Inflammation Overview and Types

Inflammation Overview

• Inflammation is a vital process in which living tissues react to injury as a protective response.
• Its goal is to localize and eliminate the cause of cell injury.

Intended Learning Outcomes (ILOs)

• Define inflammation and recognize clinical manifestations, including systemic effects.
• Explain vascular and cellular events in acute inflammation, describing its morphology.
• Compare and contrast acute and chronic inflammation.
• Recognize different types of acute inflammation and examples of each.
• Recognize pathologic changes in acute and chronic osteomyelitis.

Definition

• Inflammation is a vital process in which living tissues react to injury as a protective response.
• Actions include localizing and eliminating the cause of cell injury.

Types of Inflammation

• Acute Inflammation:
  • Rapid onset, short duration (minutes to days)
  • Exudative
• Chronic Inflammation:
  • Gradual onset, long duration (days to years)
  • Productive (granulation tissue)
  • Fibrosis

Causes of Inflammation

• Physical: Trauma, heat, cold, irradiation
• Chemical: Acids, alkalies
• Infective: Bacteria, viruses, parasites

Acute Inflammation (Detailed)

• Vascular Changes (Initial):

  • Transient vasoconstriction followed by vasodilation.
  • Increased vascular permeability (due to chemical mediators on arterioles, capillaries, post-capillary venules). This leads to inflammatory exudate and swelling.

• Leukocyte Emigration:

  • Steps of Leukocyte emigration:
    • Margination
    • Rolling (mediated by selectins)
    • Adhesion (mediated by integrins)
    • Transmigration
    • Chemotaxis
    • Phagocytosis

• Chemotaxis: Substances (chemotaxins) attract immune cells to the site of injury. This includes soluble bacterial products and components of the complement system (like C5a and C3a), as well as products of arachidonic acid metabolism (like leukotriene B4).

• Phagocytosis: Neutrophils and macrophages engulf and destroy bacteria and foreign particles.

  • Opsonization: Coating micro-organisms with opsonins (like IgG and C3b) to make them more recognizable and easier to engulf.
  • Engulfment: The immune cells engulf the targeted material.
  • Killing and Degradation: Killing of micro-organisms through Reactive Oxygen Species (ROS), Reactive Nitrogen Species (particularly NO), and lysosomal enzymes.

• Inflammatory Exudate:

  • Fluid rich in fibrinogen (clotting proteins).
  • Functions of Inflammatory exudates:
    • Diluting bacterial toxins.
    • Bringing antibodies to the inflammation area.
    • Bacteriolysins (bacteria-killing agents).
    • Agglutinins (to clump the organism).
    • Opsonins (to coat the organism).
    • Fibrinogen → fibrin (to localize infection and facilitate leukocyte movement).

• Chemical Mediators of Inflammation:

  • Cell-derived mediators (like histamine, prostaglandins, nitric oxide).
  • Plasma-derived mediators (like histamine, serotonin, substance P, bradykinin, C3a, C5a, IL-1, TNF, prostaglandins, and bradykinin).

Signs of Acute Inflammation

• Local:

  • Redness
  • Heat
  • Pain
  • Swelling
  • Loss of function

• Systemic:

  • Fever, anorexia, headache, malaise
  • Leukocytosis
  • Elevated acute-phase proteins (e.g., CRP, serum amyloid-associated protein, fibrinogen)
  • Lymphangitis and lymphadenitis
  • Shock (with severe bacterial infection).

Types of Acute Inflammation

• Local Suppurative:

  • Abscess: Localized collection of pus
  • Boil (Furuncle): Small abscess related to hair follicle or sebaceous gland
  • Carbuncle: Multiple abscesses separated by fibrous strands

• Diffuse Suppurative:

  • Cellulitis: Diffuse inflammation of subcutaneous tissue.

• Non-Suppurative:

  • Serous: Fluid with few proteins and cells (eg., blisters following burns; vesicles of herpes simplex).
  • Serofibrinous: Fluid rich in serous fluid and fibrin (e.g., acute fibrinous pericarditis).
  • Catarrhal: Excessive mucous secretion (e.g., common cold).
  • Membranous (Pseudomembranous): A true membrane forms, firmly attached to underlying tissue (eg. diphtheria). -Allergic: Characterized by excess eosinophils -Haemorrhagic: Blood in the exudate

Complications of Abscesses

• Chronic abscess
• Blood spread (toxemia, septicemia, pyaemia)
• Lymphatic spread (lymphangitis, lymphadenitis)
• Healing complications (ulcer, keloid, sinus, fistula).

Chronic Inflammation

• Persisted inflammation for weeks or months after initial injury.

• Progression from acute inflammation or recurrent episodes of acute inflammation.

• Occurs from chronic inflammation "de novo."

• Types include chronic non-specific inflammation and chronic specific inflammation (granulomas).

• Chronic Osteomyelitis : A specific type of chronic inflammation in bone

• Components of Chronic Osteomyelitis: The key structures affected and observed in chronic osteomyelitis include: Sequestrum (dead bone area), involucrum (new bone growth), and cloaca (a pathway for pus discharge).

Differences between acute and chronic inflammation (summary)

• Acute: Sudden onset, short duration, prominent vascular response, prominent local signs, acute phase proteins, prominent neutrophils, macrophages, healing or progression to chronic.
• Chronic: Gradual onset, long duration, less prominent vascular response, less prominent local signs, chronic phase proteins, chronic lymphocytes, plasma cells, macrophages, fibroblasts, fibrosis.

Fate of Acute Inflammation

• Resolution: Restoration of normal tissue structure.
• Healing/Repair: Tissue destruction and scarring.
• Progression to Chronic: Injury agent persists (e.g., tuberculosis [TB]), interfering with healing.
• Local Complications: Lymphangitis, lymphadenitis, bloodstream spread (bacteremia, septicemia, pyemia).
• Progress to Chronic Inflammation: Involves fibrosis of the affected area.