Plenary: Acute Inflammation – Medlardo Education

Cellular Response I Guide

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💡 Learning Outcomes:

Definition:
- Inflammation is a protective response of vascularized tissues to infections and tissue damage that brings cells and molecules of the immune system from the circulation to the sites where they are needed, to eliminate the offending agents.
- The primary function of the inflammatory response is to eliminate pathogenic agents and remove injured tissue components, allowing tissue repair to take place.

Types of Inflammation:
- Acute Inflammation:
  - Onset: Rapid, typically within minutes to hours.
  - Duration: Short-term response to injury.
  - Cellular Infiltrate: Mainly neutrophils.
  - Tissue Injury: Usually mild and self-limited.
  - Fibrosis: Generally absent.
  - Local and Systemic Signs: Prominent.
- Chronic Inflammation:
  - Onset: Slow, often over days.
  - Duration: Long-term response.
  - Cellular Infiltrate: Monocytes, macrophages, and lymphocytes.
  - Tissue Injury: May be significant.
  - Fibrosis: Can be severe and progressive.
  - Local and Systemic Signs: Variable, usually less intense.

Vasodilation:
- Increase in diameter of blood vessels, initiated by mediators such as histamine and nitric oxide.
- Leads to increased blood flow, causing warmth (calor) and redness (rubor) at the site of inflammation.

Increased Vascular Permeability:
- Allows proteins and leukocytes to exit the bloodstream, resulting in exudation of protein-rich fluid into tissues.
- Causes swelling (tumor) and contributes to pain (dolor) due to the pressure on nerves.

Stasis and Vascular Congestion:
- Slowing of blood flow and increased blood viscosity, facilitating the adhesion of leukocytes to the endothelium.

Leukocyte Recruitment:
- Margination and Rolling: Leukocytes move to the periphery of blood vessels.
- Adhesion: Firm attachment of leukocytes to the endothelium at the site of inflammation.
- Transmigration (Diapedesis): Leukocytes pass through the vessel wall.
- Chemotaxis: Leukocytes migrate towards the site of injury, guided by chemical signals.

Phagocytosis and Clearance:
- Recognition and Attachment: Leukocytes recognize and attach to foreign particles.
- Engulfment: The particle is engulfed, forming a phagocytic vacuole.
- Killing and Degradation: The ingested material is destroyed by lysosomal enzymes or reactive oxygen species.

Neutrophils:
- Rapidly recruited, key players in early-stage inflammation, responsible for phagocytosis of pathogens.

Macrophages:
- Arrive later (24-48 hours post-injury), contribute to prolonged inflammation, tissue repair, and release growth factors for healing.

Inflammatory Mediators:
- Initiate and regulate inflammatory responses, with various sources:
  - Cell-Derived Mediators: Produced by cells at the site of inflammation (e.g., macrophages, dendritic cells, mast cells).
  - Plasma-Derived Mediators: Produced in the liver and circulate in the plasma (e.g., complement proteins).
- Types and Actions of Major Inflammatory Mediators:
  - Histamine: Causes vasodilation and increased vascular permeability.
  - Cytokines: Promote cell signaling and communication in immune responses.
  - Arachidonic Acid Metabolites (Eicosanoids):
    - Prostaglandins (e.g., PGI2, PGE2): Promote vasodilation.
    - Leukotrienes (e.g., LT C4, D4, E4): Increase vascular permeability and aid in chemotaxis.
  - Complement System: Forms the membrane attack complex (MAC) to lyse pathogens.
- Characteristics:
  - Short-lived and tightly regulated to limit tissue damage.
  - One mediator can stimulate the release of additional mediators, amplifying the inflammatory response.

Calor (Warmth):
- Caused by vasodilation and increased blood flow to the affected area.

Rubor (Redness):
- Due to vasodilation and congestion of blood in the inflamed area.

Tumor (Swelling):
- Resulting from exudate formation due to increased vascular permeability.

Dolor (Pain):
- Arises from the release of inflammatory mediators (e.g., bradykinin, prostaglandins) that sensitize nerve endings.

Functio Laesa (Loss of Function):
- Caused by swelling and pain that limit the movement or function of the affected tissue.

Resolution:
- The injurious agent is eliminated, inflammatory mediators are cleared, and normal tissue architecture is restored.

Chronic Inflammation:
- If the injurious agent persists, acute inflammation may transition to chronic inflammation, characterized by prolonged immune activity, tissue destruction, and fibrosis.

Scarring and Fibrosis:
- When substantial tissue destruction occurs or the tissue cannot regenerate, the area heals by fibrosis, forming scar tissue.

Abscess Formation:
- Localized collection of pus, typically due to bacterial infection, where there is extensive tissue necrosis.

Ulceration:
- Occurs when an inflammatory response erodes the surface of an organ or tissue, leading to an open sore (ulcer), commonly seen in mucosal tissues.

Serous Inflammation:
- Characterized by the outpouring of thin fluid (e.g., blister).

Fibrinous Inflammation:
Fibrinous pericarditis. (A) Deposits of fibrin on the pericardium. (B) A pink meshwork of fibrin exudate (F) overlies the pericardial surface (P)
- Fibrin deposition due to increased vascular permeability, often affecting body cavities.

Suppurative (Purulent) Inflammation:
Purulent inflammation. (A) Multiple bacterial abscesses (arrows) in the lung in a case of bronchopneumonia. (B) The abscess contains neutrophils and cellular debris and is surrounded by congested blood vessels.
- Formation of pus, consisting of neutrophils and liquefied tissue debris.

Ulcer:
- A local defect on the surface of an organ due to sloughing of necrotic tissue, commonly seen in the gastrointestinal tract or skin.

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