Inflammation, Healing & Repair 1

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Questions and Answers

What is the primary aim of acute inflammation?

  • To promote tissue damage and increase pain
  • To reduce blood flow to the affected area
  • To destroy the surrounding healthy tissue
  • To contain and isolate the injurious stimulus (correct)

Which of the following is NOT a clinical sign of acute inflammation?

  • Redness
  • Loss of appetite (correct)
  • Swelling
  • Heat

What is the result of increased permeability of microvasculature during acute inflammation?

  • Pus
  • Exudate (correct)
  • Abscess
  • Empyema

Which system is activated by tissue damage and produces fibrin as an end product?

<p>Coagulation system (D)</p>
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What is the role of thrombin in the coagulation system?

<p>Increases leukocyte adhesion and fibroblast proliferation (B)</p>
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Which chemical mediator is released in response to physical injury and causes vasodilation?

<p>Histamine (B)</p>
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What is the characteristic of chronic inflammation that differentiates it from acute inflammation?

<p>Excessive macrophage accumulation (C)</p>
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What is the term for the aggregation of macrophages that form in response to chronic inflammation?

<p>Granuloma (C)</p>
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Which laboratory test is commonly used to diagnose chronic inflammation?

<p>Erythrocyte Sedimentation Rate (ESR) (D)</p>
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What is the term for the localised collection of pus surrounded by fibrous tissue?

<p>Abscess (A)</p>
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Study Notes

Acute Inflammation

  • Definition: A complex reaction of vascularised connective tissue to local injury for a short duration of time
  • Causes: Local injury
  • Aims:
    • Contain and isolate the injurious stimulus
    • Destroy, dilute, or wall off the agents and neutralise the toxin
    • Heal and repair the damage caused

Clinical Signs of Acute Inflammation

  • Heat: Hyperaemia
  • Redness: Hyperaemia
  • Swelling: Exudate
  • Pain: Neural damage, chemical mediators
  • Loss of function: Pain

Vascular Events

  • Calibre change: Rapid transient vasoconstriction followed by vasodilation
  • Blood flow change: Initial reduction of blood flow followed by increased blood flow to capillaries
  • Permeability change: Increase permeability of microvasculature -> exudate

Cellular Events

  • Transmigration towards site of infection
  • Degranulation – destroy invading microorganisms
  • Phagocytosis

Systemic Effects of Acute Inflammation

  • Fever
  • Malaise, lethargy, and sleepiness
  • Pain
  • Leucocytosis
  • Tissue damage
  • Swelling
  • Hyperpyrexia, shock, and death due to too many cytokines

Exudate, Pus, Abscess, and Empyema

  • Exudate: Protein-rich fluid that leaks out of blood vessels due to inflammation/infection
  • Pus: Inflammatory exudate rich in white blood cells and/or microorganisms
  • Abscess: Localised collection of pus surrounded by fibrous tissue
  • Empyema: Not mentioned in the text

Coagulation, Kinin, and Complement Cascade Systems

  • Coagulation System:
    • Activated by tissue damage
    • Fibrin is the end product
    • Thrombin increases leukocyte adhesion and fibroblast proliferation
    • Factor Xa increases vascular permeability and leukocyte exudation
    • Fibrin degradation acts as a chemotactic factor for leucocytes and increases endothelial permeability
  • Kinin System:
    • Activated through Factor XII
    • Product: Bradykinin – causes vasodilation, triggers pain
  • Complement Cascade System:
    • Triggers expression of adhesion molecules on leucocytes

Chemical Mediators of Inflammation

  • Vasoactive Mediators:
    • Histamine: Released from mast cells, basophils, and platelets
    • Histamine causes dilation of arterioles, increasing vascular permeability of venules
    • Serotonin: Released from platelets and enterochromaffin cells
    • Serotonin actions similar to histamine

Acute Appendicitis

  • Illustrates the processes of acute inflammation

Chronic Inflammation

  • Pathogenesis:
    • Progression from acute inflammation not totally resolved
    • Involves macrophages, lymphocytes, and plasma cells
  • Mechanism:
    • Excessive macrophage accumulation due to:
      • Continuous recruitment from circulation
      • Local proliferation
      • Immobilisation of peripheral macrophages
  • Morphology:
    • Granuloma: Aggregation of macrophages that form in response to chronic inflammation
    • Macrophages secrete IL-1, interferon alpha, and TNF
    • Macrophage elongation leads to formation of epithelioid histiocytes
    • Epithelioid histiocytes and macrophage accumulation leads to giant cell formation
    • Necrotising granuloma: Central area of necrosis, occurs in TB
    • Non-necrotising granuloma: No necrosis, occurs in Sarcoidosis
  • Granulation Tissue: New connective tissue and microscopic blood vessels that form during healing

Differences between Acute and Chronic Inflammation

  • To be identified...

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