1. Anatomy
    2. 1. General anatomy
    2. General histology
    3. General embryology
  2. Physiology
    3. 4. Functional Organization and Internal Environment
    5. Cell Membrane and Communication
    6. Bioelectricity
    7. Ageing and Yoga
    8. Blood
  3. Pharmacology
    4. 9. General Pharmacology
    10. Antibacterial agents
    11. Antifungal agents
    12. Antiviral agent
    13. Antimalarial, anti-kalazar and antifilarial drugs
    14. Anticancer drugs
  4. Pathology
    5. 15. Cellular Adaptation, Injury, and Death
    16. Inflammation and Repair
    17. Hemodynamic Disorders, Thromboembolic Disease, and Shock
    18. Neoplasia
    19. Diseases of the Immune System
  5. Microbiology
    6. 20. General microbiology
    21. Immunology
  6. Biochemistry
    7. 22. Introduction to biochemistry
    23. Metabolism
    24. Vitamins
    25. Nucleic acids DNA and RNA
Pathology
16. Inflammation and Repair
INFLAMMATION AND REPAIR

1.

Define inflammation. Describe the vascular changes in acute inflammation.

(5)

[2066, 208_suppl]

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2.

Write short notes on: a. Cytokines b. Granulomatous inflammation.

(5)

[2072, 2078]

➤

Feature
Acute Inflammation
Chronic Inflammation
Onset
Rapid (minutes to hours)
Slow, progressive (days to years)
Duration
Short (few days)
Long-lasting
Primary cells involved
Neutrophils
Lymphocytes, plasma cells, macrophages
Vascular changes
Marked vasodilation, increased permeability, edema
Less prominent; angiogenesis may occur
Tissue injury
Usually mild and self-limited
Often severe and progressive
Outcome
  1. Resolution
  2. Suppuration (pus formation)
  3. Chronic inflammation
  1. Tissue destruction
  2. Fibrosis
  3. Persistent inflammation
Examples
  1. Acute bacterial pneumonia
  2. Appendicitis
  3. Skin abscess
  1. Tuberculosis
  2. Rheumatoid arthritis
  3. Chronic peptic ulcer
Major chemical mediators
  1. Histamine
  2. Prostaglandins
  3. Bradykinin
  1. Cytokines (IL-1, TNF-α)
  2. Interferon-γ
  3. Growth factors
▢ Acute inflammation:
❖ Vascular changes:
◉ Vasoconstriction: Temporary and initial narrowing of blood vessels after injury.
◉ Vasodilation: Widening of blood vessels leading to increased blood flow (hyperemia).
◉ Increased permeability:
◈ Exudate: Protein-rich fluid that escapes due to increased vascular permeability.
◈ Transudate: Protein-poor fluid resulting from hydrostatic imbalance without inflammation.
❖ Cellular changes:
◉ Margination: Leukocytes move to the periphery of blood vessels due to slowed blood flow.
◉ Rolling: Leukocytes transiently adhere to endothelium via selectins.
◉ Adhesion: Firm binding of leukocytes to endothelium via integrins.
◉ Transmigration: Leukocytes move across endothelium into tissue (diapedesis).
◉ Chemotaxis: Directed movement of leukocytes toward site of injury via chemical signals.
◉ Opsonization: Pathogens are coated with opsonins (IgG, C3b) for easier recognition.
◉ Phagocytosis:
◈ Recognition and Attachment: Leukocyte identifies and binds to opsonized particles.
◈ Engulfment: The particle is engulfed into a phagosome.
◈ Killing and degradation:
■ Oxygen dependent killing mechanism: Involves ROS production via NADPH oxidase (respiratory burst).
■ Oxygen independent killing mechanism: Uses lysosomal enzymes like lysozyme, defensins, etc.
▢ Cytokines:
❖ IL-1: Fever inducer; promotes adhesion molecules on endothelial cells.
❖ IL-6: Stimulates acute phase protein production by the liver.
❖ IL-8: Chemotactic for neutrophils.
❖ IL-12: Activates NK cells and promotes Th1 response.
❖ TNF-alpha: Major mediator of sepsis; causes fever, cachexia, and endothelial activation.
❖ INF-gamma: Activates macrophages and promotes granuloma formation.
❖ TGF-beta: Anti-inflammatory; promotes fibrosis and tissue repair.
❖ IL-10: Suppresses inflammatory response; produced by regulatory T cells.
▢ Granulomatous inflammation:
❖ Definition: A chronic inflammatory response characterized by granuloma formation.
❖ Granuloma:
◉ Structure:
◈ Central area: Collection of activated macrophages (epithelioid cells).
◈ Surrounding rim: Lymphocytes and fibroblasts form a capsule.
◈ Multinucleated giant cells: Formed by fusion of macrophages.
◉ Types:
◈ Caseating granuloma: Seen in TB; central necrosis with cheese-like appearance.
◈ Non-caseating granuloma: Seen in sarcoidosis; no central necrosis.
❖ Causes:
◉ Infectious:
  1. Mycobacterium tuberculosis
  2. Fungi (e.g., Histoplasma)
  3. Leprosy
  4. Syphilis
◉ Non-infectious:
  1. Sarcoidosis
  2. Crohn's disease
  3. Foreign body reaction
❖ Cytokines involved:
◉ IL-2: T cell proliferation.
◉ IFN-gamma: Activates macrophages.
◉ TNF-alpha: Maintains granuloma structure.
WOUND HEALING

1.

Describe the steps in repair by scar formation. List the factors that influence tissue repair.

(4)

[2072]

➤

▢ Healing by Primary intention:
❖ Steps:
Day
Features of wound
Day 0 (At wound formation time)
Presence of blood clot in the incision
Day 1
Neutrophilic infiltration + blood clot
Day 2
Neutrophils + blood clot + continuous thin epithelial layer
Day 3
Macrophages replace neutrophils, Appearance of granulation tissue, type III collagen deposition begins but do not bridge the incision
Day 5
Abundant granulation tissue
  1. Collagen fibrils bridge the incision
  2. Neovascularisation is maximum
  3. Full epithelial thickness with surface keratinization
End of 2 weeks
Accumulation of collagen; fibroblast proliferation
By 1 month
Replacement of collagen type III with collagen type I (has greater tensile strength) due to action of collagenase enzyme
▢ Healing by Secondary intention:
❖ Definition: Occurs in large, gaping wounds with tissue loss, infection, or ulceration.
❖ Features:
◉ Wound closure: Slower due to larger defect and more granulation tissue.
◉ Scar formation: More prominent due to increased tissue damage.
◉ Wound contraction: Myofibroblasts pull edges together.
◉ Inflammation: More intense and prolonged.
◉ Granulation tissue: More abundant than in primary intention.
▢ Factors affecting Wound healing:
❖ Local factors:
◉ Infection: Most important cause of delayed healing.
◉ Blood supply: Poor perfusion slows healing.
◉ Foreign bodies: Delay healing and promote infection.
◉ Mechanical stress: Repeated trauma delays healing.
❖ Systemic factors:
◉ Nutrition: Protein, vitamin C, and zinc are crucial.
◉ Age: Delayed healing in elderly.
◉ Chronic diseases: e.g., Diabetes mellitus impairs healing.
◉ Drugs: Steroids and chemotherapy inhibit healing.
◉ Immunosuppression: Delays inflammatory and proliferative phases.