Acute and Chronic Inflammation

Acute and Chronic Inflammation - Body's Red Alert

• Inflammation: Protective response to injury.
• Acute Inflammation:
  • Rapid onset, short duration.
  • Cells: Neutrophils.
  • Features: Exudation, edema.
• Chronic Inflammation:
  • Slow onset, long duration.
  • Cells: Lymphocytes, Macrophages.
  • Features: Tissue destruction, fibrosis.
• Cardinal Signs (📌 PRISH):
  • Pain (Dolor)
  • Redness (Rubor)
  • Immobility (Functio laesa)
  • Swelling (Tumor)
  • Heat (Calor)

⭐ The five cardinal signs of inflammation were first described by Celsus (calor, dolor, rubor, tumor), with functio laesa (loss of function) later added by Galen.

Acute and Chronic Inflammation - Rapid Firefighters

• Acute Inflammation: Rapid onset, short (days). Key cell: Neutrophil. Cardinal signs: Rubor, Tumor, Calor, Dolor, Functio laesa.
  • Vascular: Vasodilation (NO, Histamine), ↑ Permeability (Histamine, Leukotrienes) → Exudate.
  • Cellular: Leukocyte Extravasation (📌 'Margie Rolls Adhesively Trans Di Chemo')

![Leukocyte extravasation cascade](https://ylbwdadhbcjolwylidja.supabase.co/storage/v1/object/public/notes/L1/Pathology_General_Pathology_Acute_and_Chronic_Inflammation/7788e856-527e-4ae6-b20a-6a738974d538.jpg)
- Phagocytosis: Opsonins (C3b, IgG). Killing: ROS, lysosomal enzymes.
- Key Mediators: TNF, IL-1, IL-6 (systemic), Chemokines (IL-8), Complement (C3a, C5a, C3b), AA metabolites (PGs, LTs).
- Outcomes: Resolution, Fibrosis, Abscess, or Chronic.

• Chronic Inflammation: Prolonged (weeks-months). Key cells: Lymphocytes, Macrophages. Tissue destruction & repair (angiogenesis, fibrosis) co-exist.

⭐ Defects in leukocyte adhesion (LAD type 1: LFA-1 integrin defect; LAD type 2: Sialyl-Lewis X defect) cause recurrent bacterial infections due to impaired neutrophil recruitment.

Acute and Chronic Inflammation - Chemical Signals & Scars

Chemical mediators (plasma/cell-derived) orchestrate vascular/cellular responses.

Key Chemical Mediators:

• Cell membrane phospholipids release AA, metabolized by COX & LOX.
• $AA \rightarrow Prostaglandins (PG), Leukotrienes (LT), Lipoxins (LX)$.

Complement System Activation: Activates via classical, alternative, or lectin pathways.

⭐ Prostaglandin E2 (PGE₂) mediates fever and pain in inflammation. (📌 Fever: IL-1, TNF, PGE₂)

Chronic Inflammation & Scarring:

• Persistent injury → chronic inflammation.
• Key mediators: Growth factors (TGF-β, PDGF from MΦ, lymphocytes) → fibroblast activation → collagen deposition → fibrosis (scar).

Acute and Chronic Inflammation - The Long War

• Chronic Inflammation: Prolonged; macrophages, lymphocytes, plasma cells. Tissue injury & repair (fibrosis, angiogenesis).
• Key Cells:
  • Macrophages: Dominant. IFN-γ (classical activation), IL-4/IL-13 (alternative). Secrete TNF, IL-1.
  • Lymphocytes: T & B cells; interact with macrophages.
• Granulomatous Inflammation: Epithelioid macrophages (activated), often with lymphocytes, Langhans giant cells.
  • 
  • Granuloma Types:

    Feature	TB	Sarcoidosis	Foreign Body	Cat Scratch
    Necrosis	Caseous	Non-caseating	Non-caseating	Stellate
    Giant Cells	Langhans	Langhans, Asteroid	Foreign body	Langhans
    Assoc.	M.tb	Schaumann bodies	Inert material	B. henselae

  ⭐ Caseating granulomas: TB. Non-caseating: Sarcoidosis, Crohn's.

• Systemic Effects (Acute Phase Response):
  • Fever (IL-1, TNF → PGE₂). ↑CRP (<10 mg/L normal), ↑SAA, ↑Fibrinogen (↑ESR).
  • Leukocytosis. Anemia of chronic disease (hepcidin).

High‑Yield Points - ⚡ Biggest Takeaways

• Acute inflammation: Characterized by neutrophils, exudation, and vasodilation. Key mediators: histamine, prostaglandins, leukotrienes.
• Chronic inflammation: Involves lymphocytes, macrophages, leading to tissue destruction and fibrosis.
• Cardinal signs of acute inflammation: Rubor, tumor, calor, dolor, functio laesa.
• Granulomatous inflammation: Features epithelioid macrophages and giant cells (e.g., Langhans).
• Tuberculosis shows caseating granulomas; sarcoidosis presents with non-caseating granulomas.
• Key cytokines: TNF and IL-1 drive acute inflammation; IFN-γ activates macrophages in chronic states.