Acute inflammation Flashcards
(34 cards)
How long does acute inflammation take to respond to cell injury or agent? What dominates it?
Immediate response
Vascular changes
What is the first inflammatory cell at the site of acute inflammation? What do lots of neutrophils suggest about the infectious agent?
Neutrophils
Lots of neutrophils suggest bacterial infection
What happens to blood vessels and blood flow during acute inflammation?
Increased blood flow
Increased vascular permeability
What structural changes happen in blood vessels?
Increased vascular permeability
Allows leakage of plasma and WBCs
What are the 3 mechanisms that caused increased vascular permeability?
Chemical mediators - e.g. histamine, causes gap formation between endthelial cells
Direct injury - e.g burns damage endothelial cells
Leukocyte mediated injury – leukocytes release proteolytic enzymes
In acute inflammation, the predominating WBC changes over time. Which cells originally predominate? What takes over?
Neutrophils - short life span
Taken over by monocytes/macropages
Chemotaxis is the movement of a cell due to a chemical gradient. What are the 2 types of chemoattrctants? Give an example of each?
Exogenous - bacterial toxins/products
Endogenous - complement system, cytokines, leukotrienes
What proteins cause chemotaxis, angiogenesis and collagen production? Are they produced by a particular cell?
Chemokines
Produced by almost all cells
Where do chemokines bind to to create a chemical gradient?
Components of ECM
How do chemoattractants cause a cell to move in chemotaxis?
Chemoattractants bind to cell receptor
Cause mobilisation of intracellular calcium
Causes assembly of contractile elements and allows cell to move
Leukocytes move in response to chemoattractants. How do leukocytes move?
Move pseudopodia
Pull remainder of the celling that direction
What cells are the 2 major phagocytes?
Macrophages (monocytes in blood)
Neutrophils
What are the 3 stages of phagocytosis?
Recognition and attachment
Engulfment
Killing or degradation
During phagocytosis, what on the target cell do they bind to?
Pathogenic associated molecular patterns (PAMPs)
What is osponisation? What molecule causes it?
Adherence of opsonins to cell to mark an antigen
Osponin is a chemoattractant - attracts immune cells
How do phagocytes engulf a cell/pathogen?
Extend pseudopodia
Form a phagosome
Phagosome fuses with lysosome to form phagolysosome
How do phagocytes usually kill cells?
Oxygen mechanisms - free radicals, relative O2 species
What degrades bacteria after phagocytosis? What pH does this work at?
Acid hyrdolases
Work at low pH
What are neutrophil extracellular traps?
Fibrous networks that prevent spread of microbes after phagocytosis
Extracellular nuclear traps can go wrong and cause injury to the tissue, possibly more severe than the original stiulus. What are the 3 ways they caused damage?
Regurgitation during phagocytsosis
Frustrated phagocytosis - attempt phagocytosis of a material bound to a flat surface
Exocytosis
What are the 4 outcomes of acute inflammation?
Complete resolution
Progression to chronic inflammation
Healing by fibrosis (scar)
Abscess formation
What happens when acute inflammation leads to complete resolution?
Return to normal vascular permeability
Drainage of fluids, proteins, cells
Phagocytosis of degenerate neutrophils and debris
Disposal of phagocytes
Why does acute inflammation progress to chronic inflammation?
Acute inflammation cannot be resolved
What are the types of inflammation?
Serous Fibrinous FIbrino-necrotising Suppurative (purulent) Haemorrhagic Necortising
