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Pathology > Chronic inflammation > Flashcards

Chronic inflammation Flashcards

1
Q

Inflammation of prolonged duration,
in which inflammatory response, tissue injury and attempts at repair coexist in varying combinations

A

Chronic inflammation

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2
Q

Causes of Chronic inflamamtion

A
  1. Persistent Infections
  2. Immune-mediated Inflammatory Diseases
  3. Prolonged exposure to endo- or exogenous
    potentially Toxic Agents (e.g. Silica → Silicosis)
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3
Q

Characteristics of chronic inflammation

A

Tissue destruction
Fibrosis
Angiogenesis
Activation of B lymphocytes

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4
Q

Dominant cellular player in chronic inflammation

A

Macrophages

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5
Q

Mononuclear system consists of

A

Blood monocytes & tissue macrophages

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6
Q

Tissue macrophages:

A

▫ Kupfer cells (liver)
▫ Sinus Histiocytes (spleen and lymph nodes)
▫ Alveolar Macrophages (lungs)
▫ Microglia (CNS)

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7
Q

How do monocytes emigrate into extravascular tissues?

A

They move in the same way as neutrophils, regulated by adhesion molecules and chemical mediators.

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8
Q

What happens to monocytes when they enter extravascular tissue?

A

They transform into macrophages.

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9
Q

What activates macrophages?

A

Microbial products, cytokines, chemical mediators.

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10
Q

What are the primary functions of activated macrophages?

A

Elimination of injurious agents (chronic inflammation and tissue injury).
Initiation of the repair process.

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11
Q

What changes occur in activated macrophages?

A

Increase in lysosomal enzymes, reactive oxygen species (ROS), and nitrogen species.
Production of cytokines, growth factors, and other mediators.

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12
Q

What are the toxic products released by macrophages?

A

Reactive and nitrogen species toxic to microbes and host cells.
Proteases that damage the extracellular matrix.

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13
Q

How do macrophages influence other cells?

A

Release cytokines and chemotactic factors to attract other cell types.
Stimulate fibroblast proliferation, collagen deposition, and angiogenesis (via growth factors).

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14
Q

How do macrophages interact with T-cells?

A

Macrophages display antigens (Ags) to T-cells and produce co-stimulators and cytokines (e.g., IL-12) to stimulate T-cell responses.

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15
Q

What do activated T-lymphocytes produce & what is their role?

A

Activated T-lymphocytes produce chemokines that recruit monocytes from circulation.

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16
Q

What cytokines do T-lymphocytes produce, and what is its function?

A

T-lymphocytes produce IFN-γ, which acts as a powerful activator of macrophages.

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17
Q

What is granulomatous inflammation?

A

It is a distinctive pattern of chronic inflammation characterized by the formation of granulomas.

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18
Q

What is a granuloma?

A

A granuloma is a cellular attempt to contain an offending agent that is difficult to eradicate.

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19
Q

What are the causes of granulomatous inflammation?

A
  • Infectious organisms:
    Mycobacterium tuberculosis (M. Tbc)
    Mycobacterium leprae
    Histoplasma capsulatum, Blastomyces dermatidis
    Treponema pallidum
    Bartonella henselae (cat-scratch disease)
  • Foreign bodies
  • Unknown aetiology (e.g., Sarcoidosis)
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20
Q

What are the microscopic features of a granuloma?

A

Aggregation of macrophages transformed into epithelioid cells.
Collar of leukocytes and sometimes plasma cells.
Rim of fibroblasts and connective tissue (in older granulomas).
Presence of giant cells formed by fused epithelioid cells, located in the center or periphery.

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21
Q

What are the two types of giant cells found in granulomas?

A

Langhans-type giant cells
Foreign body-type giant cells

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22
Q

Types of granulomas?

A

Foreign-body Granulomas
Immune Granulomas

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23
Q

Centrally located, surrounded by epithelioid and
giant cells
Refractile under polarised light

A

Foreign Body

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24
Q

What causes the formation of immune granulomas?

A

They form in response to a persistent antigen (Ag), particularly one that induces a cell-mediated immune response (Type IV hypersensitivity reaction).

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25
Q

What are the characteristics of the inciting agent for immune granulomas?

A

The agent is either poorly degradable or particulate.

