inflammation

Inflammation Overview

Assoc. Prof. Kameliya Bratoeva, M.D., PhDES of Pathophysiology, MU-Varna

Page 2: Definition of Inflammation

  • Complex Process: Inflammation is a local and non-specific pathological process.

    • Develops in response to cellular and tissue damage.

    • Consists of vascular response, cellular reaction, and systemic reactions.

Page 3: Role of Inflammation

  • Defense Mechanism: Inflammation is part of the body’s defense system.

    • Recognizes and removes harmful stimuli.

    • Initiates the healing process.

Page 4: Causes of Inflammation

  • Physical Agents: Heat, cold, radiation, mechanical injury.

  • Chemical Agents: Organic and inorganic poisons.

  • Infective Agents: Bacteria, viruses, parasites.

  • Immunological Agents: Cell-mediated and antigen-antibody reactions.

Page 5: Innate Immunity

  • Two Lines of Defense:

    • Natural barriers.

    • Inflammation as a response to breached barriers.

  • Purpose: Limits damage, protects from further injury, and promotes healing.

Page 8: Types of Inflammation

  • Classification: Based on host defense capacity and response duration.

    • Acute Inflammation: Short-term response.

    • Chronic Inflammation: Long-term response.

Page 10: Phases of Inflammation

  1. Alteration: Degeneration and necrosis of cells and tissue.

  2. Exudation: Formation of exudate.

  3. Proliferation: Restoration of tissue.

Page 11: Exudation Phase

  • Key Features:

    • Microcirculatory disturbances.

    • Increased vascular permeability.

    • Exudation of blood components.

    • Emigration of blood cells.

    • Phagocytosis.

    • Development of inflammatory infiltration.

Page 15: Acute Inflammatory Response

  • Initial Vascular Changes:

    • Vasodilation and increased capillary permeability.

    • Influx of inflammatory cells (e.g., neutrophils).

    • Systemic effects like fever.

Page 17: Vascular Changes in Acute Inflammation

  1. Vascular Caliber Alteration:

    • Initial vasoconstriction followed by vasodilation.

    • Increased blood flow leads to redness and warmth (rubor and calor).

Page 18: Microvasculature Changes

  1. Increased Permeability:

    • Plasma proteins and cells lead to swelling (tumor).

    • Fluid loss causes red blood cell concentration and slowed blood flow (stasis).

Page 19: Leukocyte Emigration

  1. Neutrophil Migration:

    • Neutrophils primarily migrate from microcirculation to damaged tissue.

Page 20: Phagocytosis Mechanism

  1. Phagocytosis:

    • Neutrophils migrate to damaged tissue via receptor interactions with capillary endothelium.

    • Endothelial cells express binding molecules (selectins) during inflammation.

Page 24: Effects of Inflammatory Exudate

  • Main Effects:

    • Dilution of damaging agents.

    • Facilitates leukocyte and antibody influx.

    • Limits spread of damage.

Page 25: Morphological Types of Exudative Inflammation

  • Types:

    • Serous: Watery, low protein.

    • Fibrinous: Thick, sticky, high protein.

    • Purulent: Pus formation with pyogenic bacteria.

    • Hemorrhagic: Vascular damage with red blood cells.

    • Catarrhal: Increased mucus production.

    • Mixed: Combination of types.

Page 30: Chronic Inflammation

  • Manifestations: Infiltration with macrophages, lymphocytes, and fibroblasts.

    • Leads to persistent inflammation and scar formation.

Page 31: Differences Between Acute and Chronic Inflammation

  • Key Differences:

    • Duration of development.

    • Cell types involved.

    • Proliferative processes.

Page 32: Functions of Macrophages in Chronic Inflammation

  • Key Functions:

    • Essential for wound healing and phagocytosis.

    • Produce proteases for foreign protein removal.

    • Release tissue thromboplastin for hemostasis.

    • Secrete growth factors for new blood vessel growth.

    • Phagocytose spent neutrophils.

Page 36: Chemical Mediators of Inflammation

  • Complement System: Enhances inflammation and chemotaxis.

  • Kinins: Increase vascular permeability and cause pain.

  • Clotting Factors: Form barriers to infection spread.

Page 42: Systemic Manifestations of Inflammation

  • Responses:

    • Fever, neutrophilia, lethargy, muscle catabolism.

    • Increased acute phase proteins (e.g., CRP).

Page 43: Cytokines in Systemic Effects

  • Key Cytokines: IL-1, IL-6, TNFα.

    • Responsible for systemic effects of inflammation.

Page 44: Liver Response to Cytokines

  • Acute Phase Proteins: Released by the liver in response to cytokines.

Page 45: Conclusion

  • **Thank You for Your