Acute Inflammation Quiz

Acute Inflammation - Overview

• Acute inflammation is the body's local response to injury caused by any agent.
• It's a protective mechanism to eliminate or limit the spread of injurious agents, and remove necrosed cells and tissues.
• Acute inflammation is innate, immediate, and early, typically lasting minutes to hours or a few days.
• Key objectives include understanding the causes and purposes of acute inflammation, its macroscopic and microscopic features (edema, vasodilation, neutrophil margination/migration), and the relationship between microscopic and macroscopic changes.

References

• Robbins basic pathology
• Muir's Textbook of pathology

Objectives

• Major causes and biological purposes of acute inflammation
• Macroscopic features of acute inflammation
• Microscopic features of acute inflammation, including edema and vasodilation
• Neutrophil margination and migration
• Relationship between microscopic and macroscopic changes

Causes of Acute Inflammation

• Microbial infections (bacterial, viral, fungal, parasitic) are common causes
• Hypersensitivity reactions (acute phase) against environmental substances or "self" tissues
• Physical and chemical agents (burns, frostbite, radiation, toxins) causing host cell injury
• Tissue necrosis (ischemia, physical/chemical injury)

Clinical Features of Acute Inflammation

• Main clinical signs include:
  • RUBOR (redness)
  • TUMOR (swelling)
  • CALOR (heat)
  • DOLOR (pain)
  • Loss of function

Acute Inflammation - Major Characteristics

• Vascular Reaction: Accumulation of fluid exudate and neutrophils in tissues
• Controlled by chemical mediators derived from plasma or cells
• It's a protective mechanism but can lead to local and systemic complications, usually followed by repair.

Vascular Changes

• Transient vasoconstriction of arterioles (few seconds)
• Vasodilation of arterioles and capillaries, leading to increased blood flow (heat and redness)
• Increased permeability of blood vessels, causing exudation of protein-rich fluid into tissues, and slowing of circulation.
• Concentration of red blood cells (RBCs) in small vessels, increasing blood viscosity (stasis)

Increased Vascular Permeability

• Increased vascular permeability leads to movement of protein-rich fluid and blood cells into the extravascular tissues.
• This causes increased osmotic pressure of interstitial fluid and more fluid outflow from the blood into the tissues.

Starling's Law and Fluid Loss

• Fluid flow across vessel walls depends on the balance of hydrostatic pressure within the vessels and the difference in colloid osmotic pressure between plasma and interstitial fluid.
• Increased hydrostatic pressure leads to increased fluid flow out of the vessels.
• Increased colloid osmotic pressure of the interstitial fluid pulls fluid into the vessels, and/or prevents fluid from leaving.

Exudate vs. Transudate

• Exudate: High protein content, specific gravity above 1.02, characteristic of inflammation
• Transudate: Low protein content, specific gravity less than 1.012, caused by hydrostatic pressure imbalance (e.g., venous obstruction)

Edema

• Edema is excess fluid in the interstitium, and can be transudate or exudate.
• Edema leads to increased lymphatic drainage.
• Pus is a purulent exudate, rich in neutrophils and cell debris.

Lymphatic Drainage in Inflammation

• Lymph flow increases during inflammation to drain edema fluid, leukocytes, and cell debris from extravascular space
• In severe inflammatory reactions, especially to microbes, lymphatics may transport the offending agent, contributing to dissemination.

Mechanisms of Increased Vascular Permeability

• Endothelial cell contraction (intercellular gaps in postcapillary venules)
• Endothelial injury (e.g., burns, infections)
• Increased transcytosis (proteins through intracellular vesicles)
• Leakage from new blood vessels (angiogenesis)

Cellular Events in Acute Inflammation (Leukocyte Recruitment)

• Stasis slows blood flow, leading to margination of neutrophils at vessel walls.
• Neutrophils roll along endothelium (rolling).
• Neutrophils adhere firmly to endothelium (adhesion).
• Neutrophils migrate through the vessel wall (emigration).
• Neutrophils migrate in interstitial tissues toward a chemotactic stimulus (chemotaxis).

Chemotaxis & Phagocytosis

• Leukocytes move towards sites of infection/injury along a chemical gradient (chemotaxis).
• Exogenous and endogenous substances are chemotactic, including bacterial products, cytokines, complement system components, and products of the lipoxygenase pathway.

Phagocytosis

• Neutrophils phagocytose microorganisms.
• Activated neutrophils release toxic metabolites/enzymes harming host tissue.

How Do These Changes Combat Injury?

• Exudation of Fluid: Delivers plasma proteins (immunoglobulins, inflammatory mediators, fibrinogen) to the injured area, diluting toxins. Increases lymphatic drainage, delivering microbes/antigens to phagocytes and the immune system.
• Infiltration of Cells: Removes pathogenic organisms/necrotic debris.
• Vasodilation: Increases blood flow/delivery to the injured area (increases temperature).
• Pain and Loss of Function: Enforces rest, reduces further trauma.