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26
Q

Describe the pathogenesis of immune granuloma formation.

A

1.Engulfment of the agent by macrophages.
2.Processing and presentation of the antigen to Ag-specific T-cells.
3/Activation of T-cells leads to two pathways:
- Pathway 1: T-cells produce IL-2 → Activates other T-cells → Perpetuates the immune response.
- Pathway 2: T-cells produce IFN-γ → Activates macrophages → Transforms them into epithelioid cells and giant cells.

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27
Q

What role does IL-2 play in immune granuloma formation?

A

IL-2 activates other T-cells, perpetuating the immune response.

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28
Q

What role does IFN-γ play in immune granuloma formation?

A

IFN-γ activates macrophages and facilitates their transformation into epithelioid cells and giant cells.

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29
Q

What are the consequences of defective inflammation?

A

Increased susceptibility to infections due to the failure of early defense mechanisms (innate immunity).
Delayed wound healing because inflammation is essential for clearing damaged tissues and initiating repair.

30
Q

How does inflammation contribute to wound healing?

A

It clears damaged tissues and debris, providing the stimulus needed to initiate the repair process.

31
Q

What is the basis of excessive inflammation in human diseases?

A

Allergies: Unregulated immune response to common environmental antigens (Ags).
Autoimmune Diseases: Immune response against normally tolerated self-antigens.

32
Q

What type of immune response characterizes allergies?

A

An unregulated immune response against commonly encountered environmental antigens.

33
Q

What defines autoimmune diseases in the context of excessive inflammation?

A

An immune response directed against self-antigens that are normally tolerated.

34
Q

What is regeneration in the context of healing?

A

The proliferation of cells and tissues to replace lost structures, resulting in complete restitution of damaged tissue.

35
Q

What is required for regeneration to occur?

A

Tissues with high proliferative capacity can regenerate if their stem cells are preserved.

36
Q

What is an example of regeneration?

A

Liver growth after partial resection or necrosis, although this is considered compensatory growth rather than true regeneration.

37
Q

What does tissue repair involve?

A

A combination of regeneration and scar formation through collagen deposition.

38
Q

What factors determine the balance between regeneration and scarring in tissue repair?

A

The tissue’s ability to regenerate.
The extent of the injury.

39
Q

What is the predominant healing process when ECM is severely damaged?

A

Scar formation, as part of tissue repair.

40
Q

What leads to scar formation in chronic inflammation?

A

Persistent injury triggers local production of growth factors and cytokines, leading to fibroblast proliferation and collagen synthesis (fibrosis).

41
Q

What are the three types of tissues based on cell proliferative activity?

A

Continuously dividing (labile) tissues.
Quiescent (stable) tissues.
Non-dividing (permanent) tissues.

42
Q

What are continuously dividing (labile) tissues?

A

Tissues where cells proliferate throughout life to replace destroyed cells, with mature cells derived from adult stem cells.

43
Q

Provide examples of continuously dividing (labile) cells

A

Squamous epithelium: Skin, oral cavity, cervix.
Columnar epithelium: GI tract, uterus.
Transitional epithelium: Urinary tract.
Bone marrow and hematopoietic cells.

44
Q

What are quiescent (stable) tissues?

A

Tissues with a low replication rate but can divide rapidly in response to stimuli, enabling tissue reconstruction.

45
Q

Provide examples of quiescent (stable) cells.

A

Cells of the liver, kidneys, and pancreas.
Mesenchymal cells (e.g., fibroblasts, smooth muscle cells).
Vascular endothelial cells.
Leukocytes.

46
Q

What is an example of regeneration in quiescent tissues?

A

Regeneration of liver cells after partial hepatectomy.

47
Q

What are non-dividing (permanent) tissues?

A

Tissues where cells cannot undergo mitotic division postnatally and are incapable of regeneration.

48
Q

How are non-dividing tissues repaired after irreversible cell loss?

A

Through scar tissue formation, such as fibrosis or gliosis.

49
Q

Provide examples of non-dividing (permanent) cells.

A

Neurons.
Skeletal muscle cells.
Cardiac muscle cells.

50
Q

Repair by connective tissue deposition includes:

A
  1. Inflammation
  2. Angiogenesis
  3. Migration and fibroblast proliferation
  4. Scar formation
  5. Connective tissue remodeling
51
Q

What happens in severe or chronic tissue injury with damage to both parenchymal cells and tissue matrix?

