Chapter 2: Inflammation
Inflammation: A Comprehensive Overview
Introduction to Inflammation
Definition: Inflammation is a protective response of the body to tissue injury, aiming to eliminate the cause of injury, remove damaged tissue, and initiate repair.
Triggers of Tissue Injury:
Chemical agents: Toxins, irritants.
Physical agents: Trauma, burns, radiation.
Pathogenic microorganisms: Bacteria, viruses, fungi, parasites.
Pathway of Inflammation:
Tissue injury occurs due to one of the above agents.
Release of mediators of inflammation.
These mediators induce a cascade of events:
Capillary dilatation: Widening of blood vessels.
Increased blood flow: Leads to localized heat and redness.
Increased capillary permeability: Endothelial cells separate, allowing fluid and proteins to leak out.
Extravasation of fluid: Accumulation of fluid in the interstitial tissue, causing swelling and tenderness and contributing to pain by pressing on nerve endings.
Attraction of leukocytes: White blood cells are recruited to the site of injury.
Migration of white cells to site of injury: Leukocytes move from the bloodstream into the injured tissue.
Systemic response: Generalized reactions like fever and leukocytosis (increased white blood cell count).
Cardinal Signs of Inflammation (Clinical Manifestations):
Heat (Calor)
Redness (Rubor)
Swelling (Tumor)
Pain (Dolor)
Loss of Function (Functio Laesa) (though not explicitly listed on page 2, it's a classical fifth cardinal sign).
Cellular Components of Inflammation
Blood Vessels: Key conduits for inflammatory cells and mediators.
White Blood Cells (Leukocytes): Crucial for host defense.
Polymorphonuclear neutrophil (PMN): Phagocytic, prominent in acute inflammation.
Basophil: Releases histamine and other mediators.
Monocyte: Precursor to macrophage, phagocytic.
Lymphocyte: Involved in specific immunity (adaptive immunity).
Eosinophil: Involved in allergic reactions and parasitic infections.
Mast cell: Releases histamine and other mediators, particularly involved in immediate hypersensitivity.
Macrophage: Highly phagocytic, antigen presentation, key in chronic inflammation.
Plasma cell: Differentiated B lymphocyte, produces antibodies.
Platelets: Involved in hemostasis and release inflammatory mediators.
Phagocytosis: Elimination of Pathogens
Definition: The process by which cells (phagocytes) engulf solid particles, such as bacteria, other cells, or cellular debris.
Mechanism (Phagocytosis of Bacteria):
Recognition and Attachment: A bacterium binds to receptors on the phagocyte's cell membrane, often via opsonins like Fc (constant region of antibody) and C3 (complement protein) (A).
Engulfment (Invagination): The phagocyte's cell membrane invaginates, extending pseudopods around the bacterium to form a phagocytic vacuole (phagosome) (B).
Degranulation and Killing: Lysosomal granules within the phagocyte move towards the phagocytic vacuole and fuse with it. This process, called degranulation, releases antimicrobial substances, including reactive oxygen species (O2, H2O_2), and enzymes into the vacuole to kill and digest the bacterium (C).
Circulatory Changes in Inflammation
These changes facilitate the delivery of inflammatory cells and mediators to the site of injury.
Transient Vasoconstriction: Initial, brief constriction of arteriolar smooth muscles.
Vasodilation: Followed by sustained relaxation of arteriolar smooth muscles, leading to:
Active hyperemia: Increased blood flow to the area, causing increased temperature (heat) and redness.
Increased Hydrostatic Pressure: The increased blood flow and vasodilation lead to higher pressure within the capillaries, forcing fluid out of the vessels.
Results in edema: Accumulation of fluid within the extravascular compartment and interstitial tissues.
RBC Rouleaux Formation: Red blood cells stack together like a