Makindo Medical Notes

Related Subjects: |Acute Inflammation

Acute inflammation is a rapid and early response of the body to harmful stimuli such as pathogens, damaged cells, or irritants. It is characterized by the classical signs of heat, redness, swelling, pain, and loss of function. The primary purpose of acute inflammation is to eliminate the initial cause of cell injury, clear out necrotic cells and tissues, and establish a repair process.

Stages of Acute Inflammation

• Initiation:
  • Triggered by the recognition of harmful stimuli by pattern recognition receptors (PRRs) on immune cells.
  • Release of inflammatory mediators such as histamine, prostaglandins, and cytokines.
• Vascular Changes:
  • Vasodilation:
    • Increased blood flow to the affected area, causing redness and heat.
  • Increased Vascular Permeability:
    • Leakage of plasma proteins and fluid into the tissue, resulting in swelling (edema).
• Cellular Events:
  • Leukocyte Recruitment:
    • Margination and rolling of leukocytes along the endothelium.
    • Adhesion of leukocytes to the endothelial cells through the interaction of adhesion molecules.
    • Transmigration (diapedesis) of leukocytes through the vessel wall into the inflamed tissue.
  • Phagocytosis:
    • Engulfment of pathogens, debris, and foreign particles by neutrophils and macrophages.
    • Formation of phagosomes and their fusion with lysosomes to form phagolysosomes.
    • Destruction of ingested material by reactive oxygen species (ROS) and lysosomal enzymes.

Chemical Mediators of Acute Inflammation

• Vasoactive Amines:
  • Histamine:
    • Released by mast cells, basophils, and platelets.
    • Causes vasodilation and increased vascular permeability.
  • Serotonin:
    • Released by platelets and enterochromaffin cells.
    • Causes vasodilation and increased vascular permeability.
• Plasma Protein Systems:
  • Complement System:
    • Activation leads to the generation of C3a and C5a (anaphylatoxins) which increase vascular permeability and attract leukocytes.
    • C3b acts as an opsonin, facilitating phagocytosis.
  • Coagulation System:
    • Generation of fibrin, which forms a clot and serves as a scaffold for migrating cells.
  • Kinin System:
    • Bradykinin causes vasodilation, increased vascular permeability, and pain.
• Arachidonic Acid Metabolites:
  • Prostaglandins:
    • Produced by cyclooxygenase (COX) enzymes.
    • Cause vasodilation, increased vascular permeability, and pain.
  • Leukotrienes:
    • Produced by lipoxygenase enzymes.
    • Cause increased vascular permeability, chemotaxis, and leukocyte adhesion.
• Cytokines and Chemokines:
  • Tumour Necrosis Factor (TNF) and Interleukin-1 (IL-1):
    • Produced by activated macrophages and other cells.
    • Induce endothelial adhesion molecules, cytokine production, and fever.
  • Chemokines:
    • Direct the migration of leukocytes to the site of inflammation.
• Reactive Oxygen Species (ROS):
  • Produced by activated neutrophils and macrophages.
  • Kill microbes and signal for further inflammatory responses.
• Nitric Oxide (NO):
  • Produced by endothelial cells and macrophages.
  • Causes vasodilation and has antimicrobial properties.

Outcomes of Acute Inflammation

• Resolution:
  • Complete elimination of the pathogen or irritant.
  • Restoration of tissue to its normal state.
• Abscess Formation:
  • Localized collection of pus due to the body’s attempt to wall off the infection.
• Chronic Inflammation:
  • Persistence of the inflammatory stimulus leads to ongoing inflammation and tissue damage.
  • Characterized by the presence of macrophages, lymphocytes, and plasma cells.
• Fibrosis:
  • Formation of scar tissue due to extensive tissue damage and incomplete healing.

Clinical Signs and Symptoms

• Redness (Rubor):
  • Caused by increased blood flow to the inflamed area.
• Heat (Calor):
  • Due to increased blood flow and metabolic activity at the site of inflammation.
• Swelling (Tumour):
  • Resulting from fluid accumulation due to increased vascular permeability.
• Pain (Dolor):
  • Caused by the release of chemicals such as bradykinin and prostaglandins that stimulate nerve endings.
• Loss of Function (Functio Laesa):
  • Resulting from the combined effects of swelling and pain.

Summary

Acute inflammation is a vital protective response aimed at eliminating the initial cause of cell injury, clearing out necrotic cells, and establishing tissue repair. It involves a series of well-coordinated vascular and cellular events mediated by a variety of chemical signals. While acute inflammation is essential for healing, it must be tightly regulated to prevent excessive tissue damage and the development of chronic inflammation.