, cold, radiation, mechanical trauma.
- Chemical agents: organic and inorganic poisons.
- Inert materials: foreign bodies such as splinters, sutures, dirt.
- Excess deposition of endogenous substances: urate crystals, cholesterol, lipids.
Inflammatory Response Players
-
Circulating Cells:
- Neutrophils
- Eosinophils
- Basophils
- Lymphocytes
- Monocytes
- Platelets
-
Connective Tissue Cells:
- Mast cells
- Macrophages
- Lymphocytes
- Fibroblasts
-
Circulating Proteins:
- Clotting factors
- Kininogens
- Complement components
-
Extracellular Matrix:
- Fibrous structural proteins (e.g., collagen and elastin)
- Gel-forming proteoglycans
- Adhesive glycoprotein (e.g., fibronectin)
-
Vascular Wall Cells:
- Endothelial cells
- Smooth muscle cells
Sequence of Events in an Inflammatory Reaction
- The offending agent is recognized by host cells and molecules.
- Leukocytes and plasma proteins are recruited from the circulation to the site of injury.
- Leukocytes and proteins are activated to destroy the offending substance.
- The reaction is controlled and terminated.
- Damaged tissue is repaired.
Acute Inflammation
-
Three major components:
- Dilation of small vessels increasing blood flow.
- Increased permeability of microvasculature allowing plasma proteins and leukocytes to leave circulation.
- Emigration of leukocytes from the microcirculation, accumulation at the site of injury, and activation to eliminate the offending agent.
Vascular Changes
- Changes in blood flow and vessel permeability are designed to facilitate the movement of plasma proteins and leukocytes out of the circulation.
- The escape of fluid, proteins, and blood cells from the vascular system into the interstitial tissue or body cavities is known as exudation.
Exudate vs. Transudate
- Exudate: fluid with a high protein content, high specific gravity, and often contains inflammatory cells, typically seen in inflammation.
- Transudate: fluid with a low protein content, low specific gravity, and usually contains few inflammatory cells, typically occurs with increased hydrostatic pressure or decreased oncotic pressure.
Changes in Vascular Flow and Caliber
- Vasodilation: Early response induced by mediators like histamine, leading to increased blood flow, responsible for heat (calor) and redness (rubor) at the site of inflammation.
- Increased Permeability: Leads to the outpouring of protein-rich fluid into the extravascular tissues causing swelling (tumor).
- Stasis: Slow blood flow due to fluid loss and increased vessel diameter, leading to a concentration of red cells and slow-moving blood.
Increased Vascular Permeability (Vascular Leakage)
- Contraction of endothelial cells: Most common mechanism, caused by histamine, bradykinin, leukotrienes, and other mediators.
- Endothelial injury: Results from direct damage to endothelial cells (e.g., burns) or microbial actions.
- Increased transport of fluids and proteins (transcytosis): May involve intracellular channels, stimulated by factors like VEGF.
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