Flashcards in MCB Lecture 58 Inflammation I Deck (30)
What are the stages of inflammation?
Differentiate between acute and chronic inflammation
Acute: short duration, neutrophils
Chronic: long lasting, macrophages and lymphocytes
What are the aims of inflammation?
Which cells are involved with inflammation?
Neutrophils, aka PMN
What is PMN?
What are the stimuli for inflammation?
Describe the recognition phase of inflammation
Which things are recognised?
Which cells recognise?
Inflammasome: contents of cells that are now seen in ECF because cells have been injured (eg. DNA, mitochondria)
Macrophages, dendritic cells and epithelial cells recognise
Describe broadly what vascular change is
Vasodilation and increase in vascular permeability to deliver more plasma protein and cells to areas of injury or infection
Describe the stages of vascular change
i. Transient vasoconstriction
ii. Arteriolar vasodilation
Describe broadly how vascular change is mediated
What is occuring during stasis?
There is congestion and very slow flow of blood. As a result, neutrophils are pushed to the margins of the lumen
Compare extravasation under normal and inflammatory conditions
Normal: no net flow in or out of the blood vessel: same amount returns at the venule end as at the arteriolar end
Inflammation: net flow out of the vessels, leading to oedema.
What is transudate?
When does it occur?
Net flow out of the blood vessels of a protein poor fluid
High hydrostatic pressure
Decrease colloid osmotic pressure
What is exudate?
What is it due to?
Net flow out of the vascularisation of a protein and cell rich fluid
It is due to an increase in permeability, mediated by chemicals
What are the two types of vasoactive mediators?
Fast and transient
Slow and prolonged
What are the immediate and transient vasoactive mediators?
Histamine, Brady Kinins, leukotrienes
What are the slow and prolonged vasoactive mediators?
IL-1 and TNF
Describe what is going on physically when vascular permeability is changed
The endothelial cells contract and separate from each other so that there is space between them for stuff to leak out
Describe how endothelial injury can lead to an increase in vascular permeability
Injury can lead to a direct change in permeability by making the endothelium leaky
What happens to the lymphatics during inflammation?
There is increased drainage, and thus the lymphatics and lymphoid organs can become inflamed
What are the stages of leukocyte recruitment?
Which molecules form the transient adhesion of leukocyte to the endothelial cells during rolling?
VCAM-1 + integrins
Sialyl Lewis + L, P and E selectins
Describe the presence of the selectins under normal and inflammatory conditions
Normal: selectins are not expressed on the endothelial cells
Inflammation: cytokine signalling causes the endothelial cells to express selectins so that there can be adhesion between the endothelium and the rolling leukocytes
Leukocyte adhesion is:
When the leukocyte and the endothelial cells form transient adhesion interactions.
What regulates leukocyte adhesion?
Cytokine signalling causes the integrins to cluster together and form higher affinity interactions
What is diapedesis?
What are the two types?
Para cellular and intracellular diapedesis.
This is the leukocyte moving across the endothelium of the blood vessel into the injured tissue
Which molecule mediates diapedesis?
What does PMN release to help it move through the ECM?
Describe chemotaxis of PMN during recruitment
1. Chemokines bind to cell surface receptors
2. Cytoskeletal changes
3. Extension of pseudopods