PATHOLOGY - Tissue Damage and Inflammation Flashcards
- What are granulomatous keratic precipitates made out of ?
- What are non-granulomatous KPs made out of
- What are mutton fat KPs made out of
- Granulomatous KPs - macrophages
- Non-granulomatous KPs - lymphocytes and polymorphonuclear leukocytes
- mutton fat - epithelioid histiocytes
Which layer do flame haemorrhages occur?
Which layer do dot blot haemorrhages occur?
Which layer do hard exudates and CMO occur?
- flame - nerve fibre layer
- dot/blot - inner/outer plexiform layers
- exudates/cmo - outer plexiform layer
Which cell type is responsible for inflammatory corneal damage?
polymorphonuclear leukocyte (PMN)s release hydrolytic enzymes that denature protein and cause tissue necrosis
What are the 3 mechanisms of acute inflammation?
NON-ADAPTIVE, NO MEMORY, NON-SPECIFIC
- Hyperaaemia - intiial vasoconstriction then dilation –> vasodilation slows blood flow, causing cells to move to the lateral walls/sides (margination)
- Exudation - protein-rich fluid moves into interstitial fluid
- Leucocyte migration - via extravasation and chemotaxis for phagocytosis
What are the chemical mediators of the vascular phase? (3)
- Histamine - from degranulated mast cells to cause increase vascular permeability (C3a/C5a) and vasodilation of venules (5-15 mins)
- Kinins - more prolonged venule and capillary vasodilation response
- Prostaglandins - dilate arterioles - more persistent response (4-24 hours)
Which cells predominate in bacterial, viral and parasitic infection?
Bacterial: neutrophils
Eosinophils: parasitic
Monocytes: viral
What is the mechanism of cellular phase of acute inflammation?
- Cell adhesion molecules expressed on activated endothelial cells
- Bonds established (by selectins on endothelium and integrins on neutrophils) between endothelium and white cells following margination
- Platelet activating factor activates neutrophils and induces beta-integrins expression on cell membrane to further promote adhesion at endothelium
- IL-8 stimulates Transmigration of neutrophils between endothelial cells
What molecules are chemotaxins? (5)
- Cytokines from leucocytes
- Complement components (C5, C5a)
- Arachidonic acid derivatives
- Pathogens
- Lymphokines (produced by T helper lymphocytes)
What is the intracellular pathway of chemotaxis?
Binding of chemotactic factors on polymorph stimulates calcium influex –> cGMP –> microtube assembly to aid migration (cAMP inhibits this)
Once within injured tissue, leucocytes can undertake phagocytosis
What are the main opsonins? (2)
- C3b
- IgG
What is the role of myeloperoxidase? What is the role of lactoferrin?
Myeloperoxidase - in lysosomes increases effectiveness of hydrogen peroxide
Lactoferrin inhibits micro-organism growth
Which clotting factor activates kinin system, clotting cascade and complement system?
Hageman factor (Factor 12)
What is the process of granuloma formation?
Granuloma represents failure of acute inflammatory neutrophils to clear inciting agent so macrophages take over
Inner core: macrophages and epithelioid cells
Outer core: activated macrophages, T lymphocytes
Outer layer: fibroblasts and multi-nucleated giant cells
What cells predominate in non-granulomatous inflammation? Which diseases? (2)
Lymphocytes and plasma cells
Behcet’s, multiple sclerosis
What is the process of corneal angiogenesis? What does it respond to?
Response to inflammation promoted by fibrin and its degradation products.
- Latent - vasodilation, vascular permeability of neighbouring vessels, stromal oedema
- Endothelial activation (24 hours), the endothelium retracts and nucleoli enlarge
- Endothelial basement membrane/basal lamina broken down by plasminogen activator which is produced by fibroblasts, macrophages and others
- Vascular sprouting - sprouts from post-capillary venules and capillaries
- Vascular maturation - deposition of ECM and laminin and basal lamina/basement membrane formation
