Inflammation, Healing & Repair 1

Acute Inflammation

• Definition: A complex reaction of vascularised connective tissue to local injury for a short duration of time
• Causes: Local injury
• Aims:
  • Contain and isolate the injurious stimulus
  • Destroy, dilute, or wall off the agents and neutralise the toxin
  • Heal and repair the damage caused

Clinical Signs of Acute Inflammation

• Heat: Hyperaemia
• Redness: Hyperaemia
• Swelling: Exudate
• Pain: Neural damage, chemical mediators
• Loss of function: Pain

Vascular Events

• Calibre change: Rapid transient vasoconstriction followed by vasodilation
• Blood flow change: Initial reduction of blood flow followed by increased blood flow to capillaries
• Permeability change: Increase permeability of microvasculature -> exudate

Cellular Events

• Transmigration towards site of infection
• Degranulation – destroy invading microorganisms
• Phagocytosis

Systemic Effects of Acute Inflammation

• Fever
• Malaise, lethargy, and sleepiness
• Pain
• Leucocytosis
• Tissue damage
• Swelling
• Hyperpyrexia, shock, and death due to too many cytokines

Exudate, Pus, Abscess, and Empyema

• Exudate: Protein-rich fluid that leaks out of blood vessels due to inflammation/infection
• Pus: Inflammatory exudate rich in white blood cells and/or microorganisms
• Abscess: Localised collection of pus surrounded by fibrous tissue
• Empyema: Not mentioned in the text

Coagulation, Kinin, and Complement Cascade Systems

• Coagulation System:
  • Activated by tissue damage
  • Fibrin is the end product
  • Thrombin increases leukocyte adhesion and fibroblast proliferation
  • Factor Xa increases vascular permeability and leukocyte exudation
  • Fibrin degradation acts as a chemotactic factor for leucocytes and increases endothelial permeability
• Kinin System:
  • Activated through Factor XII
  • Product: Bradykinin – causes vasodilation, triggers pain
• Complement Cascade System:
  • Triggers expression of adhesion molecules on leucocytes

Chemical Mediators of Inflammation

• Vasoactive Mediators:
  • Histamine: Released from mast cells, basophils, and platelets
  • Histamine causes dilation of arterioles, increasing vascular permeability of venules
  • Serotonin: Released from platelets and enterochromaffin cells
  • Serotonin actions similar to histamine

Acute Appendicitis

• Illustrates the processes of acute inflammation

Chronic Inflammation

• Pathogenesis:
  • Progression from acute inflammation not totally resolved
  • Involves macrophages, lymphocytes, and plasma cells
• Mechanism:
  • Excessive macrophage accumulation due to:
    • Continuous recruitment from circulation
    • Local proliferation
    • Immobilisation of peripheral macrophages
• Morphology:
  • Granuloma: Aggregation of macrophages that form in response to chronic inflammation
  • Macrophages secrete IL-1, interferon alpha, and TNF
  • Macrophage elongation leads to formation of epithelioid histiocytes
  • Epithelioid histiocytes and macrophage accumulation leads to giant cell formation
  • Necrotising granuloma: Central area of necrosis, occurs in TB
  • Non-necrotising granuloma: No necrosis, occurs in Sarcoidosis
• Granulation Tissue: New connective tissue and microscopic blood vessels that form during healing

Differences between Acute and Chronic Inflammation

• To be identified...

Define acute inflammation, its causes, and how it aims to reduce damage and promote healing and repair. Identify the five clinical signs of acute inflammation.