A

Repair occurs through collagen and ECM deposition, leading to scar formation.

52
Q

Restitution of tissue components.

A

Regeneration

53
Q

A fibro-proliferative response that “patches” rather than restores the tissue.

A

Repair

54
Q

What is a scar?

A

The replacement of parenchymal cells in any tissue by collagen.

55
Q

What are the three phases of scar formation?

A

Inflammation:
Injury causes platelet adhesion and aggregation → Clot formation → Inflammation.
Proliferation:
Formation of granulation tissue.
Proliferation and migration of connective tissue cells.
Re-epithelialization of the wound surface.
Maturation:
ECM deposition.
Tissue remodeling.
Wound contraction.

56
Q

What is healing by primary union (first intention)?

A

Healing of a clean, uninfected surgical incision approximated by sutures.
Limited epithelial & connective tissue damage with re-epithelialization and formation of a thin scar.

57
Q

What is healing by secondary union (secondary intention)?

A

Healing of an excisional wound with a large skin defect.
Extensive cell and tissue loss, intense inflammatory reaction, granulation tissue formation, and abundant collagen deposition → Leads to a substantial scar with wound contraction.

58
Q

What events occur on Day 1 during primary intention healing?

A

Development of a fibrin clot (haematoma).
Infiltration of wound margins by neutrophils.
Proliferation of basal cells in the squamous epithelium.

59
Q

What events occur on Day 2 during primary intention healing?

A

Movement of basal cells under the fibrin clot → Seals the wound within 48 hours.
Emigration of macrophages into the wound.

60
Q

What occurs by Month 1 during primary intention healing?

A

Collagenase remodels the wound:
Type III collagen is degraded and replaced by type I collagen, increasing tensile strength.
Formation of scar tissue devoid of adnexal structures (e.g., hair follicles, sweat glands) and inflammatory cells.

61
Q

What are the characteristics of healing by secondary intention?

A

More intense inflammatory reaction.
Increased formation of granulation tissue.
Wound contraction due to the presence of a higher number of myofibroblasts.

62
Q

What is the role of myofibroblasts in secondary intention healing?

A

Myofibroblasts cause wound contraction, reducing the size of the wound.

63
Q

What is tertiary intention healing?

A

Healing involves the treatment of contaminated wounds with:
Debridement: Removal of dead or infected tissue.
Antibiotics: To control infection.
Surgical closure of the wound after preparation.

64
Q

What differentiates tertiary intention from primary and secondary intention?

A

Tertiary intention is used for contaminated wounds and combines cleaning, infection control, and delayed surgical closure.

65
Q

Factors delaying or impeding Healing (8)

A

❖ Retention of debris
❖ Impaired circulation
❖ Persistent infection
❖ Metabolic disorders (e.g. Diabetes Mellitus)
❖ Glucocorticoids
❖ Nutritional deficiencies
❖ Malnutrition → Decreased protein
✓ Vitamin C deficiency
✓ Trace metal deficiency (e.g. Copper, Zinc)
❖ Keloids and hypertrophic scars

66
Q

What can abnormalities in the repair process lead to?

A

Complications in wound healing.

67
Q

What are the two types of deficient scar formation?

A

Wound dehiscence: Rupture of a wound, often due to increased pressure (e.g., vomiting, coughing).
Ulceration: Caused by inadequate vascularization during wound healing (e.g., ulcers in the lower extremities in patients with peripheral atherosclerotic vascular disease).

68
Q

What is the result of excessive formation of repair components?

A

Hypertrophic scar: Raised scar due to excessive collagen deposition.
Keloid: Scar tissue extends beyond the original wound and does not regress.
Excessive granulation tissue: Blocks re-epithelialization.
Desmoids/aggressive fibromatoses: Due to exuberant fibroblast proliferation

69
Q

What is the consequence of excessive granulation tissue formation?

A

It can block re-epithelialization, hindering proper wound healing.

70
Q

What are contractures in wound healing?

A

Exaggerated contraction in wound size, resulting in deformities of the wound and surrounding tissues.
Most common in areas like the palms, soles, and front of the thorax.
Typically seen after serious burns.

Pathology (26 decks)

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