Acute and Chronic Inflammation

Acute and Chronic Inflammation

Acute and Chronic Inflammation

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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) 5 Cardinal Signs of Inflammation Diagram

⭐ 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:

MediatorSourceKey Action(s)
HistamineMast cells, BasophilsVasodilation, ↑ Vasc. permeability, Pruritus
BradykininPlasma (Kinin system)Vasodilation, ↑ Permeability, Pain
C3a, C5aPlasma (Complement)Mast cell degranulation; C5a: Chemotaxis, leukocyte activation
LTB₄LeukocytesChemotaxis, Neutrophil activation
PGE₂, PGD₂, PGI₂Mast cells, EndotheliumVasodilation, Pain, Fever (PGE₂), Edema
TNF, IL-1Macrophages, Mast cellsEndothelial activation, Fever, Systemic effects
Chemokines (e.g. IL-8)Macrophages, Endothelial cellsLeukocyte recruitment & activation
Nitric Oxide (NO)Endothelium, MacrophagesVasodilation, Microbicidal, ↓ Platelet agg.
  • Cell membrane phospholipids release AA, metabolized by COX & LOX.
  • $AA \rightarrow Prostaglandins (PG), Leukotrienes (LT), Lipoxins (LX)$. Arachidonic acid metabolism pathway diagram

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 with epithelioid cells and Langhans giant cell
    • Granuloma Types:
      FeatureTBSarcoidosisForeign BodyCat Scratch
      NecrosisCaseousNon-caseatingNon-caseatingStellate
      Giant CellsLanghansLanghans, AsteroidForeign bodyLanghans
      Assoc.M.tbSchaumann bodiesInert materialB. 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.

Practice Questions: Acute and Chronic Inflammation

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Which of the following does not cause granulomatous inflammation?

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Flashcards: Acute and Chronic Inflammation

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A _____ section is done for the fixation of fats.

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A _____ section is done for the fixation of fats.

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