Lecture Notes: Inflammation and Repair
Definition of Inflammation
- Response of vascularized tissue to any cellular injury (not just infection)
- Involves cells and molecules of host defense moving from circulation to site of injury to eliminate offending agents
Types of Inflammation
Acute Inflammation
- Fast onset (minutes to hours)
- Main cells involved: Neutrophils
- Effects: Mild and self-limited tissue injury; prominent local systemic signs (e.g., fever)
- Examples: Immediate redness and swelling upon injury
Chronic Inflammation
- Slow onset (days to months)
- Main cells involved: Monocytes, Macrophages, Lymphocytes
- Effects: Severe and progressive tissue injury
- May evolve from unresolved acute inflammation or due to severe injury
Cardinal Signs of Inflammation
- Redness (Rubor): Caused by increased blood flow
- Swelling (Tumor): Due to fluid exudation
- Heat (Calor): Result of increased blood flow and inflammatory mediators
- Pain (Dolor): Stretching of pain receptors; chemical mediators
- Loss of Function: Tissue disruption; fibroplasia or metaplasia
Causes of Inflammation
- Infections (bacterial, viral, etc.)
- Foreign bodies (traumatic injury)
- Tissue necrosis (caused by ischemia or infarction)
- Immune reactions (autoimmune diseases, allergens)
Inflammatory Process Steps
- Recognition of offending agent
- Recruitment of leukocytes and plasma proteins
- Removal of agent (phagocytosis)
- Regulation of response (to prevent overreaction)
- Repair of tissue
Acute Inflammation Components
- Vasodilation: Increases blood flow to injury site
- Increased Vascular Permeability: Allows leukocytes to leave blood vessels
- Leukocyte Emigration: Leukocytes move to injury via chemotaxis
Leukocyte Recruitment
- Margination and Rolling: Leukocytes move to blood vessel walls and roll along
- Adhesion: Leukocytes adhere to endothelium
- Transmigration: Leukocytes pass through blood vessel walls
- Chemotaxis: Movement toward injury site
Cell Types in Inflammation
- Neutrophils: Predominate in acute inflammation
- Macrophages: Predominate in chronic inflammation
- Monocytes: Precursor to macrophages
- Lymphocytes: Involved in chronic inflammation
- Mast Cells and Eosinophils: Active in allergic responses
Outcomes of Inflammation
- Resolution: Complete restoration of normal function
- Fibrosis: Scar formation
- Progression to Chronic Inflammation
Chronic Inflammation
- Causes: Persistent infection, prolonged exposure to toxic agents, autoimmune disease
- Cells Involved: Macrophages, lymphocytes, plasma cells
- Tissue Destruction: Due to persistent inflammatory agents
Granulomatous Inflammation
- Formed by aggregates of macrophages
- Seen in conditions like tuberculosis, sarcoidosis
Systemic Effects of Inflammation
- Fever: Elevation caused by cytokines and prostaglandins
- Leukocytosis: Increased leukocyte production
- Elevated Acute Phase Proteins (CRP, SAA)
Tissue Repair
- Proliferation of cells and scar formation
- Types of cells: Labile, stable, and permanent
- Healing Intentions: First intention (clean, approximated wounds), second intention (large tissue deficits)
Abnormal Wound Healing
- Hypertrophic Scars and Keloids: Excessive scar formation
- Contractures: Excessive wound contraction causing deformation
- Ulceration: Poor healing due to inadequate blood supply
Conclusion
- Important to regulate inflammation to prevent damage
- Repair mechanisms aim for restoration or adaptation through scar formation
These notes summarize key points about inflammation, including mechanisms, cellular responses, outcomes, and the process of tissue repair. Understanding these concepts is crucial for diagnosing and treating inflammatory conditions effectively.