Inflammation III Flashcards

1
Q

What are the pathological effects of inflammation?

A
  • Increased endothelial permeability
  • Increased expression of adhesion molecules
  • Chemokine production
  • Fever
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2
Q

What is suppurative inflammation?

A
  • Acute inflammatory exudate rich in neutrophils
  • Common in bacterial infections
  • Mixture of neutrophils, necrotic tissue and tissue fluid in exudate
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3
Q

Describe serous inflammation

A
  • Accumulation of fluid with low plasma protein and cell content e.g pleural inflammation
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4
Q

Describe fibrinous inflammation

A
  • Pattern of acute inflammation - exudate has high plasma protein content
  • Deposition of fibrin in tissues
  • Forms mat-like sheet on membrane-lined cavities e.g peritoneum
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5
Q

Describe necrotising inflammation.

A
  • Virulent organism produces severe tissue damage and extensive cell death
  • EXAMPLE: GANGRENE - possible forms of maintenance: amputation and blood vessel construction
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6
Q

Describe chronic inflammation

A
  • CAUSES: Persistent injury and inflammatory response is insufficient to completely degrade pathogen
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7
Q

What are the causes of chronic inflammation?

A
  • Bout of acute inflammation
  • Autoimmune diseases and persistent infections
  • Response to malignant tumours and infections
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8
Q

What is the role of macrophages in chronic inflammation?

A
  • Antigen presentation to T and B cells
  • Release chemotactic factors for other leukocytes
  • Stimulates endothelium for adhesion molecule activation
  • Phagocytosis
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9
Q

What are the roles of eosinophils and basophils?

A
  • EOSINOPHILS - parasitic infections and IgE-mediated allergic reactions
  • BASOPHILS - contain mediators such as mast cells. IgE mediated reactions and histamine release
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10
Q

Describe the process of chronic inflammation.

A
  • Macrophage and lymphocyte activation
  • Growth factors cause fibroblast and endothelial cell proliferation
  • Cytokines cause increased collagen synthesis
  • Decreased metalloprotease activity = Decreased collagen degradation
  • RESULT: FIBROSIS
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11
Q

Describe granulomatous inflammation.

A
  • Type of chronic inflammation - presence of granuloma
  • GRANULOMA - accumulation of activated macrophages surrounded by rim of lymphocytes
  • Macrophages are larger than normal. Have pink cytoplasm. Called ‘epithelioid macrophages’
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12
Q

What is the outcome of chronic inflammation?

A
  • Attempt to heal by fibrosis
  • Damaged tissues unable to regenerate and replaced by fibrous tissue
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13
Q

What is tissue repair and what are its stages?

A
  • Regeneration of damaged tissue by cells of same type
  • HEMOSTASIS, INFLAMMATION, REGENERATION, FIBROSIS AND REMODELING
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14
Q

Describe the inflammatory phase. PART 1

A
  • Initiated by microbial invasion and tissue damage. Recognition of PAMPs by PRRs
  • Inflammasomes release cytokines
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15
Q

Describe the inflammatory phase. PART 2

A
  • Damaged blood vessels initiates coagulation
  • Mediators attract neutrophils and other inflammatory cells - secrete cytokines, interferons, growth factors
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16
Q

Describe the inflammatory phase. PART 3

A
  • Neutrophil polymorphs and tissue macrophages undergo apoptosis
  • Type 1 collagen replaces type 3 collagen. Cross linking stabilises wound and causes wound remodelling
  • ‘Restoration’ macrophages restore inflammatory cell types to normal levels
17
Q

f

Describe the proliferative phase.

A
  • Endothelial proliferation from existing vessels generates and secretes collagen
  • Fibroblasts mature and form collagen
  • Reduces size of injured site